“Strong

Medicine by Chris Hardy, D.O. and Marty Gallagher is an

exhaustively researched, clearly written, and practically useful guide to
improving your health.
Improving health is fundamentally different than treating disease. This
book represents the future of healthcare in our country. It requires the
patient to assume responsibility, learn the basics, and then enhance their
health through diet, exercise, sleep, and mindfulness.
If you are looking for a quick fix, this is not the book for you. If you
understand that there is no quick fix, then read this book and trust what
you read. The information is accurate and relevant, simple to understand,
and actionable.”
—Patrick Roth, M.D., author of The End of Back Pain: Access Your
Hidden Core to Heal Your Body, Chairman of Neurosurgery at
Hackensack University Medical Center and the director of its
neurosurgical residency training program.

“In the last 40-50 years we have experienced a huge rise in the chronic
diseases affecting affluent societies across the world. We are generally
fatter and less healthy than we were in the past.
In this impressive new book Chris Hardy and Marty Gallagher take the
roles of doctor and fitness coach to provide us with in-depth understanding
about why this is happening and the steps we need to take to turn this
around. This includes a comprehensive review of the latest scientific
research—which is presented in an easy to understand format. The
solution is presented as an integrated ‘Battle Plan’ which includes a
detailed and well-explained training regime along with excellent nutritional
advice, which will combine to provide a transformation to a fitter,
stronger, and healthier body. Most importantly they show us the best way
to measure the progress we are making towards this goal.
I would consider this as the most comprehensive and readable book I
have seen on this large topic, and it provides a thorough discussion of
evidence to support the nutritional and exercise advice. Some of the
research is very new, and may be considered controversial. However, this
is all presented for the reader to evaluate. What we have been doing as a
society has not been working and this book—with its many exciting new
ideas—may provide the plan to reduce the problems created by these
chronic diseases.”
—Dr. Peter Gootjes, Public Health Medicine Specialist, New Zealand

“Strong Medicine is flat-out amazing. If you ever wanted to take your

training and your nutritional theory to an elite level—better than 99.9% of
certified personal trainers—this is the book for you. It’s all in here:
genetics, gut bacteria, cutting-edge stress biology, molecular
nutrition...even better, the ‘deep science’ is all explained so clearly (with
charts, key points, photos and diagrams) that it’s almost impossible not to
understand and absorb it all fully. An automatic classic in the field, which
will surely prove impossible to surpass. I bow down to the Doc and to
Marty!”
—Paul Wade, author, Convict Conditioning and Explosive Calisthenics

“Given the sad state of our society’s health and wellness literacy, Strong
Medicine is just what the doctor should order. Chris and Marty come
together to provide the reader with sound information addressing health
and wellness from all angles. Whether it’s the impact of genetics, the use of
biomarkers, proper physical training, the importance of sleep, and/or
nutritional information, Strong Medicine has it covered.
It is time that we restore and strengthen the fabric of our society by
arming its citizens with the understanding of ‘why, instead of allowing
them to meander around in ignorance from one fad to the next. Strong
Medicine should be on the bookshelf of anyone serious about their health
and wellness. Gratitude, Chris and Marty for such a fine reference.”
—Dr. Mike Davis, DPT

“Strong Medicine is a rare gem that is a must-have for anyone who

wants to take control of their health. Chris and Marty have organized an
extremely thorough yet easy to understand encyclopedia on how to
maximize your health, fitness and genetic potential.
In a day and age where we have never been more confused about how to
eat, when to eat, how to exercise and what is right vs wrong, as well as
more unfit than ever before, this is the new Bible for taking control of your
life.
Why do I say controlling your life? Because this book is about your
health, from the inside out. No fads, no gimmicks, no “diets” to follow,
just the truth about what you need to do to truly be healthy and fit.
Without your health, you have nothing to enjoy in life.
This book is an essential resource for any fitness enthusiast, health
practitioner or coach.”
—Zach Even-Esh, author, The Encyclopedia of Underground Strength
and Conditioning

“Strong Medicine is one of the most informative books recently

published in the area of human health and fitness. The book not only
explains bare-bone principles of human biology and wellness, it actually
translates this knowledge into a practical strategy—hence ‘The Strong
Medicine Lifestyle.’ Well written and backed by science, Strong Medicine
presents important yet controversial and perhaps arguable concepts in the
area of stress response, nutrition and mental/physical conditioning. Highly
recommended to anyone interested in ‘better survival in today’s world’.”
—Ori Hofmekler, author, The Warrior Diet

“Strong Medicine is a declaration of unconventional and asymmetrical

war against mortality. The authors’ weapon of choice is information,
relayed masterfully in the form of an easy-to-understand and richly
illustrated owner’s manual of sorts. This is an owner’s manual that is
chock full of insights for every level, from the seasoned physician to the
absolute layman who is new to fitness.
For the grizzled coach who doesn’t have medical training, Strong
Medicine lays out crucial performance concepts like ‘hormetic dose’ in
ways that are easy to understand regardless of your background. Dr.
Hardy continues with insights into diet, nutrition myths, biochemistry
demystified, intestinal fine-tuning, the chronic stress connection with
disease, and then passes the baton to Marty Gallagher, who unleashes a
plethora of exercise and training tips that are centered around five basic
exercise categories. With well-shot photographs and clear diagrams to
illustrate the important points of each posture, Gallagher lays out a
beautiful plan of attack to combat weakness and mechanical decay,
including easy-to-follow training programs.
This is a book I plan to read & re-read a number of times as both a
licensed medical professional and a strength & conditioning coach.”
—Dr. MARK CHENG, L.Ac., Ph.D, contributing editor, Black Belt
Magazine

“I have had the pleasure of being with Marty Gallagher when he

delivered the ‘Beta’ version of this book—and I flew home and realized
that I needed to start from zero with my coaching of the basic movements.
Combine Marty’s great insights with the clearest explanation I have ever
read that ‘Food is Medicine’ and you have a one-two punch that changes
lives. An amazing book and well worth the time to read it and digest it
(pun intended).”
—Dan John, author, Never Let Go

“Strong Medicine demonstrates the paradigm shift that we currently

have in the world of physical development. We cannot put our fitness goals
above our health goals. Health provides the foundation for fitness to start
the process. Fitness in turn pays back health through maintenance and
sustainability. The takeaway for this book: learn as much about your
health as you do about your fitness and you’ll do just fine.”
—GRAY COOK, author, Movement, co-creator, FMS
 STRONG MEDICINE
How to Conquer Chronic Disease and
Achieve Your Full Genetic Potential

Chris Hardy, D.O. MPH and Marty Gallagher

© Copyright 2015, Chris Hardy and Marty Gallagher A Dragon Door Publications, Inc. production
All rights under International and Pan-American Copyright conventions.
Published in the United States by: Dragon Door Publications, Inc.
5 East County Rd B, #3 • Little Canada, MN 55117
Tel: (651) 487-2180 • Fax: (651) 487-3954
Credit card orders: 1-800-899-5111 • Email: support@dragondoor.com • Website:
www.dragondoor.com

ISBN 0-938045-72-5 ISBN 13: 978-0-938045-72-4

This edition first published in Fenbruary, 2015
Printed in China

No part of this book may be reproduced in any form or by any means without the prior written consent
of the Publisher, excepting brief quotes used in reviews.

Book design by Derek Brigham • www.dbrigham.com • bigd@dbrigham.com

Graphics concepts by Chris Hardy and Derek Brigham Cover illustration by Derek Rodenbeck

DISCLAIMER: The authors and publisher of this material are not responsible in any manner whatsoever
for any injury that may occur through following the instructions contained in this material. The
activities, physical and otherwise, described herein for informational purposes only, may be too
strenuous or dangerous for some people and the reader(s) should consult a physician before engaging
in them. The content of this book is for informational and educational purposes only and should not be
considered medical advice, diagnosis, or treatment. Readers should not disregard, or delay in obtaining,
medical advice for any medical condition they may have, and should seek the assistance of their health
care professionals for any such conditions because of information contained within this publication.

Digital book(s) (epub and mobi) produced by Booknook.biz.

 — CONTENTS —
FOREWORD: Honor • Courage • Commitment
by Craig D. Thorne, M.D., MPH, MBA
PREFACE: Messages from the Authors
INTRODUCTION

Phase I: Basic Training

Basic Training I—Central Themes
• Inflammation and Oxidative Stress
• The Gene-Environment Connection
• Hormesis
• The Stress Response
• Allostasis—“The Stress Cup”
Basic Training II—Nutrition and Metabolism 101
• Introduction
• Macronutrients
• Metabolism Basics

Phase II: Knowing the Enemy

Knowing the Enemy I—The Gut: Guardian at the Gate
• Gut Health: First Principles
• Triggers of Intestinal Inflammation
 • Conclusion
Knowing the Enemy II—Obesity: The Enemy Within
• Introduction: A Big Fat Problem
• The Fat Cell: Dr. Jekyll becomes Mr. Hyde
• The Plague of “Diabesity”
• How We Get Fat: the brain, hormones, and appetite
• Intervention: The 8-step program for obesity and diabetes
Knowing the Enemy III—Chronic Stress: The Silent Killer
• Mind and Body: Descartes was wrong
• Stress and Health
• Mind Interventions: Brain Training
Knowing the Enemy IV—Circadian Disruption: Thief in the Night
• The Internal Timekeeper
• Sleep Architecture
• Edison’s Folly?
• Modern Solutions for a Modern Problem

Phase 3: BATTLE PLAN

Battle Plan I—Strong Medicine Physical Training
• Introduction
• Strong Medicine Resistance Training
• Strong Medicine Basic Cardio
• Strong Medicine Advanced Cardio
Battle Plan II—Strong Medicine Nutrition
• Food Sources and Quality
 • Carbohydrate Tolerance
• Feed your activity
• A Week of Food
Battle Plan III—Putting It All Together
• Lifestyle Change: “The Neck of Roy Buchanan’s Guitar”
• Strong Medicine Lifestyle Change-Strategic Planning
Battle Plan IV—“Stuff You Can Measure”
• Introduction-biomarkers and the “Holy Grail”
• Cholesterol: What are we measuring?
• Physical Measurement
• Markers of Inflammation
• Heart Rate Variability
Epilogue
About the Authors
Acknowledgements
Index
FOREWORD

HONOR • COURAGE •
COMMITMENT

hose are the bedrock principles of the United States Navy. These

T values have guided the strong men and women of the Navy to
successfully meet all of their challenges since it began during the
American Revolution, even with a few small ships, all the way to
the large, powerful fleets and global reach of today.

The health and fitness communities are filled with many committed
enthusiasts who devote their time and efforts in educating and training the
public towards better habits and wellness. But few have the personal,
proven experience to present fact-based evidence that blends nutrition,
exercise, and psychological truths into strategies and techniques to truly
“transform” us physically and mentally. The authors of Strong Medicine
have this rare blend of foundational scientific theory and real-world
empiricism.

Chris Hardy, the ‘doctor’ co-author of Strong Medicine served in the

Navy as a medical officer for nearly a decade, and still holds those values
very closely in his personal daily mission to share his expertise in nutrition,
strength and conditioning. In addition to his specialty training in
preventive and integrative medicine, and his advanced public health
achievements, he is also a certified strength and conditioning specialist.

Marty Gallagher, the ‘coach’ co-author has been involved in high level
sports and athletics for over 50 years now, capturing his first national title
and national records as an Olympic weight lifter when he was only
seventeen year old. In May, 2013 he set his most recent national records as
a 64 year-old power lifter. Marty is not only a peerless athlete, coach, and
writer, he is also the embodiment of “successful aging”, achieving and
maintaining physical and mental abilities superior to many who are 40
years younger.

In Strong Medicine, Chris and Marty have combined their disciplines

and their experiences and have applied a modern day military theme to
provide a compelling structure to help even those of us that lead regular
lives to successfully change our lifestyle habits for the long-term.

In our own daily lives, we experience so many threats to our physical

and psychological well-being (think of them as modern day “predators”):
the pressure to succeed in stressful work environments, commuting in
traffic congestion, poor and over nutrition with processed foods, financial
pressures in a consumer-driven environment, and even the pressure to
pursue meaningful recreation and relief from anxiety. The list goes on and
on. The concomitant increasing prevalence of chronic, deadly diseases such
as obesity, diabetes, high blood pressure, heart disease, cancer and so many
more “lifestyle” conditions puts an intense spotlight on interventions that
can help turn this tide. While some of these are the result of structural and
societal changes, many are the result of individual choices and poor habits
that wreak havoc on our bodies and minds over time and rob us of our full
potential for long, healthy and productive lives.

But we have much untapped ability to change many of the antecedents

and conditions that lead to premature chronic disease and disability and
help us achieve our full genetic potential. In this information age, there are
countless guides to self-improvement, and diet fads and fitness boots
camps are abounding. Chris and Marty help us replace such “information
overload” with user-friendly “know your enemy” information and
evidence-based habits and actions so that we can commit to sustainable
and manageable change.

Think about this as you read Strong Medicine:

HONOR
“I will bear true faith and allegiance…”. For the Navy, this means that
officers need to make honest recommendations and be truthful in their
dealings with each other, and with those outside the Navy. Officers should
also encourage new ideas, take responsibility for their own actions, fulfill
and exceed their responsibilities, and be mindful of their privilege to serve
their fellow Americans. In Strong Medicine, the authors provide an in-
depth series of recommendations based on scientific literature and other
up-to-date information so that readers can honor themselves with the
correct information to make their own transformation.
COURAGE
“I will support and defend…” means to have the courage to meet the
demands of the mission when it is demanding or otherwise difficult. It also
means ensuring that the resources entrusted to officers are used by them in
a careful and efficient way. Lifestyle change can be daunting. This book
not only provides us with the knowledge needed to prevent disease and
achieve better health but also a transformational roadmap, both physical
and psychological, that can help us find the courage within to make the
changes needed, and self-program new habits without being overwhelmed.
COMMITMENT
“I will obey…” means to care for safety, professional, personal and
spiritual well-being of self and others, and be committed to positive change
and constant improvement. Commit to reading this book without rushing
any section or trying to take short cuts, and don’t reject out of hand any
parts of the holistic expert advice that it offers you.

Now take your time to read this book as I did, beginning with basic
training, then knowing the enemy, and continue reading and using the
knowledge and practical strategies presented all the way to the end (your
new beginning) to do a crucial self-assessment to build your own battle
plan. Consider all the rock-solid scientific principles presented as user-
friendly quick medical notes, take home messages, coach’s corner notes,
and even the gourmet organic recipes …. Then use all this latest
intelligence together to honor your own life. You won’t regret it!

Craig D. Thorne, M.D., MPH, MBA, Internal Medicine/Preventive

Medicine

Health Educator, Avid Runner and Lifelong Learner

Assistant Clinical Professor, Johns Hopkins Bloomberg School of Public

Health

Vice President and Medical Director, Employee Health and Wellness,

Erickson Living

Washington, D.C.

November 2014
PREFACE

et us be honest. Most of us buy diet and exercise books because we

L want to have a better body. We are motivated to become involved

with diet and exercise in an attempt to change the shape and
configuration of our physique. We are dissatisfied with how we
look and feel.

We are hard-wired by Nature. She has programed us to try to look and

feel attractive. We seek to attract mates and reproduce in order for our
species to survive. We need to recognize this underlying inborn need. The
quest for self-improvement is inherent and not rooted in vanity. This
primal drive to attract a mate and reproduce is the reason there is currently
a multi-billion dollar industry dedicated to dieting and “losing weight.”

Individuals spend large amounts of money every year looking for the
elusive Holy Grail of dieting and exercise plans. The truth is that all diets
work and all diets eventually fail. There is even documentation of people
losing weight eating nothing but Twinkies. If calories are restricted, body
weight will be lost in the short-term, but every “diet” invented eventually
fails without exception. Dieters gain their lost weight back—and then
some. The diet industry wants the cycle of losing and gaining to continue;
it is good for business.

The exercise scene is no better. Everyone wants to follow the latest

“bootcamp style beat-down” exercise program. These programs often
result in injury, burnout, or both after a couple of months. Then, the once-
enthusiastic trainee looks for the next fitness guru to whip them into shape
again to achieve the beach body of their dreams.

The real “inconvenient truth” is that the only way for sustainable
physical transformation to occur is through lifestyle change—changing
your eating and exercise habits long-term. We will show you how to
achieve your body composition goals without starvation diets or sacrificing
taste. We will show you how to build a strong and lean body, and how to
produce a physical foundation to both achieve your fitness goals and slow
the physical degeneration of aging.

The methods for achieving these physical goals are all here in Strong
Medicine, but there is a loftier purpose to this book.

Jim Morrison said, “No one here gets out alive.” Indeed the years of our
lives are a precious gift. The quality of our lives—how we live in the time
we have—is paramount. Too many of us are robbed of the irreplaceable
years of our lives, by dying prematurely from preventable chronic diseases.
An equal number live their later years in severely debilitated states of body
and mind. The epidemic of chronic disease is expanding at an alarming
rate.

The military theme of this book may

seem over the top to some. In our view
it is entirely appropriate given what we
are facing. Make no mistake, chronic
preventable disease is killing many
more people on earth every year than
the total casualties of past world wars.
Diseases such as diabetes, high blood
pressure, heart disease,
neurodegenerative disease
(Alzheimer’s), cancer, and obesity are
the true modern enemies. A battle plan is needed.

These diseases do not kill in the dramatic manner of bomb and bullet,
but are still just as deadly. These insidious killers wreak havoc on our
bodies and minds. Many of us have friends and family succumbing to these
killers. The slow metabolic destruction of diabetes or neurodegenerative
diseases such as Alzheimer’s dementia rob our loved ones of the very
essence of who they are (or were).

We need to pull our collective heads from the sand and look up from
our smartphones for just a minute. We need a call to action shocking us
out of complacency. Sustainable lifestyle change based on firm underlying
scientific principles is the only way to truly fight the epidemic of chronic
disease while simultaneously achieving the aesthetic physical changes we
desire.

To achieve sustainable lifestyle change you must understand the

foundations on which the recommended changes are built. We will teach
you the scientific and theoretical foundations for transformative lifestyle
change. If we do not take the time to teach you why we recommend
something, we are no different from the thousands of programs out there
that just say “do this” without explanation.

If you just want to be told what to do without understanding why, you

are doomed to continue being led around by the nose by the latest fitness
guru, and wandering from diet to diet in ignorance, wondering why you
continue to fail.

We will provide the tools and strategies you need to generate progress.
Those who take the plunge and institute our tactics will feel better by the
end of the first week, and will see tangible changes in body composition by
the end of the second week. Friends and family will comment on the
“incredible change” at the end of the first month. You can and will
undergo an utter and complete physical and physiological transformation
in three months—90 days—without any draconian training or
concentration camp nutrition.

This book provides a framework that regular people leading regular lives
can perform at home. Strong Medicine is a roadmap that leads the serious
individual from unhealthy and uncertain into ever-improving levels of
health, wellness and fitness.

Because we are all individuals with individual needs, we have left out a
certain amount of specificity with our recommendations. This is done for a
reason. You will have to experiment and individualize our tactics to your
needs; we are giving you a foundation.

Strong Medicine offers you the opportunity to self-assess and create a

customized template that can and will enable you to transform towards the
healthy state-of-being that has eluded you for so long. You are holding the
handbook of transformation, but you have to use it. Once you understand
the concepts and grasp the consequences (of your lifestyle choices) the
burden is on you. End the blame game; let us take responsibility for our
actions and choices.

We need one thing from those that seek radical transformation—a

burning desire to change. To change the body we must first change our
mind. Every thwarted physical and health goal you ever had lies within
your reach.

There are no shortcuts...

DOCTOR’S RX
American society is facing a bank-busting, people-crushing crisis in
which “we the people” are uniformly unfit, unhealthy, unhappy and sickly.
We continue to have skyrocketing, out-of-control growth in preventable
chronic disease. As a flat statement of fact, this bleeding artery could
bankrupt our economy. We need a reality check:

• In 1965, the United States spent 5% of the gross domestic product on

health care expenses. For every $1 produced by the USA, only a
nickel was spent on health care during this time.
• In 2010 this grew to 17% of GDP.
• In 2030 we will spend 25% of GDP on health care expenses; for
every dollar made, a quarter will be spent on medical care.
• The United States spends more on health care per citizen than any
other country in the world, but we are ranked 37th for the
effectiveness of our health care system.

We spend more money on health care and have the most advanced
diagnostic tools and technologies found anywhere in the world. But we are
still failing miserably at treating the diseases that are costing us the most,
both in human suffering and monetary cost.

The majority of health care dollars are spent on the treatment of

preventable diseases: obesity, diabetes, and heart disease. Cancer is
responsible for a significant amount of resources and suffering, yet many
cancers are preventable as well.

Health care analysts give multiple reasons why we are spending ever
more managing these diseases and predictably point to the growing aging
population, costs of medications, costs of testing, and inefficiencies in
providing medical care. An alarming number of healthcare professionals
have simply given up on the idea of preventing these diseases.

Managing diabetes, obesity, and heart disease is incredibly expensive,

but for the most part, we should not have to manage these diseases long-
term. They are preventable and for the most part, reversible.

It has not been for lack of trying. The Public Health community is filled
with many talented and dedicated people who work daily attempting to
improve public health through prevention. Billions of dollars are spent
yearly on failed (often doomed before they start) public health campaigns.
This begs the question: why do we continue to fail? It certainly is not for a
lack of funding or effort.

Why do we continue to have ever-expanding growth rates in preventable

chronic disease despite public health efforts?

Logic dictates that there are 4 possible answers to this question:

1. THE MESSAGES/RECOMMENDATIONS FOR PREVENTION ARE

WRONG
Many of the messages are sound, but there are an unacceptable number
of preventative recommendations based on outdated science that are
flawed from their foundation.

2. COMMUNICATION IS FLAWED AND INEFFECTIVE

Public health authorities seldom explain “why” people should follow the
recommendations in ways that can be easily understood, while still
maintaining a sound scientific foundation. Public health officials usually
underestimate the sophistication of the general public. The problem is not
the public’s inability to grasp physiologic concepts, it is the public health
and medical community’s inability to effectively communicate these
concepts. Let us (public health) not blame the public for our short-
comings.

3. PEOPLE ARE CONFUSED BY CONFLICTING HEALTH

RECOMMENDATIONS
There is a tremendous amount of inconsistent information coming from
“authoritative” sources, which is then further jumbled by popular media
(internet, news media, etc.).

4. PEOPLE ARE UNWILLING TO CHANGE

Stopping preventable diseases usually requires lifestyle changes that
many seem unwilling to make. In an oversimplification: many people are
addicted to the substances, foods, lifestyle and habits that created their
preventable disease.

The core essence of this book is the identification, and effective

communication of underlying causes of preventable health problems. We
then present informed, practical solutions that empower the reader. This
empowerment and resulting self-efficacy is essential, as many of us cannot
rely on our health care providers to teach us this type of information.

DOCERE?
The U.S. healthcare system is currently at a crossroads. A 15-minute
doctor’s office visit is becoming the norm, driven by the economic realities
of a failing system. There is simply not enough time available for the
physician to provide detailed preventive education in an individualized
manner. The word “doctor” is from the original Latin docere, which
means, “to teach.” Most of us who have experienced a recent visit with
their doctor would probably agree that there is very little doctor-to-patient
teaching happening in modern medicine. Most of the doctor’s time is spent
managing medications to treat lab values instead of really treating the
patient—much less providing any individualized education on prevention.
If given the time, do most physicians currently have the education to
impart this type of preventive teaching?

PRIMUM NON NOCERE (FIRST DO NO

HARM)
The public trusts the opinions and recommendations given by their
health care providers. Unfortunately, most physicians simply do not have
the expertise to give science-based recommendations regarding nutrition
and exercise; but do so anyway. It is ironic that the medical education of
our physicians devotes almost no time to learning exercise science and
nutrition. Instead, most of their time is spent learning the use of
pharmaceuticals. Chronic diseases are not cured by drugs, they are only
managed. Lifestyle changes such as proper nutrition and exercise can and
do cure many chronic diseases. Why are our physicians not better educated
to put these interventions into practice?

Too many doctors are put on pedestals by the public and viewed as all-
knowing oracles possessing papal-like infallibility. Obviously this is
nonsense, especially when it comes to exercise and nutrition. Many of my
colleagues are just parroting what they have heard about nutrition and
exercise and pass this on to their patients. They do not truly understand
the subjects from the ground up like they do pharmaceuticals.

Also, many doctors have long since forgotten the basics of biochemistry,
anatomy and physiology learned in medical school. If we are going to
practice prevention and health promotion, we as a profession have an
obligation to really learn our craft from the ground up, using basic science
as a starting point. We need to use a “first principles” foundational
approach to critically examine current orthodox recommendations.
Physicians that use basic science as a foundation for critical thinking about
wellness practice can be invaluable in this respect.

IT’S YOUR FAULT TOO...

On the flip side, there is also a serious lack of elementary scientific
literacy in our society. I do not buy the excuse that a basic working
knowledge of the human body is beyond the grasp of most people. I know
plenty of people who know EVERY detail about baseball and football
statistics—without being a pro athlete. Countless men have an extensive
knowledge of the mechanical workings of an automobile engines—yet
learning a little about how your body works is somehow past our mental
capacities? I think not.

We all NEED a basic working knowledge of the body to inform our

lifestyle choices and preventive strategies; how else can we be true partners
in our own health care?

PREAMBLE TO PREVENTION
We are all individuals with individual
needs and goals, but we all belong to the
human species. So, the underlying principles
of biochemistry and physiology still apply to
all of us. We will show you how to use these
‘guiding principles’ placed within a central
framework that still allows for individuality.
This framework also allows for the
incorporation of exciting new scientific
advances. As long as we build on a solid
foundation of underlying principles, subtle changes are easy to make. If we
need to remodel our approach as new information comes to light, no
worries—we have built our house on a strong foundation.

This is not a “lose weight quick book,” though your physical

transformation will be profound through consistent application of the
principles and tactics presented within. We are after sustainable and long-
term health, not quick fixes. The goal is to empower the reader and enable
anyone to achieve their health and fitness goals while joining the larger
fight against chronic disease.
Chris Hardy — Pacific Northwest, 2014
THE COACH’S PERSPECTIVE:
IMPROVING THE FLESH MACHINE
During the Dark Ages, trade guilds emerged as craftsman bonded
together to share trade secrets. Rather than hording information, these
men recognized that they all had a common quest and by combining their
collective knowledge, they could dramatically “up” their level of collective
expertise. A rising tide lifts all boats. When a guild is formed and
functioning, the tradecraft always improves.

Our guild is a group of likeminded individuals drawn together by a

common quest: how best to heal, detoxify, mold and sculpt the human
body while amplifying every athletic and health attribute. My little sliver of
expertise is human performance and how to improve it. My job entails
working with the world’s best strength athletes and finest spec ops soldiers.
My role is to make the best in the world better.

The irreducible core of our guild is a doctor and a coach who are of one
mind. We want to share techniques, strategies, tactics and philosophies
that actually work. The doctor and coach have seventy years of combined
experience, each operating in distinctly different worlds—but are drawn
together by the gravitational pull of physical improvement. Not imagined
or subjective improvement, but dramatic and objective improvement.

The path of progress in each of our parallel universes (medicine and high
level athletics) eventually intersected. The doctor and the coach met,
compared notes and were struck by how the knowledge gleaned from each
other’s world upped their own game—the coach became a better coach
and the doctor became a better doctor.

This book is a transformational handbook based on proven tactics and

rock-solid science. “Strong Medicine” is the result of our alliance working
in full-flight. We have a creative synergy that allows us to describe and
prescribe techniques and tactics that are immediately useable by motivated
readers.
 We are big on motivation. Give me a motivated, fired-up, morbidly
obese individual over a nonchalant elite athlete any day of the week. For
the truly motivated individual lucky enough to stumble across our
methodology, transformation is not a matter of “if,” it is “when.”

Members of our guild all seek physiological improvement—across the

board. Name a physiological benchmark or category and we will start
thinking about ways to improve that capacity or benchmark. That is what
we do for a living. In our world of uber-elite military and world-class
athletics, results are the only thing that matter and the only thing that
earns repeat business. We have a ton of repeat business.

We have extensive experience in engineering physical transformations;

we churn out renovated humans like Chrysler churns out Dodge Vipers.
Our results are based on the skillful blending of exercise, diet, psychology,
and decades of empirical experience. Our insider techniques and non-
traditional, counterintuitive tactics are unknown outside of a small circle
of uber-elite military spec ops warriors, world-class strength athletes,
outside-the-box coaches, renegade scientists, and innovative medical
professionals.

Members of our guild-alliance all are concerned with the same eternal
core problem: how do we improve the form and function of the human
body?

Any and all aspects of fitness, all of remedial medicine, every diet and
exercise tool, each and every fitness device, health profession, athletic
tactic, strategy or approach—all were created to improve the human
condition in some way. The core question is, “How exactly do we improve
the human condition?” How do we improve the form and function of—as
William Burroughs labeled the human body—“The Flesh Machine.”

Our guild is at the exact intersection of cutting-edge science and real-

world medicine melded with high-level athletics, results-producing
coaching, and elite military preparedness training.

We combine tactics from both worlds and process these volatile methods
to make them user-friendly for regular people. Our challenge was to
achieve this ‘user-friendliness’ without compromising the vital, effective
essence of each protocol. We have met this challenge by creating a
multitier system that allows anyone at any fitness level to participate.

We offer a game plan for the few with the gumption to put these ideas
into practice. It is an indisputable fact that the methods and methodologies
we are presenting work—these exact strategies are being used right now by
the best in the world.

The Tao of fitness exists and we can show you “The Way.” We can
show you how to custom design your very own transformational template
—but you need to learn some science and biology ultra-basics to be
successful. We will teach you “The Process.”

In our world you do not get to skip ahead to the training, eating, and
fun stuff without first getting the scientific, medical, and biological facts
straight. We are teaching you how to fish—we are tired of giving you fish.

Marty Gallagher — Pennsylvania, USA, 2014

 INTRODUCTION

We are at war, and we are losing. We are losing badly. This is not a
war against countries or ideologies. This war is not fought with
bullets and bombs, but with pharmaceuticals. The frontlines of the
battleground are our hospitals, clinics, and local doctors’ offices. This
is a worldwide war against chronic disease and there are few places
on Earth left untouched. The enemy is upon us in full force and the
frontlines are collapsing.

Despite being equipped with the most technologically advanced

weapons, our best soldiers—the medical professionals—seem unable to
push back and destroy the enemy. At best, they are only slowing the
advance of this faceless adversary. We are throwing more and more
resources into the war effort and are still failing miserably. The situation
seems hopeless, as the war-effort is bankrupting us.
 We need your help as the last and best hope for pushing back the
relentless advance of chronic disease. To become an effective fighter in this
war, you will need training. We have to teach you how the enemy works
from the inside out. You must understand the enemy before you can
effectively fight and decisively win. This war will be fought one small
battle at a time, by one individual at a time. You are the last line of defense
and can become the key to ultimate victory.

You will be rewarded for your courage and effort with the optimum
health of your mind and body. You will emerge from your training with
the physical appearance, fitness, and vitality that mirrors your full genetic
potential. Join us in this fight. You are needed.
PHASE I: BASIC TRAINING
Strong Medicine Basic Training is not easy, but can be accomplished by
anyone with the requisite motivation. The foundations of your training are
the central themes that underlie health and disease, and a primer on
nutritional science and human metabolism.

It is important to have a basic understanding of this section to prepare

you for the battle ahead. You will be introduced to concepts which may
not be familiar.

There is quite a bit of information in Strong Medicine Basic Training, so

spend some time here. Do not worry if you don’t get it all the first time
through, because we will reinforce this training throughout the book. We
do not expect the new Strong Medicine trainee to become a warrior
overnight.

While you are learning the fundamentals in basic training, we will also
give you an early taste of the Strong Medicine Defensive Tactics. These
tactics can immediately be put into action against the enemy—even
without the full knowledge of the adversary. The Strong Medicine recruit
who graduates from basic training will be ready for advanced training to
understand the enemy and advanced tactics to stop chronic disease and
optimize health.
PHASE II: KNOWING THE ENEMY
Your Strong Medicine trainers know the enemy. We have gathered the
military intelligence and analyzed their weaknesses. We know the chinks in
their armor. We will systematically impart this knowledge to you, as you
are no longer a recruit, but still have a lot to learn before you can lead
your own forces into battle.

You will get in-depth defensive

tactics, and will understand the
reasons behind our tactics. Our tactics
are graded as gold, silver, and bronze.
The gold tactics are particularly devastating to the enemy and should be
mastered early on. The silver and bronze tactics are very effective as well,
and will ensure chronic disease stays down once it is put down.

During this phase of your training we will periodically bring out Coach
Gallagher to give you a reality check. He is a master Strong Medicine
trainer and coach. He is rough around the edges but will give you the
brutal truth without political correctness—something we need to hear from
time to time.

Once you have gained the requisite knowledge about the enemy, you are
ready to put your training into practice. You will be able to turn the
Strong Medicine Defensive Tactics into a devastating offensive strategy
against chronic disease.
PHASE III: BATTLE PLAN
We will formulate the Strong Medicine battle plan in Phase III. This plan
will be drawn from the knowledge and tactics you learned in Phases I and
II. We will show you how to individualize a plan that is optimum for you.

Phase III will also give you a stripped down but highly effective physical
training program using original techniques and expert tactics to transform
a flaccid body into a chiseled and powerful war machine worthy of a
Strong Medicine Warrior.

You will also get a short section on measurable analytics for monitoring
the inner workings of your “flesh machine” and keeping you on the right
track.

We have included the “military intelligence” we gathered on the enemy

and the foundations for our tactics in the scientific references at the end of
each chapter for your further reading and research if desired. These
references are the sources and scientific foundation on which we have built
your training program.

The science is always kept as basic as possible in Strong Medicine

without losing the meaning, but trainees who want more should look for
the Digging Deeper and Technical Note boxes throughout the book.

Those of you willing to enlist and join us in the war on chronic disease,
let us get to it. Be a participant in this fight, not a casualty. Strong
Medicine Basic Training awaits...
 PART I

BASIC TRAINING
BASIC TRAINING I:
CENTRAL THEMES IN DISEASE AND
HEALTH

This section teaches the rules of war before you hit the battlefield. Some
of the concepts may be brand new to you, but it is important to spend
some time here before moving on. If you do not quite get this section the
first time through, do not worry, we will return to these five themes
throughout your training. These themes are the underlying foundations of
our defensive tactics against chronic disease, and form our template for
achieving your genetic potential for health and fitness.

1. Inflammation and Oxidative Stress

2. The Gene-Environment Connection
3. Hormesis
4. The Stress Response
5. Allostasis and the “Stress Cup”
 We will start with inflammation and oxidative stress. These two
processes are the underlying causes of most (if not all) preventable chronic
diseases. It is crucial to understand how they work. Get to work recruit!

CENTRAL THEMES PART I:
INFLAMMATION AND OXIDATIVE STRESS

THE 4 CARDINAL SIGNS OF INFLAMMATION:

1. Redness (Rubor)
2. Heat (Calor)
3. Swelling (Tumor)
4. Pain (Dolor)

Two interrelated physiologic processes—inflammation

and oxidative stress—are recurrent themes in this book. These two
processes are at the same time crucial to our survival as an organism and
underlying causes of disease.
INFLAMMATION
The inflammatory response is directed by cells in our immune system
and is absolutely essential to heal from injury and to combat infectious
diseases.

During an acute injury or infection, redness and heat are produced from
increased blood flow to the area. Swelling is the result of fluid and protein
“leaking” from the blood vessels into the tissue. Pain results from the
stimulation of nerve endings by certain chemical “messengers” called
cytokines released by immune cells. This process can last for several days
while the “battle” to clear the invading infection takes place, or the cells
damaged from an injury are cleared. After the “battle,” things slowly
return to normal. This is the basic process of acute inflammation.

The primary generator of inflammation (and resulting oxidative stress)

in our bodies is the immune system. A basic survey of the immune system
is in order. The immune system is incredibly complex, and we will simplify
immunological concepts without drowning in the details.
IMMUNOLOGY 101
 The cells of the Innate Immune System are like the
guards at the castle gate. They deal with anyone who
“looks or acts suspicious.” In practical terms, this The Guardian
could be an initial encounter with bacteria/viruses or
“foreign” protein fragments. The innate immune
response is not targeted at specific antigens (targets), but is a general
protective response to anything “foreign.” Innate immune cells like
dendritic cells or macrophages can “take” foreign invaders “prisoner”,
destroy them, and display pieces of the prisoners like heads impaled on
pikes mounted on the castle wall. Some of these guardians also release
inflammatory chemicals called cytokines.
 Cells of the Adaptive Immune System are
like assassins. They are known as T-cells and
B-cells. Once they encounter pieces of a
prisoner caught by the dendritic cells or
macrophages of the innate immune system,
they “adapt” themselves to become perfect
assassins for this specific type of prisoner.

The assassins target the specific patterns of

proteins (antigens) unique to this “prisoner”
The Adaptive Assassin for destruction. Then they clone themselves to
make an army of assassins with one goal—
destruction of this specific type of prisoner. These death-dealing clones
spread throughout the body and wait to encounter another invader with a
protein pattern identical to the original prisoner.
The Assassin Clone Army
These assassins are persistent, and wait in the shadows for their target to
appear again. Once they encounter their prey, they release a barrage of
destructive power in the form of antibodies and inflammatory cytokines.

It is important to note that the immune

system is not completely devoted to
destruction. There is a type of T-cell in the
adaptive immune system that helps control the
assassins and produces an anti-inflammatory
response. This type of T-cell is called a T-
regulatory cell (Treg). Treg cells are like hippie
antiwar protesters. We need a balance
between protesters and assassins to prevent The T-regulatory cell
the immune system from attacking our own hippie preaching tolerance:
body tissues. Autoimmunity is the process of “Just stop the
the immune system attacking the body. violence man!”

The immune system generates and controls the acute inflammatory

response needed for the beneficial functions of proper wound healing,
fighting infection, and recovery from exercise. Chronic inflammation is
also generated by the immune system in a process that is similar to acute
inflammation, but instead of stopping after several days, it continues for
much longer.

KEY POINT:
Chronic inflammation is the result of continuous stimulation of the
immune system. The constant release of inflammatory “cytokine”
chemical messengers wreak havoc on the body and your health.
MEDICAL TRIVIA:
It is estimated that 70-80% of our immune system lives in our
intestinal tract (our “gut”).
OXIDATIVE STRESS
Working in tandem with inflammation is oxidative stress. Most of us
have seen rust on old cars. Rust is the oxidative process at work on metal
alloys containing iron. In the presence of moisture, oxygen in the
environment reacts with iron to produce rust. Oxidation reactions also
occur in our bodies. They are essential processes in our physiology—unless
they get out of control.

The oxygen free radical (also called reactive oxygen species, ROS) is a
type of molecule that causes oxidation and oxidative stress. ROS can form
from various external and internal stressors such as pollution, infection,
radiation, and cigarette smoking. ROS molecules are also products of
normal metabolism in our cells. Many processed foods contain ingredients
prone to oxidation, and can increase oxidative stress far beyond normal
levels.

Chemically speaking, stable molecules have electrons that travel in pairs,

but a free radical is a molecule that has a lone unpaired electron. This
unpaired electron makes the molecule extremely unstable and chemically
reactive. This type of molecule really “wants” to pair another electron with
the lone electron and will take an electron from a nearby molecule.
“Stealing” an electron from a neighboring molecule will damage structures
like cell membranes and even DNA. Long-term DNA damage by free
radicals can cause mutations leading to cancer.
The Antioxidant Defense System (ADS). This is your body’s way of dealing
with free radicals (oxidative stress). They are the “bouncers in the bar.”
 The “Free Radical” drunk guy thinks he is a superhero by the end of the
night, looking for some action.

QUICK FACT:
You can think of the free radical as a drunk guy in a bar looking for a
fight. The body has mechanisms to deal with free radicals called the
antioxidant defense systems (ADS). These systems are like bouncers
in the bar who take the drunk outside before he hurts anyone.

The balance in the body between the free radicals and the antioxidant
systems determines oxidative stress. A couple of drunk guys can make the
club experience somewhat entertaining for the other patrons, but the
bouncers (ADS) will take care of them in short order.
 The ADS “bouncer” taking out the trash... a couple of free radicals are no
problem.

If the free radicals overwhelm the antioxidant defense systems (the

bouncers), there is a state of high oxidative stress. The state of high
oxidative stress is the result of free radicals starting chain reactions. The
chain reactions form large amounts of new free radicals—like a drunk who
starts a bar fight that the bouncers cannot control. A free radical chain
reaction can damage the membrane of a cell and lead to destruction of the
cell. On a larger scale, it can damage your health.
 High oxidative stress overwhelms the ADS “bouncer”

THE DELICATE BALANCE OF OXIDATIVE STRESS

The antioxidant system attempts to
counteract free radicals generated internally by
physiologic processes and externally from the
environment (food, water, toxins, etc.). This
balance is a constant push-pull process.
Tipping the balance toward free radical
generation increases oxidative stress and the
antioxidant system quickly responds. Spending
too much time in either direction is not a good
thing long-term. The body actually needs some
oxidative stress to maintain health, but not too much. Too much oxidative
stress creates disease.
 KEY POINT:
It is very important to understand that some inflammation and
oxidative stress is normal, necessary, and even beneficial. This
beneficial “dose” of inflammation and oxidative stress works through a
process called hormesis, part of the positive adaptation to stress
known as allostasis. Low “doses” of oxidative stress may even extend
our life span.

Some beneficial effects of inflammation and oxidative stress:

1. Our immune system makes use of inflammation and oxidative stress
in a controlled manner to kill invading micro-organisms.
2. Exercise and some compounds in fruit and vegetables contribute to
beneficial inflammation and oxidative stress.

Normal physiologic processes like metabolism of glucose and fats create

free radicals (ROS). Your antioxidant systems can usually deal with these
free radicals (except in the case of diabetes). A properly working immune
system generates inflammation and oxidative stress to fight microbial
invaders. Increased oxidative stress from the outside environment can also
stimulate the immune system to produce inflammation. Inflammation and
oxidative stress always travel together.

“Importing” free radicals by eating rancid fats from processed foods

adds extra oxidative stress that your system may not be able to control.
Conversely, eating organic vegetables and fruit can stimulate the body’s
internal antioxidant systems (ADS), making them stronger, more resilient,
and more resistant to inflammation and out-of-control free radicals.
KEY POINT:
Where there is oxidative stress there is inflammation. Where there is
inflammation there is oxidative stress. The two processes are
inseparable.
DURATION MAKES ALL THE DIFFERENCE...
Short-term increases in inflammation and oxidative stress are necessary,
normal, and even beneficial.

Short term, low levels of oxidative stress are beneficial.

Intermittent short-term inflammation and oxidative stress are essential

for proper functioning and defense of your body. However, if these
processes continue for long periods of time, disease develops. Long-term
inflammation and oxidative stress are the underlying causes for chronic
preventable diseases.

The “link” in the chain from the underlying sources (the enemy) to
chronic oxidative stress and inflammation resulting in chronic preventable
disease.
 You will see the central theme of chronic inflammation and oxidative
stress as underlying causes of disease throughout the book. In later
chapters, we will focus on the sources of chronic inflammation and
oxidative stress. These sources are the underlying causes “linked” to
chronic inflammation and oxidative stress and the resulting chronic
diseases. These sources are the enemy that we are fighting.
KEY POINT:
Heart disease, diabetes, cancer, high blood pressure,
neurodegenerative diseases (Alzheimer’s), asthma, and accelerated
aging all have chronic inflammation and oxidative stress as underlying
causes.
 STRONG MEDICINE
Strong Medicine is all about breaking the link between the enemy
sources of chronic inflammation and oxidative stress, thus preventing
chronic disease. We will identify the enemy in Phase II of your training.

Most chronic inflammation and oxidative stress which cause preventable

diseases are the result of our body trying to adapt to the outside
“environment.” This environment includes...

• The food we eat.

• The quality of our sleep.
• Our physical activity.
• The stress in our lives.

Our environment reacts directly with the genetic code contained in our
DNA, and affects the way our body functions in health and disease. As
modern humans, we can control many aspects of our environment,
therefore we have the potential to control how our genes are expressed in a
way to optimize health and achieve our fitness goals. The next section will
describe just how this works.

CENTRAL THEMES PART II:
THE GENE-ENVIRONMENT
CONNECTION
GENETICS AND EPIGENETICS
Our genes form a foundation that determines who we are as individual
humans. The DNA contained in our genes makes each of us unique. While
we have more similarities than differences, seemingly small genetic
variations make us unique individuals. When DNA was discovered as the
molecule of heredity in 1952, it was thought that genetic preprogramming
was set in stone, and we all had individual predestined genetic fates. The
idea that DNA is set-in-stone dominated the latter half of the 20th century.

One of the central ideas in evolutionary theory is that genetic variations

happen at a relatively slow pace. The slow evolving changes in the DNA
code are called mutations. As the 21st century began, another idea took
hold in genetic research—a concept known as epigenetics, literally defined
as “upon the gene.”

Our genes are collections of DNA—instruction manuals or “recipes” for

making specific proteins in our bodies. The proteins made from the DNA
instructions have a huge variety of functions.

• Proteins make up the physical structure of our body, including

organs, blood vessels, skin, etc.

• Proteins function as the machinery that makes the necessary

chemicals and hormones our bodies need.

• Proteins make up our immune system, which defends against

invaders.

The small sections of your DNA that contain specific instructions to

make a specific protein are called genes. You can think of a gene as a single
recipe in a cookbook that tells you how to make a specific meal. The
human genome is the total collection of genes in our DNA. The genome is
the complete cookbook containing over 20,000 “recipes” (genes) to make
specific proteins.
 KEY POINT:
The human genome is the complete DNA “cookbook” that contains
over 20,000 genes. Each gene is a specific “recipe” to make a protein.

In traditional evolutionary theory, changes to genes by mutations could

be thought of as changing the recipe. This would be like taking a cake
recipe that originally called for 4 eggs, and changing the requirement to 5
eggs. Whenever you read the cake recipe in the future you would see the
instruction to use 5 eggs. Mutations physically change the recipe. The cake
produced by the new recipe would be different than the previous cake, just
as any protein produced after a mutation would be different than the
original protein.

The epigenetic system has quite a different way of acting on genes. In

response to environmental signals (signals that originate from outside the
body), the epigenetic system will “turn off” or “turn on” different genes.
Epigenetics does not change the individual recipes; the cake will continue
to be made with 4 eggs. Epigenetic signals determine how many cakes are
made, or if they will be made at all.

TURNING
“OFF”
 Within the complete genome cookbook, epigenetic signals can make
the pages containing certain recipes “stick together” so that they
cannot be read. If you cannot read the recipe you cannot make the
specific meal. With DNA, if you cannot read the gene you cannot make
the protein.

TURNING
“ON”
Epigenetic signals can also “bookmark” a specific recipe so it is made
more often. Genes “bookmarked” by epigenetic changes will make
large amounts of their specific proteins. Similar to a favorite recipe for
pot roast or BBQ, the bookmarked recipes in the DNA cookbook are
made often.

If you could only cook meals that were in your cookbook, you would
not be able to make meals on the recipe pages which are “stuck together.”
You would make meals with the “bookmarked” recipes more frequently.

This is a simplified explanation for how epigenetics works. Different

genes (“recipes”) will be turned off or turned on to meet the internal or
external demands placed on the body.

Some recipes will have the pages stuck together, and some will be
bookmarked, depending on your “environment.”

YOUR “ENVIRONMENT”
The American Heritage Dictionary defines
“environment” as: “all of the biotic and abiotic factors
that act on an organism, population, or ecological
community and influence its survival and
development.” We refine the definition: environment
is our food and water intake, air quality, physical
surroundings, physical activity and lifestyle. Our
transformative process focuses on food selections,
activity, sleep and stress—the factors in our environment we can
control.
Epigenetic changes impact how our genes interact with what we eat,
our activity level, and how we live our lives every day. Epigenetic
changes can make profound differences in our physical wellbeing.
Handled incorrectly, our bodies will fail us prematurely. Handled
properly, we can hold back the sands of time. Beneficial environmental
changes in diet and exercise will reverse preventable diseases such as
type-2 diabetes.
Epigenetics suggests that modern maladies should be thought of as
mismatches between a person’s genetics and their environment. By
correcting mismatches, we can transform from affliction to health.
EPIGENETICS CASE STUDY
This hypothetical case study of identical twins illustrates how epigenetics
works: John and Steve are born identical twins. Their “cookbooks”
(genomes) are exactly the same down to every last recipe. In their late
teens, John decides he wants to be a bodybuilder and Steve wants to start
training to compete in ultra-endurance running. Before each man immerses
himself in his newfound athletic passion, both stand 5’ 10”, weigh 170
pounds, and have a body composition of 10% body fat.

John’s bodybuilding training consists of long hours in the gym lifting

heavy weights to self-inflict intense muscle trauma. To speed recovery, he
eats large amounts of protein. John is sending “environmental” signals to
his “cookbook” for muscle growth. The “recipes” (genes) for muscle
growth are bookmarked by epigenetic signaling.

Because of his chosen epigenetic path, John’s recipes for sustained energy
output (the kind needed for distance running) have had their pages “stuck
together” and are largely turned off. These unintended consequences
happen so John can adapt to the specific environmental stresses (lifting
weights while eating large amounts of protein) he is placing on his body.
His muscles grow significantly, but he is in no shape to run a single mile.

Steve begins his training at the same time as John. Steve stays away from
the weight room and wears out several pairs of running shoes. He is
training for a 50-mile ultra endurance race. He trains his body to maintain
high energy levels for extended periods of time. The “environmental
signals” this type of endurance training is sending his “cookbook” is for
muscle endurance, not muscle growth.

Over the months, while John is packing on muscle mass, Steve is leaning
out, shedding unneeded muscle. Steve’s high volume endurance training
enables his muscles to continue to power his running for hours on end, but
he is certainly not going to win any bench press competitions.
 KEY POINT
Epigenetic changes are not set in stone once they are made. As your
environment changes, your epigenetics will change.

After a year of training, the identical twins are no longer identical. John
is a muscled-up 200 pounds and gets winded running around the block.
Steve is down to a rail-thin 140 pounds and has lost a significant amount
of muscle mass and strength.

John and Steve still have identical genetics, but epigenetic changes
caused by different environmental stresses have made their bodies different
—they are no longer identical after a year of sport specific training.

Epigenetic changes are not “set” once they are made. Recipes that were
once stuck together can be bookmarked and vice-versa, depending on the
signals from the environment.
WOMB TO THE GRAVE
Your epigenetic changes started when you were developing in your
mother’s womb. What your mother ate, drank, and the stress she
experienced while pregnant had a direct impact on your environment in
utero. Epigenetic changes began in response to this environment and
persisted after your birth. There is actually good science now which shows
that some epigenetic changes can be passed from parent to child, much like
traditional genes.

A mother’s metabolic health and stress during her pregnancy can be

passed down to the fetus in utero. The fetus’s “environment” consists
solely of the mother’s body. If this environment is stressful, the epigenetics
of the fetus will change to adapt to the stresses. Stresses in the mother such
as gestational diabetes, psychological stress, and malnutrition WILL cause
epigenetic changes in the fetus. These changes can exist in the infant after
birth.

Recent epigenetic research on mothers who have experienced extreme

stress prior to and during pregnancy has shown that their children are
likely to develop anxiety and are less able to cope with stress later in life.
Epigenetic changes are thought to be responsible for passing stress
responses from mother to child.
 RESEARCH UPDATE
Recent research has indeed shown that gestational diabetes in the
mother during pregnancy places the child at higher risk for developing
obesity and diabetes later in life. It is also clear that this happens
through epigenetic changes in utero.

It is important to remember that epigenetic changes take place so that

we can adapt to our current environment. This is why creating the best
environment possible (the mother’s health) during pregnancy is crucial to
the future health of the child. This lifespan view of the impact of the
environment on our genes through epigenetic change has become a very
important field of scientific study in recent years.

In the “nature versus nurture” environment argument, genetics trumps

environment or environment trumps genetics. The balance tips in favor of
“nurture” based on the findings of cutting-edge epigenetics research.
“Nurture” starts in the womb.

Just as the genome describes your complete DNA cookbook, the

epigenome describes the current state of all of the recipes in the cookbook
as “bookmarked” or “stuck together.”

As your environment changes during your life, changes in your

epigenome take place to compensate. Mutations to DNA still happen and
are important, but epigenetics provides real-time adaptations to
environmental stresses that mutation-based DNA changes cannot match.
 THE HEALTHY COOKBOOK
Your environment includes nutrition, exercise, sleep and stress. These
shifting environmental characteristics “bookmark” and “stick together”
the generecipes of your genome-cookbook—every day, month, and
year.

The ability to read (or not read) the individual recipes and how much
each is made into a “meal” determines disease or health. This is highly
individual and the reason no diet or exercise plan is perfect or works for
everyone. We can optimize your epigenome by providing it with the
proper environmental signals for health.

Epigenetics has emerged as a major way that we adapt to our

environmental stressors. These stressors can change our epigenome for
better or worse. Exercise and food are beneficial in the right amounts, but
unhealthy in the wrong dose. Figuring out these beneficial doses leads us to
the concept of hormesis.

CENTRAL THEMES PART III:
HORMESIS

Stress is perceived as a negative thing. Yet exercise is self-induced stress

and can be very beneficial. A central concept, common to all organisms, is
a need for environmental stresses. In order to survive, thrive, and
ultimately live our lives to their fullest potential, environmental challenges
must be overcome.

Nietzsche’s axiom, “That which does not kill me makes me stronger” is

profoundly accurate in the world of DNA, genes and epigenetic science.
Organisms—human or otherwise—either adapt to challenges by becoming
stronger or they die. Challenges in the right amounts are not only
beneficial, but necessary. Think of the profound differences in overall
health and appearance when comparing the physique of an out-of-shape
individual to that of a life-long athlete who exercises regularly and eats a
sound diet full of natural foods.

A life devoid of physical challenges and inactivity sets a person up for an

early death from metabolic diseases, obesity, muscle loss, fractures of weak
brittle bones, etc. Unfit people degrade rapidly as they age. In our
unchallenged, unfit era, this has unfortunately become the norm.
 Physical challenges of the requisite intensity slow the aging process to a
crawl. Favorable and appropriate environmental challenges make our
bodies stronger and more resilient through a process called hormesis. The
hormesis concept originated in the study of toxicology. Although hormesis
is still considered somewhat controversial in the academic circles of
toxicology, we view hormesis as a unifying concept applicable to all
environmental stressors.

“THE POISON IS IN THE DOSE”

Paracelsus, the 16th century Swiss physician
and father of toxicology said, “Poison is in
everything, and no thing is without poison. The
dosage makes it either a poison or a remedy.” In
other words, the amount or dose of a substance
is what makes it harmful or helpful.

Hormesis is an extension of Paracelsus’

statement. It implies that there are necessary
doses of environmental challenges. The right
“doses” provide beneficial adaption, while
Paracelsus: “The
“overdoses” of the same challenges are harmful
dose makes the poision”.
in the long-term. The doses that provide
beneficial adaptation are said to be “hormetic” doses.

Hormesis readily applies to nutrition, exercise, and lifestyle. While

stressful “challenges” in the right “dose” are necessary to health,
overdosing will have the opposite effect. When it comes to dosage, while
“some” is good, “more” is not necessarily better. Overdose is as negative
and deadly as an under-dose.

Antioxidant supplements are heavily advertised and hyped, but research

studies have shown that when antioxidants are isolated and supplemented,
beneficial effects are not seen in humans. Some studies have shown that
high-dose antioxidant supplements (vitamin E for example) can actually
make some diseases worse and shorten life spans.
 As we discussed above, we need some oxidative stress to promote an
adaptive response. This increases our internal antioxidant systems, and
makes us more resilient to future stress. High-dose antioxidant
supplementation neutralizes the small amount of reactive oxygen species
(i.e. free radicals) responsible for beneficial levels of oxidative stress.
Neutralizing this beneficial oxidative stress also neutralizes the favorable
adaptive response necessary for health and longevity.

If this seems counterintuitive, think of it this way—exercise is good for

the body in the right doses, but too much can cause you harm. Eliminating
exercise altogether, because too much can harm you, is using the same
failed logic behind the idea of trying to eliminate all oxidative stress
because we know that too much oxidative stress is harmful. Just as we
need the right dose of exercise to make us stronger and more resilient, we
need some oxidative stress to thrive through the adaptive response.
 POLYPHENOLS
Polyphenols are a group of natural compounds found in fruits,
vegetables, and plant products such as olive oil. Polyphenols have been
promoted for antioxidant properties, free-radical defense, and as
helping in the battle against oxidative stress and inflammation. Recent
research has shown that their favorable action may not be directly
related to polyphenols acting as antioxidants. Instead, polyphenols
stimulate our antioxidant defense and cell protection mechanisms in
an indirect way. These compounds promote a small amount of
oxidative stress and create an environmental challenge which will
stimulate a beneficial adaptive response.

EXERCISE, NUTRITION AND HORMESIS

Coaches and athletes know how to get faster and stronger by subjecting
the body to physical demands. They are unknowingly invoking hormesis.
To become faster and stronger the adaptive response must be triggered.
There is a proper “dose” to trigger the adaptive response. Too little leads
to no beneficial changes, and too much often leads to overtraining. Sickly,
injured endurance exercise addicts are examples of overtrained individuals.

Smart coaches and athletes also know the importance of recovery in

making performance gains. Adequate recovery allows for maximum
adaptation to the “exercise dose” and promotes recovery before the next
training session. Consistent exercise overdose and inadequate recovery is
“poison” to the body.
 The right “dose” is important for both.

High quality food and nutrition also fits into our hormesis framework.
Macronutrient ratios of protein, starch, fiber and fat can be altered on a
daily basis to fuel activity levels and serve physiologic needs. We need to
account for individual genetic differences and tailor food quality, quantity
and selections based upon different “dose” requirements, goals and
preconditions such as obesity and diabetes. Both over-nutrition and under-
nutrition, outside of your individual “ideal window” can have very real
health consequences.

It will be easier to grasp the concept of hormesis visually in the diagrams

that follow...
 The above diagram illustrates the concept of hormesis. The x-axis (left
to right) measures the “dose” of environmental challenge with an
increasing dose as we move to the right. The environmental challenges can
be anything previously discussed, with food and exercise being the obvious
examples. The y-axis (top to bottom) represents the effect seen on the body
that corresponds to a given “dose,” either adverse or hormetic (beneficial).

Point A: The yellow and red sloping curve on the left could
represent inactivity (for exercise dose), or malnutrition (when looking
at food dose). The low doses of activity or food cause “adverse”
effects on the body. For food, Point A represents malnutrition. For
exercise, Point A represents sedentary/low activity.

Point B: As we move to the right with increasing doses of

environmental challenges, we see the curve turn green and rise into the
area of beneficial “hormetic” effects. This green area represents the
beneficial “doses” of environmental challenges for food and exercise
in this case.
 Point C: Continuing to the right, the higher doses start making the
curve drop into the yellow and red again, the territory of adverse
effects and eventual death with high enough doses. For food, Point C
represents over-nutrition and the resulting adverse adaptation of
obesity. As far as exercise, Point C could represent overtraining.

An alternate way of visually grasping hormesis is the arrow below. It

shows the same thing as the previous graph and the descriptions of points
A, B, and C still apply.

As you go from left to right following the arrow, the “doses” of

environmental challenges (food and exercise in our example) increases.

• Point A represents malnutrition (food) or lack of activity (exercise).

• The “just right” (hormetic) doses of point B represent beneficial
amounts of nutrition and exercise. Moving out of the green zone to
the right, you find point C.
• Point C represents too much exercise (overtraining) or too much food
(over eating).

There is a proper dose for food and exercise for each individual that
maximizes favorable adaptation without taking other external sources of
environmental stress—such as sleep deprivation or psychological stress—
into account. If we take into account these other external stresses, things
can change...
 A bad night of sleep, a stressful day at work, or a period of financial
problems, add to “environmental stress.” This decreases the ideal
“hormetic window” for things like certain types of food and exercise
because of the additional stresses on the body. What may be a good
“dose” of food and exercise while on a week long vacation may not be
right when facing a deadline at work with poor sleep.

This is your hormesis arrow after a couple of nights of bad sleep and
work stress. In this case, just a little exercise will put you in the green zone
of hormetic dose. If we did the same dose of exercise right now as we did
last week (B surrounded by the yellow box) when we were sleeping well
and on vacation, we would find ourselves in the “overdose” zone. In other
words, the dose of exercise that was beneficial for us last week will be too
much this week because of the poor sleep and job stress. A smaller “dose”
of exercise this week will be the beneficial dose.

COACH’S CORNER:
We need to be aware of all the pitfalls and landmines that can drag us
out of our “hormetic dose”—sleep deprivation, intense and prolonged
psychological stress, starvation, gluttony, too much or too little exercise
to name just a few. Hormesis is a delicate gossamer strand, a fragile
state. External stresses will rip us out of the progress zone in a matter
of hours—a night of bad sleep, a super-stressful day at work, a period
of financial problems, beating yourself to a pulp in training then
starving or stuffing yourself.

It is difficult to stay in the “hormetic zone.” But if we are able to ride

the razor’s edge and stay in the zone, we are rewarded with tangible
physical gains: measurable decreases in body fat, an increase in lean
muscle mass, health, wellness, energy, improved stamina, and
dramatic improvements in every definable athletic benchmark. It all
can be ours and this book shows you precisely how to attain and
maintain the hormetic zone—the requisite precursor to all tangible
physical progress.

In elite athletics, the combination of perfect training combined with

perfect eating, plentiful rest, copious amounts of organic, nutrient
dense foods, and stress-free living all combine to create a synergistic
zone of progress. The key is to balance the components. It is better to
have a little of all the interrelated elements and disciplines than a
whole lot of one or two at the expense of the others.
 TECHNICAL NOTE:
The graphics depicted on the previous pages show adverse effects at
low doses and high doses, with “beneficial” effects seen in moderate
doses (the green part of the curve or arrow).

Classically, hormesis as described in toxicology shows beneficial effects

at low doses with adverse effects at higher doses. The classical
hormesis graph differs from ours because we are extending the
hormesis concept to include lifestyle factors such as nutrition, stress,
and exercise—not just looking at chemical exposure.

With our expansion of the hormesis concept to lifestyle factors, we see

adverse effects at both very low doses (sedentary lifestyle, under-
eating, etc.) as well as high doses (overtraining, overeating, etc.), with a
beneficial moderate dose.

In an upcoming section we will discuss the concept of the “stress cup”

and allostasis. These ideas explain how something can be good for you one
day when your overall stress is low, and bad the next when your stress is
high. Up to this point, we have talked a great deal about “stress.” Let’s dig
a little deeper into the concept of stress, especially how your brain deals
with stress—a.k.a. the threat response.

CENTRAL THEMES PART IV:
STRESS AND THE RESPONSE TO
THREAT

One of the brain’s major roles is to

protect us from harm. A hardwired system
lives in the brain and expands to the body.
This system responds to external and
internal threats, is crucial to our survival,
and has been finetuned during the
development of the human species.

Why is this important and why is it a

central theme in a health and fitness book?
Just as we must learn the science of the body we need also learn about the
brain.
 COACH’S CORNER:
The brain can be an individual’s best friend
or worst enemy. The goal is to use the
untapped powers-of-the-mind to amplify
our training and nutritional efforts. How do
we harness the mind? How do we make it
an ally instead of a hindrance? The first
step is to understand how it works—from a
scientific perspective.

Stress is a killer. Literally. Too much stress

is the Black Plague of the modern era.
Everyone is mentally stressed trying to cope with life. Stress also kills
progress. No matter how intense the training, or strict and pristine the
nutrition, if you are over-stressed you will “go catabolic” and no
progress is possible.

Our distant ancestors’ brain circuitry was hardwired to instantaneously

respond to real or perceived threats from the environment. Dubbed “fight
or flight,” this instinctive reaction was critical for survival. Ingrained
deeper and deeper with each passing generation, the “fight-or-flight”
response was inserted deep into our collective psyche.

Early man had to respond to various “threats” including...

• Predators
• Unfriendly neighboring tribes
• Competition for resources
• Periods of scarce food
• Environmental stresses such as heat and cold
• Injury and infectious disease
 In modern society, humans are faced with a different set of “threats.”

• Stressful work environments

• Traffic
• Financial problems
• Disruption of circadian rhythm (artificial light at night, poor sleep,
shift work)
• Processed food supply
• Environmental toxicants (chemicals, pollution)
• Chronic disease

The differences between the threats to modern and primitive man may
seem very obvious to us, but in our brain’s hardwired threat response
system they are treated equally, and elicit the same threat response.

Your brain treats both types of threats in a similar manner. In an escape

from immediate danger, a “bear threat” is actually preferable to the stress
from a “traffic threat.” Daily low-level chronic stresses such as traffic can
add up to cause real health problems. We are wired to deal with the bear
using a short-term threat response, but are not as suited to handle long-
term stress associated with things like daily traffic.

The big difference between primitive and modern “threats” is that

primitive threats were mostly temporary and short-lived, while modern
threats are often continuous and long-lived. The same brain-based threat
response system that allowed our distant ancestors to adapt, survive, and
get stronger works overtime every day with modern humans. Working the
threat response system overtime has a very real impact on our health.

Chronic stress and threat response has been linked to the following
diseases:

• Heart disease
• Type II diabetes
• High blood pressure
• Autoimmune disease (see the gut chapter)
• Depression
• Chronic pain
• Cancer

QUICK FACT:
Humans are not equipped to effectively deal with the chronic threats
rampant in modern society, and it is evident in the overall poor state of
public health.

YOUR BRAIN ON “THREAT”

Anything in your environment that the brain perceives as a threat will
trigger a physiologic stress response. The racing heart, jitteriness, and
hyper-alert state we have all experienced after being startled by a loud
noise or narrowly avoiding a car accident, is the stress/threat system in
action. At the primal level, the system’s job is to prepare you to fight or
flee from danger.

There are two main components to this “fight or flight” system, the
autonomic nervous system (ANS) and the hypothalamic-pituitary-adrenal
axis (HPA axis). Both components work together to prepare the brain and
body to deal with the threat and to recover afterwards. Once a threat is
perceived, the autonomic nervous system is responsible for the immediate
preparation to deal with the threat.
I. THE AUTONOMIC NERVOUS SYSTEM
The (ANS) operates without conscious control. The ANS operates on
autopilot so that you do not have to think about raising your heart rate or
moving more blood to muscles during a threat. It happens automatically
thus the name “autonomic.” There are three main parts of this system but
only the first two are of primary importance to our discussion of the threat
response.

• The Sympathetic Nervous System (SNS) is the “flight or fight” part of

the autonomic nervous system (ANS). This is the system responsible
for increasing your heart rate when you are startled, perceive danger,
or in response to exercise. The SNS stimulates the “fast pathway”
that produces chemicals to give you energy and increase your heart
rate during danger. Adrenalin (epinephrine) is one of the chemicals
produced by the adrenal gland when danger stimulates the immediate
threat response by the brain. Another chemical similar to adrenalin
called norepinephrine is also produced.

When the SNS is dominant, processes like digestion, rest and

recovery are put on hold; you do not need them or want them while
fighting or running for your life. The main job of the SNS during a
threat response is to provide energy to maintain the high states of
alertness and increased muscle activity necessary to survive “fight or
flee” threats. The SNS has (primarily) inflammatory actions and
should only be periodically dominant to respond to danger.

• The Parasympathetic Nervous System (PNS) is the “rest and digest”

system that counteracts the SNS. This system brings your heart rate
down after the danger has passed, allows for movement of food
through the intestines during digestion, and is associated with a calm,
relaxed state. The PNS system is critical for the recovery process. The
PNS allows your body to recuperate and prepare to successfully face
another threat in the future. The PNS has (primarily) anti-
inflammatory actions. We want the PNS to be dominant most of the
time.
 QUICK FACT:
Our distant ancestors lived the majority of their lives dominated by the
“rest and digest” parasympathetic system. Their sympathetic systems
sprang into action only when a threat appeared. Stressed out modern
man lives his life dominated by the SNS.

KEY POINT:
The sympathetic and parasympathetic systems are both operating to
some degree at all times. Environmental signals determine which
system is dominant at any particular time.

• The Enteric Nervous System (ENS) is the third part of the autonomic
nervous system (ANS) that controls your gastrointestinal tract (the
gut). It is sometimes called the “second brain” due to the huge
amount of nerve cells associated with this system. We will discuss
this system in depth in the gut chapter.

II. THE HYPOTHALAMIC-PITUITARY-ADRENAL AXIS

The (HPA) is the second component to the stress/threat system. It is
responsible for the slow pathway in the response to threat, and releases
various hormones to support the threat response. The first part of the HPA
axis is the hypothalamus.
—HYPOTHALAMUS
Central to the brain’s threat response system is the hypothalamus—a
tiny area located at the base of the brain. If you drew a line starting at the
bridge of your nose and went straight backwards into your head, you
would run into the hypothalamus. This area of the brain is only about the
size of an almond, but packed into that little space is the central control
center for how we respond to stresses perceived from our environment.
The hypothalamus regulates many processes crucial to our survival:

• Sleep-wake cycle (circadian rhythm) in response to light

• Hunger
• Thirst
• Thermoregulation (maintaining a constant body temperature)
• Signals for reproduction (making babies!)
• Fight or flight response

You can see from the vital processes the hypothalamus controls, it is
logical that it is the part of the brain responsible coordinating the stress
response. The hypothalamus is responsible for initiating both the
immediate threat response through the autonomic nervous system and the
delayed response through the HPA axis.

—THE PITUITARY GLAND

In response to environmental stress, the hypothalamus releases
hormones that travel to another tiny structure “hanging” just below the
hypothalamus in the brain called the pituitary gland. The pituitary gland
acts like a relay station, taking signals from hormones released by the
hypothalamus and making its own hormones in response to these signals.
The stress hormones produced by the pituitary gland then travel outside of
the brain down to the adrenal glands.

—THE ADRENAL GLANDS

Your adrenal glands sit on top of each of your kidneys and are about the
size of your thumb. The adrenals are the third partner in the hypothalamic-
pituitary-adrenal (HPA) axis. The adrenals secrete various hormones and
chemicals in response to both the slow and fast stress response pathways.
—HORMONES PRIMARY FOR THREAT RESPONSE:
Cortisol is released in response to stress signals from the slow pathway.
Cortisol provides the fuel to help the body recover from the threat and
helps control inflammation from the threat response.

Epinephrine (adrenalin) and norepinephrine are released in response to

stress signals from the immediate, fast pathway.

THE HPA-AXIS: HYPOTHALAMUS-PITUITARY-

ADRENAL

• FAST PATHWAY:
This pathway is triggered immediately after a
threat is sensed by the brain. It bypasses the pituitary
and sends a direct signal to the adrenals to produce
epinephrine (adrenaline) and norepinephrine. This
pathway immediately puts you in an alert state, and
gets you ready to “fight” or “flee” from danger.

• SLOW PATHWAY:
This pathway is also triggered by threat but responds slowly, signaling
the adrenal gland to secrete cortisol. Cortisol helps you recover from the
threat after it has passed.

MEDICAL CONNECTION:
Prednisone is the pharmaceutical equivalent of cortisol and works
using the same mechanisms in the body. Prednisone is used in modern
medicine to control inflammation in many different diseases such as
severe asthma and autoimmune diseases.

Well-known side effects of chronic prednisone (and other similar

Well-known side effects of chronic prednisone (and other similar
medications) use is fat gain, muscle wasting, bone weakening, and
psychological side effects such as agitation.

High levels of cortisol from chronic stress/threat activation can result

in the same side effects as daily prednisone use.
ANCIENT PHILOSOPHY MIRRORS MODERN
SCIENCE
The Chinese philosophical concept of yin and yang mirrors the
interaction between the sympathetic (SNS) and parasympathetic (PNS)
systems very well as it relates to the stress/threat system. The yin/yang
graphic has become a universal symbol for good reason; it is an
overarching concept that describes our natural world from large-scale
ecology to molecular biology. We can use the yin/yang concept to illustrate
the importance of balance in the autonomic nervous system between the
SNS and the PNS.

Prolonged activation of the stress/threat system leads to dominance by

the SNS and wear and tear on the body and brain.

ANS balance is crucial to health.

HEALTH EFFECTS OF THE STRESS/THREAT

SYSTEM
The sympathetic nervous system has the potential to produce high
levels of inflammation and oxidative stress, potentially causing
significant wear and tear on our body and brain. Optimally, the SNS
should only be dominant for short periods of time. In addition to
responding to threats and challenges, the
SNS is also purposefully invoked during
intense physical training. For many of us, our
sympathetic nervous system is always on,
ramped up, agitated, and frazzled from
responding to chronic stress situations.
Chronic over-stimulation of the SNS results
in chronic inflammation.

The parasympathetic nervous system is associated with calm, relaxed

centeredness, and has anti-inflammatory effects. Bodily functions
occur optimally when operating in PNS. We want to cultivate the PNS
and have it maintain dominance most of the time.

Prolonged activation of the HPA axis can lead to abnormally high

cortisol levels. Cortisol is an essential part of the recovery from threat
and plays vital roles in our body. Modern stresses keep our HPA axis
threat system on longer that it was designed, leaving us awash in
cortisol. This damages the brain, wastes muscle, weakens bones, and
promotes fat accumulation resulting in poor health.

KEY POINT:
The sympathetic “flight or fight” nervous system (SNS) generally has
inflammatory effects.

The parasympathetic “rest and digest” nervous system (PNS) generally

has anti-inflammatory effects.

Low levels of continued SNS activity can lead to chronic

inflammation, and is a key driver of chronic diseases such as heart
disease, diabetes, high blood pressure, and cancer in modern society.
 Poor health and disease are the result of this imbalance—dominance of
the SNS over the PNS. Many modern humans live in a constant state of
low level “flight or fight” in response to modern “threats,” with very few
of these threats being a true immediate danger to life and limb. The
following point needs repeating; the brain will trigger the threat response
to both internal threats from within the body and external threats from the
environment.

• Internal threat: swollen fat cells in an obese individual causing

inflammation.
• External threat: stressful work environment.
• Internal threat: bacterial infection or injury.
• External threat: processed food causing inflammation and oxidative
stress.
• Internal threat: rumination and worry causing chronic psychological
stress.
• External threat: consistent overtraining from “boot-camp beat down”
exercise programs.
• Internal threat: inadequate sleep.

This is just a handful of examples that can activate the brain’s threat
response. You will learn more about all of these threats as you continue
your training. Notice that inflammation and oxidative stress from internal
and external threats such as obesity and processed food can stimulate the
threat response. In turn, the threat response of the “flight or fight” system
(SNS) can cause inflammation and oxidative stress. This creates a vicious
cycle that leads to poor health.

In the upcoming in-depth training on Chronic Stress, we will show you

the damage to your body and brain that results from the cycle of
inflammation and over-activation of the stress/threat system. You will also
get defensive tactics to break the cycle and restore balance to the system
and to your health.

This very brief overview of the stress response system sets the stage for
how threats from our environment and from within impact our health. On
any given day, each of us has a specific capacity for dealing with internal
and external sources of stress. This capacity is what we call your “stress
cup,” the amount of stress you can handle on any given day. The next
section expands the “stress cup” idea using the scientific concepts of
allostasis and allostatic overload, which are foundational to the Strong
Medicine view of health and disease.
CENTRAL THEMES PART V:
ALLOSTASIS: MY CUP RUNNETH
OVER…

Unlike the meaning of this phrase in the biblical context, we will use it in
reference for a way to visualize our bodies’ capacity for stress, a.k.a the
“stress cup.” You really do not want to routinely overfill this cup, as you
will soon see.

The scientists who study the adaptation of the human body to stress call
this adaptation process allostasis. This word literally means achieving
“stability through change.” Put more simply, the human body always
wants to achieve balance with the environment*, and does so by changing
and adapting.

If something in our environment (such as strength training) tries to

disrupt this balance, the body will adapt to meet the challenge, changing to
be in a new balance with the environment (in this example becoming
physically stronger in response to lifting weights).

QUICK FACT:
*As a reminder, we define environment as our food and water intake,
air quality, physical activity and lifestyle.

KEY QUESTION:
How is the concept of allostasis different than hormesis?

Answer: Allostasis is the physiologic mechanism by which hormesis

operates.

What does that mean?

• Hormesis occurs when an environmental stressor produces a

“positive adaptation” or beneficial effects in the body.

• Allostasis is how the beneficial effects (adaptations) actually

happen inside the body to achieve stability with the
environment.

Many of us have felt a sense of euphoria or wellbeing after intense

physical activity. Those in the endurance sport community call it the
“runners high.” This sensation is really a protective response to stress by
the release of natural morphine-like compounds called endorphins.

Endorphin release is part of allostasis—in this case, the brain is

attempting to decrease pain during intense physical stress.

Allostasis is responsible for other adaptations/responses seen in response

to various types of environmental stress:

• Release of stress hormones such as cortisol and epinephrine by the

brain and adrenal glands in response to stress in all forms.
• Increase in muscle size in response to weight training.
• Increased cardiovascular fitness in response to exercise.
• Stimulating the antioxidant protection system when exposed to free
radicals.

QUICK FACT:
When the environmental challenges are in a high enough dose and
frequency to consistently overload the body’s ability to adapt, the
body starts to break down from “wear and tear” and disease is the
result.

These adaptations through allostasis allow you to better cope with the
demands of any future environmental challenges and/or serve an
immediate need for survival as part of the “flight or fight” response.

FAILURE TO ADAPT: “THE STRESS CUP”

At any one time, your body has an upper limit to the amount of stress it
can handle and still produce a favorable adaptive response. This limit or
capacity for stress can change dramatically day to day, or slowly over
months and years. A night of poor sleep, a couple of fast food meals,
traffic during your morning commute, or a demanding boss can reduce the
daily capacity for stress. It may be easier to think of this visually using the
concept of the “stress cup.”

THE “STRESS CUP”

The entire cup represents your body’s capacity to
deal with stress (through allostasis) on a given day. In
this example, the environmental stress of work, poor
sleep, and bad diet fill the cup most of the way,
leaving only a little capacity (empty space at the top)
for physical stress such as strength training.
Attempting a high intensity workout session—usually
a beneficial stressor—on a day like this could
“overfill” the “stress cup” and lead to poor adaptation and even illness
or injury.

When the environmental stressors are greater than the body’s capacity to
maintain stability, scientists call this allostatic load or allostatic overload.
This overload of the system over time (the overflowing “stress cup”)
produces “wear and tear” in the body and over the long-term leads to
disease.

This wear and tear can express itself as a “broken” metabolism (as in
diabetes) or physical degeneration leading to premature aging and poor
health.

THE OVERFLOWING “STRESS CUP”

This is what happens when attempting a high intensity workout when
your “stress cup” is almost full from work stress, bad diet and poor
sleep.
 Exercise is usually a good thing, but you need to
decrease “the dose” of exercise on a day like this
day to prevent your “stress cup” from overflowing
like in the picture.

The overflowing “stress cup” is called allostatic

overload.

QUICK FACT:
The end result of allostatic overload is increased chronic inflammation
and oxidative stress, which cause damage to your body and brain.

Allostatic overload represents the health consequences of more stress

(of all types) over time than your body and brain can handle—your
“stress cup” is constantly overflowing.

As you “pour” different stresses into your “stress cup”, your body and
brain react and adapt to the stress through the process of allostasis. As
long as you do not exceed the capacity of your cup, your body and brain
will survive and thrive in response to stress.

I know what you’re thinking, “I’ve got too much stress in my life. I’ll
avoid exercise so I don’t overfill my ‘stress cup’.” This is a really bad idea
because the complete lack of exercise will make your “stress cup” smaller,
leaving you less able to handle other stresses such as injury, poor diet, poor
sleep, and work stress.
 QUICK MEDICAL NOTE:
We can measure the results of allostatic overload with medical tests
such as:

• Blood sugar tests for diabetes

• Lipid panels for heart disease risk
• Thyroid testing
• Adrenal stress indexes for problems with cortisol
• C-reactive protein (a marker of inflammation)
• Heart Rate Variability

We will go over some of these in detail in the “Stuff You Can Measure”
chapter. Just know that conceptually, we are really measuring the
markers of allostatic overload—or how our body is not adapting well
to the environment over time.

Lack of exercise will figuratively reduce your “stress cup” from a 24-
ounce cup to a 12-ounce cup. The smaller your cup, the more easily it will
overflow, resulting in allostatic overload and health problems.

KEY POINT:
It is very important to remember that a lack of stress—such as
sedentary behavior—can just as easily cause allostatic overload as
well!

Again, these stresses are necessary for a healthy body, and it is no

 Again, these stresses are necessary for a healthy body, and it is no
surprise that arthritis and degenerated joints seen in middle age often
accompany poor muscle mass and weak bones from lack of physical
training and activity.

Regular exercise can increase the size of your “stress cup”!

SLOW THE HANDS OF TIME: “SUPER-SIZE”

YOUR “STRESS CUP”
A natural part of aging is the gradual “shrinking of our stress cup.” As
we age, we do not heal or recover from physical stresses or illness as well,
and are generally less resilient than we were as children or young adults.

The good news is that we can significantly slow the “shrinkage rate” of
our “stress cups”, and armor ourselves against stress into old age.

The “stress cup” can be “emptied” with stress reduction techniques such
as the breathing exercises, mindfulness techniques, physical exercise, and
the nutritional approaches we will cover later in the book.

Those with a history of poor nutrition, exercise, and

lifestyle habits will see a dramatic increase in the size of
their “stress cup” as they adopt the comprehensive
approach to health and wellness outlined in Strong
Medicine.

THE GOOD NEWS:

 The size of your “stress cup” can be increased over time through
smart training, adequate sleep, good nutrition, and the use of stress
reduction techniques. We will slow the aging process by “supersizing”
your “stress cup”.

In this example, the stresses of poor sleep and bad diet have been
reduced through lifestyle change. There is still some work stress, but we
now have a large empty space that can be filled with intense training
without overfilling our “stress cup”.

THE FUTURE OF MEDICINE?

In our opinion, the concepts of allostasis and allostatic overload are the
best way to view chronic disease as a whole. High blood pressure, diabetes,
high cholesterol, obesity, and mental health problems such as anxiety and
depression are all examples of the body’s failure to adapt to environmental
stresses such as chronic stress, poor diet, and lack of physical activity. It is
well known that these diseases often occur together—which is no surprise
if you view them all as results of allostatic overload, overfilling your
“stress cup.”

We need to stop treating these diseases as individual issues to be treated

with drugs. Instead, the lifestyle should be aggressively modified to reduce
stress, eat well, and exercise more. If you are unwilling to do this, you are
doomed to take an ever-increasing number of drugs in an attempt to
artificially control your body’s attempt to achieve stability in a poor
environment of fast food, inactivity, and high stress. None of the chronic
diseases listed above have ever been cured by drugs, only partially
controlled at best.

Let us eliminate the causes instead of treating the symptoms. The body
has an incredible potential for self-healing. Given the right inputs of good
food, exercise, and stress reduction, it knows what to do.
USE IN DAILY LIFE
Using the visual concept of the “stress cup”, you can discover your
individual daily limits and proper “doses” of the various environmental
inputs of food, training, and lifestyle that lead to beneficial changes for
you.

What works well for you may not work well for your family members,
neighbors, or co-workers, and vice-versa. You will make mistakes in the
process of experimentation with this concept, just don’t let your “stress
cup” consistently run over. The rest of this book will give you the tools to
prevent allostatic overload and the chronic diseases that go with it.

SPOTLIGHT ON A SCIENTIST:
The work of Dr. Bruce McEwen inspired this section of Strong Medicine
with his foundational work on allostasis and allostatic overload. His
contributions to this area of research have been monumental.
“MILITARY INTELLIGENCE” (REFERENCES):
Bohacek J, Gapp K, Saab BJ & Mansuy IM. Transgenerational epigenetic effects on brain functions.
Biol Psychiatry 73 (2013): 313-320.

Calabrese, V. et al. Cellular stress responses, hormetic phytochemicals and vitagenes in aging and
longevity, Biochim Biophys Acta 1822 (2012): 753.

Calabrese, V. et al. The hormetic role of dietary antioxidants in free radical-related diseases, Curr
Pharm Des 16 (2010): 877.

Cohen, S. et al. Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk,
Proc Natl Acad Sci USA 109 (2012): 5995.

Davidson RJ, McEwen BS. Social influences on neuroplasticity: stress and interventions to promote
wellbeing, Nat Neurosci 15 (2012): 689.

Fairfield KM. Daily multivitamin supplements did not reduce risk for major CV events over > 10
years in men, Ann Intern Med 158 (2013): JC2.

Ganzel BL, Morris PA. Wethington, E. Allostasis and the human brain: Integrating models of stress
from the social and life sciences, Psychol Rev 117 (2010): 134.

Goldstein DS. Adrenal responses to stress, Cell Mol Neurobiol 30 (2010): 1433.

Gomez-Pinilla, F. The influences of diet and exercise on mental health through hormesis, Ageing Res
Rev 7 (2008): 49.

Goto S, Radak Z. Hormetic effects of reactive oxygen species by exercise: a view from animal
studies for successful aging in human, Dose Response 8 (2009): 68.

Joseph PG, Pare G, Anand SS. Exploring gene-environment relationships in cardiovascular disease,
Can J Cardiol 29 (2013): 37.

Li G, He H. Hormesis, allostatic buffering capacity and physiological mechanism of physical

activity: a new theoretic framework, Med Hypotheses 72 (2009): 527.

Maeta K, Nomura W, Takatsume Y, Izawa S, Inoue Y. Green tea polyphenols function as

prooxidants to activate oxidative-stress-responsive transcription factors in yeasts, Appl Environ
Microbiol 73 (2007): 572.

Mansuy IM, & Mohanna S. Epigenetics and the Human Brain: Where Nurture Meets Nature.
Cerebrum 2011(2011): 8.

McEwen BS. Sleep deprivation as a neurobiologic and physiologic stressor: Allostasis and allostatic
load, Metabolism 55 (2006): S20.

McEwen BS. Central effects of stress hormones in health and disease: Understanding the protective
and damaging effects of stress and stress mediators, Eur J Pharmacol 583 (2008): 174.

McEwen BS. Brain on stress: how the social environment gets under the skin, Proc Natl Acad Sci
USA 109 Suppl 2 (2012): 17180.
McEwen BS, Getz L. Lifetime experiences, the brain and personalized medicine: an integrative
perspective, Metabolism 62 Suppl 1 (2013): S20.

McEwen BS, Wingfield JC. What is in a name? Integrating homeostasis, allostasis and stress, Horm
Behav 57 (2010): 105.

Menendez JA, et al. Xenohormetic and anti-aging activity of secoiridoid polyphenols present in
extra virgin olive oil: A new family of gerosuppressant agents, Cell Cycle 12 (2013): 555.

Muscatell KA, Eisenberger NI. A Social Neuroscience Perspective on Stress and Health, Soc
Personal Psychol Compass 6 (2012): 890.

Novakovic B, Saffery R. The importance of the intrauterine environment in shaping the human
neonatal epigenome, Epigenomics 5 (2013): 1.

Nunn AV, Bell JD, Guy GW. Lifestyle-induced metabolic inflexibility and accelerated ageing
syndrome: insulin resistance, friend or foe?, Nutr Metab (Lond) 6 (2009): 16.

Ogino S. et al. Molecular pathological epidemiology of epigenetics: emerging integrative science to

analyze environment, host, and disease, Mod Pathol (2013).

Pace TW, Hu F, Miller AH. Cytokine-effects on glucocorticoid receptor function: relevance to

glucocorticoid resistance and the pathophysiology and treatment of major depression, Brain Behav
Immun 21 (2007): 9.

Pickering AM, Vojtovich L, Tower JA, Davies KJ. Oxidative stress adaptation with acute, chronic,
and repeated stress, Free Radic Biol Med 55 (2013): 109.

Pietsch K, et al. Hormetins, antioxidants and prooxidants: defining quercetin-, caffeic acid-and
rosmarinic acid-mediated life extension in C. elegans, Biogerontology 12 (2011): 329.

Puterman E, et al. The power of exercise: buffering the effect of chronic stress on telomere length,
PLoS One 5 (2010): e10837.

Radak Z, Chung HY, Koltai E, Taylor AW, Goto S. Exercise, oxidative stress and hormesis, Ageing
Res Rev 7 (2008): 34.

Ristow M, Schmeisser S. Extending life span by increasing oxidative stress, Free Radic Biol Med 51
(2011): 327.

Ristow M, Zarse K. How increased oxidative stress promotes longevity and metabolic health: The
concept of mitochondrial hormesis (mitohormesis), Exp Gerontol 45 (2010): 410.

Speciale A, Chirafisi J, Saija A, & Cimino F. Nutritional antioxidants and adaptive cell responses:
an update. Curr Mol Med 11 (2011): 770-789.

Webster AL, Yan MS, Marsden PA. Epigenetics and cardiovascular disease, Can J Cardiol 29
(2013): 46.

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meta-analysis of randomized controlled trials, PLoS One 8 (2013): e56803.
 PART II

KNOWING YOUR ENEMY

“If you know the enemy and know yourself, you need not fear the
result of a hundred battles. If you know yourself but not the enemy,
for every victory gained you will also suffer a defeat. If you know
neither the enemy nor yourself, you will succumb in every battle.”
—Sun Tzu, The Art of War
THE “PENTAVERATE” OF PESTILENCE
These are the five enemies producing chronic inflammation and
oxidative stress. They are a cabal of health calamity. We have
collected ample intelligence on each of these nefarious characters.
We will train you to understand them from the ground up, and will
give defensive tactics to protect you from their advances. Each
enemy will be briefed in the following order:

• Gut Inflammation
• Obesity and Insulin Resistance
• Chronic Stress
• Circadian Disruption

We will discuss “Inactivity” (#5) in Part 3 in our extensive coverage

of exercise.

Notice that no matter the specific enemy, the underlying cause of

most chronic disease is long-term inflammation and oxidative stress.
The Pentaverate works together to cause the diseases listed in the
black box. Those listed are only a fraction of diseases thought to be
caused by chronic inflammation and oxidative stress.
KNOWING YOUR ENEMY I:
THE GUT: GUARDIAN AT THE GATE

Our intestinal tract will likely become a primary focus as we learn more
about the underlying causes and treatment of disease in the 21st century.
Indeed the last decade has shown tremendous progress in our
understanding of just how central this organ system is for maintaining
health.

The following discussion will be fairly lengthy, but a basic

understanding of how the gut works and what happens when its function
is disrupted is extremely important to your health. If you want to attain
your body composition and fitness goals, you cannot overlook this section.

Chronic inflammation of the gut is the first member of the Pentaverate.

The intestinal tract (gut) is our first line of defense from outside “invaders”
such as pathogenic bacteria and from our modern diet.
 When the gut defenses are constantly stimulated, they can transform
from protectors into agents of chronic disease. We will show you how to
stop this insidious process with Strong Medicine defensive tactics. Proceed
for in-depth training on the inner workings of the “guardian at the gate.”
GUARDIAN AT THE GATE PART I:
GUT HEALTH: FIRST PRINCIPLES

A recent case study published in the British

Medical Journal described the results of placing a
6-year old boy on a gluten free diet after he was
diagnosed with type 1 diabetes (T1D).

For those of you that do not know, T1D is an

autoimmune disorder in which the person’s own
immune system destroys the insulin-producing
cells in their pancreas, typically the person will be dependent on insulin
injections for the rest of their life.

The results of the gluten free diet with this child were remarkable.
Within weeks of starting on the diet, he no longer needed insulin
injections. Twenty months after starting the diet, he still did not need
daily insulin treatments. Essentially, the gluten free diet put his T1D
 daily insulin treatments. Essentially, the gluten free diet put his T1D
into remission.

T1D is traditionally thought of as an incurable disease, so how was this

child apparently “cured” with something as simple as a gluten free
diet?

A “FIRST PRINCIPLES” ARGUMENT THAT

INTESTINAL TRACT HEALTH IS CRITICAL IN
ATTAINING OVERALL HEALTH:
• Our intestinal tract (gut) is where we absorb nutrients from the food
we eat.

• The intestinal tract is the first barrier through which we “interact”

with outside environmental inputs of food and water, selectively
letting in the “good” environmental inputs and keeping out the
“bad” inputs.

• This interaction is the first opportunity for the body’s defense against
outside bacterial invaders and toxins/toxicants in our food and
water.

• A large proportion of our body’s immune system is located in the

intestinal tract.

• When the gut immune system is overactive, bad things can happen.
Chronic inflammation is a result of prolonged activation of our gut-
associated immune system. This creates chronic inflammation and
oxidative stress in the body.

• Chronic systemic inflammation and the resulting oxidative stress are

the main contributors to chronic diseases including cancer,
atherosclerosis and diabetes.

• The intestinal tract and brain are closely connected. Inflammation in

the gut is communicated to the brain, creating a body-wide stress
response that can wreck our metabolism and ruin our health if left
unchecked.
THE INTESTINAL BARRIER
The intestinal tract was designed to maximize absorption within the
smallest possible space. The intestinal wall is intricately folded, creating
structures called villi. The villi themselves are comprised of individual
epithelial cells with their own folds called microvilli. The “lumen” is the
space “inside the tube” of the gut where food passes after digestion. The
epithelial cells selectively absorb nutrients—amino acids from protein,
glucose and fat—from digested food. The absorbed nutrients are sent into
the blood stream, including amino acids, glucose, short and medium-chain
fats and in the lymphatic vessels, long-chain fats are absorbed.
 This is a close-up view of the epithelial cells (light brown.) Each is
connected by tight junctions.(TJ). TJs keep large undigested particles of
protein and harmful bacteria from penetrating through to the blood
stream. This system allows nutrients (amino acids, sugars, fats) to travel
through transporters in the microvilli. The epithelial cell barrier is our first
line of defense (The Guardian at the Gate) from harmful things in our diet.
We have a system of immune cells just below the epithelial layer (in the
lamina propria) to deal with anything trying to bypass the tight junctions.
 When the tight junctions fail, this is called intestinal permeability (IP)
or “leaky gut.” IP allows harmful bacteria and undigested protein
fragments into the lamina propria and the bloodstream. The immune
system then launches its response against the interlopers, resulting in
inflammation.

The intestines contain most of our body’s total immune system, 70-
80% by many estimates. This is a strategic location for most of our
immune defenses, as it is one of the first places where the inside of our
body contacts things we bring in from the outside world—food and
water—which may include disease-causing bacteria and viruses.

The gut’s immune system is incredibly important for maintaining our

health and defending against invaders.

First, a brief review of the immune system, then a discussion on how the
immune system can get out of control and attack our own body in a
process called autoimmunity. Recent research has shown that the gut may
be the primary place where autoimmunity is triggered.
IMMUNE SYSTEM REVIEW
The immune system is highly complex. We have simplified the concepts
considerably. Please reacquaint yourself with the main players of the
immune system that we originally introduced in Basic Training. Because
the majority of the immune system makes its home in the gut, it is crucial
that you retain a basic understanding of how each member contributes to
maintaining our first line of defense against threats from the outside world.
The members of the gut immune system are truly the “guardians at the
gate.”

INNATE IMMUNE SYSTEM:

The cells of the innate immune system are like the guards at
the castle gate. They will deal with anyone who looks or acts
suspicious. This is usually the initial encounter with
bacteria/viruses and “foreign” protein fragments. Their
response is not targeted at specific individuals, but is a general
protective response to anything deemed “foreign.”

ADAPTIVE IMMUNE SYSTEM:

These assassins are called T-cells and B-cells and
once they encounter pieces of a prisoner caught by
the dendritic cells or macrophages of the innate
immune system, they “adapt” themselves. They
morph and become perfect assassins for this specific
type of prisoner. They form “clones” of themselves
to make an army of assassins once they have found a specific victim.

T-REGULATORY CELLS, AKA TREG CELLS:

Think of these cells as the “hippie” anti-war protestor that helps control the
assassins. Treg cells are the peace-loving part of the adaptive immune
system and produce an anti-inflammatory response. We need a balance
between Treg cells and the assassins to prevent the
immune system from attacking our own body tissues in
something called autoimmunity.
AUTOIMMUNITY AND INTESTINAL
PERMEABILITY
Autoimmunity occurs when our immune system (the innate guardians
and adaptive assassins) fails to recognize tissue in our body as “self.”
Instead, the immune system gets its wires crossed and recognizes “self”
tissue as foreign. As the immune system is designed to protect us from
foreign invaders, it attacks and destroys our own tissue. This can happen
in multiple tissue types.

• Celiac disease: cells lining the intestine are destroyed.

• Hashimoto’s thyroiditis: the thyroid tissue is destroyed.
• Multiple sclerosis: the “insulation” (myelin) of our nerves is
destroyed.
• Rheumatoid arthritis: our joints are destroyed.

There are many theories currently being investigated why our own
immune system turns on us. Some interesting theories involve the loss of
Treg cells (hippies). We also know that individual genetics, specifically
genetics of the immune system, play a large role in autoimmunity, but
there are environmental “triggers” that jump-start the process. One leading
researcher in the field has proposed that a third factor is necessary for the
development of autoimmunity, intestinal permeability.

The theory of intestinal permeability as the third factor required for

autoimmunity came from studying people with celiac disease. Celiac
disease is an autoimmune disease triggered by intestinal permeability.
People with this condition are known to have a much higher incidence of
other autoimmune diseases. It is proposed that whatever the environmental
trigger—bacteria, virus, food particle—it must first come into contact with
the immune system for a reaction. Intestinal permeability allows the
contact of the gut immune system with environmental triggers to take
place.
 KEY POINT:
Intestinal permeability may be the third required factor for developing
autoimmune disease.

Review the graphic from the beginning of this section showing the
intestinal barrier. Pay close attention to the tight junctions that prevent
undigested food particles and bacterial invaders from penetrating the lining
of the gut wall. When the tight junctions fail, things that should not get
past the protective gut lining take the passage that is now open between
the intestinal epithelial cells forming the barrier. Failure of the tight
junctions is the mechanism behind intestinal permeability (“leaky gut”).
When this happens, undigested food particles and bacterial invaders come
in contact with the immune system guardians that are defending the castle
wall. The gut immune system is now on alert.

DISRUPTION OF THE BARRIER:

CONSEQUENCES AND CLINICAL DISEASE
Daily exposure to things that induce intestinal permeability can lead to:

• Chronic inflammation, the precursor to developing chronic diseases—

diabetes, obesity, cancer, Alzheimer’s dementia and heart disease.

• Autoimmune diseases, which strike those who have a genetic

predisposition. Multiple sclerosis, rheumatoid arthritis, type I
diabetes, Hashimoto’s thyroiditis, celiac disease, and Crohn’s disease
are just some of the diseases influenced by intestinal permeability.
 In this diagram, the tight junctions have been disrupted, allowing
harmful bacteria and undigested protein fragments past the epithelial
barrier. The immune system is now activated (red glow) and the
inflammatory response is initiated.

Chronic intestinal permeability can also lead to reduced numbers of the

Treg cells “hippies” and increased numbers of adaptive “assassins.” New
science has shown that Treg cells are extremely important in prevention of
autoimmunity. Having enough Treg cells is critical for preventing the
adaptive assassins from getting out of control.

Chronic intestinal permeability leads to the “assassins” outnumbering

the “hippies.” This sets the stage for out of control inflammation and
autoimmunity because there are not enough hippies (Treg) to keep the
assassins in check.

We need to maintain the intestinal barrier and prevent chronic intestinal

permeability to maintain a proper balance between the “assassins” and the
“hippies.” Too many assassins leads to out of control inflammation and
autoimmunity, while too many hippies would leave us vulnerable to
invading microorganisms such as bacteria and viruses.

When the balance between “assassins” and “hippies” is disrupted,

chronic inflammation and autoimmunity are triggered, leading to disease.

Balance prevents autoimmunity and chronic inflammation.

 We will show you strategies on how to maintain this balance in
upcoming sections, but first we will show you how chronic intestinal
permeability (leaky gut) is triggered by components of processed food,
stress, and disruption of our normal population of gut bacteria.

Recent science supports the idea that although you may have the
genetics predisposing you to getting autoimmune diseases, if your gut
immune system does not come into contact with the environmental trigger,
you will remain free of disease.

KEY POINT:
Even if you are genetically predisposed to autoimmune disease,
avoiding the environmental triggers will prevent you from developing
one of these diseases.

In the next section, your in-depth training on the causes of gut

inflammation will continue. We will identify the environmental triggers of
chronic intestinal permeability and train you in defensive tactics to protect
yourself from these triggers. This is how we will bring down the first
member of the Pentaverate and keep the “Guardian at the Gate” intact,
protecting your health from the onslaught of chronic disease.
GUARDIAN AT THE GATE PART II:
TRIGGERS OF INTESTINAL INFLAMMATION

TRIGGERS OF INFLAMMATION

Potential triggers for chronic inflammation in the gut leading to disease

are the following:

1. Gluten and other dietary triggers

2. Stress, the Gut-Brain Axis

3. Dysbiosis, the disruption of gut bacteria

KEY POINT:
It is very important to keep in mind that short term increases in
intestinal permeability is a normal physiologic mechanism, and is an
 essential part of our natural defenses to fight infectious bacteria and
viruses in the gut, as well as to clear them from the body (diarrhea). It is
only when we have long-term intestinal permeability and
inflammation that we run into trouble.

TRIGGER #1: GLUTEN

In Environmental Medicine, we judge the public health impact of
potential environmental toxins and toxicants on the toxicity of the
compound and the potential for exposure. With gluten, toxicity will vary
depending on the person, but potential exposure is extremely high. Gluten
is always potentially problematic.

Inflammatory reactions to gluten proteins—found in wheat, barley and

rye food products—have received a lot of press over the last couple of
years. The gluten family of proteins have become whipping boys in the
dietary blogosphere and popular media. Although the demonization of
gluten is somewhat justified and is supported by recent research, we need
to look at this issue dispassionately.

Gluten is an ingredient in countless processed foods (and many other

products) so our potential for exposure cannot be underestimated.
GLUTEN 101
• Gluten is the main structural protein in wheat, barley and rye. Gluten
gives bread products their soft, doughy texture. Extra gluten is often
added to make bread and bagels softer.

• The toxic components of gluten proteins are called gliadins and

glutenins. Proteins are “chains” of amino acids. Different amino acid
sequences in the chains determine the shape of the protein, the ease
of digestion, and most importantly, their biologic function.

• Parts of the chains in gliadins and glutenins are

very resistant to our digestive “machinery.”
Small fragments of these proteins with amino
acid sequences containing high amounts of
proline and glutamine, are responsible for
digestive resistance. Gluten proteins are called
“prolamins” (proline + glutamine).

• Prolamin protein fragments can trigger

Amber waves
intestinal permeability and immune response
of inflammation?
resulting in inflammation and oxidative stress.

• Genetic differences in our immune systems result in individual

differences in the strength and type of immune response to these
prolamin protein fragments.
Differing immune responses to gluten create differing classifications of
glutenrelated diseases.

• Celiac disease is also called gluten-sensitive enteropathy. This

condition creates an innate and adaptive immune response.

• Gluten sensitivity is an innate, non-specific immune response.

SPECTRUM OF GLUTENRELATED DISEASE

 The spectrum of glutenrelated disorders:
your genetics (and epigenetics) determine
the reaction of your immune system to
gluten and where you fall on the spectrum.

Between points A and B: People are able to eat gluten without any
known adverse health effects. This group represents the majority of us.

Between points B and C: People with Gluten Sensitivity. Those in this

range have immune reactions to gluten. The range includes those with
no symptoms and a low level of inflammation to those with substantial
symptoms, including irritable bowel syndrome (IBS). About 20-30% of
us fall into this category.

Between points C and D: These people are afflicted with celiac disease.
About 1% of the population has celiac disease.

The variance among responses to gluten is largely genetic (and

epigenetic). Many of the scientists studying the effects of gluten on health
have come to the conclusion that there simply has not been enough time
for humans to fully adapt to grains as a food source. Widespread
agriculture has only been in existence for 10,000 years—a blip on the
historical radar.

Another interesting hypothesis holds that the increase of glutenrelated

health problems is in direct proportion to the increase in food processing.
Industrial foods are constructed using cheap, subsidized grain containing
gluten. The rise in the consumption of these artificial gluten-containing
foods mirrors the increase in glutenrelated health maladies.

Traditional cultures have long used grains without nearly the degree of
glutenrelated health problems Western cultures are experiencing. These
cultures often prepare their grains using sprouting and fermentation
processes that decrease the toxicity of gluten. (see Weston A. Price
foundation.)
 One school of thought holds that genetic modification of grains, most
particularly wheat, has changed the protein structures enough to promote
an increased immune response.

QUICK MEDICAL NOTE:

Recent research is finding links to gluten for a wide range of diseases
and metabolic disorders:

• Insulin resistance
• Leptin resistance
• Hashimoto’s thyroiditis
• Neurologic diseases
• Rheumatoid arthritis
• Irritable bowel syndrome
• Inflammatory bowel disease (Crohn’s,
ulcerative colitis)
Systemic inflammation starting in the gut may be the hidden link to
these conditions.

CELIAC DISEASE (CD)

This “disease” is not really that rare, affecting as many as 1 in 100
people. It is also under diagnosed. It is estimated that 90% of those with
celiac disease are walking around undiagnosed. Undiagnosed children with
celiac are short and scrawny for their age and are delayed developmentally.

Celiac disease is not so much a disease as it is a mismatch between a

person’s genetics and their environment. When the environmental trigger
of gluten is removed, most CD patients see complete resolution of their
symptoms.
 • The innate and adaptive immune systems each contribute to the
problems seen in CD.

• The undigested protein fragments of gluten proteins disrupt the tight

junctions of the epithelial barrier.

• The “innate guardians” intercept the foreign fragments,

ingest them and display pieces on their cell surface.
Individual genetics determine how these fragments are
displayed and the interaction with the T-cell “adaptive
assassins”.

• The adaptive assassin T-cells

recognize the displayed gluten
fragments as foreign, and form clones to
specifically recognize and unleash their destructive
arsenal.

• Unfortunately, this results in the “nuclear option”

as far as the intestinal barrier is concerned. The
assassins release large amounts of inflammatory cytokines in
response to gluten fragments.

• The massive cytokine release increases the intestinal permeability even

further, letting in more gluten fragments and foreign particles
including bacteria. The nuclear option physically destroys the
epithelial barrier in the process—akin to an innocent casualty of war.
Destruction of the absorptive epithelial barrier results in decreased
ability to absorb nutrients in the diet. This leads to malnutrition and
“failure to thrive” in growing children.
 KEY POINT:
This process will continue as long as gluten is included in the diet for
this group of genetically susceptible people. The adaptive assassins are
always waiting to pounce on gluten fragments. This is why even a tiny
bit of gluten in people with CD results in immediate symptoms of
gastrointestinal distress and diarrhea.

The intestinal permeability and immune response in CD may contribute

to the development of a variety of autoimmune and inflammatory
disorders often seen in CD patients. These include:

• Endocrine diseases such as type I diabetes, Hashimoto’s thyroiditis

(most common form of thyroid disease), and reproductive disorders.

• Neurologic disorders such as cerebellar ataxia, peripheral neuropathy,

psychosis, epilepsy (seizures), autism and migraine headaches.

• Autoimmune liver diseases such as primary biliary sclerosis and

autoimmune hepatitis.

• Anemia, osteoporosis, rheumatoid arthritis, autoimmune heart

disease (myocarditis).

• Non-Hodgkin’s lymphoma (a type of cancer of the immune system).

Gluten activates autoimmunity (celiac disease) through intestinal
permeability. Observe the destruction of the microvilli in the epithelial cells
(on the right) of the gut lining. The damaged microvilli are now unable to
absorb nutrients from food.
DIAGNOSIS OF CELIAC DISEASE
There is no clear and reliable way to definitively diagnose celiac disease.
Intestinal biopsy has been—and still is in current clinical care—the “gold
standard.” The tissue sample from the biopsy is analyzed under a
microscope to look for signs of microvilli damage in the wall of the
intestine. The problem lies in the fact that not all CD patients show
microvilli damage. The most reliable way to test for a gluten problem is by
eliminating it from the diet and monitoring symptoms over a couple of
months.

RESEARCH UPDATE:
Recent research has shown that as many as 50% of patients with CD
show no signs of microvilli destruction. This test still may be helpful as
most CD patients show infiltration of “adaptive assassin” immune cells
into the epithelial cells themselves. These are called intraepithelial
lymphocytes, or IEL.

KEY POINT:
The most reliable and practical way to determine any type of
glutenrelated disorder is to completely eliminate gluten for a period of
time and monitor your symptoms.
GLUTEN SENSITIVITY
Gluten sensitivity (GS) is gaining credence as an emerging diagnosis. GS
is distinctly different from celiac disease in how the gluten proteins within
the body cause problems.

• The epithelial cells in the small intestine are usually normal, without
signs of microvilli destruction.

• The “adaptive assassins” of the immune system do not appear to be a

key player in GS; but investigations are still under way.

• The non-specific response of the innate immune system, the

“guardians” system, produces inflammation by secreting cytokines in
response to gluten protein fragments.

• Clinically, this response leads to symptoms of bloating, diarrhea, and

cramping after exposure to gluten.

• These symptoms are often classified as irritable bowel syndrome (IBS)

by the medical profession. IBS is a catch-all diagnosis for
gastrointestinal symptoms for which a specific cause cannot be
found. The current research suggests that GS may be one of the
underlying causes of IBS.

Many people have suffered with gastrointestinal symptoms all of their

lives without a clear diagnosis. This is very frustrating for most, and most
learn to live with it, although the symptoms routinely affect their quality of
life. Some of these individuals need to plan their day to ensure they have
easy access to restroom facilities wherever they go.
 DOC’S RANT:
What has always been interesting to me is that many people suffering
with IBS-like symptoms will not “give up” foods like bread and pasta,
even when given the above information. As we discussed in previous
chapters, most gluten-containing grain products are not nutritionally
dense, and have anti-nutrients.

Since we are not missing anything nutritionally by eliminating these

products, why do people cling to their grain-based foods? You never
hear anyone say, “I won’t give up my broccoli!” A few scientists have
looked at this phenomenon and have shown that some pieces of the
gluten protein may mimic the effects of opiates (morphine-like
compounds) in the brain.

We have all heard of endorphins—our naturally produced feel-good

substances. Some scientists are now referring the specific pieces of
gluten proteins as “exorphins,” and think these molecules may be
responsible for the craving some people have for gluten-containing
grain products.

Most of us do not have celiac disease or gluten sensitivity. However, if

you have any chronic gastrointestinal problems such as IBS, reflux disease
(chronic heartburn), gallbladder problems, or inflammatory bowel diseases
such as ulcerative colitis or Crohn’s disease, gluten may be a significant
contributor to these diseases. Gastrointestinal problems often have an
inflammatory origin, so why not eliminate a potential source of gut
inflammation by eliminating gluten.

Without a clear and definitive test for determining whether you have CD
or GS, the most rational approach is to eliminate gluten from your diet.
How do you feel after a week or a month? Is your heartburn better? Are
IBS symptoms decreased? If you have an autoimmune disease, a glutenfree
trial period is a must do. You have nothing to lose (other than bread) and
everything to potentially gain. There is no nutritional benefit to eating
gluten, and for as many as 30% of us, there are significant health
consequences for continuing to eat gluten-containing products.
 RESEARCH UPDATE:
The focus on gluten in wheat is admittedly a bit reductionist on our
part. Gluten is certainly potentially problematic and the best studied,
but it may not represent the whole story.

New research shows that other proteins in wheat aside from gluten are
potential culprits in stimulating intestinal permeability and
inflammation and may be the underlying cause of problems previously
attributed to gluten.

STRONG MEDICINE TACTICS:

Eliminate gluten-containing grains for 1-2 months to assess their
potential effects on your individual health.

TRIGGER #2:
STRESS AND INTESTINAL PERMEABILITY
Many of us are familiar with clichéd sayings such as, “I’ve got a gut
feeling about this”, “Show some intestinal fortitude!” or “Gut it out!”
Most of us have experienced a “nervous stomach” or “butterflies in the
belly” before stressful events.
 There is very strong scientific and anatomical basis for a gut-brain
connection. The intestinal tract has its own nervous system that can
operate independently from the brain. This gut-based nervous system is
known as the enteric nervous system (ENS) and has been called our
“second brain” by some scientists.
THE SECOND BRAIN
The ENS is extensive and contains as many nerve cells as our spinal
cord. Like the brain, the ENS has sympathetic (flight or fight) and
parasympathetic (rest and digest) systems. These systems can and do
operate independently from the brain. Also similar to the brain, the ENS
has nerve cells responsible for sensation, controlling muscle movement
(peristalsis) and neurotransmitter production. Neurotransmitters are
molecules that carry messages between nerve cells. You may be familiar
with neurotransmitters such as serotonin (depression) or epinephrine
(adrenaline). The ENS alone produces over 30 different neurotransmitters!

DIGGING DEEPER:
Enteric Glial Cells
Yet another similarity between the ENS and the brain are the presence
of specialized cells that act in support of nerve cells. In the brain these
cells are known as astrocytes. These cells have a multitude of functions
and act to regulate the function of nerve cells.

Astrocytes are the primary component of the blood-brain barrier. This

barrier is crucial in preventing things from getting into the brain that are
potentially harmful. There are very specific transport systems in the
blood-brain barrier that only allow certain things (like nutrients) to pass
through.

The ENS has a cell similar in type to the astrocyte, the enteric glial cells.
These cells support the ENS nerve cells and help control gut function.
EGCs are responsible for helping maintain intestinal barrier function by
reducing intestinal permeability.
“THE GUT-BRAIN AXIS”
Even though the ENS can operate independently from the brain, there is
a strong communication link between the two, the gut-brain axis. Through
this two-way communication network, signals are passed from gut to
brain, and from brain to gut. The system of how stress is communicated
between the brain and gut explains how psychological stress can produce
physical symptoms such as diarrhea.

As a system, the gut-brain axis orchestrates processes such as:

As a system, the gut-brain axis orchestrates processes such as:
• Gastrointestinal function
• Appetite control
• Body weight control

The vagus nerve is the direct connection of the gut-brain axis. The
vagus nerve carries sensory information from the gut to the brain. The
vagus also controls motor signals for gut muscle contractions.

KEY POINT:
Higher levels of parasympathetic activity (as in relaxed states) have
been shown to decrease inflammation, and protect the gut from
intestinal permeability. This is how stress reduction can protect your
gut.

High sympathetic (fight or flight) states reduce parasympathetic

signaling leading to increased inflammation and intestinal
permeability. If you are “stressed” constantly, think how this may
affect your gut!
THE BRAIN RESPONSE TO STRESS
The vagus nerve is the primary carrier of parasympathetic (rest and
digest) signals from the brain to most of our internal organs, including the
gut.

During psychological stress or physiological

stress (poor sleep, overtraining, etc.) the brain
releases a signaling hormone called
corticotropin releasing hormone (CRH) from
the hypothalamus. This triggers the pituitary
gland to release a hormone called
adrenocorticotropic hormone (ACTH). ACTH
then acts on the adrenal glands to release the
stress hormone cortisol.

Cortisol is released to combat stress, and decreases inflammation. It does

so by depressing the immune system. This process is your body’s way of
defending itself after a stressful event. This works well for short-term
stresses, but the system breaks down if it is constantly stimulated from a
lifestyle of daily stresses. Chronically high cortisol levels lead to weight
gain and poor blood sugar control—a risk factor for diabetes. Stress leaves
you susceptible to sickness from bacteria and viruses.
THE GUT RESPONSE TO STRESS
The “second brain,” the ENS, also releases its own CRH in response to
stress signals. The effects are different from CRH released by the brain.
This CRH acts directly on immune cells of the “innate guardian” type, the
mast cells. Mast cells are known in medical circles as cells that release
histamine in allergic reactions. It is now known that mast cells also release
a full complement of inflammatory cytokines. These cytokines increase
intestinal permeability by altering the function of the tight junctions shown
in the pictures at the beginning of this chapter.

GUT INFLAMMATION FROM STRESS LEADS TO

CHRONIC DISEASE
1. Psychological and/or physical stress
leads to high sympathetic (fight or
flight) nervous system activity.
2. The brain responds by decreasing
parasympathetic (rest and digest)
signaling to the gut by the vagus
nerve.
3. Decreased parasympathetic signaling by the vagus nerve leads to
increased intestinal permeability.
4. Increased intestinal permeability activates the gut immune system.
“Invaders”—foreign bacteria and protein fragments—lead to
inflammation.
5. Inflammation of the gut leads to impaired function resulting in
symptoms such as diarrhea and bloating.
6. Chronic stress leads to chronic intestinal permeability, which leads
to chronic inflammation.
 7. Chronic inflammation leads to diabetes, cancer, high blood pressure
and heart disease.

Locally in the Gut:

1. Stress activates the ENS to produce CRH.
2. CRH activates mast cells that release inflammatory cytokines.
3. Inflammatory cytokines disrupt tight junctions leading to intestinal
permeability.
4. Intestinal permeability leads to inflammation.
5. Chronic stress leads to chronic inflammation.
6. Chronic inflammation leads to diabetes, cancer, high blood pressure
and heart disease.

STRONG MEDICINE TACTICS:

Stress reduction is crucial to improving your gut health and will help
prevent chronic disease. Use the stress reduction techniques in the
Chronic Stress chapter.

TRIGGER #3. DYSBIOSIS: CHAOS IN THE GUT “ZOO”

“This consortium of bacteria contains tenfold more cells than the human
body, 100 times the number of genes than the human genome, and has the
metabolic capacity of the human liver.”

The quote above is from an article published in 2009 from a very

prestigious scientific journal, describing the bacteria that live in our gut.
We have known for a long time that vast amounts of bacteria call our gut
home, but we are only recently beginning to learn the profound effect they
have on our health.

The gut really is a “zoo” in the truest sense of the word:

• There are approximately 100 trillion bacteria in our intestines.

• There are approximately 1,000 separate bacterial species capable of

colonizing the human intestinal tract.

• At any one time, a healthy adult has 150 to 200 of these bacterial
species inside them.

• Which specific species are present depends on the human host’s

environment. A study has recently shown that gut bacteria species in
children from rural African communities are very different from the
species found in European city dwellers.

Just as a large diversity of species is good for our planet’s ecosystem, a

large diversity of bacterial species has been shown to be an indicator of
good health in humans. In fact there has been shown to be a direct
correlation with loss of gut bacteria diversity and poor health. Sickly and
obese people have fewer types of bacteria in their guts than healthy people.

DIGGING DEEPER:
What is a Microbiome?
Many of us have heard the term, human genome. Our genome is
simply the total collection of our genes. We each have approximately
20,000 different genes. Each gene represents a message encoded in
our DNA that when activated, produces a protein of a specific structure
and function. These proteins include—among other things—
hormones, enzymes, signaling and structural proteins. The metabolic
“machinery” in humans is also made from these proteins encoded by
DNA. The machinery that creates (and breaks down) carbohydrates,
protein, and fat, are all made from specific genes.

The gut bacteria microbiome, is simply the total amount of different

genes found among the bacteria that live in our intestinal tract. There is
a key difference between the human genome and the gut bacteria
microbiome:
• The human genome completely resides within a single organism—a
human.
• The gut bacteria microbiome is comprised of separate genes in each
species of bacteria. When we group the species of bacteria together
(150-200 species in our guts), we then get the total collection of
genes known as the microbiome from the populations of separate
bacterial species.

You and I can have different species of bacteria present in our gut
“zoo”, but our gut microbiomes can still be similar to one another,
because similar genes will be present in a diverse population of
separate bacterial species.

This is why high diversity (many different types) of gut bacteria is

important. Sick and obese people have less species, and this lower
diversity means that the microbiome in these people is probably
lacking some bacterial genes that are important to the person’s health.
So now when we refer to the microbiome, you know what we are
talking about.
FROM CRADLE TO GRAVE
When you were still in your mother’s womb, your insides were a sterile
place, free of any bacteria. Bacteria began to colonize your gut during and
after the birthing process. Recent science suggests that the time during and
immediately after birth is crucial for development of a diverse population
of bacteria. Certain practices in Western society affect this process with
potentially profoundly negative health consequences.

The results of a study in the Netherlands published in 2006 showed that

the specific gut bacterial species found in infants depended on a number of
factors including: gestational age (how long the fetus was carried in the
mother before delivery), type of delivery (C-section vs. vaginal), location of
delivery (hospital vs. home), type of feeding (breast milk vs. formula), and
antibiotic use.

The results showed that infants born at home and breastfed exclusively,
showed the highest amount of beneficial gut bacteria and the lowest
amount of potentially pathogenic bacteria.

Hospitals are certainly appropriate places to monitor delivery of

pregnancies. Formula feeding is sometimes the only option and C-sections
can be lifesaving. That said, it seems whenever possible and safe, “natural”
birth environments and processes promote a healthy and diverse gut
bacteria population for the baby. Breastfeeding has been shown to be
especially beneficial in this regard.

It is thought that the gut bacteria population has matured to mirror that
of an adult by three years of age. The first few years of life are crucial for
forming a balanced gut bacteria population.

The early development of our immune system during infancy and

childhood is influenced by gut bacteria composition. Disruption to the
normal “balance” of gut bacteria may change the way our immune
systems develop, possibly leading to increased susceptibility to:
• Allergic disease such as asthma
• Autoimmune diseases such as type I diabetes

RESEARCH UPDATE:
Some scientists think that early in life, our gut bacteria may “program”
our metabolisms, helping determine whether we will develop
metabolic disorders such as obesity or type II diabetes. One scientist
suggests that we can help prevent obesity and diabetes in adulthood
by identifying and correcting gut bacteria imbalance in early childhood
and even during childbirth!
THE DELICATE BALANCE
It turns out that a balance exists
between bacteria species beneficial to our
health and those that are potentially
problematic. In medical lingo, we call the
latter “opportunistic pathogens.” They
don’t cause problems if there are enough
beneficial (good guy) bacteria around, but
if the population of good guys is reduced
for some reason, the opportunistic
pathogen bad guys will take over with chronic inflammation as the result.

THE HEALTH BENEFITS OF OUR “INTESTINAL

TENANTS”
The beneficial species of bacteria can do great things for us as long as
we treat them well.
• When we eat fermentable fiber—fibrous carbohydrate material
mainly from fruits and vegetables—the bacteria uses the fiber for
food, metabolizes it for us, and produces a “waste” product of anti-
inflammatory short-chain (SC) fats. Our colon uses SC fat as a
primary energy source. These SC fats are powerful and exceedingly
effective at reducing inflammation. Short-chain fat boosts the
immune system and has been shown to have anti-cancer properties.
• Our beneficial gut bacteria detoxify potentially harmful compounds
in our food and water.
• They prevent the overgrowth of infectious “pathogenic” bacteria.
• They are crucial for proper development of our immune system.
• They can help prevent insulin resistance and diabetes.
• Beneficial gut bacteria can even help protect against autoimmune
diseases.
DIGGING DEEPER:
T-Regulatory Cells and Gut Bacteria
New research has shown that beneficial gut bacteria provide the signal
for formation of new Treg cells (the “hippies”) in the gut. Remember
that the Treg cells keep the “assassin” T-cells in check, preventing
them from getting out of control and damaging our body tissues. The
beneficial gut bacteria need to be present in the proper balance to
keep the “assassins” and “hippies” in proper balance.

This signaling function to form new Treg cells by beneficial gut bacteria
may be behind the following findings in recent research:
• Beneficial gut bacteria have been shown to help prevent our immune
system from becoming overactive, thus preventing chronic
inflammatory disease.
• Specific types of beneficial gut bacteria may protect against
autoimmune disease, including inflammatory bowel diseases such as
ulcerative colitis and Crohn’s disease.
• People with inflammatory bowel diseases often show a loss of
certain types of beneficial gut bacteria.
• Beneficial strains of gut bacteria have been shown to help maintain
our intestinal barrier, protecting against chronic intestinal
permeability.
• Butyrate produced from fiber (vegetables and fruit) fermentation by
beneficial gut bacteria makes more Treg cells (“hippies”) to help
control inflammation.
RESEARCH UPDATE:
Deficiencies in beneficial gut bacteria lead to deficiencies in
Treg cells
Recent research has shown that deficiencies in Treg cell populations in
humans may predispose us to asthma, inflammatory bowel disease,
type I diabetes, and multiple sclerosis.

The importance of the balance between the “beneficial” gut bacteria

(green) and the opportunistic pathogens (red) is illustrated here. Certain
types of beneficial bacteria stimulate formation of the Treg “hippies”
while the pathogens stimulate formation of T-cell “assassins.”
Imbalance resulting in an overgrowth of pathogens is called dysbiosis.
 It can lead to too many assassins around which can cause chronic
inflammation. At the same time, too many hippies and not enough
assassins can lead to a poor immune response to an infection when
necessary. Just like real life, we need both the warriors and anti-war
protesters in balance so we do not go too far in either direction.

THE BALANCE DISRUPTED: DYSBIOSIS TAKES OVER...

The term “dysbiosis” refers to any altered state of normal bacteria
balance associated with disease. A feature common to all types of dysbiosis
is the loss of bacteria species diversity. We need balance between
“beneficial bacteria” and “opportunistic pathogens.”

TECHNICAL NOTE:
The definition of dysbiosis we are using is greatly simplified. Indeed,
recent research shows that there are significant differences in the
composition and balance of gut bacterial species between obese
individuals and non-obese and between diabetics and non-diabetics.
Classifying gut bacteria as “beneficial” or as “opportunistic pathogens”
is not as black and white in reality. We use this distinction to
communicate a concept, but it is important to note that some bacteria
associated with inflammation in the gut may not be “pathogenic” in
the technical sense. We are still classifying them under “opportunistic
pathogens” because they can promote inflammation and contribute to
chronic disease when the normal balance is disrupted, when there is a
loss of bacterial diversity, and in cases of intestinal permeability.
DYSBIOSIS HAS BEEN ASSOCIATED WITH NUMEROUS
DISEASES AND DISORDERS
• Autoimmune disorders (including inflammatory bowel disease)
• Allergic disease including asthma
• Irritable bowel syndrome
• Obesity
• Type II diabetes
• Colon cancer
• Fatty liver disease
• Atherosclerosis (heart and vascular disease)
• Acne (not surprising, acne is an inflammatory condition)

Dysbiosis—the opportunistic pathogens

outnumber beneficial gut bacteria. This leads
to an imbalance between “hippie” Treg cells
and “assassin” T-cells. With more assassins
around, we are more prone to out-of-control
inflammation and autoimmune disease.
There are not enough hippies to balance the
assassins.

WHAT CAUSES DYSBIOSIS?

The shift to dysbiosis has been associated with multiple factors, but the
primary influence on gut bacteria populations seems to be diet, with
environmental exposures such as antibiotic use also contributing.

“Diet is the most powerful influence on gut microbial communities in

healthy human subjects” —Stig Bengmark (2012)

Evidence is mounting that processed foods containing large amounts of

flour, refined oils, and sugar may be a primary culprit in development of
dysbiosis. We are used to thinking about food in terms of carbs, fat, and
protein—the macronutrients. Diet books are best sellers and each
champions a diet strategy promoting one nutrient while damning another,
i.e. “low fat/high carb” or “high fat/low carb.”
 It is interesting that many traditional cultures eat a wide range of diets,
including high fat/low carb (the Inuit tribe) and high carb/low fat (the
Kitavans). These cultures have extremely low rates of “Western” diseases
such as diabetes, obesity, and heart disease, despite the large variability in
types and ratios of macronutrients.

When people from these cultures begin eating processed Western diets,
high in refined grains, sugar, and refined oils, they quickly lose their tribal
health and vitality. Obesity, formerly unheard of, becomes epidemic. The
tribal members eating “Western” succumb to “Western diseases”.

An intriguing hypothesis was put forward recently in the scientific

literature by Dr. Ian Spreadbury. He suggests that processed grain-based
carbohydrate foods affect gut bacteria very differently than natural, non-
processed “whole food” carbohydrate sources, such as root tubers (sweet
potatoes,) stem tubers (potatoes) and fruit. Dr. Spreadbury suggests that
the carbohydrate density of a food is important to how our population of
gut bacteria respond.

If you are having a hard time conceptualizing density, think of how

many people are in one square mile in rural Montana versus a square
mile in New York City. As far as carbohydrate density, tubers and fruit
are more like Montana, while processed grain foods are like New York
City.

Dr. Spreadbury suggests that high-density carbohydrate foods promote

dysbiosis, the overgrowth of specific inflammation-promoting gut bacteria.
He further suggests that once this type of dysbiosis has been cultivated and
takes root, high dietary fat intake (especially refined oils, corn oil,
vegetable oil) promotes further inflammation. This suggests that the fat
intake in the diet may only become harmful if processed grain foods are
eaten. For promoting dysbiosis, the worst dietary sin would be combining
lots of processed grain-based foods with lots of refined dietary fat. This
combination describes the composition of most fast food.
 Do not worry about eating tubers, vegetables, and fruit. These foods
contain high amounts of “fermentable fiber.” They are excellent food
choices, containing the type of fiber our beneficial gut bacteria use for fuel.

These foods will not lead to dysbiosis because the “waste” product of
fiber fermentation is short-chain fatty acids (SCFA). Butyrate, propionate,
and acetate are all SCFAs that are anti-inflammatory and have numerous
health benefits, including promoting the growth of beneficial gut bacteria.

FERMENTABLE FIBER AND GUT HEALTH: FIRST

PRINCIPLES
Current scientific thought—eating foods high in fermentable fiber
encourages the growth of beneficial bacterial species in our guts,
helping maintain the balance. “Western” processed food, largely
devoid of fermentable fiber, encourages the growth of opportunistic
pathogens leading to dysbiosis. This hypothesis of processed food
leading to dysbiosis makes sense for many reasons:
• There are several examples of traditional
cultures eating no processed food, but
otherwise a relatively high fat diet without
apparent health consequences.
• Processed, grain-based high-density
carbohydrates coupled with refined oils and
fats is the definition of the health-killing
“Western Diet.”
• Several traditional cultures eat a diet high in unprocessed
carbohydrates from tubers such as sweet potatoes without
succumbing to metabolic diseases such as obesity or diabetes.

Here again we see the trend of “food quality,” not ratios of carbs or
fat, being crucial for health. Real food trumps processed food every
time.
STRONG MEDICINE TACTICS:
To prevent dysbiosisrelated diseases such as type II diabetes, fatty liver
disease, and obesity, cut out processed, grain-based high-density
carbohydrates, and replace them with low-density carbohydrates like
vegetables, tubers and fruit.

DIGGING DEEPER:
The Link Between Obesity, Diabetes, Atherosclerosis, and
Fatty Liver Disease?
One of the ways microbiologists group some bacteria is by how well
they absorb a special type of dye—a Gram stain—in their cell walls
when viewed under a microscope. Gram-positive bacteria take up the
stain well and look purple in color under the microscope. Gram-
negative bacteria do not take up the stain, and have a light pink color.
Gram-negative bacteria have an outer membrane surrounding their cell
wall, which prevents the stain from coloring the cell wall.

Gram-negative bacteria have something called lipopolysaccharide

(LPS) in their outer membrane. LPS is also known as a bacterial
“endotoxin”. When LPS gets through our intestinal barrier and into the
blood stream, our immune system goes crazy and produces a large
inflammatory response. This is called endotoxemia. Also the epithelial
cells lining our gut have a system to recognize LPS. When LPS is
 recognized either in the blood stream by immune cells or in the gut
wall, inflammation is the result.

People with type II diabetes, fatty liver disease, and obesity have been
shown to have a greater proportion of Gram-negative bacteria in their
gut (dysbiosis), and thus more LPS than healthy individuals. It is
probably no coincidence that many type II diabetics are overweight or
obese, have fatty liver, and accelerated atherosclerosis.

In fact, there is a hypothesis that is strongly supported by recent

research that links chronic low levels of LPS in the bloodstream
(chronic endotoxemia) with Type II diabetes, obesity, atherosclerosis
and fatty liver disease. Scientists suggest that constant low levels of
LPS are getting into the bloodstream from chronic intestinal
permeability.

“After millions of years of co-evolution, have societal advances

paradoxically and adversely affected human health by reducing our
exposure to health-promoting bacteria?”

The quote above is from a study published in 2009 and brings to light
another possibility for a dietary source of dysbiosis. Many people in
modern society have been “sheltered” from exposure to bacteria in our
food starting early in childhood. Our modern foods have been largely
sterilized compared to traditional cultures. There are a variety of
potentially beneficial bacteria present in naturally grown fruits and
vegetables. Traditionally these vegetables are an early source of beneficial
bacteria in our diets.

We have become obsessed with food hygiene as we have modernized,

and for good reason. Our modern large-scale farming and distribution
methods have led to frequent contamination of our food supply by
pathogenic bacteria. News stories about salmonella contamination of
produce or E. coli in meat are common. A recent study showed significant
differences in gut bacteria found in rural African children versus those in a
group of city-dwelling European children. The African children had a large
and diverse population of beneficial gut bacteria able to ferment fiber,
while the European kids showed decreased diversity and small amounts of
beneficial gut bacteria. A sanitized food supply in Europe was thought to
be one of factors accounting for this difference.

ANTIBIOTIC USE: A DOUBLE EDGED SWORD

Another potential contributor to dysbiosis is the use of antibiotics. The
discovery and widespread medical use of antibiotics in the 20th century
has saved countless lives. Use of these wonder drugs has become incredibly
common in recent years. Some argue that though they are clearly effective
and beneficial, in many circumstances, antibiotics may have unintended
health consequences.

Antibiotic use significantly alters the balance of your gut bacteria, and in
some cases leads to dysbiosis. The main job of antibiotics is to kill bacteria
that are causing infections; unfortunately beneficial bacteria are mowed
down in the process—like innocent bystanders killed in a gang drive-by
shootout. Killing beneficial bacteria leads to imbalance and dysbiosis.

It is often the opportunistic pathogens that are resistant to antibiotics.

Left to fester, dysbiosis spins out of control, and left unchecked leads to
chronic inflammation. Pseudomembranous colitis occurs when antibiotics
kill beneficial bacteria, leading to overgrowth of an opportunistic pathogen
known as Clostridium difficile (CD). CD overgrowth leads to
inflammation of the colon and diarrhea.

Pseudomembranous colitis is an extreme example of dysbiosis caused by

antibiotics. Recent science has shown that antibiotic use generally results in
significant changes in bacterial balance; the clinical significance of this
change is unclear. We know that antibiotic use changes the composition of
gut bacteria, but we have not studied it long enough to determine how or if
it affects your health. Disrupting gut bacteria equilibrium with frequent
antibiotic doses is likely to have unintended consequences.
 RESEARCH UPDATE:
A new article in the journal, Pediatrics, has started to illustrate these
unintended consequences. The study found that while following a
group of 464 children for 15 years, the children who received courses of
antibiotics early in childhood had a significantly higher risk for
developing inflammatory bowel disease (IBD) as they got older. The
authors correctly state that other factors are involved in developing
IBD, but early antibiotic use clearly seems to be a significant factor.

The following is clear from current research:

• A single course of broad-spectrum antibiotics (those that kill a wide

variety of types of bacteria) causes changes in gut bacteria
populations lasting from three months to two full years.

• Combination antibiotic therapy, as used to treat Helicobacter pylori

infections (a cause of stomach ulcers), has been shown to alter gut
bacteria populations for up to four years after treatment in extreme
cases.

• Widespread antibiotic use is creating strains of bacteria resistant to

current antibiotic treatment.

Many people go to their doctor’s office demanding antibiotics for

relatively minor maladies such as upper respiratory infections. A significant
number of these patients are successful in getting their doctor to prescribe
antibiotics, even though the majority of upper respiratory infections are
due to viruses unaffected by antibiotics.

Frequent and inappropriate use of antibiotics may end up contributing

to long-term health problems from the impact on
beneficial gut bacteria. Not to mention, it creates
problems for the rest of us by developing resistant
strains of bacteria.

We also unintentionally get low levels of antibiotics

from environmental sources such as meat and dairy
from feedlot animals. Eighty percent of all antibiotics
sold in the U.S. are currently used for chickens, cows,
and pigs to prevent infection in the crowded
environments in which they are raised. Many of these
antibiotics eventually find their way to your dinner Antibiotic source?
table, and most are not destroyed in the cooking
process.

Some studies have even found antibiotics in produce such as lettuce,

carrots, and potatoes grown in fields treated with manure-fertilizer from
antibiotic-treated animals. It is currently unclear how these sources of
antibiotics affect gut bacteria and human health, but it seems logical to do
your best to avoid them if possible.

Knowing where your food comes from is the best way to start. Choose
locally grown organic produce and choose meat from pastured animals,
free from antibiotics.

STRONG MEDICINE TACTICS:

To prevent dysbiosis and antibiotic resistance, avoid frequent
treatment with antibiotics for minor conditions.

Also choose meat and produce that is free from antibiotics by

demanding organic, pastured, and locally grown food.
“Let food be thy medicine and medicine be thy food”

—Hippocrates

The best way to restore bacterial balance is through diet. First and
foremost—avoid processed food. For people with dysbiosis (and gut
inflammation) consumption of probiotics in fermented foods has been
found to be extremely beneficial. The treatment of disease with probiotics
is a hot topic in current medical research and deserves further discussion.
PROBIOTICS AND FERMENTED FOODS
The World Health Organization defines probiotics as, “Live
microorganisms which, when administered in adequate amounts, confer a
health benefit on the host.” Fermented foods containing live
microorganisms (such as yeast and bacteria) have been part of traditional
diets for thousands of years. It has been known for 150 years that the
bacteria and yeast in fermented foods are responsible for chemical changes
that result in health benefits.

Fermentation is defined as a biochemical change in carbohydrates—

microorganisms such as yeast, bacteria or mold use the carbohydrate for
food. The microorganisms metabolize carbs and create “waste products.”
Beneficial gut bacteria transforms fiber into short-chain fatty acids and
these short-chain fat “waste products” (from bacterial fermentation of
vegetable and fruit fiber) are crucial for the overall health of our intestinal
tract.

The product of microorganism fermentation most us are most familiar

with is alcohol. Alcohol is the waste product from yeast fermenting sugars.
Alcohol is not considered a probiotic because the yeast is filtered out of
alcoholic beverages before consuming.

For thousands of years, traditional tribal cultures have made fermented

foods from vegetables, fruit and dairy products. These primal tribesmen
were not concerned one wit about health benefits—fermentation allowed
foods to be stored for later consumption in the hard winter months.
Fermented foods can be stored for years: Korean kimchi is aged like wine.
Fermented foods are always widespread when refrigeration is not common
or available. Fermented foods are still regularly part of millions of people’s
daily diets worldwide.

The medicinal and health benefits of fermented foods were recognized

by ancient cultures and used as medicine. With the advent of industrial
food processing, modern society has relegated fermented foods to the trash
heap. Recently there has been a resurgence in interest in fermented foods,
driven largely by research into the health benefits of probiotics.

The supplement industry has discovered probiotics and is attempting to

commercialize and popularize their usage. This is yet another example of
inappropriate reductionism. The supplement industry grows bacteria
species thought to be beneficial, isolates and processes them, puts the
anemic concoction into a capsule, then makes exaggerated claims for the
product. Traditional cultures obtained these beneficial bacteria in their
diets—not from a pill—in the form of fermented foods.

The most common beneficial bacteria species found in traditional

fermented foods produce lactic acid as a waste product during the
fermentation process. Using this type of bacteria for fermentation is thus
called lacto-fermentation, or lactic acid fermentation. Lacto-fermentation
is used on a wide variety of fruits, vegetables, and dairy products to
produce fermented foods.

LACTO-FERMENTATION
There are vast amounts of bacteria that
naturally make their homes on vegetables and
fruit. Even with a thorough washing, bacteria
clings to produce in large numbers. We all have
seen fruits and vegetables “go bad” quickly or
spoil if left out in the air at room temperature for
a period of time. The produce will stay fresh
longer in the refrigerator, but decomposition and
rot are inevitable. Fruits and vegetables
decompose because of bacteria. Surface bacteria
begin to quickly break down the host when left
exposed to oxygen at room temperature.
Lacto-Fermented Escabeche (jalapeño, sweet peppers, carrots, onions,
garlic). www.thenourishinggourmet.com

Lacto-fermentation works because the lactic-acid-producing bacteria on

the fruits and vegetables thrive in the following conditions:
 • In an acidic environment

• In the presence of relatively high salt concentrations

• Without the presence of oxygen

DO IT YOURSELF!
To start the fermentation process,
vegetables and/or fruit are placed in
a container and filled with water to
ensure no air is present. Salt is added
and the container is left in a dark
place with the temperature between
68 and 72 degrees. This environment
encourages the growth of the lactic-
acid-producing beneficial bacteria. As these bacteria multiply, they
start to use the vegetables and fruit as a fuel source and give off lactic
acid as a waste product (this is the fermentation process). The lactic
acid reduces the pH of the surrounding fluid, making it more acidic. The
other bacteria present (the ones involved in the rotting process) die
because they are not able to survive the high salt and acidic
environment. This leaves the lactic-acid-producing bacteria alone to
continue the fermentation process until the lactic acid builds up
enough to slow their growth. The resulting fermented vegetables and
fruit now can be stored for long periods of time because the high acid
and salt content prevent the decomposing (rotting) bacteria from
growing.

Health benefits of lacto-fermented fruits and vegetables:

• Increased vitamin content—lacto-fermenting bacteria concentrate

large amounts of vitamins (especially B vitamins) during the
fermentation process.
 • Better digestibility: fermentation breaks down the indigestible parts of
plants, allowing humans to utilize them. Many traditional cultures
use fermented foods to wean young children from breast-feeding.

• Removal of natural plant toxins and anti-nutrients: many plants have

their own defense mechanisms to prevent them from being eaten. The
process of fermentation breaks down many of these defensive toxins
and anti-nutrients, leaving the plants safe to eat.

QUICK DEFINITION:
Anti-nutrients are compounds found in many plants that bind to
nutrients such as vitamins and minerals. This binding process prevents
us from absorbing these beneficial nutrients when we eat the plant.
Fermentation destroys many of these anti-nutrient compounds
allowing us to better absorb the vitamins and minerals found in the
plant.

LACTO-FERMENTING BACTERIA AND OUR HEALTH

Recent science has shown that lacto-fermenting bacteria are extremely
beneficial to our health. These bacteria shore up our immune system.

• Lactic acid fermenting bacteria (Lactobacillus) have been shown to

directly induce formation of Treg cells in the gut. Treg cells (the
“hippies”) control the “assassins” and reduce inflammation.

• Lactic acid fermenting bacteria increase tight junction formation in

the intestinal epithelial cells and reduce intestinal permeability. They
also were found to protect the tight junctions from further
disruption.
 It is now thought that the lactic acid fermenting bacterial species from
fermented foods do not stay in the gut as long as previously thought. We
used to think that these probiotics “repopulated” the gut bacteria directly.
Current science seems to show that most of them just “pass through” but
still exert considerable beneficial effects on our immune system and health.
This is why regular consumption of fermented foods is necessary. This may
partially explain the fact that most cultures still eating fermented foods as
a regular part of their traditional diets are free from chronic inflammatory
diseases such as heart disease and diabetes.

The best way to restore the “balance” in your gut bacteria is primarily
through eating foods with plenty of fiber such as fruits and vegetables.
These types of foods provide a fuel source, and encourage the growth and
reproduction of beneficial bacteria living in your gut. Lacto-fermented
fruits and vegetables not only provide an anti-inflammatory effect from the
probiotic lactic acid fermenting bacteria in the food, but the food itself
helps the beneficial bacteria that are already in your gut multiply. Thus,
taking probiotics in a pill only gives you half of the solution to
dysbiosisrelated inflammation.

Specific preparation methods for

fermented foods are beyond the scope of
this book. There are several excellent
resources in books and on the internet. A
comprehensive book on the subject is The
Art of Fermentation by Sandor Katz and
for beginners, Cultured: Making Health
Fermented Foods at Home by Kevin
Gianni. Both are highly recommended. Go
try some kimchi!

STRONG MEDICINE TACTICS:

Eat fermented food 2-3 times per week to control intestinal
 Eat fermented food 2-3 times per week to control intestinal
permeability, inflammation of the gut, balance the immune system,
and improve digestion.

THE GUT-BRAIN-BACTERIA TRIUMVIRATE: WHO’S IN CHARGE?

Recent research indicates that bacteria may influence our mood and
behavior. The idea that mute bacteria living within us can affect our
behavior is, well, strange. In the last several years, some intriguing research
(in animals) has shown that specific bacteria can measurably change levels
of anxiety and alter responses to stress.

Scientists have shown that anxiety-related behaviors were increased in

mice when they were given small doses of “opportunistic” pathogen-type
bacteria. They also showed that when given certain probiotic strains of
beneficial bacteria, the mice’s anxiety levels plummeted. Researchers have
shown that alterations in the normal gut bacteria in young mice left them
with exaggerated responses to stressful events later in life as adults.

Our brain and “second-brain” (enteric nervous system) communicate

through the vagus nerve—our internal communication “super highway”.
We also know that our gut bacteria can directly affect and change the
function of our enteric nervous system via intestinal permeability and
dysbiosis. Our enteric nervous system communicates these changes to our
brain (primarily) through the vagus nerve.

Somehow this complex organic communication system is able to

differentiate “good” from “bad” bacteria and sends signals to decrease or
increase anxiety states in the brain.
 FIRST PRINCIPLES PERSPECTIVE
An overgrowth of opportunistic pathogen-type bacteria could be
considered a “threat” to the body. No matter the source, our brain
responds to “threats” (any potentially dangerous situations) by
stimulating our “flight or fight” sympathetic nervous system. Increasing
our “flight or fight” system can certainly increase anxiety. Think about
narrowly avoiding a car accident or being confronted by a dangerous
wild animal. These two examples are external threats and produce
large flight or fight responses compared to comparatively minor
“threats” such as increased bacterial pathogens in our gut. But a minor
threat to the body that happens chronically every day can constantly
keep the brain in a low state of flight or fight. Over time, this constant
low-level “threat” response can lead to negative effects in the brain
and body.

We know that chronic stress can lead to anxiety and depression, so

given our discussion above, it is not far fetched to consider that
imbalances in gut bacteria (a low level chronic stress) may contribute
to mental health problems.

Interestingly, an alternative (FDA-approved) treatment for intractable

depression is vagus nerve stimulation. As gut bacteria can stimulate the
vagus nerve pathway, it is plausible that there could be a connection
between gut bacteria composition and mood disorders like depression.

RESEARCH UPDATE:
A recent study from 2011 provided early evidence that probiotics
improved anxiety and mood within 30 days of use. More research
 improved anxiety and mood within 30 days of use. More research
needs to be performed, but these results are very interesting.

In addition to communicating with the brain through the vagus nerve,

intestinal bacteria may also affect several hormones that act directly on the
brain to regulate appetite, the sleep/wake cycle, memory retention and
metabolism. These hormones include leptin, ghrelin, gastrin, orexin, and
many others.

Recent work by a French research team has shown that our immune
system produces “auto-antibodies” that actively work against some of
these hormones.

QUICK DEFINITION:
Autoantibodies are antibodies produced by our adaptive immune
system (assassins) against our own tissues. See our discussion on
autoimmunity for more on this.

The team of researchers hypothesized that these auto-antibodies are

produced by our immune system in response to “signals” sent by specific
gut bacteria. The signaling mechanism is thought to be “molecular
mimicry.” Molecular mimicry is when a certain protein sequence found in
bacteria is chemically similar to a protein sequence found in our own
tissues. The immune system recognizes the bacterial protein sequence and
produces antibodies for defense against the bacteria.

The problem is that these antibodies will also bind to tissues in our body
(in this case the hormones) that have a similar protein sequence as the
bacteria. By binding to the hormones inappropriately, these antibodies
(now called auto-antibodies) can affect the way the hormones deliver their
messages to the brain. Depending on the hormone affected, signals for
functions like hunger, sleep, and mood can be altered by these auto-
antibodies. The resulting hormonal chaos contributes to inappropriate
eating behavior, sleep disturbances, and depression.

The composition of gut bacteria influences what type of auto-antibodies

are produced by the immune system and what hormones are affected.

These ideas are relatively new and more investigation is needed before
jumping to any conclusions, but they were included here to illustrate
another way bacteria may profoundly influence our health and behaviors.
Basic physiologic processes like sleep, hunger and mood are regulated by
chemical-signaling hormones in the brain. Anything that can alter these
processes (such as gut bacteria) will affect how the brain functions.

Based on recent science, the idea that our gut bacteria can affect our
outward behavior may not be as far-fetched as it once seemed. One more
reason to hedge your bets and follow the Strong Medicine Defensive
Tactics in this chapter to prevent dysbiosis.
GUARDIAN AT THE GATE PART III
CONCLUSION

Chronic inflammation is a central cause of

diseases such as heart disease, high blood
pressure, diabetes, and cancer. We have shown
chronic intestinal permeability and gut
inflammation from a variety of sources is not
only a potential source of chronic inflammation,
but perhaps a necessary component for
developing and perpetuating autoimmune
diseases (such as type I diabetes).

Using the basic dietary

and lifestyle interventions
given in this chapter’s
Strong Medicine Defensive
Tactics can “break the
link” to chronic
inflammation in the gut
and the diseases and
conditions resulting from
it.


TYPE I DIABETES CASE STUDY

REVISITED
Let us resume our initial case study of the 6-year-
old with type I diabetes from the beginning of this
chapter. Although speculative, a rational way to
explain his fantastic results with a gluten free diet
is as follows:
• Gluten was likely triggering intestinal permeability.
• Chronic intestinal permeability was setting off his adaptive immune
response by exposing the immune system to “foreign” molecules
daily.
• His individual genetics left him predisposed to an “agitated” adaptive
immune system accidently targeting his own cells—in this case the
insulin producing cells in the pancreas—and started to destroy them.
Again we speculate, but it is plausible that he had dysbiosis, leaving
him with fewer Treg cell “hippies” to tame the out-of-control
immune response from the “assassins.”
• We know that proper gut bacteria balance is especially important to
the development of the immune system in infants and children.
• Removing the gluten trigger before all of his insulin-producing cells
were destroyed by the out-of-control immune attack allowed him to
recover. Without the gluten trigger, the vicious cycle of chronic
intestinal permeability and the resulting immune response stopped.
• His condition was caught and treated early enough to save sufficient
insulin-producing cells in his pancreas. He no longer needs insulin
injections.
Early intervention with a gluten free diet eliminated the problem
before it was too late. Most type I diabetics are not that lucky, and
the damage is already done by the time gluten sensitivity is caught.
In my opinion, there are no benefits in including gluten in a child’s
diet—and everything to gain by adhering to a gluten free diet at an
early age. Most children are not genetically predisposed to develop
type I diabetes, but is it worth the risk with your child?

COACH’S CORNER:
 Gut Health and Body Composition
If you are focused on fat loss and muscle gain, take heed. High cortisol
levels from the HPA-axis threat response promote fat gain and muscle
loss. Inflammation and oxidative stress in the gut are interpreted as a
threat by the brain, leading to activation of the cortisol producing HPA-
axis. Stopping the threat response by controlling inflammation in your
intestinal tract will improve your health, as well as accelerate your fat
loss and muscle building efforts.

Now that you have adequate training on the devastating health effects of
chronic gut inflammation, prepare yourself to learn about one of the most
powerful members of the “Pentaverate,” obesity.
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KNOWING YOUR ENEMY II
OBESITY: THE ENEMY WITHIN

A nuclear explosion is an uncontrolled chain reaction leading to a

devastating outcome. The obesity epidemic is an out of control chain
reaction that is devastating to both our health and healthcare system. By
contributing to creating a legion of people with chronic diseases, obesity is
also killing us economically.

Obesity and its resulting health consequences, may represent the single
biggest threat to 21st century public health.

Obesity transforms our fat cells into an “enemy within.” We will show
you how to reverse this transformation and stop the metabolic corruption
that ultimately results in a devastating assault on your body and brain.

The Strong Medicine Defensive Tactics learned in this section will repel
this assault and restore the flesh machine to state of optimum function. We
will overthrow the enemy within.
KNOWING YOUR ENEMY II
INTRODUCTION: A BIG FAT PROBLEM...
THE NEWEST MINORITY
A couple of years ago, I was preparing for job interviews after my time
in the military and needed to buy a new suit. For the previous 13 years, I
wore military uniforms for formal occasions and had not bought a
business suit in years. I went to a well-known men’s clothing store,
thinking it would be relatively easy to purchase a decent suit, without
spending a fortune on custom tailoring. I was wrong.

The salesman worked with me for more than 2 hours, trying on suit
after suit, before he said with a look of dismay, “Even with extensive
tailoring, I don’t have anything here that I can make fit you. There is just
too much extra material around the waist.” I was somewhat taken aback
by his statement. At the time, I had a 44-inch chest and a 32-inch waist—
hardly freakish proportions. He said there was too much of a difference
between my chest and waist size, making off-the-rack suit purchases
“impossible.”

He directed me to a competitor who carried a brand that was “athletic

cut” and which could probably be tailored to fit me. After spending an
entire day looking for a suit, I eventually found something to fit my
apparently “rare” proportions. I had no idea that my body type had
become a rarity, as I had been around military men and women—who
were far fitter than the general population—for more than a decade. I did
not truly grasp the extent of the obesity problem until my sheltered bubble
was burst while shopping for a suit.

The actual statistics for the proportion of U.S. adults that are overweight
or obese—almost 3/4ths of our population—are sobering. The remaining
1/4th of us who are not overweight or obese are the newest minority.
 Data compiled by the American Heart Association, 2013.

COSTS: HEALTH AND THE ECONOMY

Excess body fat ranges from overweight to obese to morbidly obese. The
health consequences mirror the individual’s degree of obesity. These
chronic diseases and poor health outcomes are inexorably linked to
obesity:

• Type II diabetes
• High blood pressure
• Heart disease
• Cancer

The current economic cost of obesity-related disease is estimated at over

$250 billion each year. By 2030, it is predicted that the health care costs
from obesity could rise to over $950 billion.

Obesity and chronic disease are linked very strongly since obesity is a
source of chronic inflammation and oxidative stress. We will present what
you can do to fight your own battle with obesity—and win.

QUICK FACT:
Health care costs related to obesity could reach as high as $950 billion
per year by 2030.
TECHNICAL NOTE:
Someone is defined as overweight or obese by an indictor called the
body mass index (BMI). BMI is calculated using a person’s height and
weight:

BMI = mass(kg) / height(m))2 Metric version

BMI = mass(lbs) / height(1n))2 X703 English version

There are several online BMI calculators on the internet, which will
automatically calculate the BMI from your height and weight
measurements.

A BMI from 25.0 to 29.9 indicates being overweight.

A BMI of 30 or over indicates obesity.

Many will correctly point out that lean,

muscular people may have a BMI in the
overweight range when they are not actually
overweight. For example, I am 5’9’ tall and
weigh 175 lbs. I am fairly lean—about 8-9%
body fat. My BMI is calculated as 25.8, which is
considered overweight even though I have
little body fat.

Lean individuals who carry more muscle mass

may find that the BMI is not the most accurate assessment. For the
general population, it is a decent measurement for being overweight or
obese. We will discuss some new body measurements that have
shown to be superior to BMI in the Analytics Section.
OBESITY: THE ENEMY WITHIN I
THE FAT CELL: DR. JEKYLL BECOMES
MR. HYDE

The fat cells, or adipocytes are the major storage sites for fat in the
body. We all have fat in our body, and we all need fat to survive.

QUICK DEFINITION:
The word adipocyte comes from: “adipo”= fat and “cyte”= cell.
Adipocyte literally means “fat cell.”
 Adipocytes do much more than just store fat. They provide crucial
signals to the brain regarding energy storage. These fat cells regulate
appetite, adjust metabolism and lower inflammation when they are
functioning properly.

When fat cells are stuffed to capacity from overeating, the adipocytes
undergo a metamorphosis from being benefactors of good health into
aggressive, bloated monsters spewing inflammation and oxidative stress.

How does a fat cell transform? Why does an excessive intake of

industrial, processed food and drink transform mild-mannered Dr. Jekyll
into evildoer Mr. Hyde? The following diagram (from the Central
Concepts chapter) shows chronic inflammation and oxidative stress
contributing to chronic diseases.

The over-stuffed adipocytes in an obese person are one source of chronic

inflammation and oxidative stress that “links” obesity to cancer, heart
disease, diabetes, and high blood pressure as well as accelerated aging and
neurodegeneration.
The “link” between obesity/insulin resistance and chronic disease.

THE METAMORPHOSIS OF A FAT CELL

The normal fat cell seeks to store excess energy in the form of
triglycerides—the storage form of fat. The adipocyte, functioning correctly
(as found in lean individuals) secretes an important hormone, adiponectin.
This little-known hormone performs several health-promoting functions:

• Decreases inflammation - adiponectin controls

inflammation caused by the immune system. It
decreases the number of inflammatory
cytokines, the messengers of inflammation.

• Increases insulin sensitivity - adiponectin

decreases levels of inflammatory cytokines. This allows insulin to do
 its intended job: pulling glucose into the cells to prevent a toxic
buildup of glucose in the blood stream.

• Increases fat burning for energy - adiponectin stimulates the

machinery that breaks down fat for energy.

The healthy adipocyte stores just the right amount of fat, and because it
is not overworked, it functions properly. When we eat food during the day,
we stockpile nutrients and have a good supply to use for energy while we
sleep. The healthy adipocyte produces high amounts of the beneficial
hormone adiponectin regularly.

When we take in more calories than we can

use for energy, the adipocyte starts to grow in
size. It swells to capacity as it tries to store
excess triglycerides. When excess dietary fat and
triglycerides made from extra glucose combine,
they overwhelm the storage and processing
capacity of the fat cells.

Now, the bloated adipocyte starts to attract the attention of the immune
system. The immune system exists to defend us from “threats” and the
bloated adipocyte has appeared on the immune radar as a potential health
threat. A very interesting process involving an immune cell called a
macrophage begins in our fat cells as they get jam-packed with fat.

QUICK DEFINITION:
Macrophage literally means “big thing that devours”. Macro = “big”
and phage = “thing that devours” (from Greek phagos).
 The macrophage is an “innate guardian” cell that “eats debris” when a
cell dies. Macrophages also fight invading bacteria and other foreign
material. A type of macrophage called an M2 macrophage “stands guard”
inside an adipocyte in case something bad happens.

When the adipocyte starts to swell with triglycerides (fat), the M2

macrophage senses a threat and goes on “alert,” then starts to arm itself
with weapons. Like prison guards who get assault rifles and tear gas ready
when they sense a riot may start, the M2 macrophage “arms” itself by
transforming into a deadly M1 macrophage. The M1 macrophage prepares
for battle by secreting inflammatory messengers called cytokines.

The swelling adipocyte, stuffed with

triglycerides triggers the
transformation of the M2
macrophage to the inflammation-
producing M1 version.

The adipocyte starts secreting inflammatory cytokines as a “911 call”

summoning immune reinforcements.

If more food is eaten—despite the fact that enough fat to fuel the body
for weeks may be available for energy—the normal cellular processes break
down.

Inside the swelling adipocyte fat cell, the

mitochondria work overtime and produce large
amounts of oxidative stress in the form of free
radicals. More of the M2 macrophages are
converted into the M1 variety, as the immune
system registers a “prison riot” in full swing
inside the swollen fat cell. Higher amounts of inflammatory cytokines are
sent into the bloodstream as the fat cell tries to protect itself from the
excess energy and resulting oxidative stress.

The immune system responds by sending in more soldiers, triggering and

increasing intense, prolonged and devastating inflammation. Stressed and
bloated adipocytes create obesity-related inflammation.
 Intense inflammation causes the fat cells to reduce secretion of the
beneficial hormone, adiponectin. Without the antiinflammatory effects of
adiponectin, the inflammatory momentum picks up even more steam.

The body considers fat deposited next to vital organs—the liver,

intestines, and blood vessels—as especially threatening. This is called
“visceral obesity,” as viscera means internal organs. People with visceral
obesity have the classic “apple shape” with the majority of the fat stored in
the abdominal cavity around the organs. This type of visceral obesity is
seen with the classic beer belly. People proudly sporting a beer belly often
brag that it is “hard as a rock” and not squishy like superficial fat. This is
the absolute worst type of fat and nothing to be proud of, as it is highly
inflammatory.

QUICK MEDICAL NOTE:

Visceral obesity (also called abdominal obesity or central obesity) is
highly associated with a variety of diseases related to inflammation:
• Type II diabetes
• Heart disease
• Fatty liver disease
• Cancer
• Alzheimer’s dementia
• Accelerated physical aging

Given what you now know about fat cell transformation and
inflammation, these associations should not be surprising.

The swollen adipocytes surrounding the vital organs in visceral obesity

are no longer recognizable as the innocent fat cells found in lean
 individuals. These monsters truly have become
Mr. Hyde. They spew forth massive amounts of
inflammatory cytokines into the rest of the body
like an oil rig fire. These beasts often end up
dying in their attempt to protect themselves,
leaving the M1 macrophages to clear their bodies
away. This dying and clearing process is also
highly inflammatory.

Recent research has shown that swollen fat cells can be a substantial
source of chronic inflammation and oxidative stress. As we mentioned at
the beginning of this section, the inflammation and oxidative stress
produced daily by these bloated fat cells is likely the link between obesity
and the chronic diseases of cancer, heart disease, diabetes, and high blood
pressure.

QUICK MEDICAL NOTE:

It was once thought that by adulthood, you had all of the fat cells
(adipocytes) you would ever have, and people got fatter only by over-
stuffing their existing fat cells in a process called hypertrophy.
Hypertrophy simply means “growing bigger”.

It turns out that an overweight or obese person can actually grow new
fat cells. This process is called hyperplasia. People can increase their
fat mass by storing fat in existing fat cells (hypertrophy) AND by
producing new fat cells (hyperplasia).

Drawing on the ideas from the Central Concepts chapter, obesity can be
viewed as a process of allostasis—trying to achieve stability in a changing
environment. In this case, your body attempts to adapt to the
environmental stimulus of overeating. It increases your fat storage as a
protective mechanism to keep high levels of damaging glucose and certain
fats (palmitate) out of your bloodstream. Over time, this protective
mechanism becomes problematic, causing excessive inflammation and
contributing to disease. The diseases caused by this process can be viewed
as part of allostatic overload, or the body’s failure to adapt (long-term) to
an environmental stress such as overeating.

The following sections will cover obesity’s contribution to chronic

diseases, including an appropriately detailed discussion of diabetes, given
its current impact on public health.
OBESITY: THE ENEMY WITHIN II
THE PLAGUE OF “DIABESITY”

Obesity and type 2 diabetes (T2D) have a powerfully negative

relationship. Obesity and T2D occur together so often, that amongst
medical professionals the combined affliction is often referred to as
“Diabesity.” Diabetes + Obesity = Diabesity.

Massive public health campaigns, an increased focus on diabetes

prevention, and diabetes management in clinical settings have not been
able to turn the tide. The evil combo of diabesity is a health Armageddon
—a literal tsunami leaving death and destruction strewn in its wake. The
statistics for T2D are disturbing evidence that we are losing this fight.
According to the latest update from the American Diabetes Association
(2013), 26 million people in the US have diabetes, and an additional 79
million people are prediabetic.

• The economic cost of diabetes has risen to $245 billion per year in the
US alone.
 • If current trends continue, it is estimated that one in three adults will
have diabetes by the year 2050.

Although we know a genetic component contributes to a person’s risk

for developing diabetes, genetics do not account for the dramatic increase
in diabetes over the past half-century.

The massive increase in T2D is parallel to a radical change in our daily

environment—degradation of food quality, lack of physical activity,
increased stress, and detrimental habits. Recent science reveals epigenetic
changes—the way environmental signals turn our genes on and off—are at
the center of the T2D epidemic. Borrowing from our earlier analogy in
Basic Training (Central Themes), we are “bookmarking” recipes that
wreck our metabolism long-term.

RESEARCH UPDATE:
Recent research has shown that exposure to high amounts of glucose
in utero (in the womb)—as in gestational diabetes—will produce
epigenetic changes making the fetus much more likely to develop T2D
as an adult. Even our earliest environment (the womb) affects our
epigenetics and life-long health.

Epigenetic changes produced by the modern environment predispose us

to disaster. Left unchecked, the metabolism “breaks”—the smooth
efficiency of a normal metabolism is shattered. When a healthy adipocyte
turns into a bloated monster of a fat cell, massive amounts of
inflammation and oxidative stress are produced. These two culprits are
largely responsible for the loss of insulin sensitivity that leads to T2D over
time.
 Inflammation and oxidative stress cause a loss of insulin sensitivity in
two main ways:

1. Inflammatory cytokines (in this case from adipocytes) “break” the

signaling mechanism of the insulin receptor. The doorbell ringer on
the “door” to the cell is an insulin receptor, a protein on the surface
of the cell to which insulin can “dock.”

When insulin docks to the insulin receptor, it “rings a doorbell” on the

cell. Usually, a special kind of door called a glucose transporter opens and
allows glucose into the cell from the bloodstream. The inflammatory
cytokines “short-circuit” the insulin receptor. Once the insulin receptor is
short-circuited, insulin can still normally bind to the receptor, but the
signal to open the glucose door does not get through. More and more
insulin is required by the malfunctioning receptor over time. These
“broken” receptors will eventually require the pancreas to produce a tidal
wave of insulin to clear glucose from the bloodstream.

KEY POINT:
Inflammatory cytokines “short-circuit” the insulin receptor. This is one
of the primary ways inflammation causes loss of insulin sensitivity and
leads to T2D.

Your body doesn’t know how to fix the receptor, it just responds to the
problem by producing more insulin to “ring the doorbell harder.” Fixing
the problem requires stopping the chronic inflammation from the bloated
adipocyte-monster, not putting more insulin into the bloodstream.

The analogy is a doorbell with a short-circuit that someone keeps

hitting harder to ring—instead of just fixing it!
 Swollen adipocytes reduce beneficial secretions of adiponectin, the
inflammation-reducing hormone. Reduced adiponectin production leads to
increased numbers of inflammatory cytokines.
INSULIN SENSITIVE
The healthy adipocyte helps ensure insulin sensitivity by keeping
inflammation (inflammatory cytokines) low. The insulin receptor is sensitive
to the signal generated when insulin “docks” to the receptor.

This signal opens the “door” of the glucose transporter, allowing glucose into
the cells from the bloodstream. Glucose will not build up in the bloodstream,
and proper blood sugar levels will be maintained.
INSULIN RESISTANT
The bloated adipocyte “monster” spews forth inflammatory cytokines, which
“short-circuit” the insulin receptor. The insulin receptor is now resistant to
sending a signal to the glucose transporter when insulin docks to the
receptor.

The signal does not get through and the glucose transporter “door” remains
closed. Glucose can no longer enter the cell and builds up in the bloodstream.
As you become more insulin resistant, diabetes begins to develop. Chronic
inflammation drives diabetes. In this case, the bloated adipocyte is the source
of the inflammation.

2. Increased oxidative stress in the mitochondria. The second major way

obesity causes insulin resistance is through elevated stress levels in cell
energy factories. This cause of insulin resistance is similar to a smoke
detector sounding an alarm if your house catches fire. The overheated,
over-stressed mitochondria are simply overwhelmed by a flood of
food/fuel.

Mitochondrial energy factories produce ATP, the vital “energy

currency” generated from the fuel obtained from food. During normal
circumstances, we eat enough food to fuel our body’s requirements for
energy—but not so much that we overwhelm the capacity of our
mitochondria energy factories. We need to eat enough but not too much to
operate within mitochondrial limits and capacities. How do we determine
such a minute and finite thing as cellular fuel capacities? Sounds more like
a biophysics equation! In more earthy terms, it is similar to running your
car’s engine at low to moderate RPMs.
 DIGGING DEEPER:
What Exactly is a Cytokine?
We have referred to cytokines extensively in this section and in
“Immunology 101.” Cytokines are signaling molecules, carrying
messages from cell to cell throughout the body. Cytokines are best
known as messengers of the immune system. A very simplified way of
looking at cytokines is to classify them by the messages they carry.

As you might have guessed, inflammatory cytokines carry the message

of inflammation. Inflammatory cytokines are generated during
infections or injury, and signal the immune system to attack an invader
such as a foreign bacteria or virus, or to start the healing process in
response to an injury. As we have just seen in chronic diseases like
diabetes, inflammatory cytokines can also disrupt normal metabolic
“machinery” such as the insulin receptor. Oxidative stress can also
trigger inflammatory cytokines.

There are also antiinflammatory cytokines produced to keep the

immune system “in check” and to stop the inflammation response.
The Treg cells we discussed in Immunology 101 and the Gut Chapter
are examples of cells that produce antiinflammatory cytokines. The M2
macrophage also produces this type of cytokine.

Cytokines communicate the current “stress state” of the body between

cells and organs. In this way, the liver “knows” if there is an infection or
injury in the right leg because it is communicated by inflammatory
cytokine messengers.
It is important for the various organs to “know” what is happening in
other parts of the body so they can respond appropriately.
Cytokines allow this to happen.

Even running at safe and moderate RPMs, the mitochondria will

naturally—like a engine’s exhaust—produce free-radicals (oxidative stress).
As long as the free radical production is relatively low, our body’s
antioxidant systems can take care of this “green level” of oxidative stress.
 Eating just enough food to fuel your
energy requirements will keep your
“Mito-RPM” in the green.

If
you

consistently take in more fuel than your body needs by overeating, the
mitochondria factories go into overdrive trying to process the extra fuel.
The energy-producing machinery in the mitochondria will start to heat up
and produce high quantities of free radicals. Oxidative stress reaches “red”
danger levels. The increased oxidative stress starts to overwhelm the
antioxidant systems and triggers a stress response within the cell, similar to
a 911 “call for help.”

High oxidative stress triggers alarm systems within the cell when
“smoke” (free radicals) is detected from the overheating mitochondria. The
alarm system carries the message that something bad is happening in the
mitochondria, alerting the cell to damage from large amounts of free
radicals.

The absolute best way to stop a fire is to remove the fuel source, and
that is exactly what the cell tries to do. When we eat starches and other
glucose-containing carbohydrates, insulin is produced and docks to the
insulin receptor (ringing the doorbell). This signal would usually open the
glucose transporter (door), allowing glucose into the cell to be utilized for
energy production by the mitochondria. The cell tries to shut this door-
opening signal down to protect itself.
INSULIN RESISTANCE FROM THE INSIDE
When the “Mito-RPM” is in the red from processing too much fuel, the
overload of free radicals (oxidative stress) “turns off” the insulin receptor
signaling mechanism, which stops the glucose transporter from opening.
This removes the fuel source by stopping glucose from entering the cell.
The cell is trying to protect itself from too much fuel.

TECHNICAL NOTE:
The “nuts and bolts” of how insulin resistance actually happens on the
molecular level is an active area of research. We have just presented
simplified versions of two mechanisms supported by current research.

TAKE HOME MESSAGE:

A malfunctioning insulin receptor, broken by inflammatory cytokines
or oxidative stress in the mitochondria, is called insulin resistance (or
loss of insulin sensitivity). Insulin resistance will slow the entry of
glucose into the cells, allowing glucose to build up in the blood stream.

Any environmental stimulus that provokes long-term increases in

oxidative stress and inflammation will result in insulin resistance. This
also includes sleep deprivation and psychological stress.

As chronic inflammation and oxidative stress get worse, insulin

 As chronic inflammation and oxidative stress get worse, insulin
resistance gets worse, and blood sugar levels get higher, resulting in
type 2 diabetes.

CONSEQUENCES OF OBESITY AND CHRONIC

INSULIN RESISTANCE
Insulin is a storage hormone. Insulin’s job is to store glucose and fat
when food is plentiful. When the insulin signal is not transmitted to the cell
due to insulin resistance (the doorbell is broken) several things start to
happen simultaneously:

1. Stored fat in fat cells (adipocytes) starts to break down. In normal

circumstances, insulin signals the storage of excess energy as fat in
the adipocyte. Insulin usually signals the storage of fat and stops it
from breaking down. Since the insulin signal is interrupted because
of chronic inflammation and oxidative stress, the brakes are taken
off. Fat is released from the adipocyte into the bloodstream.

This release of fat is not a good thing, considering that there is no

place for this fat to go. The body already has a fuel excess at this
point and there is nowhere to “burn” the fat. The liver grabs the fat
from the bloodstream and transforms it into triglycerides before
placing it on a lipoprotein carrier circulating in the bloodstream
looking for a place to drop the fat. It is like an ever-growing group
of people riding a bus with no destination and no one ever gets off
the bus.

Instead of the fat getting stored in adipocytes as triglycerides, it is

aimlessly circulated in the bloodstream on lipoproteins. This
inevitably causes real problems. The trapped, endlessly circulating
triglycerides are the reason diabetics almost always have high
triglycerides when their doctor checks their blood-work.
 COMING ATTRACTIONS >>>
See the cholesterol section in the Analytics Chapter to learn how high
triglycerides in diabetes and metabolic syndrome can lead to heart and
vascular disease.

2. The liver “banker” starts making glucose.

When the insulin signal is not getting
through, the liver starts to do something
unthinkable—it starts making new glucose
(gluconeogenesis) and releasing it into the
bloodstream. The liver is pouring fuel on
the fire by making and releasing glucose
when the bloodstream is already highly
saturated with glucose. Adding fuel to the fire...

As far as the liver is concerned, the body is in a state of stress, and

the liver needs to ensure that the brain has adequate supplies of
glucose—especially when stressed. Insulin resistance “fools” the
liver into thinking that the body is starving and needs more glucose.

QUICK MEDICAL NOTE:

The anti-diabetic drug Metformin works by stopping gluconeogenesis
in the liver. Metformin helps stop this source of extra glucose in the
 blood, and decreases blood sugar levels.

3. Insulin resistance puts the pancreas in overdrive. When the insulin

signaling system is broken and glucose builds up in the blood, the
pancreas responds to its programming by producing more insulin.

Chronic inflammation and oxidative stress short-circuit the insulin

receptor “doorbell button” mechanism. The pancreas responds by
making more insulin (more doormen to hit the button).

Because the person will not change his or her lifestyle and eating
habits to decrease inflammation and oxidative stress, the body has
no choice but to produce more insulin. Unfortunately, producing
large amounts of insulin to cope with insulin resistance burns out
the pancreas over time. Eventually, the pancreas will fail and lose
the ability to produce insulin at all. A type II diabetic reaching this
stage will have major health problems. They need to take insulin at
higher and higher doses as their disease progresses.

DIGGING DEEPER:
Beta-Cell Failure in the Pancreas
The cells which produce insulin in the pancreas are called beta-cells.
They detect glucose and respond by producing insulin. As insulin
resistance develops from chronic inflammation and oxidative stress,
the beta-cells compensate by producing more insulin.

They can only compensate for so long, and the stress of constantly
producing high amounts of insulin will wear out the beta-cells. They
eventually break down and die, leaving fewer beta-cells to carry the
work-load of insulin secretion. When many beta-cells fail, the
 work-load of insulin secretion. When many beta-cells fail, the
remaining ones can no longer effectively compensate to keep blood
sugar in check. Then, blood sugar rises into diabetic levels, and things
just get worse as the process continues.

4. Muscle wasting occurs when our lean muscle mass starts to

disappear. Insulin resistance causes muscle wasting. Recent research
on muscle wasting—as it relates to obesity and diabetes—has
focused on a protein, myostatin. Myostatin’s function is to reduce
muscle mass by stopping muscle growth (myo= muscle; statin= stop
or inhibit).

Myostatin is secreted by muscle, and is thought to be the central

player in muscle loss associated with aging (sarcopenia).

A recent study has shown myostatin production is elevated in obese

and insulin resistant people. The horrific combination of chronic
inflammation and insulin resistance was found to increase
myostatin production levels. The elevation of myostatin is thought
to be a major contributor to the loss of muscle mass often seen in
severe cases of obesity and diabetes.

Obesity, insulin resistance, and diabetes act as “age-accelerators”

for loss of muscle mass. All humans lose muscle mass as we age, but
obese people and diabetic people experience muscle loss at an
accelerated rate. The body will break down its own muscle tissue to
strip it of amino acid content. The cannibalized amino acids will be
used to feed the now-deranged “liver-banker,” in its mad quest to
make more glucose when none is needed. In addition to muscle-
wasting myostatin secretion, the chronic inflammation associated
with obesity and diabetes directly contributes to muscle wasting.
Insulin stimulates building new protein, but the “building” signal is
not getting through. As insulin resistance increases, muscle building
grinds to a halt.
 KEY POINT:
Obesity, insulin resistance, and diabetes create a perfect storm for
muscle wasting.

FIRST PRINCIPLES-BASED SPECULATION:

MYOSTATIN
It makes sense that myostatin increases in cases of
insulin resistance from chronic inflammation. The
body is reacting to the “threat” of chronic
inflammation and insulin resistance much like it
reacts to the threat of starvation.

Myostatin is also elevated in times of starvation to

decrease muscle mass. From a survival perspective,
maintaining muscle mass has a very “expensive” energy cost. If the
body can decrease muscle mass, it will have more energy to keep the
brain going. We can survive with reduced muscle mass, but we don’t do
well without brain function. Insulin resistance and diabetes are
interpreted by the body as a state of starvation and/or stress—even
though plenty of fuel is available—and it will decrease muscle mass to
conserve energy for the brain.

5. Fat without a home... When the adipocytes (fat cells) are too full
and unable to store excess energy as fat, the liver and muscle will
start to retain some of it, simply because it has nowhere else to go.
Excess fat contributes to development of fatty liver disease. The fat
will also start to replace the muscle mass lost to myostatin.
 Large amounts of fat circulating in the bloodstream amplify the
inflammatory response and insulin resistance. Fat cells store a
significant amount of fat in the form of palmitate. In the Nutrition
101 section, we learned palmitate is a 16 carbon saturated fat that
gives saturated fat a bad name.

Palmitate is the primary fat liver cells make from excess glucose. When
palmitate is released into the bloodstream by malfunctioning fat cells or
when the liver produces it from large amounts of excess glucose, it
activates alarm systems normally reserved for detecting foreign invaders
such as bacteria.

The alarm system activated by palmitate ramps up the immune system

promoting increased inflammation, oxidative stress, and further increasing
insulin resistance. The fact that this specific saturated fat activates this
alarm system shows that large amounts of palmitate are a threat to the
body. High amounts of palmitate occur with obesity and insulin resistance
—your body is trying to protect itself!

The middle picture is an MRI cross section of a 74 year

old sedentary man’s thigh muscle. The view in the
pictures is the same as if the thigh was cut in half, and
we looked down at the stump.

You can see the fat (adipose) tissue surrounding the

shrinking muscle, as compared to the large muscle
mass in both of the pictures above and below. If you
are insulin resistant or diabetic, this process is
happening to you right now. If you are not exercising, this process will
happen even faster.

Unfortunately, many young diabetics are exhibiting the dramatically

decreased muscle mass associated with much older people.

PALMITATE—GIVING SATURATED FAT A BAD

NAME:
Without fail, almost every scientific study examining the effects of
saturated fat uses palmitate for testing—as if it were the only saturated
fat in existence. It is perplexing how very smart scientists continually
overlook this fact and in their research, generalize palmitate’s effects to
represent all saturated fat.

As previously stated, palmitate indeed has some bad effects on

metabolism and contributes to chronic disease. Of importance to this
chapter, please note that a significant amount of fat produced in the
liver from excess glucose and fructose in the obese and diabetic
person is specifically palmitate.

In high amounts, palmitate can wreak metabolic havoc:

• Palmitate causes inflammation, oxidative stress, and increases insulin
resistance.
• Palmitate decreases adiponectin secretion by fat cells, increasing
insulin resistance.
• Palmitate has been shown to increase inflammation in the
hypothalamus, which disrupts appetite regulation (causes hunger
when the body already has enough energy.)

Look back at the saturated fat section in Nutrition 101. Most saturated
fats have very beneficial effects, don’t judge them all by the actions of
palmitate.
 Remember that it is normal for low levels of palmitate to be stored in
healthy fat cells, and it does not cause any of the above problems.

6. Obesity and chronic insulin resistance increase the risk of cancer.

Cancer is not a single disease, like diabetes or heart disease. Each
type of cancer is very different, depending on the original cell type.
The triggers for cancer development are just as diverse. For
instance, liver cancers can be caused by infections, exposure to
chemicals, and chronic alcohol use. Since cancers come in many
different varieties, there is no one “cure for cancer.”

However, there are several characteristics that some—and in some cases

all—cancers have in common that are important to obesity, insulin
resistance, and diabetes:

• Cancerous cells show uncontrolled, aggressive cell growth and have

transformed from previously normal cells.

• Many cancer cells become dependent on glucose as their only source

of energy (called the “Warburg Effect”).

• Some cancers such as breast and endometrial cancer are sensitive to

estrogen.

• A common trigger for many cancers is chronic inflammation and

oxidative stress.

We’ll tackle these characteristics individually to show you why cancer

loves obesity, insulin resistance, and diabetes.

“Cancerous cells show uncontrolled and aggressive cell growth, and

have transformed from previously normal cells.”

Uncontrolled cell growth is the hallmark of all cancers. These cells no

longer respond to normal, healthy “check and balance” signals that
control growth and reproduction. Insulin resistance creates a “growth
favorable” environment. During insulin resistance, the pancreas responds
by producing more insulin. People with insulin resistance have relatively
high insulin levels all the time. Because insulin is a “growth, building, and
storage” hormone, the presence of high insulin levels helps cancer grow
out of control.

“Many cancer cells become dependent on glucose as their only source of

energy.”

Nobel prize winner Otto Warburg first described the phenomenon of

cancer cells switching their metabolism to only use glucose without the
need for energy production from mitochondria. At first glance, this does
not make sense, because much more energy can be generated if the
mitochondria finish burning glucose. (See Metabolism Basics.)

Most cancer cells only break glucose down to lactate, generating a paltry
2 ATP, compared to the 38 ATP they could get from glucose if they used
the mitochondria.

The area shaded in pink is the energy

pathway that cancer cells use, showing the
“Warburg Effect.” Only 2 ATP is generated
because the mitochondria are not used.

Scientific speculation holds that because

cancer cells are fast growing, they need
rapid energy production, and the
mitochondria take too long. The cancer cells don’t care if they are wasting
energy, they want fuel immediately and don’t care about sloppy
inefficiencies.

Cancer cells become the ultimate glucose hogs; a raging cancer cell will
burn through glucose 200 times faster than a normal cell. They are like
500-horsepower muscle cars that get 7 miles per gallon. They do not care
about fuel efficiency, they just go very fast. Normal cells are like Smart
Cars by comparison, they use glucose for fuel in a reasonable and highly
efficient way.
 The fact that cancer cells become dependent on glucose is important for
those with insulin resistance and diabetes:

• A diabetic’s high blood sugar levels give cancer cells a huge supply of
glucose to survive and thrive.

• Most cancer cells use glucose transporters (doors) that do not need to
be opened by insulin. The cells can scarf up large amounts of glucose
from the bloodstream without relying on insulin.

QUICK MEDICAL NOTE:

If some cancer cells are dependent on glucose through the Warburg
Effect, it would make sense that a low carbohydrate diet would be a
valuable part of treatment. Most cells in the body can use fat as an
energy source, so a low carbohydrate diet could potentially “starve”
and weaken the cancer cells that need glucose to survive, allowing
traditional treatments to be more effective. This could be a “one-two
punch,” weaken the cancer cells by starvation, then kill them with the
drugs.

For some reason, low carbohydrate diets have not seen widespread
use in the treatment of cancer. Recent research has shown some
promise using low carbohydrate (ketogenic) diets in conjunction with
 promise using low carbohydrate (ketogenic) diets in conjunction with
traditional cancer treatment. Widespread use of both therapies
together could potentially help save many lives.

If the specific cancer is dependent on glucose for energy, low

carbohydrate diets really have no potential negative side effects for
cancer patients. If you are newly diagnosed with cancer, discuss
starting a low carbohydrate diet with your doctor to see if it is
appropriate for your type of cancer.

STRONG MEDICINE TACTICS:

If you have cancer, discuss the use of a low carbohydrate or ketogenic
diet with your doctor as part of your treatment plan.

“Some cancers such as breast and endometrial cancer are sensitive to

estrogen.”

The point applies to obesity in general. Adipocytes (fat cells) produce an

enzyme called aromatase. Aromatase converts hormones such as
testosterone into estrogen. The more fat you have, the more aromatase
present, and the more estrogen you are producing (this also applies to
men).

Cancers such as endometrial cancer, and some breast cancers are

“estrogen sensitive.” This means estrogen can trigger them to grow. Losing
fat mass will reduce the amount of estrogen in your body, which may help
reduce the growth of breast and endometrial cancers.

If you attempt a fat-loss plan when you have one of these cancers, make
sure to discuss it with your doctor first.
 STRONG MEDICINE TACTICS:
Losing fat mass through a well-constructed weight loss plan may help
reduce the trigger for breast cancer and endometrial cancer growth.
Discuss this approach with your doctor as a potential part of your
treatment plan.

“One of the triggers for many cancers is chronic inflammation and

oxidative stress.”

As we have covered extensively, obesity is a disease which produces

chronic inflammation and oxidative stress. The inflammatory cytokines
produced by the bloated “monster” adipocytes are the same ones known
to trigger the development of several types of cancer. The constant barrage
of inflammatory cytokines from deranged fat cells encourages the survival,
growth, and spread of cancer cells.

The high levels of free radicals that accompany oxidative stress damage
DNA in normal cells. Under some circumstances, free radicals can
transform normal cells into cancer cells. This DNA damage caused by free
radicals, will mutate the normal cell into cancer.

Obesity, insulin resistance and diabetes are all inflammatory diseases

linked to an increased risk of cancer. Being highly inflamed is the ideal
cancer hothouse.

7. Obesity and chronic insulin resistance increase the risk of heart and
vascular disease.

Obesity and diabetes greatly increase your chances of heart and vascular
disease. The statistics for this association are frightening:
 • A diabetic is twice as likely to have a heart attack or stroke than a
non-diabetic.

• 66% of diabetics end up dying from a heart attack or stroke. Only

1/3 of diabetics die from other causes.

• A recent study showed that obese men had a 60% greater chance of
dying from a heart attack than non-obese men.

• Diabetics are up to four times as likely to have vascular disease in the

lower extremities (legs, feet) than non-diabetics.

• Diabetes also causes a type of heart failure called diabetic

cardiomyopathy.

• Diabetes leads to small blood vessel damage which causes nerve

damage and can lead to amputation.

These statistics are not surprising if you know that the main trigger for
heart and vascular disease is chronic inflammation and oxidative stress.
Obesity and diabetes are sources of chronic inflammation and oxidative
stress.

KEY POINT:
Heart and vascular disease are triggered primarily by chronic
inflammation and oxidative stress.
 COMING ATTRACTIONS >>>
The cholesterol section in the Analytics Chapter contains a thorough
discussion on why the cholesterol carriers (lipoproteins) directly cause
problems in heart and vascular disease, instead of cholesterol itself.

8. Obesity and chronic insulin resistance can lead to accelerated aging.

Chronic oxidative stress from obesity and insulin resistance/diabetes can

cause premature aging (accelerate the rate at which you age).
Dysfunctional mitochondria in the fat cells of obese and diabetic people
can produce large quantities of free radicals. These free radicals can
damage specific parts of DNA called telomeres. Telomeres are the “caps”
on the ends of chromosomes.
TECHNICAL NOTE:
We have represented the telomeres as multi-colored “caps” on the
tips of the chromosome for clarity. In reality, the telomeres look
exactly like the regular genetic DNA that contains your genes.

The telomere DNA “caps” function to protect the genetic DNA from
damage. Bad things happen when your genetic DNA is damaged,
namely cancer and accelerated aging.
 Telomeres are made from DNA and protein. They function to protect
DNA that contains your genes—your genetic material.

When most cells divide to make new cells, some of the telomere
structure is lost. After a certain number of cell divisions, the telomere no
longer exists. The cell is unable to divide any further and often dies.

Most of the cells in the body do not divide often enough for this to be a
problem. The issue for people who are obese and/or diabetic is that the
constant onslaught of free radicals from chronic oxidative stress has been
shown to shorten telomeres by damaging the telomere DNA.

The telomere DNA is more susceptible to free radical damage than gene-
containing DNA. Telomeres are much like a “sacrificial lamb” when high
amounts of oxidative stress are present as in diabetes and obesity.

BIOLOGICAL VERSUS CHRONOLOGICAL AGE:

Chronic oxidative stress and
inflammation result in accelerated
telomere loss and more rapid aging. Most
of us have seen obese and diabetic
people who look older than their actual
age.

Biological age is how old the cells in your

body are based on telomere length, while chronological age is based
on the year you were born. This is how a 50-year-old diabetic can have
the body of a 70-year-old (similar to a rusty car) based on telomere
length.
This graphic shows a single “arm” of a chromosome with the telomere cap
in place. Chronic oxidative stress from the mitochondria in diseases such
as obesity and diabetes, shorten the telomeres over time. Chromosome A
shows a normal telomere length before any damage takes place. The
telomere shortening is shown in the picture as the chromosome passes
through the stages shown in B, C, D, and E. Chromosome E is unprotected
by the telomere and the DNA containing your genes can now be damaged.
(Notice the free-radical “drunk guys” wreaking havoc.)

Cells that have DNA like chromosome E can no longer divide to produce
new cells. Old worn-out cells are not replaced. This is really the definition
of aging—when your cells can no longer divide to replace the worn-out
cells. Eventually the “worn-out” cells in your organs such as the liver,
pancreas, heart, kidneys, brain, begin to die and are not replaced because
they no longer have functioning telomeres.

Shortened telomeres are seen in people with many diseases associated

with oxidative stress such as heart disease, diabetes, Alzheimer’s dementia,
and obesity, as well as environmental exposures such as smoking, air
pollution, and stress.
 Researchers are now using telomere length to analyze the rate of aging
and even predict lifespans.

MITOHORMESIS: EXTENDING LIFESPAN WITH

OXIDATIVE STRESS?
Recent research has shown that when mitochondria
are not overloaded with fuel, they increase their
efficiency in producing energy. Free radials are
produced during this efficient energy production, and
result in oxidative stress.

Periodic reduction of glucose in the diet, physical

exercise, and calorie restriction all create short-term
stress to the metabolism. Specifically, these conditions
increase oxidative stress in the mitochondria.

The result of these stressors and the increase in

oxidative stress is an increase in our cells’ antioxidant defense
systems capacity for dealing with free radicals. These increases can
protect us from aging—specifically they can stop telomeres from
shortening from free radical damage. Mitohormesis is the stimulation
of mitochondria by oxidative stress.

It is very important to point out that taking antioxidant supplements

has not been shown to improve health or slow aging. They may even
be detrimental because antioxidant supplements stop the beneficial
dose of oxidative stress in the mitochondria and prevent the increased
capacity in our natural free radical defense system.

In fact, most of the beneficial “antioxidants” (such as polyphenols)

found in plant products do not act directly as antioxidants. They only
stimulate our free radical defense system.

In keeping with the concept of hormesis, periodic stresses that

increase short-term oxidative stress are beneficial, while chronic
 increases in oxidative stress from obesity and diabetes overwhelm the
mitochondria and the free radical defense system. Keep your “Mito-
RPM” in the green to stimulate mitohormesis with regular exercise, and
the nutritional strategies we will cover soon. Your telomeres will thank
you!

RESEARCH UPDATE: ALL IS NOT LOST

Learning how obesity and especially diabetes can accelerate aging can
be pretty discouraging. Before you update your life insurance policy, let
us discuss some findings in recent research showing that loss of
telomere length can be slowed dramatically. A study on diabetics
showed that total loss of telomere length was prevented in diabetics
who maintained good blood sugar control. In the upcoming sections,
we will give you the tools and knowledge to maintain good blood sugar
control, slow down premature aging, and perhaps even reverse the
disease.

STRONG MEDICINE TACTICS:

Maintain good blood sugar control to prevent accelerated aging.

9. Obesity and chronic insulin resistance can lead to “brain wasting.”

Paralleling the increase in obesity and diabetes, neurodegenerative
 diseases such as Alzheimer’s disease (AD) are reaching epic
proportions. AD is the most common cause of dementia in our
aging population.

We all have heard horror stories about friends, relatives and parents
succumbing to AD or other neurodegenerative diseases. The financial and
emotional burden it places on families is catastrophic. Family members—
non-professionals—provide 80% of home care for AD patients. AD has
become more and more common in recent years and strikes people at an
age when they should be enjoying life the most. Spending the last decades
of life in a tortuous existence, marked by a slow fall into mental and
physical decay is occurring with increasing regularity. Why?

“TYPE 3 DIABETES”
In 2005 a research group from Brown University Medical School
described Alzheimer’s disease as type 3 diabetes. Their research showed
AD to have characteristics of both type 1 (decreased insulin production)
and type II diabetes (insulin resistance). Proper insulin regulation is highly
important for brain cell neurons—they die very quickly when insulin is not
properly regulated.

Ketogenic diets and supplementation of ketone-producing substances

(such as medium chain triglycerides) are showing very promising results in
early clinical studies on nutritional therapies for AD. Short-term ketogenic
diets and low carb diets can also be very effective in reversing type II
diabetes—a result which supports the metabolic similarities between T2D
and AD. Additionally, chronic inflammation, oxidative stress, and
formation of advanced glycation endproducts (AGE) are common to the
development of both Alzheimer’s disease and type 2 diabetes.

Obesity and the resulting insulin resistance greatly increase your chances
of succumbing to neurodegenerative diseases such as Alzheimer’s disease.
STRONG MEDICINE TACTICS:
Prevent Alzheimer’s disease by reversing obesity and insulin resistance
using strategies in the upcoming intervention section.

CENTRAL THEMES CONNECTION:

Most of us who have a parent or close relative with AD often wonder if
we will be likely candidates for AD and dementia.

There is no greater nightmare than for a functioning, able, independent

and intelligent adult to—without warning—begin a slow and
inexorable descent into a state of mental infancy.

While there is a lot of talk about the “genetic risk factors” associated
with Alzheimer’s disease, we need to look at AD and genetics through
the lens of epigenetics.

Recent research has shown a strong connection between development

of AD and diseases such as type II diabetes (T2D), cardiovascular
disease and high blood pressure. T2D was found to double the risk for
dementia. Individuals requiring insulin therapy are four times more
likely to acquire AD.

These diseases are associated with metabolic syndrome and can

(often) be prevented by altering lifestyle factors. Altering our habits and
 environment can dramatically reduce the chances of acquiring brain
atrophy—no matter how strong our genetic predisposition. Alzheimer’s
and other causes of dementia follow the same pattern: they have a
strong genetic component, but need the right environmental triggers
to germinate and take root.

STRONG MEDICINE TACTICS:

Cook with coconut oil for a “dose” of medium chain triglycerides to
help keep your brain cells healthy, especially if you have a family
history or early signs of Alzheimer’s disease.

HOW DO I KNOW IF I HAVE DIABETES?

Do you have diabetes? Are you starting to show signs of developing
diabetes or insulin resistance? A person just does not wake up one morning
with type II diabetes. T2D and the broken metabolism that accompanies it
takes years to develop. But, there are early signals of which to be aware.

Insulin resistance and diabetes involve increases in blood sugar from

malfunctioning insulin receptors. The laboratory tests for diabetes and
“prediabetes” analyze blood sugar levels and how well you “handle” a
glucose load in the diet.

1. The first test used to diagnose diabetes (and prediabetes) is the

hemoglobin A1c (HbA1c) test. Hemoglobin is a protein inside red
blood cells that carries oxygen. Depending on how much glucose is
in the blood, a certain amount of glucose will stick to the
hemoglobin. Higher concentrations of glucose in the blood (as seen
in diabetics) results in more of the hemoglobin getting glucose
“stuck” to it. The percentage of hemoglobin that has glucose stuck
 to it gives the HbA1c value.

The average red blood cell has a lifespan of 120 days, so the
hemoglobin in the cell is exposed to blood glucose for the same
length of time. This allows the HbA1c measurement to give an
average level of blood sugar for the past 3 months.

The percentage amounts of HbA1c is used to classify someone as

normal, prediabetic, or diabetic:

The values in this table were taken from the American Diabetes
Association (ADA). Notice that there is a “no-man’s land” for values
between 5.1 and 5.6. Our personal bias is that although this area is not
officially prediabetes, the numbers in this range may indicate a developing
problem with insulin resistance. My personal bias is the closer to 5.0 (or
lower), the better.

2. The next commonly used laboratory test for prediabetes and

diabetes is fasting blood sugar. This is our least favorite test because
is it only represents a brief snapshot in time—your blood sugar at
the time of the blood draw. Other factors, such as a night of poor
sleep can elevate this number even if you do not have diabetes.
Nevertheless, the official values for this laboratory test, again taken
from the ADA guidelines, are as follows:
 3. The third test is called the Oral Glucose Tolerance Test (OGTT).
The OGTT is performed by fasting for 8 hours, then drinking a
glucose and water mixture containing 75 grams of glucose. After
drinking the liquid and waiting 2 hours, your blood glucose is
measured. The diagnosis is based on the ADA guidelines below:

The idea behind the OGTT is to test your tolerance for glucose.
Remember, when people have insulin resistance (diabetes or prediabetes),
the insulin signal does not get through to allow glucose into the cells. Then
the glucose builds up in the bloodstream. Depending on how severe your
insulin resistance is, and how well your pancreas is secreting insulin, the
more of the 75 gram glucose solution will stay in your bloodstream.

As we will discuss later, when figuring out how much carbohydrate a

prediabetic or diabetic can tolerate, performing a home version of the
OGTT using real food can help you track improvement of insulin
sensitivity, and figure out what kinds and quantities of foods cause trouble
for you in terms of blood sugar. We will talk much more about this in the
Intervention section.

For convenience, here is a chart compiling all three tests:

 All of these charts show very definite divisions with ranges of numbers
indicated as “normal”, “prediabetic”, or “diabetic”. Insulin resistance
leading to diabetes is a long process that takes years before most people are
officially classified as diabetic by a blood test.”

A - This point represents good insulin sensitivity. Oxidative stress and

inflammation are in the green zone. But, you start to eat processed
food and stop exercising due to a hectic work schedule.
B - 2 years later your lifestyle is beginning to catch up with you. Your
blood tests are still in the “normal” range, but you are gaining
weight around your midsection. Your blood tests are normal
because your pancreas has started to go into overdrive to produce
more insulin to deal with the start of insulin resistance.
Inflammation and oxidative stress are increased and your
telomeres are likely shortening. Age acceleration has begun.
C - 3 years later you are upset after your annual checkup because your
doctor said your blood tests show you have prediabetes. The
insulin secreting cells in your pancreas are starting to fail, resulting
in increased blood sugar. You have gained 20 more pounds over
the last 3 years. Oxidative stress has further increased and your
telomeres continue to shorten, accelerating aging.
 D - 2 years later you are shocked when your doctor tells you are
“borderline diabetic.” You have not gained any more weight but
your blood pressure has gotten worse, and your telomeres are
quickly shrinking.
E - Your doctor says your HbA1c is 6.8 and that you have diabetes. You
now make a resolution to change your lifestyle because you “have
diabetes”, but wonder how it happened so fast.

Do not be the person at point E, and wait too late to do something

about your disintegrating health. By the time a person has attained
prediabetes status, a significant amount of damage to the insulin-secreting
beta-cells has likely already occurred. This person will likely never regain
full function of these cells—but they always have the power to halt the
damage.

The time for action is at point A and B, before much damage takes
place. Use the Strong Medicine prescriptions in the intervention section to
prevent chronic insulin resistance and diabetes.

If you have no symptoms and normal blood tests (points A and B) how
do you know if you are at risk? The following groups of people should be
focused on prevention, as they are at higher risk for developing diabetes:

• A family history of diabetes—your parents, brothers, or sisters have

diabetes

• Recent diagnosis of high blood pressure

• High triglycerides and low HDL on blood tests
• History of polycystic ovarian syndrome (PCOS)
• History of gestational diabetes
• Sedentary lifestyle
• Ethnic groups including African Americans, Hispanics, Native
Americans, or Pacific Islanders
• Overweight or obese, especially abdominal obesity
CENTRAL THEMES CONNECTION:
Revisiting the “stress cup” from Central Themes V (Allostasis), the
graphic below is a “stress cup” overflowing from a poor diet of
processed food filled with sugar, flour, and vegetable oils. The obesity
and diabetes resulting from this type of daily diet has overfilled the
individual’s “stress cup,” and caused allostatic overload. For the obese
and diabetic, the “stress cup” does not have the capacity to handle
poor sleep and job stress. Those additional stresses will only cause
more overflow. This chronic allostatic overload—an overflowing “stress
cup”—plus the inflammation and oxidative stress that goes with it, will
lead to accelerated aging, heart disease, high blood pressure,
neurodegenerative diseases (such as Alzheimer’s), and cancer.

STRONG MEDICINE TACTICS:

Find out if you have risk factors for developing diabetes. If so, start a
program of early prevention.
DRIVEN TO EXCESS
We have talked extensively about the health risks of obesity, and
especially diabetes. The $64,000 question is why are so many of us getting
overweight and obese? After all, the majority of Americans are overweight
or obese.

Why are we consistently eating so many of the wrong calories? Have we

all become gluttons and hedonists in the last 50 years? That is what social
critics would have us believe! Dietitians would urge us to count our
calories, and limit the amount we eat, in the attempt to gain some control
of our growing waistlines. Counting calories is not natural or sustainable,
and it does not get to the root of the underlying problem.

It turns out there are some very real problems in the modern brain—
problems that drive us to eat beyond our physiologic need for calories.
Some of these problems are coming from within our bodies and others are
from our environment. Appetite is controlled in the brain. Ergo, the brain
can become our worst enemy or best friend in our efforts to shed body fat
and add lean muscle mass.

We will decrypt the hunger communication system’s “black box” and

understand how the brain controls our drive to consume food. Without
understanding this system we are doomed to fight a losing battle against
hunger. Counting calories and other neurotic practices are all destined to
fail in the long term. Obesity, the “enemy within,” will never be
vanquished without an understanding of the drive to eat.

OBESITY: THE ENEMY WITHIN III:
HOW WE GET FAT: THE BRAIN,
HORMONES, AND APPETITE
THE DRIVE TO EAT
Humans are hardwired to find high-energy foods to fuel our body. This
primordial survival mechanism is built into our brains and resides just
below conscious thought. “Hunger” is an urge created by a sophisticated
communications system in the primitive parts of our brain. Once the
hunger message is received, humans use their superior problem-solving
abilities—that other animals do not possess—to find creative ways to
acquire and make decisions about food.

The hunger drive is indeed a primal one. It is based on a complex

communications system of hormones and chemical messengers within the
brain—neurotransmitters. These hormones and neurotransmitters interact
with the primitive structures in the brain responsible for the “reward
system.” The reward system in the brain produces feel-good
neurotransmitters to create a pleasurable response to eating food. This
pleasure response helps us survive as a species.

For ancient hunter-gatherers, there was a caloric cost associated with the
acquisition of food. They would expend thousands of calories bringing
down and butchering an elk—and even more calories transporting the
carcass back to camp on foot. We no longer have to expend energy to
hunt, gather, or cultivate our food. We purchase our artificial, industrial
foods without burning a single additional calorie. We need to readjust our
thinking and our actions; we need reexamine our relationship with food.
Let us stop being slaves to the subconscious primordial impulses and urges
from a broken metabolism and short-circuited reward system. If we let it,
hunger can turn us into a ravenous saber-tooth tiger on the hunt. We have
to understand our drive to eat before we can exert some control.
THE HUNGER COMMUNICATION SYSTEM
“The regulation of appetite” is exceedingly complex. To faithfully
describe all the players in the system and their interrelations would quickly
lead to confusion. We want to explain new ideas and scientific
breakthroughs in a simplified way so we can gain control of our
nutritional destiny.

1. FAT IS TALKING—SO LISTEN UP!

Fat is not just a storage site for excess energy, it is an active participant
in metabolism. In the past, fat was thought to be inert material. Then
scientists discovered that normal, healthy fat cells (adipocytes) secrete a
substance called adiponectin. As discussed previously, this fat-hormone
keeps inflammation down and insulin sensitivity high throughout the body.
Recent research supports that fat tissue is highly active. Healthy fat
secretes several different compounds that have effects on the body and
brain.

A major player in the hunger communication system is a hormone called

leptin. Leptin is secreted by fat cells. The more fat mass you have, the more
leptin is pumped into the bloodstream.

KEY POINT:
The more fat you have (and the larger your fat cells), the more leptin is
produced.

The more fat you have (and the larger your fat cells), the more leptin is
produced.
 Leptin travels from the fat cells and
communicates with the brain by docking
on leptin receptors located on certain
brain cells. This is similar to how insulin
docks to insulin receptors. Leptin
communicates with specific cells located
on the hypothalamus (part of the
Stress/Threat system we discussed earlier).

The hypothalamus is the central

receiving and command center in the human brain which responds to
environmental signals. The hypothalamus is at the center of the brain’s
hunger communication system.

The brain is normally protected from the rest of the body by the “blood-
brain barrier” (BBB). Part of the hypothalamus is located at a “crack in the
wall” of the BBB and has direct access to the bloodstream. Leptin crosses
into the brain through a specialized transport system after being released
by fat cells.

When leptin “docks” with the leptin receptor on the hypothalamus, the
hunger communication system generates a signal to stop eating.

The brain knows how much energy is available from fat because of the
leptin system. As fat stores decrease (from fasting or starvation), less leptin
is available to signal the hypothalamus. This results in the feeling of intense
hunger. As body fat increases, leptin increases and the signal to stop eating
will be stronger.

TAKE HOME MESSAGE:

 Leptin functions as a signal to keep body fat at optimum levels. When
it is working correctly, the leptin signal from fat cells to the hunger
communication system—controlled by the hypothalamus—will keep a
person’s body fat amount in an ideal range.

Low body fat = low leptin = signal to eat (hunger)

Higher body fat = high leptin = signal to stop eating

(satiety)

Leptin is secreted into the bloodstream by adipocytes

(fat cells). Leptin travels through the bloodstream to
the brain and docks with leptin receptors on the
hypothalamus through the break in the blood-brain
barrier.

The hypothalamus receives the signal that the body

has plenty of energy, and the hunger communication
system tells the body to “stop eating.”

When the leptin system is working correctly, you

should be less hungry as you collect more body fat.
More body fat = more leptin. More leptin = a stronger signal to stop hunger.

Based on what we now know about leptin and the hunger signal, how
does anyone get fat? The overweight and obese have higher leptin levels
than lean people. If the communications system was working properly,
people with more fat should get a strong signal to stop eating.

The reason overweight and obese people are still hungry even with high
leptin levels is leptin resistance. As with insulin resistance, the signal that
leptin is supposed to carry (stop eating) is not getting through to the
hypothalamus.
KEY POINT:
Despite high leptin levels, the obese and overweight do not get the
“stop eating” signal because of leptin resistance.

DIGGING DEEPER:
Leptin and Having Babies...
Although we are discussing leptin’s role as a signal to stop eating when
body fat is high, this is only a piece of its greater role, that ensures
survival of not just the individual, but the human species.

One of leptin’s primary functions is to signal the brain when energy

levels are high enough to sustain a pregnancy. When there is an
appropriate level of body fat, the leptin signal from fat cells to the
hypothalamus is relatively strong. The hypothalamus “knows” body fat
is adequate and sends a signal to the pituitary gland which secretes the
sex hormones controlling ovulation, menstrual cycles, and fertility.

It is important that women have an adequate supply of energy stored

as body fat to successfully carry a fetus to term. If a woman’s body fat
levels fall, the leptin signal to the hypothalamus decreases, and fertility
hormones from the pituitary gland also decrease. This is why some
young women with very low body fat (endurance athletes, women
with anorexia nervosa) stop having their menstrual cycles and certainly
have fertility problems.

There is an ideal level of body fat for the optimum leptin levels needed
to maintain fertility. Infertility is not just a problem for women with
very low body fat. Overweight and obese women with high levels of
leptin also have fertility problems. But, should not high levels of leptin
from the extra fat mass give a strong signal for fertility based on what
we just said above? The overweight and obese develop leptin
resistance, and the signal doesn’t get through despite high levels of
leptin. This concept should sound familiar to insulin resistance in the
previous section. No leptin signal = no fertility signal.
KEY POINT:
It is important to understand that overweight and obese people
(especially diabetics) truly feel hungry most of the time, despite the
large amounts of body fat they carry.

Because leptin is not functioning correctly, their brain behaves as if

they have low body fat and sends the signal to eat. This creates a
vicious cycle of eating, more weight gain and inflammation, and more
leptin resistance, leading to more eating.

Knowing about this process can help an obese person understand why
they are always hungry, which can give them some control.

It is very helpful for friends, family members, and medical providers to

also understand this process to support the obese or diabetic person in
your life without dismissing their eating habits as gluttony or lack of will
power.
LEPTIN RESISTANCE
The bloated adipocyte “monster” is secreting high amounts of leptin and
inflammation. The inflammation breaks the transport system and short-
circuits the receptor. Now, very little leptin reaches the receptor, and the
small amount that gets through cannot transmit a signal through the broken
receptor.
Without the “stop eating” signal from leptin, the hypothalamus sends the
message to eat more!

You can see from the graphic that despite high body fat and high leptin
levels, the brain “thinks” that body fat is low because the leptin signal is
not received. Why? The bloated adipocyte (fat cell) “monster” is producing
large amounts of inflammation and oxidative stress which interrupts the
leptin signal.

2. THE GUT TALKS TO THE BRAIN

Having just read through the gut chapter, you know that the digestive
tract communicates to the brain through the gut-brain axis.
Communication hormones and messenger molecules are produced by our
digestive system in response to the food we eat. Trying to describe their
myriad functions and how they interrelate is beyond the scope of this
book. The complexity of how the gut-brain axis works is truly mind-
blowing; even the scientists researching these amazingly complex biological
functions are mystified as they nibble around the edges of understanding.

What are the practical considerations? How does the digestive system
signal the hunger communication system? How does the brain’s response
to food vary depending on the food in question?

Most of the digestive tract signaling messengers send a message of satiety

to the brain. Satiety is defined a feeling of fullness and satisfaction after
being fed. Once the digestive tract (stomach, intestines, gall bladder, liver,
and pancreas) senses a meal has just been eaten, it sends multiple signals—
all designed to promote a feeling of satiety—to the brain. The satiety signal
stops intake of more food—the goal is to allow time for digestion, and to
prevent overeating. Most of the satiety signaling in the digestive tract is
designed to control short-term eating behavior. This is an important
distinction, leptin is not a short-term satiation solution, it is more effective
at exerting long-term control over eating behavior.

The feeling of being full after a big dinner, but

still being hungry the next morning is a short-
term eating signal. Digestive tract signals are
mostly concerned with stopping continued
eating in the short-term to allow for digestion.
But, the digestive tract will signal for more food
when digestion is nearing completion from the
previous meal.
Long-term eating signals (leptin) control the
quantity of what you eat over multiple meals.
Routinely eating large amounts of food at every
meal—greater than the fuel requirements of your body—is an
example of disrupted long-term eating signals. An example of proper
long-term eating behavior from correctly functioning long-term eating
signals is routinely eating the right amount of food to supply your
body’s energy needs without much excess.

TECHNICAL NOTE:
There are many specific digestive tract messengers that send a “stop
eating” (satiety) signal. They include: Peptide Tyrosine (PYY), Pancreatic
Polypeptide (PP), Glucagon-Like Peptide (GLP-1), and Cholecystokinin
(CCK).
 One of the only messengers from the digestive tract that triggers the
hunger response is ghrelin. Ghrelin is produced in the stomach and is
active between meals. When the stomach is empty, ghrelin is secreted
to stimulate hunger.

PROTEIN PRODUCES THE LARGEST AND LONGEST SATIETY

SIGNAL TO THE BRAIN.
Amino acids from protein digestion are sensed in the intestine. A signal
is sent to the brain through a variety of messengers, and produces a strong
signal of satiety.

The satiety signal from protein is the strongest of all the food satiety
signals. Many studies have shown that high protein diets result in lower
intake of total calories throughout the day. This is because protein triggers
the best short-term signal to stop eating. People that eat a good quantity of
protein with each meal are less hungry and naturally eat less throughout
the day—without discipline. Their protein-satiated brain tells them that
they do not need food.

Eating 20-30 grams of protein as part of your breakfast will keep you
from being hungry later in the morning and resorting to “snacking.” Many
people succumb to sweet, sugary snacks because they did not provide the
right satiety signal to the brain first thing in the morning with a high
protein meal.

KEY POINT:
Remember this for the rest of your dietary life: protein produces
satiety. It generates the largest and longest satiety signal to the brain of
any and all nutrients. Want to kill an appetite? Eat protein!
 STRONG MEDICINE TACTICS:
Eat 20-30 grams of protein as part of breakfast to provide a strong
satiety signal to the brain first thing in the morning. This will help
decrease the calories you eat for the rest of the day without feeling
hungry.

Protein is the only macronutrient that consistently produces satiety

signals in the brain. Carbohydrates and fat can produce satiety as well, but
the specific types of carbohydrates and fat are important. In some forms,
carbohydrates and fat can produce a hunger and food craving response.
That leads us to our next point...

3. “PALATABLE” FOODS CAN STIMULATE

THE REWARD CENTERS OF THE BRAIN,
INCREASING APPETITE.
“Palatability” of food can be a confusing topic, and should not always
be equated with good tasting food. Palatability refers to the feeling of
satisfaction or “reward” coming from eating a particular food at a
particular time. A good way to explain this is the immediate satisfaction
and “comforting” feelings you may get by eating ice cream after a stressful
day. Although ice cream generally tastes good to most people, it may not
always be satisfying to eat depending on the circumstances. For instance, if
you have not had ice cream with chocolate syrup for a month, it may be
extremely palatable because you have not had it for so long. It generates
the “feel-good” response and satisfaction. If you have ice cream nightly, it
may still taste good but you may not have the intense “feel-good”
satisfaction response you experienced after being deprived of it for a
month. Having ice cream every night has made it less palatable.

Palatability of food is very individual, but in general, caloriedense foods

that contain sugar and fat are generally palatable to most of us. Fast-food
and other processed foods are very palatable to many people for this
reason.

Palatable foods that stimulate our

reward system can override our normal
“stop eating” signals. A good way to
tell if a food falls into this category (for
you) is if you feel driven to eat the food
even when you are full—and will go out
of your way to acquire this specific
food. The normal “stop eating” signal
that emanates from the digestive tract’s
communication system will often be
silenced or overruled by the food Palatable foods?
reward system. There is a chemical
reason you continue eating certain foods even when full.

The reward system in the brain is the same area activated by drugs such
as cocaine.

When the reward system is stimulated, “feel good” chemicals like

dopamine and endorphins are produced. Stimulating the reward pathway
makes us feel good and can encourage us to stimulate it over and over.

THE REWARD SYSTEM HAS CHANGED IN OBESE PEOPLE.

Two main parts of the reward system are in the brain, and recent
research has shown that the reward system functions differently in an
obese person than it does in a lean person. The two parts of the reward
system are interconnected and influence one another.

• The first part of the reward system is controlled by the parts of the
brain involved in the actual experience of pleasure. Palatable food
 signals this part of the brain to produce a chemical called dopamine.
Other chemicals that increase dopamine include opiates such as
morphine, heroin, and prescription pain-killers, as well as drugs like
cocaine.

• The second main part of the reward system is the part of the brain
involved in organizing and planning actions to obtain a reward.
Once something like palatable food stimulates dopamine release (in
the first part of the reward system) the second part of the system
plans how to obtain the palatable food again. This part of the reward
system is involved when you leave your house, get in your car, and
travel to the store to pick up your favorite ice cream when a craving
hits. It is also the system that helps you imagine how good the ice
cream is going to taste before you eat it.

One current theory holds that the overeating seen in overweight and
obese people is due to the two parts of the reward system changing in a
very similar way to what is seen in drug addiction.

In an obese person, the first part of the reward system involved with
experiencing pleasure from dopamine release is suppressed. This means
that just like developing tolerance to a drug, a higher amount of the
palatable food is needed to get the same “feel-good” pleasure response.

While the “pleasure-part” of the reward system is suppressed in the

obese person, the second part of the system involved with planning to
obtain palatable food, and predicting how much pleasure will be involved
with eating it, is overactive.

This broken reward system may explain why some people are compelled
to seek out palatable food more often and in larger amounts. It is a
subconscious attempt to stimulate the pleasure part of the reward system.

People will literally fantasize about how good favorite foods will taste—
only to feel unsatisfied when they actually eat the food. This creates a
vicious cycle of fantasy, fulfillment, and continuing to forage and eat
because nothing satisfies. Many people continually seek out highly
palatable foods in a futile attempt to feel pleasure and satisfaction.
 FIRST PRINCIPLES PERSPECTIVE: WHY THE
REWARD SYSTEM?
The brain’s food reward system makes sense as a system to ensure
survival when food is scarce. Ancient humans did not have grocery
stores and fast food chains available when they were hungry. Access to
large quantities of caloriedense food was not a common occurrence in
a hunter-gatherer society. When these groups obtained a large source
of calorie dense food, the ability to override the “stop eating” signal
may have had some advantages.

Periodic overeating to store excess energy as body fat would be a

valuable stored energy source to draw from when food became scarce
again. In this way, the ability to override the “stop eating” signal could
be a survival advantage.

The same food reward system that helped ensure survival of primitive
humans is ironically contributing to the poor health of modern humans.

The fat cells and the gut communicate with the brain (especially the
hypothalamus) to signal when we have eaten enough or, conversely, if we
need to eat more to derive additional energy from food. The energy system
that drives us to eat can be overridden by the reward system. An obese
person may continually have the urge to eat—even though there is no need
for more energy from food—because the reward system is in control.

TAKE HOME MESSAGE:

An obese or overweight person has two strikes against them in their
battles to control how much they eat:
battles to control how much they eat:
1. The “energy” hunger communication system involving leptin is not
working. They are not getting the “stop eating signal” from leptin
and are hungry.
2. The “reward” hunger communication system is broken, which will
cause overeating in the attempt to feel satisfied.

If you are overweight or obese, hopefully this information can help you
realize that you are not “weak-willed,” but have a real drive to eat—
even when your body does not need the energy. This may help you
gain some control over these urges when they hit.
“...knowing is half the battle.” —G.I. Joe (1985)

KEY POINT:
The reward system can override the “energy” system for control of the
drive to eat.

DIGGING DEEPER:
Processed Food, Palatability, and Reward
Fast food and processed food tastes good to most of us. That is why
multi-billion dollar food industries are a major contributor to the
obesity epidemic. Why does this type of food maximally stimulate our
food reward centers in the brain?

Food processing removes much of the

natural flavors present in whole food
ingredients. Most of the ingredients—
that most of us cannot pronounce—
seen on processed food labels are
preservatives to keep the food from
spoiling or flavor and color additives.
Color additives make the processed
food more visually appealing, and flavor additives are engineered to
make the food palatable.

There is a whole profession of “flavorists,” chemists who specialize in

creating flavors to add to processed food, and which maximally trigger
the reward centers in the brain. Flavorists are highly trained individuals
with the primary goal of making processed food extremely palatable.
Many of us are very loyal to products like specific soft drinks (from
particular manufacturers) because of the unique and reward-
stimulating flavors created in laboratories. These flavors are
manipulating your behavior through your reward system. If they can
“hook” you with a flavor, they have a loyal customer for life.
Unfortunately, the reward system “hooked” on artificial, laboratory-
concocted flavors contributes to the rampant overeating that underlies
the current obesity epidemic.

COUNTING CALORIES: ISSUES WITH CONTROL

Daily, I overhear dieters’ conversations about the latest strategies,
gadgets, and resources for determining the calorie count of every meal.
They are counting calories in an attempt to gain some control over a
broken hunger communication system. They are not addressing the
underlying problem.
 The healthcare community (especially dietitians)
has promoted counting calories in a big way. This
practice has done a disservice to the public and
their health. Sure, counting and restricting
calories will work for short-term weight loss, but
it is not sustainable for the long-term. It is not
sustainable because we are trying to exert
control over a primal hunger system that is
hardwired in our brain to ensure survival. We
cannot restrain it for prolonged periods of time.

A properly working hunger communication system will not let you

overeat. We have to restore proper operation of the hunger system
with the right food, sleep, stress-reduction and exercise. It will take
some time to fix the hunger system but it can be done following the
Strong Medicine approach.

Restricting calories while still eating the wrong type of food (processed
foods, etc.) will not restore the hunger communication system. The
brain thinks you are starving the body and will activate the stress-
threat system producing cortisol, interrupting the actions of leptin. The
result is constant hunger and a losing battle to maintain calorie
restriction. Calorie counting often becomes a neurotic and self-
defeating practice in the long term. Have some patience when working
to restore your hunger communication system. The rest will take care
of itself.

This has been a very simplified overview of what drives us to eat, and
what can go wrong when the hunger communication system breaks down
with obesity and diabetes. Now that you understand what is going on
“under the hood” with obesity, diabetes, and the drive to eat, the
interventions we will discuss to fix and prevent these problems should
make a lot more sense. We are going to put obesity “on the ropes” and
prepare to deliver the knockout punch.

OBESITY: THE ENEMY WITHIN IV:
INTERVENTION: THE 8-STEP PROGRAM
FOR OBESITY AND DIABETES

How do we reduce the chronic inflammation and oxidative stress that

promotes obesity and diabetes? Both obesity and type II diabetes can be
treated and reversed with nutritional and lifestyle interventions. Our
approach is geared towards the systematic reduction of body fat and
proven methods for controlling blood sugar.

QUICK MEDICAL NOTE:

 Please work with your health care provider when implementing the
recommendations that follow in this section—especially if you are
taking medications to treat diabetes. Your medications will likely have
to be adjusted as you change your diet and lifestyle, so it is important
that your healthcare provider is in the loop. You are encouraged to take
this book with you to your appointment to help with the conversation.

If your clinician is unwilling to support these interventions as part of

your treatment plan, consider finding another healthcare provider to
work with. There are plenty of us out there who are willing and able to
help a motivated patient.

Let’s dive right in to our stepwise approach to losing fat and controlling
blood sugar...
STEP 1

DETERMINE YOUR TOLERANCE FOR STARCH

AND SUGAR.
Reducing starch and sugar to “tolerance levels” is fundamental. If you
are obese, but without a diabetes diagnosis, it is a safe bet that you are on
your way to insulin resistance, so this step will also apply to you.

Insulin resistance—malfunctioning insulin receptors—caused by chronic

inflammation and oxidative stress leads to poor entry of glucose into
muscle and fat cells. As insulin resistance gets worse, the amount of
glucose in your bloodstream increases, damaging your blood vessels and
accelerating aging. Someone with insulin resistance cannot tolerate the
same amount of glucose from starch and sugar that a healthy person with
good insulin sensitivity can tolerate.

After a meal, a healthy person with good insulin sensitivity will rarely
experience blood sugar exceeding 140 mg/dL, even directly after a starchy
meal. For the insulin resistant obese person or diabetic, small amounts of
starch and sugar may increase their blood sugar well above 140 because
they cannot “dispose” of the glucose. They cannot get it into muscle or fat
cells because of malfunctioning insulin receptors. A long-term diabetic
likely has twice the problem–broken insulin receptors and a burned out
pancreas. A damaged pancreas cannot produce enough insulin to help
handle significant amounts of dietary starch or sugar.

KEY POINT:
Someone with insulin resistance cannot tolerate the same amount of
glucose from dietary starch and sugar that a healthy person with good
insulin sensitivity can tolerate.
 insulin sensitivity can tolerate.

Depending on the severity of your insulin resistance, your tolerance for

glucose will vary. To achieve optimal results, you will have to consistently
measure your blood sugar after meals to assess your tolerance for the
amounts and types of specific foods.

Even regular people can benefit from identifying how certain foods (and
amounts of those foods) react within their bodies. I recommend purchasing
a glucose meter from your local pharmacy. Meter technology has improved
considerably over the last several years and most glucose devices are
inexpensive and require very little blood.

Remember that starches are just thousands upon thousands of glucose

molecules “linked” together. Digestion rapidly turns starch into glucose,
and insulin is then needed to clear the glucose from the bloodstream so it
doesn’t stay at high levels.

Many people do not know which foods are large sources of starch and
glucose. You can favorably manipulate blood glucose and insulin by
making expert use of food. We need to understand some basic
biochemistry to intelligently discern which foods are beneficial or
detrimental.
 KEY POINT:
STARCH = GLUCOSE
An important point to make is that not all of the foods listed are
necessarily “bad” for you. Tubers, root vegetables, and fruit are nutrient
dense and can have high nutritional value. The whole point of the list is to
identify sources of starch and glucose in your diet so you know what to
eliminate or reduce if your blood sugar readings are too high after a meal.

Ideally, you should eat the amount of starch/glucose that your insulin
system is able to effectively clear from the bloodstream with relative
immediacy after a meal. Using the blood sugar monitor, you can perform
your own glucose tolerance test. We will test your individual ability to
clear glucose from many different types of meals instead of just testing
with a glucose solution at your doctor’s office.

You have the power to experiment with many different food

combinations to find out what foods (and in what amounts) are beneficial
or detrimental. An oral glucose tolerance test is used to diagnose diabetes
and prediabetes. You can use this as a food tolerance test to help you plan
your meals and keep blood sugar under control.

COMMON SOURCES OF STARCH AND

GLUCOSE:
• Rice is basically starch and not much else.
• Flour includes favorites such as bread, pasta, pastries, bagels, and
tortillas. ANYTHING made with flour is a large
 source of starch.
• Cereals are a grain-based processed breakfast
food packed with starch.
• Tubers and root vegetables include potatoes
and sweet potatoes, etc.
• Soda and “fruit beverages” have high
amounts of glucose and fructose—especially in the form of high
fructose corn syrup.
• Fruit juice is really the concentrated sugar from fruit and water. A
glass of orange juice contains the juice of several oranges without
much of the beneficial fiber.
• High sugar fruits include bananas, mangos, apples, pears, grapes, etc.
Dried fruit is even higher in glucose!
• Candy, sweets, pastries—enough said!

Self-testing is simple, take two readings after each meal. Use the blood
glucose meter one hour after a meal, then two hours after a meal. This will
take the guesswork out of the process—no more guessing how that
lunchtime sandwich affects your blood sugar.

A healthy person with normal insulin sensitivity will rarely have their
blood sugar elevate above 140 after a meal, so we will use 140 as a
“normalcy benchmark.” We offer these goals for appropriate (normal)
amounts of starch/glucose in the bloodstream after consuming a food or a
meal or a beverage.

QUICK MEDICAL NOTE:

Why are these goals stricter than the Oral Glucose Tolerance
Test?
The first reason is that we are using real food instead of a glucose
solution. Most importantly, the “normal” ranges in the OGTT (and
diabetic testing in general) are not adequate for achieving optimal
health in my opinion. The traditional tests set the bar too low and
categorize too many people with early insulin resistance as “normal.”
 REAL LIFE EXAMPLE
“Joe” was recently diagnosed with
prediabetes. He is using our self-
monitoring program and wants to
find out how the baked potato he is
having for lunch today will affect his
blood sugar. He eats a whole baked
potato and measures blood glucose
at 180 at the first hour and 142 by
the second hour. Obviously he
cannot tolerate that much starch in a meal, as these readings are
outside the goal values in the chart above.

The next day Joe has 1/3 of a baked potato for lunch. His 1-hour blood
glucose measurement is 136, and his 2-hour measurement is 118. Now
he knows that generally, he can tolerate the amount of starch in 1/3 of
a baked potato. He moves on and does the same experiment with
more of his favorite meals so he can make the necessary adjustments.

For most overweight, obese, and type II diabetics early in their disease,
these goals are achievable. You will need to reduce the amounts of
starch/glucose in your meals appropriately. How insulin sensitive (or
resistant) you are will determine how much you need to reduce the starch
load in your meals. You will also notice which foods are problematic for
you.

The amount of starch you can handle will also change depending on
what you eat with the starchy food in the meal. For instance, eating
fermentable fiber with the starch will slow the release of glucose in the
bloodstream allowing you to tolerate more starch with the meal.

Measure your blood sugar this way for a while to get a sense of which
specific foods you can handle and which ones you cannot. It can also help
you identify which foods to eat with a starchy food help control blood
sugar (i.e. fiber from vegetables). There is no guesswork. Things you
thought were “healthy” might shoot your blood glucose through the roof.
You will never know unless you use this testing protocol.

Over time, you will not need to measure as much. You will have
assembled enough empirical data to intuitively know what kind of foods
you should avoid. All you need is an inexpensive glucose monitor to get
started. We will now refer to what you are measuring with this method as
your individual glucose tolerance (IGT).

WHOLE GRAINS FOR DIABETICS? SERIOUSLY?

Somewhere, somehow, someone got the bright idea that whole grains
were good for diabetics. This has never made any sense to me, and
sometimes makes me a little crazy when I hear that a well-meaning
health care provider has told a diabetic person “to eat more whole
grains” as nutrition advice to help their diabetes.

While it is true that the starch in whole grains is converted to glucose a

little slower than processed flour, eating whole grains still results in a
large glucose load the body must clear from the bloodstream. If you
don’t believe me, eat a sandwich made of “healthy whole grain” bread
and check your one and two hour blood sugars. Try a plate of “whole
grain” pasta and do the same blood testing protocol and see what it
does to your blood sugar.

Unprocessed whole grains such as oats and pseudo-grains such as

quinoa can definitely be part of a healthy diet for someone with good
insulin sensitivity, but even these foods in large amounts will often
present too much of a starch load for most diabetics and prediabetics
to effectively process.

Diabetic educators and other well-meaning clinicians keep parroting

the whole grain mantra they learned in their training, but it is not doing
their patients any favors, believe me. It drives me a little nuts when
whole grains are recommended to diabetics, and everyone wonders
 why the patient’s blood sugar is not well
controlled.

Sometimes I feel like Inspector Dreyfus in

the old Pink Panther movies with the
“whole grain” issue. The bumbling Inspector
Clouseau’s antics torment Dreyfus over the
years, and eventually land him in an insane “Stop recommending
asylum. I am not yet in a mental health whole grains for
institution, but I do get the occasional eye diabetics!!!!”
twitch.

As you get leaner and healthier, you will be able to tolerate more starch.
Along the way it is your duty to experiment and verify the changes. If you
have excellent insulin sensitivity, and can tolerate high starch levels, eat it,
enjoy it, and clear it with no worries. Do not lie to yourself about having
high insulin sensitivity if you do not. The IGT will not lie to you.

QUICK MEDICAL NOTE:

Type II diabetics (especially those who have had the disease for a while)
may need additional help from pharmaceuticals to control their blood
sugar. Drugs like Metformin control the release of glucose the “liver
banker” produces from gluconeogenesis (see item #2 in the
Consequences of Obesity and Insulin Resistance from the previous
section) and can definitely help some achieve their blood sugar goals.

Again, if you are currently on diabetes medication, please work with

your doctor while implementing the starchy carbohydrate reduction as
described in step one. Your medication may need adjustment to keep
your blood sugar from falling too low.

Type I diabetes can be more complicated to manage. Type I diabetics

Type I diabetes can be more complicated to manage. Type I diabetics
definitely need medical supervision if they try dietary changes.

COACH’S CORNER:
Recent research strongly supports the contention that restricting
starchy carbohydrates and sugars is of substantial benefit for the type II
diabetic and the insulin-resistant obese.

Welcome to the orthodox elite who showed up to the party 30 years

late to proclaim that starchy carbs, grains, liquor, man-made industrial
food and artificial chemically poisoned proteins are BAD for us and
contribute to obesity and type II diabetes. Thank you for confirming
what the athletic elite already knew in 1983!

Individuals with a broken insulin system should reduce stress on the

system by decreasing dietary glucose (created from starch and sugar)
to an amount that their system can effectively process. It is so simple!
Again, the amount each person can tolerate will differ between
individuals.

The more insulin resistant you are, the less starch and sugar you will be
able to tolerate. Get serious about regaining your health and use the
science and technology available for identifying your individual glucose
tolerance.
REAL LIFE EXAMPLE
“Sally” has had the diagnosis of type II
diabetes for 4 years, and probably had
insulin resistance developing for more than
a decade. She could not figure out why her
blood glucose kept reading high after her
lunch. She had switched from making her
sandwiches with bread to making wraps
with corn tortillas. Her glucose readings
improved but were still considerably high
after lunch. Lettuce wraps are a
great alternative to
During a clinic visit, Sally was reminded
reduce the amount of
that corn tortillas are made with corn flour
starch in your favorite
and are mostly starch. Since Sally has had
wrap recipe.
her condition for a while, she cannot
Maintaining healthy
tolerate much starch with her meals while
blood sugar levels
keeping her after-meal glucose within the
can still be tasty.
goal range. Switching from corn tortilla
wraps to lettuce wraps did the trick and now her after-lunch blood
glucose readings are well within the goal range.
STEP 2

STOP EATING FOODS THAT CONTAIN

GLUTEN!
Obesity and diabetes are inflammatory disorders. For many individuals,
gluten adds fuel to the inflammation fire by causing gut irritation,
intestinal permeability, and inflammation. Gluten-containing products
provide no nutritional advantages. There is no downside to eliminating
gluten from your diet.

“GLUTENFREE” DOES NOT NECESSARILY

EQUAL HEALTHY!
I have seen plenty of people cut out gluten from
their diets only to run to the glutenfree section
of their grocery store to buy a bunch of
processed glutenfree replacement products.

Many of these processed products are far from

healthy. Most are just highly dense sources of
starch with very little nutritional value. A
glutenfree cake is still a cake, and a glutenfree cookie is still a cookie—
the only difference is they do not contain a potentially gut-irritating
protein (gluten).

These glutenfree processed products will wreak havoc on your blood

sugar and waistline. Do not fool yourself into thinking that these are
health foods!

Do glutenfree the right way and stay away from these processed
products.
STEP 3

ELIMINATE PROCESSED SEED OILS FROM

YOUR DIET
Processed seed and vegetable oils are some of the largest contributors to
inflammation and oxidative stress in modern society. These rancid
concoctions are in 99% of all processed (man-made) foods. Fast food
manufacturers find ways to include seed and vegetable oils in nearly every
food product they make—from milk shakes to burger “meat,” from the
hot apple pie crust, to the bacon bits sprinkled over your salad, these bad
fats are everywhere.

Processed seed and vegetable oils are high in omega-6 PUFA and
contribute to chronic inflammation and oxidative stress.

• High dietary intake of omega-6 PUFA can disrupt the omega-

3/omega-6 balance leading to a chronic inflammatory state.

• Omega-6 PUFA, like all polyunsaturated fats are prone to free radical
damage because of their multiple double bonds. This leads to free-
radical chain reactions in the body, which quickly produce large
amounts of oxidative stress.

This is linoleic acid (LA) an omega-6 PUFA. High amounts of LA are

found in many processed foods and in the vegetable/seed oils used to
cook fast food.
 Free radicals are attracted to double bonds!

The last thing you need if you are obese or diabetic is to “import” more
oxidative stress and inflammation from vegetable and seed oils found in
processed food and fast food.

KEY POINT:
Insulin resistance is triggered by chronic inflammation and oxidative
stress. Do not make it worse by “importing” more inflammation and
oxidative stress by eating high amounts of omega-6 PUFA from fast
food and processed foods. Read your labels!!

OMEGA-6 CONTENT OF VEGETABLE AND SEED

OILS
Corn Oil
• 24% MUFA
• 60% Omega-6 PUFA
• 12% SFA
Sunflower Seed Oil
• 19% MUFA
• 65% Omega-6 PUFA
• 10% SFA
Safflower Oil
• 14% MUFA
• 75% Omega-6 PUFA
• 6% SFA
 Soybean Oil
• 23% MUFA
• 51% Omega-6 PUFA
• 6% Omega-3 PUFA
• 14% SFA

You can see the high percentage of omega-6 PUFA in each of these
oils. Check processed food packages and salad dressings for these oils.
Many of them are even advertised as being healthy for you!
• MUFA = monounsaturated fatty acid
• PUFA = polyunsaturated fatty acid
• SFA = saturated fatty acid

WHAT SHOULD I USE FOR SAUTÉING FOOD OR FOR SALAD

DRESSING?
Why not use the choice of the world’s elite chefs, olive oil or coconut
oil? Do you really think the world’s best chefs use trashy, highly processed
vegetable oil for sautéing top quality ingredients? Of course not! They use
the finest extra virgin olive oil, or the purest of high MCT coconut oil—
these magnificent fats are highly beneficial and introduce great flavors into
your foods.

If we are going to ask you to stop using something, we will give you
substitutes:

Use extra virgin olive oil to make your own homemade salad dressing
instead of using store-bought dressings. I challenge you to find a store-
bought salad dressing low in omega-6 PUFA.

For cooking, coconut oil is superb. It is high in medium-chain

triglyceride saturated fats (including lauric acid) that have amazing health
benefits. Because it contains saturated fat, coconut oil will not oxidize and
produce free radicals when you cook with it. Medium-chain saturated fats
aid in weight loss and provide some benefit to people with Alzheimer’s
disease. They are “heart safe” and do not aggravate risk factors for heart
and vascular disease.

Medium-chain triglycerides go to the head of the fuel-burning line as

soon as they are consumed; MCTs are used directly for energy instead of
being stored as excess body fat. MCT consumption is especially helpful for
insulin resistant individuals cutting back on starchy carbohydrates. The
medium chain-fats can provide “replacement energy” for the “lost”
starchy carbs. Ironically, this is the identical strategy (replace starch
calories with MCT calories) used by competitive bodybuilders leading up
to competitions where 5% body fat percentages are common.

Overall, the high content of medium chain saturated fats makes coconut
oil an excellent alternative to vegetable oil for most cooking needs.

Also, coconut oil does not impart a strong coconut flavor to food as you
might imagine. Try it when making a vegetable stir-fry and see for
yourself.

STRONG MEDICINE TACTICS:

As alternatives to processed seed and vegetable oils, use olive oil for
homemade salad dressings and coconut oil for cooking.
STEP 4

EAT AT LEAST 20-30 GRAMS OF PROTEIN

WITH EVERY MEAL
Every time you eat, consume some protein: at least 20 grams if you are
smaller and 30 grams if you are a larger person. Protein provides the
amino acids critical for maintaining (or increasing) lean muscle mass, and
protein is also an appetite suppressor. Protein satiates, nourishes, and
quells hunger. Quality protein triggers the brain’s satiety (the “fullness”)
centers, and eating protein throughout the day will quench hunger.

Determining how much protein you are eating with a meal is relatively
easy using the following “rule of thumb” estimates for protein. All you
need is a kitchen scale that measures cooked protein sources in ounces.

PROTEIN ESTIMATOR: THE EASY WAY

The following are good “rules of thumb” for figuring out protein
amounts from animal sources. For plant sources, we recommend using
the National Nutrient Database
(http://ndb.nal.usda.gov/ndb/search/list) since plant sources are
highly variable in protein amounts.
• Cooked chicken, turkey, beef, or pork have about 7 grams of protein
for every 1 ounce of meat. Four ounces of any of these cooked meats
provide approximately 28 grams of protein, and are well within the
20-30 gram goal.
• Ground meats such as hamburger are less dense, and have about 7
grams of protein for every 1.5 ounces of cooked meat. You will need
6 ounces of cooked ground meat for the same 28 grams of protein.
• 1 egg has about 7 grams of protein. So, 4 scrambled eggs provide 28
grams of protein.
• Fish and fatty poultry (duck) have
about 7 grams of protein for every
1.5 ounces. Six ounces of fish or duck
contain 28 grams of protein.
Over time you should be able to
literally “eye-ball” the amount
of food you need to get within
the 20-30 gram protein goal for each meal.
STEP 5

INCREASE PLANT-BASED FOODS FOR

FERMENTABLE FIBER AND ANTIOXIDANT
DEFENSE.
Fruit and vegetable fiber is fermented (broken down) by our gut
bacteria. This process produces beneficial “waste” products including
short chain saturated fats like butyrate.

Unlike our digestive machinery, the beneficial

bacteria that live in our gut can break the connecting
bonds in fiber and they can feed on the released
glucose. These bacteria secrete the short chain fats
(butyrate) as “waste” products, but these waste
products have amazing antiinflammatory properties.

Here is a quick review on the benefits of butyrate:

• Butyrate has potent antiinflammatory properties.

Obesity and diabetes are inflammatory conditions,
therefore substances like butyrate and other short
chain fatty acids produced from the fermentation of fiber help
counteract the chronic inflammation produced from bloated fat cells.

• Butyrate has been shown to have anti-cancer properties, and potential

anti-cancer action—especially with colon cancer.

KEY POINT:
The main health benefits from fiber result from the short chain fat
 The main health benefits from fiber result from the short chain fat
(butyrate) production from fermentation of fiber by the gut bacteria.
Fiber from many types of grains (especially wheat) is not as
fermentable.

WHAT ABOUT THE FIBER IN WHOLE WHEAT?

The fiber found in whole wheat is not nearly
as fermentable as the fiber in most fruits
and vegetables. The beneficial gut bacteria
cannot break down the whole wheat fiber
as well, so very little butyrate is produced.

The main health benefits from fiber result

from the short chain fat (butyrate)
production, so fiber that is not as
fermentable (like whole wheat) is not the
best choice.

Whole wheat is also very dense with starchy carbohydrates, making it a

poor choice (like many of the whole grains) for people with obesity and
diabetes.

STRONG MEDICINE TACTICS:

To help stop chronic inflammation, choose vegetables and fruit over
grains as your sources of fermentable fiber.

Eating fermentable fiber from a wide variety of fruits and vegetables can
help decrease the level of glucose in your bloodstream after meals. This
will help you meet the one-hour and two-hours after-meal glucose goals
discussed in step one. Make fibrous vegetables and fruits a cornerstone of
your nutrition.

Fermentable fibers can slow the rate in which food is moved from the
stomach during digestion. This can help create a feeling of satiety
(fullness).

The following list is some of the best sources of fiber from fruits and
vegetables, but it is not nearly a complete list.
GOOD SOURCES OF FERMENTABLE FIBER
The Vegetables:
• Leafy green vegetables such as kale, spinach,
and chard
• Stem tubers such as potatoes
• Root tubers such as sweet potatoes
• Root vegetables such as carrots, turnips,
rutabaga, daikon, radish, parsnips, jicama

Fruit:
• Berries such as strawberries, blueberries, blackberries, raspberries
• Avocados
• Pears, apples, oranges, bananas (be aware of the sugar content)

INCREASING ANTIOXIDANT DEFENSE WITH

PLANT-BASED FOOD
There are certain health-promoting compounds found
only in plant foods. Many of these compounds
stimulate our body’s antioxidant defense systems and
counteract the chronic oxidative stress linked to
obesity and diabetes.

Many fruits and vegetables are “edible pharmacies”

containing hundreds of different compounds to
combat inflammation and oxidative stress—especially
important for diabetics and the obese.

For a long time it was thought that these plant

compounds acted as antioxidants, scooping up free radicals and
preventing them from damaging the body. Some of these compounds
may work in this fashion to a limited extent, but current research shows
 that many of these chemicals work primarily by stimulating our
natural antioxidant defense and detoxification systems. Some of
these plant-chemicals also work by stopping inflammation.

Some grains such as oatmeal do contain a relatively high amount of

fermentable fiber, but also have a pretty high starch load, so use with
caution if you are diabetic.

Legumes such as beans, peas, and lentils have high amounts of fiber, but
can cause gut inflammation in some people. If you are going to use
legumes as a fiber source, make sure you soak them for 24 hours then cook
them thoroughly to reduce some of the toxic compounds found in dried
legumes. If you tolerate legumes, they can be an excellent source of fiber if
prepared correctly. Vegetable and fruit-based fiber generally causes less
irritation than legumes and is generally preferable from a gut health
perspective.

There are thousands of plant-derived chemicals, and many have positive

health benefits. Some are outstanding and deserve to be singled out
because they are especially beneficial to the insulin resistant obese or
diabetic person.

SULFORAPHANE: BROCCOLI’S BOUNTY

Sulforaphane is a chemical found in all
cruciferous vegetables (broccoli, cauliflower,
cabbage, bok choy, horseradish, mustard seed,
wasabi, rutabagas, radishes, turnips and others).

Sulforaphane stimulates the central controller of

the antioxidant response system, which fights
oxidative stress from the free radicals inside your
cells. It also directly helps to stop the inflammatory response.

Since obesity and diabetes are diseases of chronic inflammation and

oxidative stress, sulforaphane can be especially helpful for diabetes in
particular.
particular.

Sulforaphane has also shown potent anti-cancer activity in some types

of cancer, and may inhibit the growth of the ulcer-causing bacteria,
Helicobacter pylori.

Additionally, sulforaphane can stimulate the body’s natural

detoxification system, helping to detoxify certain types of toxins and
toxicants from the air, water, and food.

The best dietary source of sulforaphane is from broccoli sprouts (3-5

day old broccoli plants). Broccoli sprouts have 20 times the
sulforaphane content as full-grown broccoli plants.

TECHNICAL NOTE:
Sulforaphane is produced from a chemical building block in broccoli
called glucoraphanin. A special enzyme in the plant is needed to
convert glucoraphanin to sulforaphane. You must damage the plant
through chopping or chewing for the conversion to sulforaphane to
take place directly from the plant. Glucoraphanin can also be converted
to sulforaphane by the gut bacteria.

KEY POINT:
Broccoli sprouts must be damaged by chewing or cutting to get
sulforaphane directly from the plant.
sulforaphane directly from the plant.

RESEARCH UPDATE:
A recent study has shown that sulforaphane can alter the epigenetic
programming of certain cancer cells. Researchers found that
sulforaphane “turns off” a gene responsible for growth in these cancer
cells. This is important, since cancer is uncontrolled cell growth.

This research suggests that sulforaphane can stop uncontrolled growth

in some cancer cells by “switching off” growth genes, through an
epigenetic process.

If you need a review on the epigenetic process, go back to the Central

Concepts section on Gene-Environment Interaction.

RESEARCH UPDATE:
Of special interest for diabetics—new research has shown that adding
foods with high sulforaphane content such as broccoli sprouts to the
diets showed substantial benefit for diabetics.

All of the diabetic patients in the study showed improvements in

insulin resistance, and overall decreased oxidative stress and
inflammation after adding broccoli sprouts to the diet.
DO IT YOURSELF!
Broccoli sprouts are easy to grow at
home. An internet search will yield
several sites with instructions on how to
grow your own sprouts. Given the
benefits of sulforaphane, having your
own indoor broccoli sprout garden is well
worth the effort, and they will be fresher
and more effective than sprouts from the grocery store.

STRONG MEDICINE TACTICS:

Eat cruciferous vegetables such as broccoli, cauliflower, cabbage, bok
choy, horseradish, mustard seed, wasabi, rutabagas, radishes, and
turnips to get the benefits of sulforaphane. Broccoli sprouts are the
best source.

POLYPHENOLS: DARK
CHOCOLATE ANYONE?
Polyphenols are a large group of plant-chemicals
found in most plant species. Laboratory studies
have shown they have strong antioxidant effects
and inhibit inflammation.
Studies in a test tube (called in vitro) show that polyphenols act as
antioxidants, scavenging free radicals. However, recent research has
shown that in the body, polyphenols do not have as much direct
antioxidant effect themselves, but activate the antioxidant defense
system (see the “bouncers in the bar” from the Central Concepts
chapter).

Polyphenols are found in many plant-based foods, but the highest

concentrations are found in cocoa beans, coffee, red wine, green tea,
black tea, and olive oil. The bitter taste in many of these foods comes
from the polyphenol content. The higher the polyphenol content, the
more bitter the flavor.

Pure cocoa has one of the highest polyphenol contents of any food,
but is inedible because of the bitter taste. 85% dark chocolate is an
excellent source of polyphenols and tastes pretty good once you are
accustomed to the flavor (and lack of sugar).

Research on polyphenols is still ongoing, but recent studies have

shown that polyphenols may be of some benefit for diseases of
inflammation and oxidative stress such as diabetes, heart disease,
cancer, and Alzheimer’s dementia.

Incorporate a variety of polyphenols in your diet—there are plenty of

sources to choose from.

STRONG MEDICINE TACTICS:

Incorporate polyphenol-rich foods like dark chocolate (80-85% cacao),
coffee, red wine, green tea, black tea, and olive oil into your diet.
FIRST PRINCIPLES PERSPECTIVE: PLANT
CHEMICALS AND HEALTH
There are multiple theories as to why so many plant-based chemicals
show health benefits. But, the theory that these chemicals act as direct
antioxidants is slowly losing favor.

Plant-based chemicals such as polyphenols are produced inside the

plant in response to environmental stresses on the individual plant.
Poor soil nutrients, insect predators, and lack of water can all produce a
stress response in plants, increasing polyphenols.

Recently an intriguing hypothesis was put forward—chemicals such as

polyphenols, produced in plants during stressful conditions, are known
to activate stress defense mechanisms (antioxidant defense) in our
bodies when eaten, and they act as an environmental stress sensor.
The authors of this hypothesis think that these plant-chemicals (when
eaten) allow us to sense stress in the food supply (stress to the plants)
and prepare our bodies for an upcoming threat to the food supply such
as a drought or insect infestation.

In the hunter-gather societies of our distant ancestors, the ability for

our body to prepare for a food shortage by “sensing” stress in the food
supply would be a survival advantage. It may be one reason why so
many chemicals in plants have health benefits for humans.

This is still just a hypothesis, but it makes sense through the first-
principles lens.
STEP 6

CUT OUT HIGH FRUCTOSE CORN SYRUP AND

SUGAR.
Like alcohol, fructose can only be metabolized in the liver. The liver
does two things with fructose—converts it to glucose or body fat for
storage at one of the many fat-storage depots dotting the bodily landscape.

The amount of fructose in the fruit we eat is relatively small and can be
easily processed by the liver without causing problems. It is the added
sugar and high fructose corn syrup in processed foods causing the health
problems in many modern societies.

When the liver has stored as much glucose as

possible in the form of glycogen, it will convert the
extra glucose into fat, specifically triglycerides.
Usually these triglycerides are transported to fat cells
for storage, but if you are somewhat insulin resistant,
the fat cells are not storing triglycerides well. The
liver and muscles become the new “storage sites” for
fat. This process damages the liver leading to “fatty
liver disease”, also known as NonAlcoholic Fatty
Liver Disease (NAFLD). Overloading the liver with
glucose and fructose leads to NAFLD.

KEY POINT:
The primary causes of NAFLD are:
• Insulin resistance
• Intestinal permeability (see Gut chapter)
 • Excess sugar in the diet

Recent research has shown that a combination of insulin resistance,

intestinal permeability, and excess dietary sugar (especially fructose) causes
NAFLD.

High-fructose corn syrup continues to get bad press as a “dietary devil.”

Some of this portrayal as a nefarious character is deserved, but further
discussion in the following “Digging Deeper” section is warranted to
establish its role in health problems in a scientific context.

DIGGING DEEPER:
Why the fuss over high-fructose corn syrup?
High-fructose corn syrup (HFCS) is almost identical to table sugar
(sucrose) when you compare them as chemicals. Most HFCS is 55%
fructose and 45% glucose, while sucrose is 50% fructose and 50%
glucose. Eating either in large quantities can cause health problems,
especially if you have insulin resistance or outright diabetes.

The reason behind the bad press on HFCS is because food

manufacturers add it to most processed foods and fast food to
improve taste and palatability. The primary reason they can do this is
because the government subsidizes farmers growing corn, which
makes HFCS very cheap. Processed food manufacturers can use large
amounts of HFCS in their products more cheaply than sucrose
harvested from sugar cane or sugar beets.

The body can handle small amounts of HFCS or sucrose, but the
amount consumed by the average American is causing health
problems.
 The average American eats an estimated 80 to
100 pounds of added sugar in the forms of sucrose
and HFCS annually. “Added sugar” simply means
sugar not naturally present in real foods. It is a large
part of processed and fast food.

This staggering amount of added sugar in our diet

is certainly contributing to NAFLD, obesity, and
diabetes. HFCS is not chemically different from
sucrose, but the large amount we are exposed to in
processed food is the real issue.

SUGAR AND “AGE”

Sugar, consumed in large amounts over a protracted period of time,
inevitably creates serious health problems, especially for diabetics. Table
sugar and HFCS are large concentrations of glucose and fructose. Large
amounts of these simple sugars leads to increased formation of Advanced
Glycation Endproducts (AGE). AGEs are formed when glucose and
fructose undergo chemical reactions that allow them to “stick” to proteins
inside and outside cells.

Low amounts of AGEs are normal. They are naturally produced on a

constant and ongoing basis as part of a healthy metabolism. Health
problems occur when large amounts of AGEs form in part from high
amounts of sugar and HFCS in the diet, then trigger inflammation. If the
cause is dietary, then we can control it.

Just as there is a receptor, or “dock”, for insulin, leptin, and countless

other molecules in the body, there is a receptor for AGEs as well. This
receptor is the Receptor for Advanced Glycation Endproducts (RAGE).

When AGEs “dock” with RAGE, an inflammatory response is

generated. The more AGEs present in the body, the more inflammation is
produced when they dock with RAGE. The chronic inflammation from
high levels of AGEs, contributes to accelerated aging of the body. AGE
makes you age faster, but we can control this with diet.
 KEY POINT:
As the amount of AGEs increase in the body, so does the level of
inflammation. This worsens chronic diseases and contributes to
accelerated aging.

Fructose forms AGEs eight times faster than glucose. Some organs in
your body—kidneys, brain and blood vessels—will produce AGEs rapidly
when subjected to high levels of glucose and especially fructose. High
amounts of glucose and fructose (as found in high fructose corn syrup)
damage these organs and turn them into AGE-producing machines.

The kidneys and blood vessels prone to AGE-caused inflammation are

damaged in diabetes. Kidney failure, vascular, and heart disease are often
seen in long-term diabetes.

KEY POINT:
When overall sugar is high, the blood vessels and kidneys are especially
prone to forming AGEs. Chronic inflammation from AGEs in these
organs contributes to the high incidence of heart disease and kidney
disease seen with diabetes.
ADVANCED GLYCATION END PRODUCTS IN
FOOD
We have just discussed how levels of
sugar can lead to AGE formation inside
your body, but AGEs can also be
preformed in the food you eat, even
before it gets into your body.

The type of food and cooking process

greatly affects how much AGE is
present. High temperature cooking, such as deep frying, can elevate
AGE formation by up to 100 times.

Animal-based foods are protein-rich and are especially vulnerable to

AGE formation with cooking methods such as frying. Processed foods
often contain sugar and proteins subjected to high temperatures during
the manufacturing process. They are often loaded with AGEs.

Alternate cooking methods can greatly reduce the amount of AGEs in

your food. So-called “moist” cooking methods using water and lower
temperatures (slow cookers/crock pots) are excellent for reducing AGE
formation. Also, adding acidic liquids such as lemon juice and vinegar
will also reduce AGEs formed from cooking.

Making stews, soups, and slow cooker meals are all great ways to
prepare your food to avoid high levels of AGEs, especially if you are
diabetic.

STRONG MEDICINE TACTICS:

 Reduce AGEs by decreasing sugar and HFCS in your diet and follow
low-AGE cooking methods.

HOW TO ACCELERATE DISEASE AND AGING:

THE NUCLEAR OPTION
If you are diabetic or overweight/obese, the
best way to accelerate disease and aging is to
continue to eat fried fast food and processed
food. There is no doubt that fried chicken and
French fries from your favorite fast food restaurant taste amazing. It is
why the fast food industry makes billions of dollars per year from
consumers. But, these foods are inflammation/oxidative stress nuclear
weapons in your body:
• The processed vegetable oils (PUFA) used to fry the food create huge
amounts of free radicals.
• The breading (starch) and protein cooked at high temperatures
creates AGEs by the bucket-load.
• Most of these foods have added sugar and HFCS to make them more
palatable, which potentially increase the AGEs produced in your
body.
• Most of these foods have large amounts of gluten that can contribute
to inflammation in the gut if you are sensitive.

These foods taste great and generate strong reward signals in your
brain, but are deadly to your health. If you are obese or diabetic and
continue to eat these foods regularly, you are simply not serious about
getting healthy.

The following graphic summarizes how preformed AGEs in processed

and fried food, as well as AGEs generated in the body from high glucose
levels—seen with diabetes and insulin resistance—lead to chronic
inflammation and oxidative stress.

SOFT-DRINKS, ENERGY DRINKS, FRUIT

DRINKS: HEALTH-KILLING SMART BOMBS
Soft drinks, energy drinks, and “fruit-flavored” drinks are devoid of any
nutrition and will slowly wreck your metabolism. If you already have
prediabetes, diabetes, or obesity, you need to steer clear of these
beverages.

They are all filled with sugar and HFCS. They are taste-engineered to
stimulate your food reward system. Many of us have “soda addictions”
which are hard to kick. Clever marketing is also involved in fruit-drink
labeling such as “made with real fruit”, yet they are all loaded with
sugar! Some children are even showing signs of fatty liver disease in
their early teenage years largely due to soft-drinks, fruit beverages, and
energy drinks.
Energy drinks are hugely popular with teenagers and
young adults. Not only are they loaded with
caffeine, but some have almost 3 times the sugar
as a soft drink! Here are some numbers:
• One 12-ounce can of soda can have between 10-15
teaspoons of sugar. A 20-ounce bottle has 16-25
teaspoons of sugar depending of the brand.
• Energy drinks can have as much as 40 teaspoons of sugar in one can!
Most brands have 25 to 30 teaspoons of sugar per can.

Fruit drinks marketed to children can have just as much, if not more
sugar than soft drinks.

WHAT ABOUT FRUIT JUICE?

It is a big shocker for most people, but fruit juices can
have just as much sugar (glucose and fructose) as soft
drinks. While juice has some nutritional value in the
form of vitamins and minerals, they also have huge
sugar loads for the body:
• One glass of orange juice is equivalent to 10 teaspoons
of sugar.
• One glass of apple juice has 10-12 teaspoons of sugar.
• One glass of grape juice can have up to 15 teaspoons of sugar.

Fruit can be a part of a healthy diet and is a good source of fermentable

fiber, vitamins, and minerals. Remember that it takes 4-6 good-sized
whole oranges to make one 8-ounce glass of orange juice.
whole oranges to make one 8-ounce glass of orange juice.

Eat the whole fruit rather than the juice to get the nutrition without
the huge sugar load.

HOW DO I KNOW HOW MUCH SUGAR IS IN A

FOOD OR DRINK?
1. Read the label to find the amount of sugar in grams.
2. Divide the number in grams by 4 (there are about 4 grams in 1
teaspoon of sugar). For example, 40 grams of sugar, divided by 4,
equals 10 teaspoons of sugar.
3. Watch “serving size.” This is a small deception often used by food
and beverage marketers. The amount of sugar is labeled by serving
size. If a beverage is labeled as having 40 grams of sugar in a 16 oz.
bottle, but with a serving size of 2, you are really consuming 80
grams of sugar if you drink the whole bottle.

STRONG MEDICINE TACTICS:

Limit the amount of soft drinks, energy drinks, and fruit juice in your
diet. If you are obese and/or diabetic, cut them out completely.
 STRONG MEDICINE TACTICS:
Read food labels to determine how much sugar is in the processed
foods you are eating (If you are eating unprocessed food without a
label, you generally do not have to worry).

STEP 7
INCREASE INSULIN SENSITIVITY WITH
EXERCISE.
Step 7 is probably one of the most powerful ways to increase insulin
sensitivity and help normalize blood sugar for a type II diabetic or insulin
resistant obese person.

Even the conservative Centers for Disease Control (CDC) recommends

at least 2.5 hours per week of “moderate intensity” aerobic exercise or 75
minutes per week of “vigorous intensity” aerobic exercise. They also
recommend 2 or more days of resistance training in addition to aerobic
exercise. These recommendations are often lacking when it comes to
exercise specifics—but we have them for you. We can show you how to get
fit with maximal time efficiency.

Out-of-shape people avoid fitness and exercise for a variety of reasons.

Some of their reasons are legitimate—mistreatment by fitness professionals
and personal trainers, incompetent exercise instruction, or from using
exercise modes incapable of producing results. We will guide you through
setting up a proven exercise template used to this day by elite athletes.
Every intelligent exercise program needs a cardiovascular training regimen
(builds and strengthens heart and lungs, flushes arterial highways), and a
resistance training regimen (builds and strengthens the 600 + muscles on
the human body.) We will successfully blend these two exercise modes.

Exercise is one of the best ways to restore insulin sensitivity.

You do not have to spend hours in the gym to obtain the insulin-
sensitizing benefits of exercise. Recent research shows the possibility of
getting these benefits using short exercise protocols—if the protocols are
sufficiently intense. Exercise intensity is measured by the percentage of
maximal heart rate achieved during the exercise.

As a preview to our exercise approach, we will present an abbreviated

exercise protocol that has been tested in a lab with actual diabetic patients,
and which showed excellent results. The key to the success of this protocol
is the intensity of the exercise.

In this case, we are measuring exercise intensity of exercise by the

percentage of maximal heart rate achieved during exercise.

Let’s back up a bit to explain more about exercise intensity before we

dive into the protocol. The CDC defines “moderate intensity” exercise as
anything that gets your heart rate between 50% and 70% of your
maximum. “Vigorous intensity” is defined as exercise that causes heart
rates between 70% and 85% of maximum.

WHAT IS MAXIMUM HEART RATE?

The maximum heart rate (HRmax) is the highest heart rate you can
expect to achieve during exercise. HRmax is mostly affected by a
person’s age—the older you get, the lower your maximal heart rate. In
other words, a younger person can generally achieve a higher heart rate
during exercise than an older person.

HRmax varies considerably among individuals, but some general

formulas have been developed to provide reasonably good estimates
of your personal maximum heart rate. We used to rely on the simple
“220 minus age” formula to calculate HRmax, but that was found to be
relatively inaccurate.

Some of the more recently developed formulas will better suit our
purposes for determining your HRmax:

For men: 208 - (0.7 X Age) = HRmax

For women: 206 - (0.88 X Age) = HRmax

Example 1: Chris is 43 and wants to calculate his maximum heart rate.
He will multiply his age (43) by 0.7, which equals 30.1. He will then
subtract 30.1 from 208 to get 177.9 (we will round to 178). So Chris’s
HRmax is about 178 beats per minute.
 Example 2: Carrie is 46 years old. To calculate her HRmax, she would
multiply her age (46) by 0.88 to get 40.5. She would then subtract
40.5 from 206 to get 165.5 (we will round up to 166). Carrie’s HRmax is
166 beats per minute.

Following the CDC’s recommendations for “moderate” intensity

exercise, Chris needs to keep his heart rate between 50% and 70% of his
maximum heart rate during exercise. He will take the HRmax of 178 that
he just calculated and multiply that number by 0.5 (50%) and 0.7 (70%):

• 178 X 0.5 = 89 beats per minute

• 178 X 0.7 = 125 beats per minute

When Chris is exercising at “moderate” intensity for 2 1/2 hours per

week as recommended by the CDC, he will keep his heart rate between
89 and 125 beats per minute.

Carrie decides she doesn’t have 2 1/2 hours per week to devote to
exercise, so she is going to exercise with a little more intensity. She wants
to go into the heart rate zone the CDC classifies as “vigorous.” With this
intensity she only needs to exercise for 75 minutes (half the time of the
moderate exercise goal) per week.

Carrie uses the HRmax she just calculated and figures out her
“vigorous” target zone of 70% to 85% of her HRmax. She takes her
HRmax of 166 beats per minute and multiplies this number by 0.7 (70%)
and 0.85 (85%):

• 166 X 0.7 = 116 beats per minute

• 166 X 0.85 = 141 beats per minute

When Carrie is exercising at a “vigorous” intensity for 75 minutes per

week as recommended by the CDC, she will keep her heart rate
 between 116 and 141 beats per minute.

Exercising 3 times per week, Chris will need to work for 50 minutes per
session to get his 2 1/2 hour total at moderate intensity.

Carrie will schedule 25 minutes per exercise session, 3 times per week
for her 75 minute weekly total at a vigorous intensity.

EXERCISE TIP:
Do not rely on the heart rate monitors built into the handles of exercise
machines. They are notoriously inaccurate. Invest in a personal heart
rate monitor with a chest strap and watch receiver. This is a worthwhile
investment if you are serious about your fitness.

HIGH INTENSITY BEATS MODERATE OR VIGOROUS INTENSITY

High intensity, short duration exercise protocols have more
physiological benefits than the “steady-state” exercise recommended by the
CDC. One of these protocols, High Intensity Interval Training (HIIT), is
especially beneficial to people who are insulin resistant. As the name
implies, HIIT is exercise ramped up to a high intensity for short bursts. For
example, a burst or sprint, stop and recover, burst or sprint again, over
and over until the session is complete. This method has been shown to
reduce high blood sugar as seen in type II diabetes and prediabetes.
 HIGH INTENSITY INTERVAL TRAINING
PROTOCOL
The HIIT protocol involves pushing your heart rate to approximately
90% of your maximum heart rate for short periods of time with rest
breaks in between. Let us use Carrie as an example:

Carrie has already calculated her HRmax at 166 beats per minute, then
she multiplied her HRmax by 0.9 (90%) to get approximately 149
beats per minute.
• 166 X 0.9 = 149 beats per minute (her target
heart rate).
• While wearing her heart rate monitor, Carrie will
choose a piece of cardio equipment such as a
bike, elliptical, treadmill, stair climber, etc.
• She will start at a slow pace for 2-3 minutes to
get her muscles warmed up.
• She starts exercising as hard as possible to get her heart rate up to
her target of 149 beats per minute, and continues until the 60 second
interval is complete.
• After the 60-second exercise interval, she will rest for 60 seconds (or
pedal/walk very slowly).
• After resting for 60 seconds, she will start another 60-second
exercise interval to achieve her target heart rate of 149 beats per
minute.

Carrie will repeat this pattern for a total of 10 60-second exercise

intervals before cooling down for 2-3 minutes.

The HIIT protocol is only 10 total minutes of exercise (10 60-second

intervals), and 10 total minutes of rest (10 60-second rest periods). These
intervals combine to only 20 minutes in total—and you are done. “I don’t
have time for exercise” is no longer a valid excuse.

KEY POINT:
The most common excuse for not exercising is “I don’t have enough
time...” If that is the case, then use the HIIT protocol.

Short bursts of activity at a high intensity, followed by rest periods has

been shown to be just as—and in many cases more—effective as traditional
sustained lower intensity exercise. While Chris is plugging away for 50
minutes of “moderate” intensity exercise, Carrie has finished her workout,
showered, and is back to the day’s business. Despite the short duration of
her workout, she has also gained some advantages that Chris won’t get
from “moderate” intensity workout.

The benefits of short duration high intensity training come from the
effect it has on glucose storage in muscles.
 FLASHBACK
Quickly review concept #3 and #10 in the Metabolism Basics section,
before reading onward.

As intensity is increased from “moderate”, “vigorous”, and finally to the

90% HRmax seen in our HIIT protocol, more glucose is used by the
muscle for energy. This is because the body cannot supply oxygen to the
muscle fast enough to keep up with the demands of high intensity exercise.
As a result, the muscle is forced to use glucose without oxygen for energy.
This produces lactic acid buildup as a waste product, and starts to empty
the muscles of their stored supply of glucose. Fat needs oxygen to be used
as fuel, so the low oxygen in the muscles during intense exercise shifts the
primary fuel source to glucose.

Wait a minute! I want to burn fat with exercise. You are saying
that I will mostly be burning glucose with the HIIT protocol, and I
want to get rid of fat!

You will burn plenty of fat during the rest periods and after this
workout, especially. This type of high intensity workout will keep your
metabolism working at a higher rate for the next 24 to 36 hours, and will
primarily burn fat as fuel. The point of burning up all of this glucose will
become evident in the following discussion.

The reason we want to use high intensity interval exercise to empty the
muscles’ storage supply of glucose is because of what happens after the
exercise. As far as your body and brain are concerned, the high intensity
exercise may have happened because you ran from a wild animal to escape
getting killed. Your body wants to replenish the supply of glucose in case
you need to escape from an animal again in the near future. You know
that you are riding a bicycle, and not running from a predator, but your
body responds to the high intensity stimulus as a threat and wants to make
sure you are prepared to survive for another day.

In response to the high intensity exercise “threat,” the muscle does a

neat trick and bypasses the insulin signaling mechanism we saw in the
“Diabesity” section. After intense exercise, muscle cells do not need an
insulin signal to open the glucose transporters to let glucose in from the
bloodstream. Even if you have substantial insulin resistance, after intense
exercise the glucose transporters are “unhooked” from the insulin signal.
Going back to our “electronic door” analogy, high intensity exercise is like
installing a manual door-opening mechanism which bypasses the insulin
receptor’s electronic door system.

High intensity interval exercise not only opens the glucose transporters,
but it also signals the muscle to make more glucose transporters. This
allows the glucose that has been accumulating in a diabetic’s bloodstream
to push its way into the muscle cells, thus lowering blood sugar.

KEY POINT:
After intense exercise, muscle cells do not need a signal from insulin to
open the glucose transporters to let glucose in from the bloodstream.

The great thing about high intensity exercise is that the benefits continue
for the next 1-2 days after a single 20-minute session. Glucose transporters
stay active well into the next day. When this protocol was tested on
diabetics, not only was their fasting blood sugar lower the following day,
but their blood sugar levels after meals were also lower for 24-36 hours
after the workout.
This is the normal state of a type II diabetic (let’s call him Jim) with bloated fat
cells spewing out inflammation which blocks the insulin signal from opening
the glucose transporter. Glucose is left in the bloodstream and builds up to
toxic levels.

Jim is not engaging in any exercise at this point because he thinks that he
doesn’t have time to spend hours in the gym.
Jim has now started a high intensity exercise protocol. He likes the fact that
he only has to spend 20 total minutes a day, with only 10 minutes of actual
exercise. Jim has calculated his HRmax and is using the HIIT protocol with a
target heart rate of 90% of his HRmax.

The high intensity intervals are decreasing his muscle glucose storage, and
the muscle responds by “unhooking” the glucose transporters from the
insulin signal, and by making more transporters.

The fat cells are still shooting out inflammation which block the insulin signal,
but it does not matter since the transporters have “bypassed” the insulin
signal. Glucose from his bloodstream is now pouring into his muscles and is
decreasing his blood glucose levels.
To grasp the concept, it may be easier to think of your muscles as
“containers” that store glucose (as glycogen) for emergencies like running
from a bear. HIIT depletes muscle glucose and creates an open storage area
for the glucose from the bloodstream. If you did not deplete the muscle
glucose with HIIT, the extra glucose would build up in the bloodstream
causing high blood sugar, or it would be converted and stored in the fat cells
as fat.

For these reasons, HIIT is a very powerful protocol for diabetes and
prediabetes. It can substantially help keep your after-meal blood glucose
levels within the target ranges discussed in earlier sections.

If you consistently apply this protocol with a proper diet, over time the
better blood sugar control will result in increased insulin sensitivity. The
pancreas will now secrete less insulin because there is less glucose in the
bloodstream for it to process.

Also, now that the extra glucose will be stored in the muscles, the fat
cells will not need to process the excess glucose and turn it into fat for
storage. The fat cells will start shrinking, and return to their “happy state”
with decreased inflammation.
This is how you lose fat with HIIT
 As fat cells return to their normal size over time, the decrease in
inflammatory cytokines will also increase insulin sensitivity. Chronic
inflammation is a major cause of “broken” insulin signaling. You can
modify the HIIT protocol to fit any type of exercise. You just need to
ensure your heart rate is sustained at 90% of your HRmax for 60 seconds.
Find the exercise or equipment that works for you.

In the exercise chapter we will discuss other high intensity exercise

strategies and resistance training extensively. Resistance training coupled
with HIIT will give diabetes and prediabetes a knockout punch!

IMPORTANT MEDICAL NOTE:

As beneficial as high intensity exercise is for diabetes, it is extremely
important that you first discuss it with your doctor before starting a
protocol like HIIT. This is especially true if you have had prior heart
attacks or chest pain with physical exertion. If you fall into these
categories, you MUST get approval from your physician first for safety
reasons. There are plenty of other exercise routines that you can safely
do and that will still be beneficial. We will cover some of these in the
exercise chapter.

HIIT is highly beneficial, but make sure your heart can tolerate high
intensity exercise before you dive in.
STRONG MEDICINE TACTICS:
Once cleared by your doctor, high intensity interval training is a great
method if you are short on time. Incorporate three sessions a week of
HIIT in your exercise program.
STEP 8

FIX YOUR SLEEP AND USE STRESS

REDUCTION TECHNIQUES.
If you are not getting at least 7-9 hours of restful sleep per night, your
fat loss and blood sugar control goals will come to a screeching halt.

We are going to extensively discuss sleep and stress reduction in

following chapters, but will get started with the main points.

Studies have shown that more than a third of adults in the U.S. are
getting inadequate sleep—and the health consequences are more than just
being tired the next day.

Sleep deprivation is a large stressor and turns on the body’s “threat

response.” Part of the threat response due to poor sleep is increased
oxidative stress and inflammation.

KEY POINT:
Poor sleep triggers your body’s threat response.

Just 1-2 nights of poor sleep have been shown to put healthy people into
a nearly diabetic state of insulin resistance! Imagine what this would do to
someone who is already obese or has prediabetes or diabetes. Poor sleep
also promotes weight gain as a likely effect of chronic insulin resistance.

Although the amount of sleep one needs can be substantially different

among individuals, The National Sleep Foundation recommends between
7-9 hours of sleep per night for adults.

KEY POINT:
Inadequate sleep leads to inflammation and oxidative stress, making
insulin resistance and other chronic diseases worse.

STRONG MEDICINE TACTICS:

To stop making insulin resistance and weight gain worse, ensure you
are getting between 7-9 hours of sleep per night.

We are not going to delve any deeper into sleep here, since there is a
whole chapter devoted to it later in this book. Just be sure to make sleep a
priority; you will not achieve your weight loss goals or healthy blood sugar
levels without consistent, adequate sleep.

Chronic psychological or “life stresses” also activate the threat response

in the brain, leading to chronic inflammation and oxidative stress. Stress
reduction techniques are crucial for the chronically stressed and will be
covered in detail in a forthcoming chapter devoted to chronic stress.
 COMING ATTRACTIONS >>>
Make sure you read the Chronic Stress and Sleep chapters to fully
understand the concepts, then incorporate the recommendations from
those chapters into your 8-step plan.

PARTING THOUGHTS ON THE 8-STEP

PLAN:
In closing, make sure you pay close attention and adhere to as many of
the 8 steps as possible. In doing so, you will achieve better and faster
results. It is important to note that use of Step 1 will vary depending on
your situation. If you are not diabetic, testing your blood sugar after meals
a couple of times can still give you valuable information. If you have
prediabetes or diabetes, Step 1 is extremely important to follow until you
figure out what foods consistently put you out of the target ranges for
blood sugar.

The key to this 8-step program is consistency, and the enemy of the
program is convenience. Preparing good food is time consuming, and
getting fast food is convenient.

KEY POINT:
 Consistency is your friend with the 8-step plan.
Convenience is the enemy.

Spend a couple of hours on a weekend to prepare a large quantity of

food for your lunches the following week. Soups and stews work well
because they are relatively easy to make in large quantities. We will cover
more of these ideas in the Strong Medicine Nutrition: Individualized
Strategies chapter near the end of the book.

Over time, consistency with the 8-step plan will lower chronic
inflammation and oxidative stress, fix your leptin signaling, restore insulin
sensitivity, and help you achieve your weight loss and blood sugar goals
without counting calories and being constantly hungry.

“BREAKING THE LINK”

The Strong Medicine 8-Step Program for Obesity and Insulin Resistance will
“break the link” in the chain between obesity/insulin resistance and chronic
disease, thus defeating the “enemy within.”
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KNOWING YOUR ENEMY III:
CHRONIC STRESS: THE SILENT KILLER

Chronic psychological stress affects us all to varying degrees.

Psychological stress is a serious problem that can lead to physical maladies.

Sustained stress in particular causes tangible, medically definable harm

to the body and brain. Chronic stress causes premature ageing while those
who have conquered stress look years younger than their chronological
age.

Very real physical changes occur to those who have continual chronic
stress. Chronic stress can be overcome by using proven stress-relieving
strategies and methods. Stress has been called the silent killer, but can be
overcome with knowledge and a game plan.

Chronic stress is a master assassin that kills with a thousand small cuts
over time. He will worm his way inside your brain and wreak havoc. As
you will see, this silent member of the Pentaverate will actually change
your brain and affect your body from the inside.
 The Strong Medicine training team has studied the ways of this killer
and devised effective defenses against him.
CHRONIC STRESS AND DISEASE
Recent research has linked chronic stress to a multitude of diseases. For
many of these diseases, stress is either thought to be the actual cause of the
disease, or at the very least, stress makes any disease worse.
 DISEASES ASSOCIATED WITH CHRONIC
STRESS
• Obesity
• Diabetes
• Alzheimer’s dementia and other
neurodegenerative diseases
• High blood pressure
• Heart disease
• Depression and anxiety
• Chronic pain
• Cancer

Even with the association of chronic stress to the above diseases, most
patients do not bring up their chronic stress when discussing their health
concerns with their doctor, and most doctors don’t ask their patients about
stress levels. There are roadblocks for having this crucial discussion...

• Many physicians feel they are physical custodians, not mental

custodians, and refuse to offer advice or recommendations regarding
stress reduction.

• Most physicians don’t have specific advice or recommendations to

give their patients to effectively reduce stress.

• Chronic stress is still not recognized as a serious risk factor leading to

disease.

• Historically there have been no good medical tests to evaluate chronic

stress. This is starting to change.

• Mental health and physical health are still viewed as separate and
distinct and obviously that is flawed thinking.
 Your mental health is really an extension of your physical state. Mind
and body need be addressed as an organic whole. Chronic stress will
prevent us from attaining any and all body-composition and fitness goals.
CHRONIC STRESS I
MIND AND BODY: WAS DESCARTES
WRONG?

Rene Descartes (1596 - 1650) was a brilliant 17th

century mathematician and philosopher widely
considered the father of modern philosophy. One of
his central philosophical tenets is the idea of dual
nature—we have a mind and we have a body.
Descartes proposed the theory of mind-body dualism
—the body and the thinking, conscious mind exist in
separate parallel universes. For Descartes, the body
Rene Descartes
was a material object following the laws of nature,
while the thinking conscious mind was (1596-1650) French
“nonmaterial,” and not subject to these laws. He mathematician and
philosopher
contended that the body and mind can influence each other, but ultimately
remain separate and distinct.

Descartes’s philosophy founded the idea that psychology and

neuroscience are separate and distinct disciplines—and should remain that
way. Psychology deals with the “nonmaterial” thinking mind while
neuroscience explores the actual mechanical workings of the physical
brain. Increasingly, modern science is discovering that this is not how the
mind and body function. Both form an intertwined, indivisible whole. New
fields of study such as neuropsychology and psychoneuroendoncrinology
explore this mind/body connection.
UNION OF MIND AND BODY
Our conscious and subconscious mind is responsible for so many things
on many levels. The brain is Command Central, Headquarters, the place
where projection and reflection reside. It is able to switch tasks, compute,
calculate, interface ongoing changes in our environment, then determine
our next actions and reactions. Consciousness always occurs in the exact
present time.

The brain monitors critical operations of the body, such as the second to
second function of the heart and lungs for example. Though the brain itself
is a physical organ, it has produced the non-physical consciousness of our
mind and is able to manifest our intellect, personality and behavior. The
actual physical brain is constantly shaped, changed, and literally
reconfigured, based on our experiences, thoughts and perceptions.
THE CHANGING BRAIN
Ideas, thoughts, attitudes and perceptions can literally change the brain’s
“hardwiring.” New technology now allows us to track these brain circuitry
changes. Brain plasticity is not new age nonsense designed to fleece hippies
—technical advances are allowing us to actually see how the human brain
can rewire itself. If the rewiring is in response to repeated, ongoing
physical and psychological stress, then it is a bad thing—but, if the
rewiring is in response to activating new and exciting areas of the
untapped brain, then it is a fabulous thing.

Change to the physical structure and function of the brain in response to

internal and external stimuli is known as neuroplasticity. The original
definition of the word plastic is, “Easily modeled or molded, capable of
adapting to various conditions.” The human brain is “plastic” as well, and
can mold or adapt itself to various conditions throughout a lifetime.

KEY POINT:
Neuroplasticity refers to the brain’s ability to physically change its
structure and function to adapt to changing environmental conditions.

The most current research shows that the human brain contains
approximately 86 billion nerve cells (neurons) and almost an equal amount
of “support cells” (glial cells). There are about 25 times more cells in a
single human brain than there are people on the planet. Even more mind-
blowing is the fact that each of the 86 billion nerve cells can form up to
1000 connections with other cells in the brain. The total number of
potential connections formed between nerve cells has been estimated at
several hundred trillion. The possibilities are literally endless.
 Let us take a look at the nerve cells and how they make these trillions of
connections.

The synapses, or “connections” between axons and dendrites of

neighboring nerve cells are “made” and “unmade” constantly, depending
on environmental circumstances. The making and unmaking of these
connections is the definition of neuroplasticity.

The picture above is a drawing of a nerve cell (neuron):

• The cell body of the neuron is the cell’s “control center” and the
location of the energy-producing machinery keeping the neuron
alive.
• The dendrites receive signals from the other nerve cells. You can
think of them as satellite dishes receiving incoming transmissions to
the neuron cell body.
• The axons transmit signals from the nerve cell to other nerve cells in
the brain, and also to other cells (like muscle cells) in the body.

The light blue “blocks” covering the axon in the picture above act as
insulation allowing the signals transmitted by nerve cells to travel
farther. This insulation is called myelin, and acts just like the insulative
coating around electrical wires, which allows electricity to flow without
“short circuits.”
 THE ULTIMATE WIRING DIAGRAM
Billions of nerve cells communicate with each other via the dendrite
“receivers” and the axon “transmitters.” This graphic only shows 6
nerve cells (neurons) connecting and communicating. Imagine the
complexity of billions of nerve cells each forming up to 1000
connections!

The yellow glow at the connection (synapse) of an axon “transmitter”

between one neuron to the dendrite “receiver” of another neuron
illustrates the communication signal passed along the chain of neurons.

This is how your brain communicates within itself and the rest of the
body. When you want to move your leg, this is how the signals pass
from the brain all the way to your muscles to tell them to move. This
system is also how the body communicates changes in your outside
environment to the brain. This is how signals about touch, taste, smell,
sight, hearing, heat, cold, and danger are communicated from body to
brain.

KEY POINT:
Neuroplasticity occurs because of nerve cells making and unmaking
connections. This process can start just minutes after a new stimulus to
the brain.

Like a muscle, the human brain has a “use it or lose it” quality. When
we stop performing regular physical activity, our muscles shrink, and
bones become brittle. Stressing our body purposefully and intelligently
with exercise halts these negative physical processes. The brain is no
different.

Your brain will adapt to the challenges you give it by forming new
connections. Without challenges, the circuit connections wither away. We
challenge the brain by taking on new and mentally complex tasks outside
our normal scope of activities. This includes difficult tasks like learning a
foreign language, taking up a musical instrument, reading classical
literature, composing poetry, sculpting, painting, or mastering another new
and different skill. There are two elements critical to invoking positive
brain plasticity. First, the new skill needs to be different from the skills you
already possess—new skills activate new regions of the brain. Second, the
skill needs to be sufficiently complex—we need intellectual stimulation, not
moronic “stupefaction.”

Mental challenges cause an “adaptive response” to take place in the

brain, just like a muscle. Challenges build axon-dendrite “transmitter-
receiver” connections. Passive activities such as watching “reality”
television do not stimulate or build these connections. We need to be
actively involved with our activities, instead of being passive observers.
Making and unmaking nerve cell connections (neuroplasticity) dictates
how well the brain can handle stress.

THIS IS YOUR BRAIN ON STRESS

Stress actually changes the brain’s structure and function through
neuroplasticity. Brain cell changes and alterations will affect how you
think, act and behave. The duration and intensity of psychological stress
makes a huge difference in how the brain responds to stress.

• Isolated, short-term stresses such as an argument with your friend or

spouse, final exam week at college, or an unexpected expense
temporarily causing financial stress, can all actually lead to resiliency.
Resiliency means that after the short-term stresses, you rebound and
are able to deal with future stresses that come along much better.
Think of the difference between a college freshman going through
her first exams, versus a graduate student who has spent the last 4-5
years dealing with exams. The graduate student is much less stressed
about exams than the freshman. The grad student has survived the
short-term final exam stress many times before and is now more
resilient. Her brain has made axon-dendrite “transmitter-receiver”
connections that allow her to deal with the stress of final exams
better. The freshman is just starting the process of building the brain
connections that enhance exam resiliency.
 FLASHBACK
Do a quick review of Central Themes IV, “Stress and the Response to
Threat,” before you read on.

The freshman has never encountered this level of exam stress before
and her brain registers the exams as a significant threat. This
produces the threat response. The graduate student’s brain, fortified
against the stress of final exams from years of experience, perceives
the exams as far less of a threat. Short-term, intermittent stressors of
relatively low intensity will build resiliency to future stress and
decrease the threat response.

KEY POINT:
Occasional, relatively low intensity stressors will build resiliency and
protect you from future stress through “rewiring” the brain
(neuroplasticity).

• Chronic stress, or high intensity stress alters the brain much differently,
and much more radically—in a negative, detrimental way—than short
term, low intensity stress. Chronic stress and high intensity stress (such as
combat stress, auto accidents, or other traumatic events) alter brain
“transmitter-receiver” connections that strengthen the stress response
over time to threats. The connections that strengthen the stress response
do not make you more resilient to future stress; instead you become more
vulnerable to the effects of psychological stress. Intense trauma makes you
more sensitive to threats in your daily life.
 Many of us under chronic stress can relate
to having “little things” set us off, and not
being able to handle minor stresses that
we used to take in stride. This feeling of
being always “stressed out” is because our
brain’s threat system has been rewired in
response to chronic stress. From a strictly
survival standpoint, your brain is trying to protect you from a persistent
threat. Remember from Central Themes IV that the brain’s threat
response doesn’t know if your “threats” are a nasty boss at work,
financial worries, or dealing with a troubled teenager. All it knows is that
you are under a daily “threat” and it responds by strengthening your
threat response. The problem is, the strengthened long-term threat
response is not good for your health.

KEY POINT:
Chronic stress “rewires” the brain to strengthen the stress response to
threat. This physical change in the brain will make you more sensitive
to future stress with poor long-term health effects.

We will diagram the “rewiring” of the brain to help you visualize what
happens to certain regions of the brain during chronic stress. The
Hypothalamic-Pituitary-Adrenal axis (HPA axis) is a “hardwired” stress
response system. The HPA axis and the Sympathetic Nervous System
produce stress hormones such as cortisol, epinephrine, and norepinephrine.
These hormones are released when preparing for a “fight or flight”
situation.

THE HPA-AXIS:
HYPOTHALAMUS-PITUITARY-
ADRENAL
• The fast pathway is triggered immediately after
the brain senses a threat. It bypasses the
pituitary and sends a direct signal to the adrenals
to produce epinephrine (adrenaline) and
norepinephrine. This pathway immediately puts
you in an alert state, and prepares you to “fight”
or “flee” from danger.
• The slow pathway is also triggered by threats, but responds slowly,
signaling the adrenal gland to secrete cortisol. Cortisol helps you
recover from the threat after it has passed.

The HPA axis induced hormones—cortisol, epinephrine, and

norepinephrine have the following actions on the body and brain:

• They increase the energy available to the body by increasing blood

sugar.
• They increase heart rate and blood pressure.
• They increase blood flow to muscles
• They produce hyper vigilant behavior (watchfulness, anxiousness,
alertness)

The HPA axis—both slow and fast pathways—is triggered in response to

any stress perceived as a threat by the brain. It is a well-designed system,
but is only meant to operate in response to “threats” in our environment.

The fast pathway triggers the sympathetic nervous system (flight or

fight). The result is the release of epinephrine (adrenaline), and a hormone
that closely resembles epinephrine called norepinephrine. Both of these
hormonal messengers increase alertness, release stored glucose from the
liver into the bloodstream, increase heart rate, stop digestion, and increase
blood supply to the muscles—all in anticipation of either fighting hard or
running away fast. This particular pathway will make you jittery after a
heated confrontation or disoriented after a car accident.

The slow pathway goes through the pituitary gland on the way to the
adrenal glands. This pathway is the most active about 30 minutes after the
threat has passed. Cortisol is the primary hormone that helps you recover
from the threat, and it prepares the body and brain for any future threats.
Cortisol releases glucose from the liver to ensure the brain has enough fuel
to deal with the threat. Cortisol will also “assist” in breaking muscles
down (muscle cannibalism) so the amino acids in the muscle protein can be
used to make more glucose for the brain. In certain circumstances, cortisol
helps the body eat itself. One reason many marathon and ultra-marathon
runners look emaciated is they are awash in cortisol to the point that
caloric shortfalls are fed with the runners’ own muscles.

This system was never meant to be used

daily. A majority of the population overuses
and over-works this system in response to
modern threats such as abusive bosses, snarled
traffic, domestic relationship and financial
problems or poor sleep.

As far as our brain is concerned, many of us

are “chased by bears” daily. While the degree
to which the system is activated will not
register as high as actually being chased by a
As far as our
bear or an assailant, we still activate it in
brain is concerned,
lesser degrees when responding to the constant
many of us are
daily stresses of modern life. Our stresses add
“chased by bears”
up to the proverbial “death of a thousand
daily.
cuts.”
THREAT AND THE STRESS RESPONSE
What determines if the HPA axis is activated to produce the stress
response? Anything the brain perceives as threatening from within the
body or from our external environment will activate the HPA and produce
a stress response.

• Potential threats arising within the body include infection, injury,

toxins or sickness. Internal threats do not have to be processed by
higher levels of the brain. The subconscious perceives the internal
threat and triggers the HPA axis to greater and lesser degrees.

• Higher levels of the brain process external threats that arise in our
environment and enter into our consciousness. External threats
require a series of “decisions” which need be made—the seriousness
of the threat is assessed, and a course of action is devised.

KEY POINT:
Potential threats from our external environment are first processed by
higher levels of the brain before they are determined to be threatening
or non-threatening.

Degree of threat and threat response will vary radically from individual
to individual. What is perceived as threatening to one person is considered
no threat whatsoever to a harder type. The difference between individuals
in the perception of threat is experiential: a Navy SEAL under fire during
combat will show a lower threat response and less agitation than a
distraught teenager dumped by a boyfriend or girlfriend.
 For simplicity’s sake, our discussion will be
limited to the three parts of the higher brain
instrumental in perceiving threats and initiating
the stress response. The workings of the brain
are staggeringly complex, and the following is
substantially simplified from the current science
of the brain and threat response. Let’s meet the
main players in this game:

• The Prefrontal Cortex (PFC)

• The Hippocampus
• The Amygdala

THE PREFRONTAL CORTEX (PFC)

The PFC is the area in the front of your brain (behind your forehead)
responsible for what brain scientists call “executive function.”
Executive function is the description given for tasks such as:
• Assigning “value” to something (“good” versus “bad”).
• Paying attention to something.
• Controlling your behavior (you lose this when you are drunk).
• Solving complex problems, and task switching (commonly called
multi-tasking).
• Distinguishing “same” versus “different” when viewing two objects.

The PFC can help stop a stress response by the HPA if executive
function is intact. The PFC is one of the brain structures that separates
us from animals. It helps us evaluate a potential environmental threat
by “thinking” about it before deciding if it is threatening or not. Animals
don’t have the executive function, and react to potential threats
instinctively without “thinking” about it.
THE HIPPOCAMPUS
This part of the brain is thought to be
responsible for functions such as:
• Putting short-term memory into long-term
memory (learning).
• Forming memories of “new” situations or
environments.

The hippocampus is one of the only areas in an

adult brain that regularly grows new nerve
cells. The hippocampus also helps stop stress
responses from the HPA axis by recalling memories about your
environment when you come across a potential threat you have seen
before.
 THE AMYGDALA
The amygdala is an area of the brain in charge of:
• Forming memories associated with strong emotions.
• Controlling aggressive behavior.
• Controlling emotional reactions.

The amygdala can activate the stress response by the HPA axis. It is
also the structure of the brain responsible for “learned fear.” For
example, hearing a bell does not provoke fear for most people.
However, if every time you heard a bell ring you received a painful
electric shock soon after, you would quickly learn to “fear” the sound of
a bell. This is an example of a learned fear produced by the amygdala.

When working properly, the PFC hippocampus and amygdala act

together to produce stress responses appropriate to the threat. The three
will also halt the stress response when the danger has passed—an
overactive stress-response system is counterproductive and detrimental.

The PFC and hippocampus can stop the stress response by using
executive function and memory to determine that something is not
really a “threat.”

The amygdala triggers the stress response to external stimuli in the

environment that are perceived to be “threats.”
 This is the normal “threat-stress circuitry” in the brain of a healthy person.

The PFC and hippocampus can stop the stress response by using
executive function and memory to determine that something is not
really a “threat.”

The amygdala triggers the stress response to external stimuli in the

environment that are perceived to be “threats.”


CHRONIC STRESS REWIRES “THREAT-

STRESS” CIRCUITRY
The hippocampus is especially sensitive to overactivation of the HPA-
axis. Over time, the high levels of cortisol from chronic stress will actually
shrink the hippocampus, reducing its function. Studies using special types
of MRI have shown that people under chronic stress (and people with
depression) have smaller, shrunken hippocampi, which are decidedly
smaller than those in healthy people. The mechanisms and rationale for
how and why stress shrinks the hippocampus include:

• Decreased dendrite “receiver” and axon “transmitter” connections

between bundles of nerve cells.

• Decreased formation of new neurons in the hippocampus. The

hippocampus is one of the few regions in the adult brain that
regularly produces new nerve cells (neurons). The hippocampus relies
on the formation of new nerve cells to maintain its numbers. When
fewer new nerve cells are formed, the overall population decreases,
shrinking the entire hippocampus.

The shrinking hippocampus results in poor short-term memory and

problems when coping with new situations and environments. A shrunken
hippocampus is woefully ill prepared to deal with stress, and does a poor
job of controlling the activation of the HPA axis.

The nerve cells in the prefrontal cortex (PFC) also shrink. The dendrite
“receivers” shrink, due to high cortisol levels released by chronic stress.
When the dendrite “receivers” shrink, they cannot form as many
connections with other nerve cells. These connections are critical for cell
communication. The “executive function” of the PFC is also diminished.
Without good executive function, we have trouble paying attention,
controlling our behavior, solving complex problems, organizing thoughts
and distinguishing “good” from “evil.”

Chronic stress changes the amygdala in a opposite way as compared to

the PFC and the hippocampus. “Receiver-transmitter” connections
between nerve cells in the amygdala will grow stronger and more
numerous in response to continual chronic stress. High fear and anxiety
levels increase the activation of the HPA-axis. The strengthened amygdala
can result in increased aggressive behavior.

Physical changes due to chronic brain stress include:

• Non-threatening stimuli are perceived as “threatening” to the
stressed-out brain. Tension and stress provoke the HPA-axis stress
response causing a decrease in function of the PFC and the
hippocampus. Stress strengthens the amygdala and these effects
combine to create stress responses to events that were previously
non-threatening. Many of us in modern society are “set off” over
trivialities, which causes us to engage in aggressive behavior like
“road rage”, overreacting, or snapping at friends and family over
minor issues.

• The poorly functioning PFC and hippocampus do not allow us to

evaluate situations well using our higher brain functions. We start
reacting to things much like animals do. One way to view the
physical changes of chronic stress is that our brains will function in a
more “animal-like” way.

• More stress leads to higher threat perceptions, which leads to more

activation of the HPA-threat system. More HPA-axis activity leads to
higher cortisol and adrenaline, which leads to poorer function of the
PFC and hippocampus. This is a vicious cycle of chronic stress and
has real health consequences.
 THE “STRESSED-OUT BRAIN”
Notice the shrinking of the PFC and the hippocampus along with the
strengthened amygdala. These changes will result in an overactive threat
response and HPA-axis activation.

The environment can physically alter our brain. It not only affects our
physical health, but can alter our behavior and even our personality. If
Descartes were living in our modern age, would he change his assessment
based on what modern science has discovered in respect to the mind/body?
FIRST PRINCIPLES PERSPECTIVE: STRESS AND
BRAIN CHANGES
What advantage would physical changes in the brain
in response to chronic stress give us? If you take us
out of modern society for a minute and think about
what chronic stress might mean in a different
environment, these brain changes may make more
sense.

If an individual from a primitive society was under a

constant threat from his or her environment—
predators, aggressive neighboring tribes—it would
make sense for the brain to change to help this person survive. If the
brain changes to interpret most things in the environment as a
potential threat (whether they are or not), the person will never be
caught off guard.

They will always be alert and anxious about every noise in the woods at
night, and it would be unlikely that a predator or human enemy could
sneak up and kill them. They are always ready for “fight or flight.”

In this primitive, survival situation, it seems better for them to react to

the unknown like an animal, instead of using any higher brain functions
(PFC and hippocampus) to further evaluate the “threat.” In the long-
term, this is bad for their overall health, but it could certainly help them
live another day in a dangerous environment.
CHRONIC STRESS II
STRESS AND HEALTH

THE “NEGATIVITY BIAS”

Human beings are hardwired to react more strongly to negative things in
our environment than positive things. Due to our higher brain function, we
are generally much more capable at evaluating potential threats than an
animal, but we still carry a “negativity bias.”

In psychology, a negativity bias means that a negative stimulus (pain,

conflict, criticism) will elicit a much stronger reaction and memory
formation than a positive stimulus (comfort, reassurance, compliment) of
equal intensity. Many of us intuitively know this is true from our own
personal experiences.

• One critical comment from a supervisor can erase ten previous

compliments from your mind.
• One argument or fight with a friend can end a friendship that has
existed for years.
• We learn more from making mistakes than we do by “getting things
right.”
 The negativity bias exists, and our brain reacts this way for a reason.

FIRST PRINCIPLES PERSPECTIVE: NEGATIVITY

BIAS
We already discussed the survival advantage for the brain changes
from chronic stress. These changes can be thought of as an extension
of the negativity bias. The negativity bias helps us survive when
exploring a new environment or situation.

If a situation is perceived by the brain

to have an equal amount of negative
and positive characteristics—such as
a potential source of food located
close to an aggressive bear’s home—
the potential danger from the bear
gets a stronger response from the
brain than the potential benefit of
getting the food. Even though food is necessary for survival, the
potential danger from the bear may stop you from pursuing this food
source. Starvation is surely a threat, and acquiring the food is a
powerful positive reward, but the bear is potentially an immediate
danger to life and limb. The negativity bias wins the day for immediate
survival.

Knowing about the negativity bias may help you moderate your
reactions to negative events and stimuli. Our higher brain functions allow
us to override systems like the negativity bias, once we understand them.

Many of us know people whom seem unfazed by genuinely stressful

situations. “Nerves of steel,” “courageous” and “crazy” are how others
view the rare few who have learned how to put non-life threatening and
life-threatening stresses into the proper context. Let’s not have a total
freak-out over a traffic jam; or grossly overreact when confronted by
everyday modern stressors.
 KEY POINT:
Understanding the negativity bias can help you react less negatively to
things that are not life or limb dangers.

EARLY LIFE EXPERIENCES SHAPE THE

STRESS RESPONSE
Traumatic events experienced in childhood (abuse, loss of a parent,
hunger, neglect) have a profound impact on a child’s developing brain—
especially the developing stress-threat system. As these children enter
adulthood, they are disproportionally afflicted with depression and
anxiety. Their brains are physically and functionally different than a
normal adult who did not have traumatic childhood experiences. The
developing brain of a child is much more susceptible to stress—from
childhood into adulthood.
FLASHBACK
Do a quick review of Central Themes II, “The Gene-Environment
Connection,” before continuing further.

CENTRAL THEMES CONNECTION:

 Early life Stress and Epigenetics
In Central Themes II “The Gene-Environment Connection,” we
discussed how epigenetic changes alter how a gene is expressed. Some
changes “bookmark” the gene, causing it to be turned on all of the
time, and other changes “stick the pages of the recipe together,” in
effect turning the gene off.
Early life stress causes these types of epigenetic changes in the areas
of the brain involved in the stress-threat system.

Specifically, early life stress “turns on” many of the genes involved with
making the HPA-axis function more often. This leads the HPA-axis to
be very sensitive to any “threats” in the environment, and will turn on
very easily. Adults with a history of significant early life stress can have
their stress systems turned on most of the time, even in response to
minor stresses.

Remember from the previous section that the prefrontal cortex (PFC)
and the hippocampus normally function to help stop the stress
response of the HPA-axis. Adults with a history of early life stress have
epigenetic changes that interfere with normal PFC and hippocampus
function. For these people, the PFC and the hippocampus don’t stop
the stress response well, and it can get out of control.

Research has also shown that children raised with abuse or other
significant stresses have epigenetic changes affecting the function of
the amygdala, making it strongly trigger the stress response of the
HPA-axis.

Recent research shows how continual and repeated stress rewires the
brain to make it even more susceptible and inclined to trigger stress. There
are epigenetic mechanisms responsible for these changes. Epigenetic
changes can be reversed over time. If you are an adult with a history of
childhood stress, seek to normalize the stress-threat system. This is
accomplished with consistent and dedicated brain plasticity training. The
adult brain is still very “plastic” or changeable, if you give it the right
inputs.

BRAIN CHANGES AND “MENTAL HEALTH”

Epigenetic changes to the brain of those afflicted with chronic stress
(particularly childhood stress) have been shown to increase depression,
anxiety and other mental health conditions. The brain is a physical organ
that is adversely affected, literally changed by chronic stress. This leads to
mood and behavior changes. Thus, “mental health” is just another aspect
of your physical health and should be treated as such.

Supporting this notion, people with major depression have been shown
to have smaller hippocampi than non-depressed individuals. These are
physical brain changes associated with depression and other mental health
disorders, not just a “mental” defect.

It should be no surprise that many of the self-treatment approaches

covered in following sections for chronic stress, have also been shown to
be effective in treating disorders traditionally thought of as mental health
problems.
STRESS AND CHRONIC DISEASE
The long-term health consequences of chronic
stress are primarily related to chronic
inflammation and oxidative stress. It is therefore
no surprise that chronic stress has been linked
to...

• Heart disease
• Diabetes
• Accelerated aging
• Autoimmune disease
• Cancer
• Obesity
• Depression-new research is showing that depression is an
inflammatory disease!

CENTRAL THEMES CONNECTION:

A primary mechanism behind how long-term stress leads to chronic
inflammation and oxidative stress is overactivity of the sympathetic
(“flight or fight”) nervous system. We covered this at the beginning of
the book in Central Themes IV, but it bears repeating. Activation of the
“flight or fight” (sympathetic) part of the nervous system can lead to
an increase in inflammation and oxidative stress.

Short-term activation of the sympathetic nervous system from stimuli

such as exercise produces short-term inflammation and oxidative
stress, which is beneficial for health through hormesis, as we have
discussed extensively.

Long-term, low level activation of the sympathetic (flight or fight)

Long-term, low level activation of the sympathetic (flight or fight)
nervous system from chronic stress leads to the chronic inflammation
and oxidative stress that is the underlying cause of many diseases.

Cortisol produced as part of the stress response is supposed to help

with recovery by decreasing inflammation and oxidative stress, after a
short-term stress such as exercise, injury, or escaping a predator. In
short, cortisol “puts the brakes on” inflammation and oxidative stress
produced by the “flight or fight” system after the “danger” has passed.

This system of checks and balances between the sympathetic nervous

system (inflammation) and cortisol (anti-inflammation) works
extremely well with short-term stressors. The problem lies when
cortisol (HPA-axis) is activated constantly. New research proposes that
the body develops “cortisol resistance” similar to insulin resistance
and leptin resistance. Similarly, it also leads to uncontrolled
inflammation.

TECHNICAL NOTE:
Cortisol receptor resistance is a relatively new area of research, but the
idea seems conceptually sound. Receptor resistance—as found with
insulin receptors in diabetes, and leptin receptors in obesity—is
commonly found in bodies with disease. It is not surprising that
another hormone, like cortisol, could follow this same theme.
DIGGING DEEPER:
Cortisol Receptor Resistance
Chronic stress and resistance to the effects of cortisol is a new area of
research. As discussed before, cortisol usually has anti-inflammatory
effects on inflammation produced by cells of the immune system
(both the “innate guardian” and “adaptive assassin” types). To make
this anti-inflammatory effect happen, cortisol binds to receptors on
the immune cells to signal for them to stop producing inflammatory
messengers (cytokines).

Remember from the Obesity chapter, we discussed how in insulin

resistance, the insulin receptor stops working and the normal signal
from insulin does not get through to the cell. Cortisol resistance is
similar to insulin resistance in this manner. With chronic stress, the
receptors for cortisol on the immune cells start functioning
insufficiently over time. When this happens, the immune cells no
longer get the signal to “turn off” inflammation after a threat has
passed. This results in long-term uncontrolled inflammation and
oxidative stress leading to chronic diseases such as heart disease,
diabetes, obesity, autoimmune disease and cancer.

In summary, chronic stress causes the “flight or fight” sympathetic

nervous system to trigger chronic inflammation from our immune
cells. The normal anti-inflammatory “checks and balances” produced
by cortisol are working insufficiently due to cortisol resistance.
 FLASHBACK
Remember the hunger communication system with its food reward in
the obesity chapter? High levels of cortisol produced by chronic stress
also trigger the food reward pathway. This causes hunger and cravings
for high-calorie, palatable foods. This makes since from a survival
perspective.

As far as your brain is concerned, cortisol means that you just survived
a significant stress and need to refuel. High calorie sources of fuel
would be desirable to prepare you for the next “fight or flight.”

Unfortunately in modern society, most of our “threats” don’t require

refeeding for recovery. The stressed out brain is more “animal-like”
and gets the signal to refeed anyway. When you are stressed,
recognize what is happening and don’t “feed the beast.”

BODY AFFECTS BRAIN; BRAIN AFFECTS

BODY
From the Gut Chapter, we saw that problems with our body can affect
the function of our brain. Recent research shows that metabolic diseases
such as diabetes can affect both the structure and function of the brain
over time. Studies have shown that diabetes can have the same “shrinking”
effects on the hippocampus as chronic psychological stress.

This should not be too surprising as diabetes is an “internal” physical

stress recognized as a threat by the brain, in the same way as a chronic
“external” environmental stress is seen as threatening. Diabetics
experience chronic activation of the HPA-axis because the brain thinks the
body is starving since the leptin and insulin signals not getting through to
the brain. The inflammatory “threat” of diabetes perceived by the brain
creates a vicious cycle…
 • The internal threat of inflammation triggers the HPA-axis, producing
cortisol. This process shrinks the hippocampus.

• High cortisol triggers the hunger communication system, signaling

you to eat more.

• Eating more makes the diabetes condition worse.

• As the diabetes gets worse, it produces more inflammation, which

triggers the HPA-axis, ad infinitum...

Diabetes makes people more susceptible to depression since a shrunken

hippocampus and inflammation are indeed contributors to depression. The
physical brain changes generated by continual chronic external stress are
made worse with the addition of chronic internal stress from diabetes.

KEY POINT:
No matter the source (external or internal), chronic stress makes the
brain change in ways that activates the threat-stress system (HPA-axis)
more often. This leads to chronic diseases and increased susceptibility
to future stress—a vicious cycle.
CHRONIC STRESS AND PREMATURE AGING
Chronic stress has been associated with accelerated aging in humans.
Chronic stress activates the HPA-axis/sympathetic nervous system’s threat-
stress response system. Long-term and continual activation of the threat-
stress response system leads to chronic inflammation and oxidative stress.
One of the consequences of chronic inflammation and oxidative stress is
damage to the protective “caps” (telomeres) on your chromosomes (DNA).
Losing telomeres leads to DNA damage. Damaged DNA eventually stops
your cells from dividing to regenerate the tissues and organs in your body.
When your tissues and organs can no longer regenerate, they start to fail—
leading to death. Chronic stress accelerates this process.

Many of us know people who’ve seemed to age before our eyes during a
period of intense stress. The perfect example of this is how a U.S. President
will appear to rapidly age during their term in office.
 The most health-damaging and age-accelerating aspects of chronic stress
are two stress behaviors—rumination and worry.

STRESS FROM “NOTHING”—RUMINATION

AND WORRY
Rumination and worry are stress-related behaviors that amplify the
negativity bias. The stress-threat system perceives rumination and worry as
two sides of the same coin. These behaviors are the largest contributors to
chronic stress.

Rumination is defined as having persistent negative thoughts about past

experiences. Rumination is a negative process that adversely impacts self-
image and self-worth. Rumination can be caused by critical comments or
embarrassing situations. Insecurity triggers rumination.

If you find yourself mired in continual and ongoing rumination, be

aware that this will have a devastating impact on your mental and physical
health over time. Rumination is in some ways “stress over nothing.”
Rumination is created in the mind, and in the same way, the mind can kill
rumination by not engaging in it, or silencing rumination before it has an
opportunity to fester and grow. We want to avoid reliving stressful
situations over and over in the mind, since this prolongs activation of the
HPA-axis. The ruminator is creating “stress from within” when there is no
real stress currently present in the environment.

Worry is the opposite side of the same stress coin. Worry is the
anticipation of a future stressful or threatening event. With worry, the
stressful event has not actually happened yet, but you are activating the
stress-threat response system when the brain “worries” about the future
event.
CENTRAL THEMES CONNECTION:
 Hormesis and Chronic Stress
The arrow below should look familiar. It was taken from Central
Themes III, Hormesis. The stress of rumination and worry follows a
hormesis-like response:

Point A represents an individual with no worry or rumination. Finding a

human without any worry or rumination would be extremely difficult.
Many animals fall into this category. As previously discussed, having no
worry or rumination would not be a survival advantage.

Point B represents an individual with occasional, short-term worry and

rumination. This “hormetic dose” of worry and rumination provides a
survival advantage by making this individual more resilient against
future stress.

Point C represents an individual with chronic daily worry or rumination.

The stress-threat system (HPA-axis) is constantly activated by “stress
from nothing”, leading to chronic diseases such as heart disease,
diabetes, obesity, depression and anxiety.

Scientists call this the anticipatory threat response. In effect, we are

anticipating a future stressful event, but causing a stress response in the
present moment—without an actual environmental stressor. This is why
we also classify worry as “stress from nothing.”

A certain amount of short-term periodic rumination or worry can make

us resilient to future stresses. Rumination and worry provide humans a
survival advantage over animals. With reasonable and appropriate worry,
we anticipate and prepare for future stresses.
 RESEARCH UPDATE:
Recent research has shown that anticipatory stress (worry) activates
the stress-threat system more than experiencing the actual future
stressful situation you are worrying about! Rumination and worry are
very hard to control with the environmental stresses of modern
society.

THE 24-HOUR NEWS MEDIA, CHRONIC

STRESS, AND THE NEGATIVITY BIAS
The modern news media is now operating 24/7, constantly reporting
on war, murders, plane crashes, abductions, economic forecasts, and
other negative events and subjects to anyone tuned in. Negativity
brings good ratings and feeds our negativity bias. Over time, habitual
watchers of the modern news media have increased chronic stress that
keeps their “flight or fight” system constantly in low-level activity.
Worriers seem to be the most affected.

Most people don’t even know what has happened to them until they
“unplug” for a period of time. Many people who voluntarily restrict
their viewing of the 24-hour news cycle for a week or so report lower
levels of anxiety and depressive thoughts. Taking a “news holiday” is
always a good idea.

Rumination allows us to learn from past threats—specifically, how to

adapt and better deal with similar threats in the future. But, long-term,
chronic rumination and worry over-activate your stress-threat system
(HPA-axis), fill your stress cup and eventually lead to chronic disease.
 Modern stresses amplify our inborn, human negativity bias to such a
degree that our health is negatively impacted by the thoughts, ideas,
projections, and reflections which occur in our consciousness.
Understanding this mental stress is the first step. The second step is
developing “mental antidotes”. Awareness of potential triggers or mental
land mines, that over-activate the stress-threat system empower you to
avoid, temper, or alleviate stress when it first appears.
CHRONIC STRESS III
MIND INTERVENTIONS

BRAIN-TRAIN:
WHERE EASTERN MEDITATION TACTICS
MEET WESTERN HIGH TECHNOLOGY
The previous chapters showed that chronic stress physically changes the
structure and function of the human brain by over-activating the stress
response, filling the stress cup to overflowing, contributing to age
acceleration, and developing chronic disease.

What if there was a mental approach or strategy that you could

consistently use to relieve stress, and minimize projection, reflection,
rumination and worry? Additionally, this same brain-train mind method
can be used to improve discipline, adherence, steadfastness and human
performance.

Training the brain will have a beneficial carry-over to physical effects

with the body. Training the body will beneficially affect the structure
 and function of the brain.

We live in the information age where there are no more

secrets. If you want to learn details about anything under the sun, just
Google it. Mental training techniques used by Eastern mystics and
shrouded in mystery for centuries are now available to anyone. Want to
learn Dogen Zenji’s tactical approach to meditation? No problem! Want to
learn about the breakthrough mental preparation of elite athletes in the old
Soviet Union? Google Dr. Aladar Kogler and read about his pioneering
work with autogenic and auto-suggestive practices.

Experts in the East and West have offered up complex and effective
systems for transforming the human mind from an individual’s worst
enemy into their best friend. Our user-friendly mind methodology is a
blend of Eastern contemplative techniques and Western athletic and
technological techniques and tools. All the religiousness and supernatural
aspects of Eastern meditational techniques, and overly mechanistic
shortcomings of the uber-rational Western approach have been stripped
away. Our synthesis of East and West—with understanding and practice—
will be immediately applicable for you in your current life situation.

View the interventions in this chapter as mental exercise—we are

literally training the brain in the same way we train to make our bodies
stronger and more resilient with physical exercise. Just as we need
consistency in our physical exercise, we need consistency in our brain-train
protocols.

The three main interventions are:

1. Mindfulness practice
2. Biofeedback
3. Physical exercise
I. MINDFULNESS PRACTICE
Mindfulness training originated in traditional Buddhist meditation
practices, but has been used extensively in modern medicine for well over
20 years.

WHAT IS MINDFULNESS?
In its simplest definition, mindfulness means focusing your attention
and awareness on the present moment. With mindfulness, you are
aware of internal processes like breathing, and external stimulus from
the environment—while not “holding on to” any thoughts or
experiences after they pass from the present moment.

Focusing your attention and awareness to the

present moment sounds easy until you try it for a
couple of minutes. At first, it is common for
beginners in mindfulness training to have intrusive
or distracting thoughts—that have nothing to do
with the present moment—pop into their heads.

Thinking about what you need to get at the store

for tonight’s meal, or the jerk that cut you off on
the way home from work, will take you away from
your focused attention on the present moment. You
Seamus the
can be aware of what goes on in your environment
“mindful cat”
moment to moment, but don’t hold on to or make
judgments on these stimuli, just label them as what they are and let them
pass. For instance, during mindfulness practice you can be aware of the
sound of a jet passing overhead, but don’t think about how annoying the
sound is, or how you wish you hadn’t bought a home so close to the
airport.

Being consistently mindful for even a couple of minutes can be

challenging at first. Try this simple breathing exercise to get you started.
MINDFUL BREATHING
Many mindfulness meditation techniques involve focusing on your
inhalation and exhalation during slow breathing. The way you breathe in
these exercises is critical to the desired effect on your nervous system. It is
important that you primarily breathe “into your belly” instead of your
chest. In other words, we are trying to almost exclusively use our
diaphragm for breathing instead of the chest and neck muscles.

There are scientific reasons for breathing in this specific way:

• Inhalation (breathing in) activates the sympathetic nervous system.

Breathing in using your chest and neck muscles strongly activates the
flight or fight sympathetic system. This makes sense when you are
running away from danger or fighting—you will take in huge gulps
of air by using your chest and neck muscles to assist your diaphragm.
This helps your muscles get the maximum amount of oxygen during
the physical stress of a flight or fight situation. The brain associates
“chest and neck breathing” with the flight or fight response and
increases sympathetic nervous system activation. Many people under
chronic stress habitually breathe this way without the presence of
immediate danger to life and limb. Breathing this way causes chronic
low-level sympathetic nervous system activation. We have previously
mentioned that constant high levels of sympathetic flight or flight
activation result in high alert levels, increased inflammation, and
oxidative stress that can lead to chronic disease. For this reason,
don’t use your chest and neck muscles for breathing.

• Exhalation (breathing out) activates the parasympathetic nervous

system. We want you to breathe with slow exhalations that are
longer than inhalation so we can tip the balance of your autonomic
nervous system in favor of the parasympathetic system, which has
anti-inflammatory and calming effects on your body. By breathing
out for a longer time than breathing in, we are spending a longer
time activating the parasympathetic system and a shorter time
activating the sympathetic system. The effect over time is less
 activation of the stress-threat system that we discussed in the
previous section. Try to practice breathing like this throughout the
day so it becomes a natural way to breathe. Many of us with chronic
stress have fallen into the “chest and neck” breathing pattern
without even realizing it.

• Find a comfortable position, either

seated or somewhat reclined.
• While you are first learning to breathe
correctly, place one hand on your belly
and the other on your chest.
• Breathe in slowly through your nose,
and make sure that you mostly feel the
hand on your belly move during inhalations, and only minimal
movement in the chest area.
• Exhale slowly. The time spent breathing out (exhalation) should be
longer than the time spent breathing in (inhalation). If you are
having problems exhaling slowly, purse your lips at the beginning of
the exhalation. This makes your mouth smaller and it will be easier to
control the air passing out of your mouth.
• Focus on the sensation of the air passing in through your nostrils,
filling your belly, and then passing out of your mouth.

Mentally count each cycle of inhalation and exhalation, attempting to

reach 10 without any “intruding” thoughts other than the sensation of
breathing. If you find your mind has wandered before you get to 10
breaths, start over.

• Focusing on the sensation of breathing without letting your mind

wander with distracting thoughts has the benefit of directly attacking
rumination and worry. Remember that your prefrontal cortex is
involved with maintaining attention. By focusing attention on
breathing, you are strengthening the connections in this area of the
 brain. By not allowing rumination, worry, and negative thoughts
—“stress from nothing”—we decrease activation of the stress
response. Decreasing chronic activation of the threat-stress system
over time with this type of mindful attention to the present moment
and breathing will strengthen the prefrontal cortex and hippocampus
while weakening the amygdala. The downstream effects of this
seemingly small breathing exercise performed routinely over time can
slowly physically rebuild the stressed brain so it functions normally
again.

With proper breathing, we can maximize our

time with high parasympathetic activation,
and only using the high level activation of the
sympathetic “flight or fight” system sparingly
when necessary.

Review Central Themes IV for more on the balance of the autonomic

nervous system.

The following graphic shows the “rebuilding” process of the brain

through daily mindful breathing exercises:

• Decreased rumination and worry, which decreases the activation of

the threat-stress system.

• Decreased activation of the sympathetic system with increased

activation of the parasympathetic system caused by slow “belly
breathing” with long exhalations, reduces overall activation of the
threat-stress system.

• Prolonged reduction of the stress-threat system activation allows the

prefrontal cortex and hippocampus to strengthen their connections.
 The bottom picture illustrates how regular mindfulness
breathing restores the healthy brain over time. The
previously overactive amygdala from the top image of the
“stressed out brain” is now “shrinking” and has a smaller
activation signal to the stress-threat system. Now that the
prefrontal cortex and hippocampus are strengthened, they
can stop the stress response better with stronger inhibition
signals. This will give you more resilience against future
stress. Mindfulness not only helps with present time stress
reduction, it prepares you to cope with future stress by
physically rebuilding and restoring the stress-threat system
to a healthy state.

This is how brain training with mindfulness practice is similar to

strength training for your muscles. In both cases, regular training causes
beneficial physical changes.
 KEY POINT:
Regular mindfulness practice can physically rebuild your brain in the
same way that regular strength training can build your body.

Start out by trying to spend at least 10 minutes each day with

mindfulness breathing, working up to 30 minutes a day over time. You
may begin to sleep better, have less depression and anxiety, and cope with
daily stresses more easily. Make time for mindfulness breathing whenever
you can. The benefits are too great to be ignored. Make the time to
practice.

STRONG MEDICINE TACTICS:

Start with 10 minutes a day of mindfulness breathing practice and
work your way up to 30 minutes a day over time.

THE BODY-SCAN
This is not a high-tech device at airport security checkpoints! Body
scanning refers to systematically visualizing and “paying attention” to each
part of your body. Like mindful breathing, you can perform this exercise in
a relaxed seated or reclining position.

Start by focusing your attention on one of your big toes for 20-30
seconds and register all of the sensations coming from this toe. Don’t let
any “intrusive thoughts” take hold and cause your mind to wander. Move
on from your big toe to the rest of your foot and proceed slowly up your
ankle, leg, knee, and thigh. At all times, focus on the sensations coming
from those specific areas. Then start at the big toe on the other foot and do
the same thing until you get to the waist area. Next, move up your torso
with the same focus on your abdomen, rib cage, and chest. When you get
to your neck, start with individual fingers on one hand and move up the
arm to the shoulder. Then begin with the other hand, moving up to the
shoulder on that side. Lastly, move up the neck into your head until you
reach the top of your scalp.

STRONG MEDICINE TACTICS:

Add the body-scan technique as part of your mindfulness training after
you have worked up to 20-30 minutes of mindful breathing practice.

The body scan may seem strange, but it is similar to the mindful
breathing exercise. Both exercises involve being in the moment while
focusing on the immediate sensations coming from your body. While doing
the body scan, if your mind wanders—especially with negative thoughts of
rumination and worry—stop, then start again at the big toe.

Focusing on the three dimensional space in and around your body

during the body scan is an additional strategy recommended by Dr. Les
Fehmi in his book, The Open-Focus Brain. In this approach, with your
eyes closed, imagine the three dimensional space occupied by each body
part as well as the distance between them. Dr. Fehmi asserts that focusing
on 3-D space further assists the mindful-state and enhances the body scan.

The body-scan technique is a somewhat advanced mindfulness

technique, and should be added after you have trained with the
mindfulness breathing technique for several weeks or months. Once your
breathing technique has become automatic, you can continue breathing
properly while performing the body scan.

With either the mindfulness breathing or the body-scan, you should

attempt a total 20-30 minutes of mindfulness training daily.
 This is just the very tip of the iceberg with mindfulness training. You
may find many other techniques that work better for you. There are some
fantastic mindfulness systems and books to explore if you like the results
you get from the basics:

• Jon Kabat-Zinn, PhD, brought mindfulness practice into mainstream

medicine. He founded the Mindfulness-Based Stress Reduction
(MBSR) course currently taught around the world. His books and
programs are excellent resources.

• Rick Hanson, PhD, is a neuropsychologist and author of Buddha’s

Brain. He has some excellent audio-based mindfulness programs that
are definitely worth looking into. He also discusses the science
behind mindfulness in a very clear and easy to understand way.

• Les Fehmi, PhD, is a pioneering scientist in the field of neurofeedback

(biofeedback for the brain) and the author of The Open-Focus Brain.
His scientific perspective on mindfulness is a great place for a
beginner to start.

Mindfulness “brain training” is no longer just for Buddhist monks or

Zen masters. It has become mainstream in a big way over the past 10-15
years along with very strong scientific evidence for health benefits. This
type of training interrupts the vicious negative mental thought cycles of
chronic rumination and worry. As rumination and worry are large
contributors to chronic stress, it’s no surprise that recent research shows
very promising results with mindfulness training for chronic “body”
diseases such as diabetes, heart disease, high blood pressure, and
autoimmune disease.
 You can’t try mindfulness exercises once and decide “they don’t work for
you.” That would be like going to the gym once and saying “exercise doesn’t
work for me.” This is brain training, and daily mindfulness practice is key if
you want to rebuild a stressed brain.
II. BIOFEEDBACK
Biofeedback is a technique for stress reduction in which you use devices
to monitor your body’s heart rate, muscle tension, or skin conductance in
the attempt to exert some type of control over these processes. A
biofeedback device will give you instant “feedback” so you can be aware
of your body’s state in real time. For instance, a device monitoring your
muscle tension can give you instant feedback to your stress state, since
increased muscle tension equals increased stress. You can also monitor the
sweat response in your skin with skin conductance biofeedback. Increased
stress leads to increased sweating, causing increased electrical conductance
measurable by the device. Monitoring muscle tension and skin
conductance provides a real-time window to your current state of stress—
second by second.

The idea of biofeedback is to use real-time information in an attempt to

change your stress level. If the device shows increased muscle tension—that
you might not be aware of—then you can actively try to relax your
muscles to change the muscle tension readings. You will be able to change
your behavior based on the feedback.

KEY POINT:
Biofeedback uses monitoring devices to train you to reduce stress-
related body responses.

Many of us walk around during the day with high amounts of muscle
tension from underlying stress. We may “carry” the stress in our neck or
chest muscles. Biofeedback brings this muscle tension to your awareness so
you can change it by relaxing. Once we are aware of the behavior, we can
eventually “catch” ourselves and stop the tensing behavior without using
the biofeedback device.

Monitoring muscle tension and skin conductance can require expensive

equipment and technical expertise. These types of biofeedback sessions are
best done in a clinic with a biofeedback professional.

A type of biofeedback many of us can perform at home with relatively

inexpensive equipment monitors something called heart rate variability.

Heart rate variability (HRV) does not measure the slowing down and
speeding up of the heart rate as the name might imply. HRV measures the
variation in the time between each heartbeat.

The best way to illustrate this concept is to show how the heart behaves
in a person with a resting heart rate of 60 beats per minute (one beat every
second).

Low Variability: the heart beating

exactly once every second. The time
between each beat is exactly the same
(in this case 1 second). This machine-like
precision is not how a healthy person’s
heart beats. Low variability is a marker
of poor health.

High Variability: the heartbeats do not

happen on exactly every second.
Sometimes the time between
heartbeats is less than a second, or more
than a second. This person would still
have 60 heartbeats in a minute on
average, but would not have a heart beat exactly every second. High
variability is a marker of good health.

LOW HRV = BAD

 Low HRV, the machine-like heart, has been linked to a high amount of
sympathetic nervous system (“fight or flight”) activity. Low HRV is seen
in people with chronic diseases and indicates poor health overall.
Chronic stress and activation of the stress/threat system causes the
heart to beat in a more “machine-like” way, causing low HRV.

HIGH HRV = GOOD

High HRV corresponds to higher activation of the “rest and digest”
parasympathetic nervous system. High HRV is associated with good
physical health and low stress states.

New technology has allowed for portable HRV biofeedback devices that
you can use at home. These devices monitor your HRV moment to
moment by tracking your pulse with different types of sensors.

Using the mindful breathing techniques covered earlier in this section,

biofeedback can track how proper breathing reduces “flight or fight”
system activation and raises your HRV. The device will also alert you if
your attention drifts into worry or rumination which both raise your
anxiety levels and lowering your HRV.

Biofeedback devices that use HRV are useful for daily practice at home
to reduce your stress levels. There are plenty of portable systems on the
market, but our current favorite personal HRV biofeedback system is Inner
Balance made by HeartMath. It is an application and ear sensor that works
with the iPhone.

With biofeedback, you can train your brain to maintain low stress states
with real effects on your body. Give it a try...

STRONG MEDICINE TACTICS:

Try a personal HRV biofeedback device to reduce chronic stress and
raise your heart rate variability. Use it daily for maximal health benefits.
III. EXERCISE
Similar to mindfulness practice, exercise decreases activation of the
stress-threat system (HPA-axis). But, it also helps to regrow stress-
shrunken brain structures such as the hippocampus by stimulating the
release of Brain Derived Neurotrophic Factor (BDNF).

DIGGING DEEPER:
Exercise, BDNF, and the Hippocampus
Exercise stops the shrinking hippocampus by not just decreasing the
excess cortisol from stress activation of the HPA-axis, but by
stimulating the growth of the hippocampus by an additional
mechanism.

Exercise is a potent stimulator of Brain Derived Neurotrophic Factor

(BDNF). BDNF is a protein that stimulates nerve cell growth and is a
central player in neuroplasticity (adaptive brain changes to
environmental stimuli). Exercise stimulates BDNF, which stimulates the
growth of nerve cells in the hippocampus, rebuilding this part of the
brain that was “shrunken” by stress. Recall that the hippocampus is a
key player in preventing the stress-threat system from getting out of
control. Regrowth is good for controlling stress.

Exercise has proven to be beneficial for stress relief. Recent research

shows that exercise specifically decreases rumination and worry—both
major contributors to chronic stress. Exercise has been shown to be
extremely effective for reshaping the stressed brain through neuroplasticity.
Reshaping the brain connections with exercise is
 thought to be responsible for helping the anxiety
and depression-related symptoms that often
accompany chronic stress.

Exercise is a true mind-body intervention.

While you can train both the body and the brain
directly, not all exercise is optimal for targeting
brain training.

COACH’S CORNER:
We love outdoor exercise such as chopping wood, running or biking
steep mountain trails, running along the seashore, swimming, intense
games and sports. Think big athletic cardio—not being stuck indoors
like a gerbil riding or operating an aerobic stationary bike or machine
while watching the built-in TV to distract you from the horror of the
mindless activity you are doing.

Meanwhile the mountain biker or runner—tearing along wooded trails

of serene natural beauty—is having a transcendental, altered-state
experience while working his lungs until they sear and generating
innumerable rivulets of sweat.

Outdoor exercise gives maximum stimulus from the environment. It is

superior for keeping you in the moment, mindful of what you are doing. It
is easy to fall back into worry or rumination when you are plodding away
on a treadmill or elliptical machine.

Chris has always been drawn to sports such as mountain biking, rock
climbing, trail running, and surfing. There is no room for rumination or
worry while flying downhill on a narrow mountain bike trail, or when
dropping in on a big wave. Marty is a life-long
powerlifter. He is not thinking about anything but
the present moment while pulling a 500lb deadlift.
Both of us have been drawn to sports such as these
because of the mindful aspects built in to the
performance of these activities.

You certainly do not have to engage in

powerlifting or rock climbing to tap into physical The authors engaged
mindfulness activities. A short hike in the woods can in “physical
quickly reset your stress-threat system. Also, yoga mindfulness”
and the ancient Chinese internal martial art of T’ai chi ch’uan (known as
tai chi in the West) are embodiments of physical mindfulness and can be
practiced by anyone regardless of fitness level or athletic experience.

STRONG MEDICINE TACTICS:

Get regular exercise for stress relief. Outdoor exercise and “physical
mindfulness” activities are especially beneficial to reverse stress-
related brain changes. Let Nature be your trainer, get outdoors!

COMING ATTRACTIONS >>>

There will be extensive coverage on the Strong Medicine exercise
approach in Part 3, Battle Plan.
KNOWING YOUR ENEMY IV:
CONCLUSION

Chronic stress causes structural and functional changes in the brain that
“link” to significant health consequences and leads to premature aging.
The human mind and body are not separate entities, but tied together
inextricably.
 Chronic stress can also affect other organs such as the gut, multiplying
chronic inflammation and oxidative stress. Remember the Gut-Brain Axis?
 The triumvirate of brain training—mindfulness, biofeedback, and
exercise—will repair the damage of the stressed brain and combat chronic
disease by reducing inflammation and oxidative stress.

If you still think this is all new-age nonsense, be aware that recent
research using sophisticated brain imaging techniques has shown that brain
training does indeed physically reshape the brain. Several studies show that
people who exercise and practice mindfulness regularly have structurally
and functionally different brains than those who do not. People who
exercise and practice mindfulness also have much lower rates of stress-
induced chronic disease and mental health disorders. Just as weightlifters
grow their muscles, and runners improve their cardiovascular fitness
through training, brain training does the same for the brain.

In our stressed-out modern world, brain training can help prevent

chronic disease and is truly part of the fountain of youth for your mind
and body.
BREAKING THE LINK
The Brain Training Triumvirate (mindfulness, biofeedback, and exercise) can
stop chronic stress in its tracks, “breaking the link” between chronic stress and
chronic disease. The Strong Medicine Defensive Tactics in this section will
expose the lurking “Silent Killer” and stop his subversive plan to destroy your
health.

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KNOWING YOUR ENEMY IV
CIRCADIAN DISRUPTION: THIEF IN THE
NIGHT

Our body and mind follow a natural rhythm of activity and rest that few
of us appreciate or follow. The modern environment is at odds with this
ancient internal rhythm that developed at the origin of our species.

Failure to follow this circadian rhythm creates dissonance and

disruption in the internal workings of our body—with profound
consequences to our health that modern science is just now beginning to
appreciate.

Circadian Disruption is one of the more slippery members of the

Pentaverate. He operates in ghostly silence and attacks relentlessly. You
cannot touch, taste, smell, or hear him. The only evidence of his attack is
constant fatigue and the slow destruction of your health.
 We will show you how to spot him and stop him in his tracks. We have
his number.
CIRCADIAN DISRUPTION I
THE INTERNAL TIMEKEEPER

A master clock resides deep inside the brain. It governs cycles of

sleeping, waking, eating, fasting, body temperature, and controls the ebb
and flow of the various hormones that control our metabolism.

This clock is not constructed of metallic gears, it is a molecular clock

made of genes and protein located within specific nerve cells of the
hypothalamus. Recall that the hypothalamus is the control center of the
brain that responds to signals from the environment. It controls many of
the body’s processes, so it makes sense that the hypothalamus houses the
master clock.

QUICK DEFINITION:
Circadian is from the Latin circa = “about” dies = “day”. Processes that
follow circadian rhythm fluctuate over a time period of approximately
 24 hours or “about a day.”

The inner workings of our master molecular clock are just now being
understood by very sophisticated cutting edge science and will not be
covered in Strong Medicine due to the extreme complexity.

Science has recently shown that most cells in the body contain their own
circadian clocks, but only the master clock in the hypothalamus can
maintain a circadian rhythm without external influences from the
environment. Scientists have removed master clock cells and locked them
away from environmental influences like light and dark, fueling and
fasting, and yet they maintain their rhythm of slightly more than a 24-hour
cycle (between 24.2 and 24.5 hours).

The master clock in the hypothalamus regulates all of our major organs
including the liver, lungs, heart, kidneys, gastrointestinal tract, and our
muscles. Each organ has its own internal clock that is influenced by the
master clock. This ensures that each organ system is adjusted to meet the
metabolic and functional demands of activity during waking hours, and
allows for “sleep mode” regeneration during rest and sleep. This rhythm of
the metabolic and physiologic ebb and flow allows for maximal efficiency
in operation and repair of the “flesh machine.”
THE CONDUCTOR OF THE ORCHESTRA
The master clock in the hypothalamus coordinates the activity and
regeneration rhythms of the organs in the body. The individual organs’ clocks
also communicate with each other through hormonal signals to coordinate
optimum functionality for activity during the day, and repair and regeneration
at night.

This timing system and the organs’ coordinated rhythms are crucial for
ensuring precious energy is not wasted and each organ system is prepared
to function individually and in harmony with the other organs.

The whole system must be coordinated to deal with the extremes of the
circadian cycle: full throttle physical activity during the day, and deep sleep
during night time hours.

The master clock is the conductor of this symphony orchestra. The

various organ clocks are the musicians who must listen to each other while
following the conductor. One organ clock out of sync with the system is
like a violist playing a different tune than the rest of the orchestra—
disastrous to the overall performance, and in the body, this is disastrous to
long-term health.

Peripheral body “organ clocks” are set by the “master clock” in the
hypothalamus. Each organ clock controls organ functions during activity
and regeneration modes. They are crucial in ensuring the organ systems
work together in a synchronized manner. As we will see, desynchronized
(broken) clocks lead to chronic disease.

The adrenal gland’s clock helps maintain the timed

secretion of cortisol in the early morning to prepare
for activity by increasing glucose release from the
liver. It reduces cortisol levels in the evening and
through the night to promote rest and regeneration.
 The heart clock helps prepare the heart for daytime
by making it more responsive to the demands of
physical activity with heart rate and strength of
contraction. At night, the clock allows the heart to be
less responsive during sleep.

The liver clock helps control the “glucose banker” so

that the liver can store glucose during daytime
activity and meals, then release and make glucose at
night during fasting to supply the brain.

The pancreas clock sets insulin secretion at the

highest during daytime activity to allow for energy
storage. At night, insulin secretion is set low to
ensure the brain receives a steady supply of glucose
for regeneration.

The fat clock controls the release of the hormones

adiponectin and leptin. Adiponectin is higher during
daytime activity to increase insulin sensitivity,
allowing the storage of nutrients. Leptin is higher at
night, delivering the “stop eating” signal necessary
for fasting during regeneration.

The muscle clock helps prepare our muscles for optimum performance
during the day. The clock sets a metabolic rhythm, making it easier for
 muscle to burn glucose during the day, then using fat
for energy at night.

The immune clock has the

immune system on alert for
threats such as bacteria and viruses
in the daytime, then at night the
adaptive assassins create “immune
memories” for the threats
encountered during the day.

The kidney clock helps control fluid and electrolyte

balance in the body. To support daytime activity,
blood pressure is increased, then at night there’s a
10-20% drop in blood pressure during regeneration.

The gut clock regulates gastrointestinal function to

increase digestion, absorption of food, and motility
(movement of digested food) during the day. It
signals for repair of the gut lining at night when
digestive processes are minimized.
 During daylight hours, hormone levels are controlled by the master
clock in the hypothalamus to support increased physical activity.
• Cortisol levels are highest in the morning. This increases glucose
after nighttime fasting, making energy available for the brain and
body. It also helps “wake you up”.
• Leptin levels are low in the morning and during daylight hours, this
gives the brain the “GO” signal to eat. Hunger is high with low leptin
levels, this promotes eating to satisfy the energy requirement for
physical activity during the day.
• Melatonin levels are suppressed by light, which brings the brain and
body out of resting/sleep mode to prepare the mind and body for
activity.
• Growth hormone is low, suppressed by increased cortisol in the
morning as the body comes out of the regeneration/repair mode of
sleep.

During the onset of night, hormone levels are controlled by the

master clock in the hypothalamus to support repair and regeneration.
• Cortisol levels are lowest at this time to prepare the body and brain
for sleep. Low cortisol allows for growth hormone secretion during
sleep.
• Leptin levels are high at night, giving the brain the signal to “stop
eating”. Hunger is low with high leptin levels, which promote fasting
 during the repair/regeneration phase and allow for uninterrupted
sleep (no need for midnight snacks).
• Melatonin levels start to rise as the sun sets, giving the brain and
body the signal to slow down in preparation for sleep and the repair
and regeneration that happens during this time.
• Growth hormone is high especially during deep sleep in the first part
of the night. Growth hormone increases the burning of body fat for
energy during fasting, and increases muscle repair and regeneration.

Because the organs in the body function differently if we are in the

activity or regeneration phases of the circadian rhythm, are there optimal
times to perform activities such as exercise and eating so these activities
match up with the rhythm of organ function?

• Is it better to exercise in the morning or evening?

• Is a late night snack a good idea?

• Are there any health consequences to shift work?

We’ll answer these questions in upcoming sections, but they are

important to consider now.
LIGHT RESETS THE MASTER CLOCK
While the master clock in the hypothalamus can keep running without
any external influence, the clock can be reset to match the external
environment through outside influences such as light. It is important to
reset the clock daily as most people’s internal master clock runs in a cycles
a bit longer than 24 hours. The majority of the general public has an
internal timekeeper genetically set to about 24.5 hours. Some people may
have longer cycles up to 26 hours.

Without external cues from the environment (such as light), the internal
timekeeper would slowly advance out of sync with the environmental 24
hour cycle ruled by the rising and setting of the sun. Most people’s internal
time would end up being about 30 minutes off “environmental time” each
day, adding up to over 3 hours out of sync in a week.

KEY POINT:
Most people’s master clock is genetically set for a cycle of about 24.5
hours. We need external “cues” from the environment to “reset” our
clock each day.

The external environmental clock setters are called “zietgebers,” which

is German for “time givers.” Light is the most powerful zeitgeber that
resets our master clocks on a daily basis.
 KEY POINT:
Light is the most powerful environmental cue to reset the master clock.

The circadian master clock regulates our daily rhythm of activity and
regeneration through key hormones as shown in the previous diagram. Of
these hormones, melatonin is of particular importance to how we enter
and exit the body’s regeneration mode.

When light—especially short-wave length blue light—hits our eyes in the

morning, specialized cells in the back of our eyes transmit this signal to the
hypothalamus (master controller). The hypothalamus transmits the “light
signal” to a tiny structure in the brain called the pineal gland, which is
responsible for producing melatonin. The “light signal” tells the pineal
gland to stop producing melatonin so we can enter the activity phase of the
circadian cycle.

KEY POINT:
Light signals the pineal gland to stop producing melatonin. Decreased
melatonin levels send a message to the master clock and the organ
clocks to prepare for the activity phase.

After the physical and mental stress of our daily activities, the body and
brain desperately need time to regenerate and repair. Our flesh machine
enters regeneration mode primarily through the actions of the hormone
melatonin. The dimming light—with longer wavelengths of red and orange
—in the evening signals the hypothalamus to tell the pineal gland to start
making melatonin. Melatonin production starting at twilight is the
gateway into regeneration mode.

KEY POINT:
The dimming light of the evening sky signals the pineal gland to start
producing melatonin. Melatonin is the gateway into the regeneration
phase.

MELATONIN: THE GATEWAY TO

REGENERATION MODE
 Melatonin is indeed the “gateway” hormone for entering the
regeneration mode, and it is essential for overall health with multiple
actions in the body:

• Melatonin prepares the brain and body for sleep, allowing a smooth
transition between waking and sleeping.

• Melatonin signals the organ clocks to start shifting from activity

mode into regeneration mode.

• Melatonin is a potent antioxidant and greatly increases the body’s

internal antioxidant defense system to decrease oxidative stress.

• Melatonin has antiinflammatory properties that can counteract

chronic inflammation.

• Melatonin is a crucial signal for cellular and DNA repair. This is

important because damaged cells and DNA contribute to accelerated
aging and cancer.

Given the many actions of melatonin which enhance regeneration of the

flesh machine, and protect against chronic disease, anything that decreases
melatonin during the evening and night has the potential to cause health
problems. Melatonin interacts with the master clocks as well as the organ
clocks to help keep the flesh machine “orchestra” perfectly synchronized as
the brain and body weave in and out of the activity and regeneration
modes in the 24 hour circadian rhythm.

KEY POINT:
Interrupting the natural cycle of melatonin secretion at night has far-
reaching health consequences and contributes to many chronic
diseases.
 One of the gravest consequences of low melatonin at night is sleep
disturbance. Poor sleep has emerged as one of the most important public
health issues of the modern age. Chronic poor sleep doesn’t just result in
fatigue during the day, it plays havoc on the regeneration mode at night.
Recent research shows that poor sleep is a major contributor to chronic
disease. Building a perfect night’s sleep is a challenge in a modern world
polluted by artificial light. Read on for a description of sleep in its
optimum form.
CIRCADIAN DISRUPTION II
SLEEP ARCHITECTURE: BUILDING A
GOOD NIGHT’S SLEEP

There is a lot happening in the body and brain from the time you lay
your head down at night until you wake in the morning. Sleep is much
more than escaping the conscious world when the lights go out. The health
benefits of the regeneration mode happen during high quality sleep.

An episode of sleep is actually a very structured process built on a cycle

of sequential stages that repeat approximately every 90-120 minutes, with
four to five total cycles during a night of sleep. The structured cycle of
sleep is called sleep architecture.
BUILDING BLOCKS
There are two distinct types of sleep that occur during the night—non-
rapid eye movement sleep (NREM) and rapid eye-movement sleep (REM):

• NREM sleep makes up about 75% of total sleep time during the
night. It is divided into 3 distinct stages: NREM-1, NREM-2, and
NREM-3. As you fall asleep you descend down through the stages:
awake NREM-1 NREM-2 NREM-3. The electrical activity
of your brain slows as you descend through the stages to NREM-3.
Brain electrical activity is very slow at NREM-3, also named slow
wave sleep (SWS). Slow wave sleep happens mostly in the first part
of the night.

TECHNICAL NOTE:
Non-rapid eye movement sleep (NREM) was traditionally broken up
into four separate stages. In 2008, the American Academy of Sleep
Medicine merged stages three and four—both characterized by slow
wave sleep (SWS)—into one phase. The NREM-3 we refer to in this
book is the combination of stages three and four, to be consistent with
the new classification system.

• REM sleep makes up about 25% of total sleep time. In this type of
sleep, the brain shows electrical activity similar to waking states.
REM sleep is also known as “active sleep.” REM sleep is when most
dreaming takes place, The length of time spent in REM sleep
increases at the end of the night.
IMPORTANCE OF SLOW WAVE SLEEP (NREM-3)
Slow wave sleep (SWS) during the first part of the night has some very
important functions in the regeneration mode of circadian rhythm:

• Most of the daily supply of growth hormone is released during slow

wave sleep. Recall that growth hormone is essential for sparing muscle
mass while burning fat for energy during the fasting period at night.
Reduced slow wave sleep leads to reduced growth hormone. Reduced
growth hormone leads to muscle wasting, and slows fat loss to a crawl.

• Events from the previous day are stored in long-term memory during
slow wave sleep. This is especially true for storing new information
learned during the day into long-term memory for later recall.

• Much of the cellular and DNA repair in the body and brain is
performed during slow wave sleep.

COACH’S CORNER:
You will not achieve your body fat reduction or muscle gain goals if you
are not getting enough sleep—no matter how dialed-in your nutrition
and exercise plans. Inadequate sleep = reduced slow wave sleep =
reduced growth hormone= poor body fat loss and increased muscle
wasting.
 THE FIRST HALF OF THE NIGHT—(NREM-3)

The first half of the night is dominated by slow wave sleep (NREM-3).
Notice that as you descend into sleep, you spend a relatively brief time
in NREM-1 and NREM-2 before spending the majority of time in the
deep SWS of NREM-3. The mind is quiet with slow electrical activity.

Much of the restorative and healing processes of the regeneration

mode happen during NREM-3 in the first part of the night. Disrupting
NREM-3 has significant health consequences of which few are aware.

THE SECOND HALF OF THE NIGHT—(REM)

The second half of the night is dominated by REM sleep, when

dreaming takes place. During this time, the mind is very active with
electrical activity similar to waking states. During REM sleep, although
the mind is active, the muscles of the body are paralyzed.

REM sleep is extremely important for health, but for different reasons
than SWS as we will discuss shortly. Most people don’t appreciate the
potential health consequences of reduced dreaming.
 IMPORTANCE OF REM SLEEP
The importance of rapid eye movement (REM) sleep to human health
and function is less clear than that of slow wave sleep, but some
theories are emerging from recent research...
• In REM sleep, we can play out stressful situations in the safe
environment of dreaming. This process is thought to give us
resiliency, leaving us less vulnerable to the effects of actual stresses
encountered during waking hours. Recall from the Stress Chapter
how stress can cause significant health problems. REM sleep may
help shield us from actual stressful events by “rehearsing” stressful
situations in our dreams.
• REM sleep is thought to significantly enhance creativity and problem
solving. Historically, great works of art and scientific breakthroughs
have been reported as happening after dreaming. Recent science has
shown us that REM sleep activates areas of the brain thought to be
responsible for problem solving and creativity.

Sleep research is still in its infancy and we are only beginning to crack
the surface of what happens at night in the mind and body when we leave
the conscious world. But, the nasty health effects of sleep deprivation are
already well defined. Before we launch into the health problems caused by
poor sleep, it is crucial to understand what causes us to fall asleep, and the
transition from activity mode to regeneration mode. We cannot fix sleep
problems such as insomnia if we do not understand the internal processes
that allow us to fall asleep under ideal circumstances.
THE DRIVE TO SLEEP
There are two primary processes that work together to promote falling
asleep and staying asleep. If these two systems are synchronized, we will
enjoy a smooth plunge into a restful and regenerative sleep period. If these
systems are uncoupled, insomnia and restless, fragmented sleep may occur.

SLEEP DRIVE #1: THE CHEMICAL SYSTEM

The first sleep system is the “chemical system” because it is primarily
driven by the build up of a certain chemical—adenosine—in the brain. The
name of this chemical may seem familiar; it is part of the “energy
currency” molecule adenosine triphosphate (ATP) introduced in the
Metabolism 101 section.

Recall that the brain is an “energy hog” and

uses 20% of the body’s supply of ATP even
though it is only 2% of the body’s weight.
When adenosine triphosphate (ATP) is used
for energy it loses its phosphates and becomes
adenosine. Adenosine could be understood as
an energy waste-product. The brain goes
through a mountain of ATP during the high
activity of waking hours. Adenosine, the
energy use “waste-product,” begins to build
up in certain parts of the brain. This build up of adenosine is the chemical
signal that produces fatigue and drives sleep as night approaches.

KEY POINT:
 The “energy waste product,” adenosine, accumulates in the brain
during the day. Once adenosine builds up to a certain level in the brain,
it triggers the drive to sleep.

Adenosine building up during the day

is analogous to adding debt on an
“awake-time credit card.” Once this
credit card reaches its awake-time
spending limit for adenosine, it must be
paid off. The only way to pay off this
credit card is by sleeping. After several
hours of sleep, a large amount of the
adenosine will have cleared out—the “credit card” will be close to paid off,
and waking is triggered.

SLEEP DRIVE #2: THE CIRCADIAN SYSTEM

The second sleep system is the one driven by the circadian rhythm. The
circadian sleep system follows the light-dark cycles of your environment
and works side by side with the chemical (adenosine) system. The circadian
system sets the threshold of how much adenosine can be accumulated on
the chemical system’s “awake-time credit card” before triggering sleep.

The circadian sleep system sets the adenosine threshold (“credit-limit”)

primarily through the actions of melatonin. During darkness, the circadian
system secretes melatonin and sets the adenosine “credit limit” low. Lower
amounts of adenosine will easily trigger sleep with the lower “credit limit”.
When daylight hits the eyes, the circadian system stops secreting melatonin
and the adenosine credit limit is set higher. Now it will take higher
amounts of built up adenosine to trigger sleep.
 KEY POINT:
The adenosine “credit limit” is the amount of adenosine build-up
necessary to trigger sleep. This “credit limit” is set by the circadian
sleep system.
• A high “credit limit” requires a large amount of adenosine to trigger
sleep.
• A low “credit limit” only needs a small amount of adenosine to
trigger sleep.

The morning sunlight triggers the

circadian system to stop secreting
melatonin. The circadian sleep system
issues a high credit limit “gold card”
for adenosine for use during the day.

The adenosine gold card issued by the circadian system allows the brain
to accumulate relatively high amounts of adenosine during the day without
triggering sleep.

As the sun sets, low light levels

trigger melatonin. At this time, the
circadian sleep system issues a low
credit limit “gray card” for use at
night.

The low credit limit gray card issued by the circadian sleep system
lowers the amount of adenosine necessary to trigger sleep.

The card switch from gold to gray as the sun sets allows the amount of
adenosine that accumulated during the daylight waking hours to trigger
sleep under the low adenosine credit limit of the gray card. The gray card’s
lower credit limit requires that the adenosine “debt” be paid immediately
by sleeping.

The card switch from gray to gold as the sun rises allows the brain to
accumulate adenosine during waking hours without reaching the high
credit limit. The gold card’s high credit limit prevents the accumulating
adenosine from triggering sleep during the day, so we can wait to pay the
sleep debt.
SLEEP SYSTEM SYNERGY
The chemical and circadian systems are synergistic for a reason. It makes
sense to sleep when the master clock and organ clocks of the circadian
system are primed for the regeneration mode. Using the circadian sleep
system, the brain will allow sleep to be triggered more easily by the
chemical sleep system if the master clock and organ clocks are prepared to
enter regeneration mode.

It also makes sense to wake up when the master clock and organ clocks
are primed for activity mode. The brain will resist the chemical signal
(adenosine) to sleep if the circadian master clock and organ clocks are
primed for activity mode.

When working properly, the circadian system will keep you asleep under
the effects of melatonin even though your levels of adenosine are
decreasing during sleep. The regeneration mode of the circadian system
will set the low gray card “credit limit” for adenosine. This means you can
clear out adenosine to relatively low levels by sleeping and remain asleep
because the low adenosine levels are still triggering sleep because of the
“low credit limit.”

During waking hours the circadian system in activity mode counteracts

the rising levels of adenosine as the day progresses, allowing you to stay
awake. The circadian system in activity mode sets the adenosine “credit
limit” high with the gold card so you can accumulate adenosine without
falling asleep during the daytime.

The two sleep systems ensure that our circadian clocks and organ clocks
are optimized to our activity levels. We should be awake during the
circadian activity mode and asleep during circadian regeneration mode. To
do otherwise will cause significant stress on our mind and body. Out of
phase sleep systems result in using a gold card at night and a gray card
during daytime. This is called circadian disruption and leads to poor sleep
and eventually chronic disease.
 We are going to cover the health consequences of inadequate sleep in the
next section, but first we will describe how the circadian system gets out of
sync with the chemical-adenosine sleep system. Before we can fix
something, we have to know the cause of the problem. The alternative is to
try treating sleep symptoms with medications without addressing the
underlying causes.
CIRCADIAN DISRUPTION III
EDISON’S FOLLY? THE CONSEQUENCES
OF A BROKEN CLOCK

Thomas Edison, the prolific American

inventor of the late 19th century, brought us
the first electric light bulb suitable for
widespread consumer use. Edison also
patented an early electrical distribution
system, paving the way for the accessible
electrical power we enjoy in our homes and
businesses today.
Thomas Edison,
American inventor
 There is no doubt that Edison’s American inventor
contributions to the Industrial Age have allowed the transition to the
modern Information Age, supported by trillions of kilowatt-hours of
electrical power annually. Businesses can now operate around the clock,
and we can engage in late night recreation because of the ubiquitous bright
electrical lighting in our world.

Prior to electric light, the world primarily woke and went to sleep with
the light and dark cycles from the rising and setting of the sun. Prior to
130 years ago, our circadian rhythms were entrained with the sun since the
origin of our species. Electric light has enabled us to live out of sync with
our natural circadian rhythm by extending waking activity well into the
night. It has also enabled us to start working well before the sun comes up
in the morning.

From a circadian perspective, the regeneration mode has been

significantly shortened in exchange for extended activity time. Science is
now starting to understand that the artificial disruption of the circadian
system may not be so good for our health.

Light is the most powerful stimulator of the circadian system. Natural

light is broken up into a spectrum of different colors, each corresponding
to different wavelengths. You can see the light spectrum when it is
refracted by water droplets in a rainbow or when viewed through a crystal
prism. Otherwise, you cannot distinguish the full spectrum of colors hiding
within daylight.

The short wavelength—primarily blue light—portion of natural light

stimulates our circadian system. Blue light signals the brain to stop
melatonin production and prepare us to enter the activity mode of the
circadian cycle.
 The blue light from the sun rising in the morning signals the master
clock and the organ clocks to prepare the mind and body for the increased
energy demands of activity. Natural light’s effects on melatonin keep us in
activity mode during the day. The circadian system issues us a high credit
limit “gold card” to prevent the build up of adenosine from triggering
sleep.

KEY POINT:
Blue light, the short wavelength part of natural light, is the primary
stimulator of the circadian cycle. Blue light turns off melatonin
production and signals the activity mode to start.
 Before incandescent light bulbs were widespread, the setting sun reduced
the blue light signal that triggered melatonin production. The circadian
system issued the “gray card” with the low credit limit as melatonin
increased and the adenosine build-up triggered sleep. Light from candle
flames and fire have less blue light in their spectrums and did not
significantly affect the circadian systems of preindustrial citizens.

In modern times, widespread use of indoor electric light at night has

effectively extended the daylight. Although indoor electric light is lower in
intensity than sunlight, it still has a significant amount of blue in its
spectrum. It does not take much blue light to stop melatonin production,
and recent science has shown that most nighttime indoor light significantly
reduces melatonin production. This light at night (LAN) extends the
activity mode of the circadian cycle at the expense of the regeneration
mode. Computer screens and television sets also give off significant
amounts of blue light.

Light at night (LAN) is not just from indoors. If you live in or around a
metropolitan area, it will be difficult to see the starts at night. Many places
in our country simply no longer have true darkness at night. Street lamps
and illuminated signs shine through bedroom windows, potentially
disrupting melatonin production and sleep. This constant outdoor electric
light at night is known as light pollution.
FALLING ASLEEP WITH LAN
The light at night (LAN) exposure many of us have produces an
abnormally long activity mode with no gradual transition from wake to
sleep. Without exposure to LAN, melatonin production starts
approximately 2-4 hours after natural light starts to dim at sunset. This
delay in melatonin production 2-4 hours after sunset corresponds well to
bedtime for many people who do not have the influence of artificial light at
night.

Recent research has shown that exposure to artificial light at night not
only delays the onset of melatonin production, but also reduces the total
amount of melatonin produced overnight. Many of us try to go to sleep
right after exposure to artificial light for most of the evening hours. Even
though we have turned off the lights, we will have to wait an additional 2-
4 hours for melatonin production to start in full swing. Since melatonin is
the gateway to the regeneration mode for the mind and body, we have
delayed and shortened the time for recovery and repair.

Light at night (LAN) also makes it difficult to fall asleep. Recall that
melatonin generated by the circadian sleep system issues the low-credit
limit “gray card” for the adenosine sleep system. In this way, melatonin
allows the built-up adenosine to trigger sleep. If we have delayed melatonin
production with LAN, we are still in the activity mode of the circadian
sleep system. We are still carrying the high credit limit “gold card” for the
adenosine sleep system while trying to fall asleep. The gold card credit
limit will not allow the adenosine built up during the waking hours to
trigger sleep. Insomnia is the result.

Compounding the problem, light at

night decreases the melatonin produced
when we finally enter the regeneration
phase. The low levels of melatonin do
not produce a strong “keep sleeping”
signal as adenosine levels of the chemical
sleep system drop during sleep. The
 Using the adenosine result is frequent waking during the
“gold card” night, especially towards the early
at night = insomnia morning. Valuable sleep is lost.

Many people in modern society wake before dawn to a home

illuminated by low intensity artificial light. Then they go to offices with
only low intensity artificial light which does not completely shut off
melatonin production. To truly reset the circadian system in the morning
and strongly enter the circadian activity mode, we need the high intensity
natural light from outdoors. Outdoor natural light has a high enough
intensity and a significant amount of blue light in its spectrum to
absolutely turn off melatonin.

KEY POINT:
High intensity natural outdoor light is the best way to reset the
circadian system and enter into activity mode.

While anemic indoor light is enough to stall the start of melatonin

production at night, it does not sufficiently shut off melatonin production
in the morning once the regeneration mode has picked up steam during the
night. The low intensity indoor lighting sends mixed signals to the master
clock and organ clocks. The internal clocks do not fully initiate the activity
mode, and your brain and body are not optimized to meet the challenges
of the day.

Many people who suffer from disrupted circadian systems and the
resulting poor sleep at night turn to stimulants like caffeine to keep them
going during the day. The out-of-sync circadian sleep system lets relatively
small amounts of adenosine build up and trigger an intense feeling of
fatigue and need to sleep. It is no surprise that caffeine works by
interfering with adenosine signaling.

A significant number of us carry around enough chronic adenosine sleep

debt that we need caffeine and other stimulants on a daily basis to keep
functioning.

QUICK MEDICAL NOTE:

Caffeine keeps you alert for activities such as all night study sessions,
late night parties, or to help you get through your day after poor sleep.
It stimulates us and delays sleep by stopping the actions of adenosine
in the brain.

In effect, caffeine—and the theophylline in tea—slows down the

chemical sleep drive system, keeping you awake. Unfortunately you
will have to pay your sleep debt at some point after the effects of the
caffeine wear off.
LAN AND CIRCADIAN DISRUPTION
The end result of high amounts of indoor light at night and the lack of
outdoor natural light in the daytime is a broken circadian system. This
shortens the duration of restorative sleep at night and leaves us struggling
to survive the day without falling asleep. Over time, this pattern leads to
chronic disease through allostatic overload.

Noted scientists and chronobiologists Michael Terman, PhD, and Ian

McMahan, PhD, state in their groundbreaking book Chronotherapy,
“Most of us live a twilight existence.” They are describing modern life
with no true daylight in indoor offices during the day, and light pollution
obscuring true darkness at night creating perpetual twilight.

Circadian disruption and the accompanying lack

of restorative sleep are major contributors to filling
your daily stress cup. Light at night (LAN) allows us
to uncouple the synergy between the circadian cycles
of activity and regeneration modes, and our actual
patterns of waking and sleeping. The long-term
health effects of this circadian disruption cannot be
underestimated—the clocks are broken.
Circadian disruption
and poor sleep
significantly fills
your stress cup
CONSEQUENCES OF A BROKEN CLOCK
Long-term circadian disruption often leads to chronic poor sleep with
significant health consequences. It is hard to separate the adverse health
effects of circadian disruption from those of inadequate sleep as they so
often occur together.

Circadian disruption leads to sleep problems, and poor sleep can

negatively effect the circadian system. Not all sleep disorders are caused by
circadian disruption but these sleep problems do impact the circadian
system. Trying to tease out the cause of these long-term health effects is
like the “chicken or the egg” argument. We do know that long-term
inadequate sleep is strongly associated with the following conditions:

• Obesity
• Insulin resistance and diabetes
• Cancer
• High blood pressure
• Increased susceptibility to infectious disease
• Heart and vascular disease
• Depression
• Aggravated symptoms of autoimmune disease
• Accelerated aging

The chronic disruption of the circadian system seen in long-term night

shift workers has also been associated with all of the conditions listed
above. This supports the strong reciprocal link between sleep disruption
and circadian disruption regarding health consequences.
THE MALFUNCTIONING MASTER CLOCK
When the master circadian clock in the hypothalamus is “broken”, it has
far reaching effects on the mind and body. Recall that the hypothalamus is
the master controller for many functions of the flesh machine including:
metabolism, reproduction, stress-threat response, hunger, thirst, and body
temperature. The master circadian clock orchestrates the timing of all of
these crucial processes in the hypothalamus based on anticipated activity
and regeneration cycles.

When the master clock is out of phase it affects the body’s organ clocks
as well. With overall direction by the hypothalamus, the organ clocks are
finely tuned with functions optimized to activity or regeneration,
depending on their place in the circadian cycle. Exercising when the organs
clocks are in regeneration mode, or sleeping during activity mode places
stress on the body.
 When the organ clocks are out of sync with your waking and sleeping
activity, they are not prepared to function optimally to support your
activity. Waking activity during circadian regeneration mode leads to poor
physical and mental performance as well as wear and tear on the body.
Attempting to sleep in circadian activity mode promotes poor mind and
body repair and regeneration. Some possible scenarios are outlined below.

Cortisol timing is off and may peak when you are

trying to go to bed at night instead of the normal
time—just before waking. Cortisol at night is
stimulating to the mind and body and will disrupt
sleep.
A heart clock still in regeneration mode while you
begin the increased activity of the day is not
prepared to respond to the increased demands of
physical activity. Wear and tear on the heart is the
result.

A liver clock still in regeneration mode while you are

having a meal in the morning will cause the liver to
mishandle glucose or fat. Insulin resistance, diabetes
and fatty liver disease are possible long-term
consequences.

A pancreas clock still in regeneration mode during

the day may not produce adequate insulin to handle
food intake, contributing to diabetes. If the clock is in
activity mode while you are sleeping, the
inappropriate insulin release may make your blood
sugar too low at night.

A disrupted fat clock will cause adiponectin and

leptin to be released at the wrong times. The result
will be hunger at night, disrupting sleep and loss of
insulin sensitivity leading to diabetes.
A muscle clock still in regeneration mode during
physical activity will lead to poor athletic
performance. Muscle clock dysfunction can also
cause improper glucose handling leading to insulin
resistance and diabetes.

A broken immune clock can lead to a poor defense

against “invaders” during the day and poor formation
of long-term immunity. It may also lead to out of
control inflammation which contributes to heart
disease, diabetes, cancer, and autoimmunity.

A broken kidney clock can cause poor regulation of

fluid and electrolyte balance contributing to high
blood pressure, a risk factor for heart disease and
stroke.

A gut clock still in regeneration mode during a meal

can lead to poor digestion and poor movement of
food through the GI tract. A gut clock in activity
mode during sleep leads to poor intestinal barrier
regeneration contributing to chronic inflammation.
 TECHNICAL NOTE:
The organ clocks can adopt circadian rhythms independent of the
master clock with signals such as food intake and exercise. This can
cause problems with various organ clocks being on their “own
schedule,” and out of sync with each another. That is why the
orchestrating function of the master clock is so important, it ensures
that the organ clocks work together optimally.

THE MELATONIN CONNECTION?

One of the primary ways exposure to artificial light at night may slowly
destroy your health and vitality is through diminishing the amount of the
hormone melatonin. We previously described the potent effects melatonin
has during the regeneration mode as a powerful antioxidant and
antiinflammatory agent. In addition to acting as a direct antioxidant to
scarf up free-radicals, it also strongly stimulates the body’s own
antioxidant defense system, protecting against oxidative stress. Melatonin
has been shown to protect against cancer and accelerated aging. There are
melatonin receptors (“docks”) in almost every type of cell in the body.
Melatonin truly has a long reach, potentially affecting every part of the
mind and body during its activity after dark as the gateway hormone to
regeneration.

The benefits of melatonin are not a surprise given its protective effects
against oxidative stress and inflammation. Diminished melatonin at night
due to circadian disruption and reduced sleep is likely a primary
mechanism through which sleep and circadian disruption contribute to
chronic inflammation and chronic oxidative stress. These two processes are
the well-known deadly duo leading to chronic disease.
 This is not to say that melatonin deficiency is the sole cause of all
chronic diseases arising from circadian disruption and poor sleep. It is a
likely major contributor, but circadian disruption and poor sleep activate
the brain’s stress-threat system on their own. The stress-threat system
greatly increases the flight or fight sympathetic nervous system activity
level, resulting in inflammation and oxidative stress.

KEY POINT:
Circadian disruption and poor sleep result in decreased melatonin
production, chronic activation of the stress-threat system, and
physiologic “wear and tear” on the internal organs.

This all adds to the growing pool of chronic inflammation and oxidative
stress which lead to chronic disease.
CIRCADIAN DISRUPTION, SLEEP, AND
DIABETES
When the body’s organs are forced to operate out of phase with their
own individual circadian clocks, the resulting metabolic derangement and
physiologic stress causes additional inflammatory responses and oxidative
stress. This is especially true of the liver, muscles, and the pancreas.
Disruption of the natural daily rhythm of these three organs is thought to
contribute significantly to the development of insulin resistance leading to
diabetes.

The effects of circadian disruption and poor sleep on the development of

insulin resistance and diabetes can be profound. Several recent scientific
studies have shown that even a couple nights of poor sleep can increase
insulin resistance to prediabetic levels in healthy young people.
 It was found that the loss of slow wave sleep (NREM-3) is the biggest
contributor to insulin resistance.

KEY POINT:
A couple nights of poor sleep have been shown to increase insulin
resistance in healthy young people to prediabetic ranges.

Loss of slow wave sleep seems to be the most damaging.

If circadian disruption and reduced slow wave sleep can give a healthy
young person insulin resistance to prediabetic levels, imagine what
metabolic havoc poor sleep can have on an obese or diabetic person. For
diabetes, we often focus on nutrition and exercise to help control blood
sugar levels. This is hugely important, but a diabetic with disrupted sleep
will have great difficulty meeting blood sugar goals no matter how good
they are doing with their nutrition and exercise.

QUICK MEDICAL NOTE:

If you are obese and/or diabetic, fixing your sleep must be a top
priority. Good nutrition and exercise are a great start, but you most
likely be unable to reverse type II diabetes without mastering your
circadian rhythm and getting recuperative sleep.

The next section will give the Strong Medicine Tactics to fix your sleep.
OTHER EFFECTS ON THE BRAIN AND BODY
Circadian disruption and sleep loss result in poor long-
term memory formation and difficulties with
concentration. Both can also lead to anxiety and
depression due to their effects on the brain. Slow wave
sleep (NREM-3) and REM sleep are crucial for the brain’s
recovery after a day of activity. During sleep, memories
and information are stored, emotional events are processed
to promote resiliency, and irrelevant “mental debris” from
the previous day is cleared away.

Circadian disruption tears away the carefully structured

sleep architecture, often reducing slow wave sleep and REM time in favor
of lighter sleep stages such as NREM-1 and NREM-2. This results in light,
non-regenerative, restless sleep. You can get a full eight hours of this non-
recuperative sleep and still feel like a truck hit you in the morning.

BODY FAT, MUSCLE, AND SLOW WAVE SLEEP

Remember that slow wave sleep is the primary time for growth
hormone release. Growth hormone is a major player in fat burning,
muscle growth, and muscle repair during the regeneration mode.
Circadian disruption leads to reduced slow wave sleep, a one-way
ticket to body fat gain and muscle wasting.

You will not reach your body composition goals unless you fix your
sleep.

A night of poor sleep will limit your productivity the next day, make it
difficult to concentrate or make decisions, and will decrease your ability to
handle stress. Your reaction time will slow to the equivalent of having a
blood alcohol level above the legal limit. A sleep-deprived driver can be
just as dangerous as a drunk driver with impaired ability to react in traffic.
Make sure you get your slow wave sleep before you drive.
 QUICK FACT:
A sleep-deprived driver can be just as dangerous as a drunk driver.
Studies have shown that sleep deprivation results in reaction times as
slow or slower than a person with a blood alcohol level above the legal
limit of 0.08 g/dL.

It’s likely that there are many more sleep-deprived drivers than drunk
drivers on the road. Driving while sleep-deprived is a real safety
concern and public health issue.

Spending time to fix circadian disruption can be especially important for

people suffering with depression. One of the interventions shown to be
effective for improving depressive symptoms is bright light therapy (BLT).
We will discuss BLT in the next section as a method to reset the circadian
rhythm. The anti-depressive effect of BLT in the morning supports the
theory that a significant contributor to depression may in fact be circadian
disruption.

A final note to dieters struggling to control cravings and food intake.—

circadian disruption and sleep loss stimulate the drive to eat. The
threat/stress response that results from poor sleep puts the food reward
system into overdrive. Poor sleep results in a strong drive for palatable and
rewarding foods that are often the same foods a dieter is trying to avoid.
Fixing your sleep and circadian system will put the reigns on food cravings.
 KEY POINT:
Circadian disruption and poor sleep put the food reward system into
overdrive. Your goals of sustained lifestyle change will be sabotaged by
cravings if you do not address circadian and sleep issues.

SHIFT WORK: A CIRCADIAN NIGHTMARE

Part of the formal training in Occupational and Environmental Medicine
(OEM) includes chronobiology. Chronobiology is simply the study of
natural biological rhythms such as the circadian system. OEM physicians
apply the knowledge of chronobiology to shift workers. As much as 20%
of the U.S. workforce participates in some type of shift work.

Night time shift work is the ultimate circadian nightmare. It puts the
worker at complete odds with the natural cycle of the sun’s rising and
setting for activity and sleep.

• The nightshift worker starts his or her day during the darkness of
night. They are gearing up for physical and mental activity when the
mind and body should be entering regeneration mode.

• They are exposed to relatively low-intensity indoor light during their

work shift. This somewhat suppresses melatonin but does not give
the strong circadian signal for activity mode that high-intensity
natural light provides. They often rely on caffeine to block the sleep
promoting effects of the adenosine which accumulates while they are
working.

• The nightshift worker often finishes their work shift as the sun rises in
the morning. During their drive home, the high intensity outdoor
light is stops melatonin production and places them in the circadian
 activity mode. The circadian system issues them a “gold card” for
adenosine with a high credit limit, and prevents the accumulated
adenosine in the brain from their time at work from triggering sleep.

• The worker will go home and attempt to sleep while their circadian
system is in activity mode. The outside daylight seeps into their home
during sleep and decreases melatonin. The adenosine build up
becomes so high that it is able to override the circadian system to fall
asleep but only for a short while. Most night shift workers report
only getting 5-6 hours of sleep at best in the daytime. The sleep they
do get has a significantly disrupted sleep architecture with shortened
slow wave recuperative sleep.

• The nightshift worker wakes in the afternoon and prepares for the
physical and mental activity of their upcoming “day”. The sun sets
during the hours when they are preparing for work.

• These workers often eat their meals during the regeneration mode of
the circadian system, a time that the organs are not prepared to
process and store nutrients from food. This leads to metabolic
derangement such as insulin resistance.

The extreme circadian disruption and poor sleep of the shift worker
results in significant health consequences. Nightshift workers are at greater
risk for developing chronic diseases such as diabetes, obesity, high blood
pressure, heart disease, depression, accelerated aging, and cancer. In fact,
the World Health Organization has classified shift work as a carcinogen
(cancer-promoting).

Many people have no choice but to perform shiftwork to make a living

and provide for their families. In the next section, we will show some easy
strategies shift workers can implement to minimize the circadian disruption
of and improve their health.

EDISON’S FOLLY?
The point of this section was not to blame circadian disruption in
modern society on Thomas Edison’s amazing invention. There is no doubt
that artificial light in the modern world has dramatically altered how we
live our lives and has allowed increased productivity and an exponential
rate of technological advancement over the past century. Unfortunately,
substantial negative impacts to our individual and public health have
resulted from this advancement as a tradeoff.

Modern problems require modern solutions. We will now provide some

very simple and science-based interventions that can go a long way in
fixing your broken clocks and restore the healing power of circadian
regeneration mode.
CIRCADIAN DISRUPTION IV
MODERN SOLUTIONS TO A MODERN
PROBLEM

U.S. citizens are working longer hours than the citizens of any other
industrialized nation in the world. We are taking full advantage of artificial
light at night to work longer hours, making us especially vulnerable to
circadian disruption. Many other countries are not far behind us, with
sleep disorders and circadian disruption emerging as a worldwide public
health problem—if not an epidemic. Fueled by artificial light, our
recreational activities are extending further into the evening hours as well,
with time spent in front of computer and television screens constantly
increasing.

Statistics from the National Sleep Foundation support the notion of

inadequate sleep as a public health epidemic.
 • Over 60% of American adults experience sleep disruption on two or
more nights per week.

• Approximately 40 million Americans report chronic sleep problems.

• Approximately 30% of Americans report routinely getting only 6

hours or less sleep per night.

Additionally, the increased hours Americans are working do not

translate into increased productivity on the job. Sleep deprived workers are
not efficient or productive. An estimated $18 billion is lost every year in
decreased productivity from sleep loss in the U.S. alone.

We rely on stimulants such as caffeine during the day to keep us going

while adenosine levels keep piling up in the brain. Caffeine does not solve
the problem and we carry the accumulated adenosine as sleep debt, since
we’ve artificially stopping the sleep trigger. Most of us put off this sleep
debt all week with stimulants and try to repay it on the weekends by
“sleeping in.” This pattern is hard on the body and brain, and overfills our
stress cup (allostatic overload).

We switch off the bright lights as we hit the bed, already well into the
night. Then we are frustrated that we can’t fall asleep immediately, as we
struggle against a circadian system disrupted by light at night. We resort to
alcohol or prescription drugs as sleep aids instead of fixing the underlying
problem, a disrupted circadian rhythm.

Alcohol and many of the drugs used to help people fall asleep
dramatically alter sleep architecture. Slow wave restorative sleep time
(NREM-3) is reduced and replaced by an increased time in the “light
sleep” stage of NREM-2. You may fall asleep faster, but you are missing
the period of slow wave sleep crucial for your health.
 KEY POINT:
Alcohol and many of the sedative prescription medications alter sleep
architecture, reducing time spent in slow wave sleep.

Sending your circadian system the right signals at the right times can
reset your clock and will help break the cycle of using stimulants to keep
you going and sedatives to make you sleep. Stop fighting your broken
internal clock. There are some simple ways to realign your internal clock
with your personal wake-sleep needs, even if you are a shiftworker.
FIXING YOUR CLOCK
We can use light (even artificial light) to “train” your circadian system
to match up with your waking and sleeping schedule. Training the
circadian system with light exposure is what chronobiologists call
entrainment. The timing of meals, body temperature, and exercise can also
be used to entrain the circadian rhythm, but light remains the most
powerful “trainer”.

The goal of training your circadian system is having your activity mode
fall inline with your time awake, and the regeneration mode synchronized
with your sleep. This is more difficult with extreme situations such as
nightshift work, but still doable to some extent. We will begin by showing
you how to use light as a “circadian trainer.”

KEY POINT:
Fixing your clock involves getting the activity mode of the circadian
cycle to fall inline with your time awake, and the regeneration mode
synchronized with your sleep.

LIGHT AS THE MASTER-TRAINER

Recall that short-wavelength light in the “blue range” is a potent signal
to turn off melatonin and start the activity mode of the circadian system,
while the dimming light at the end of the day will trigger melatonin release
in preparation for regeneration. The following interventions will get you
started in becoming a master of your circadian rhythm...
 • Use a dawn simulator to make the
transition from sleeping to waking gentle
and natural. Most people experience a
startling transition from sleeping to
waking with the piercing sound of an
alarm clock. Often they are in the middle
of REM sleep and the sudden loud noise
rips them out of their dream state,
leaving them disoriented and with an Dawn simulator
elevated stress/threat system response. This is not an ideal way to
start your day. A relatively new technology allows a light to
gradually increase in intensity starting about 20-30 minutes before
you plan to wake. This technology is called a dawn simulator and is
very valuable for those who have to rise before the sun comes up.

The idea behind using a dawn simulator is to provide a very gradual

transition from darkness to light, mimicking the sun rising at your planned
time to wake. The gradual increase in light (even through closed eyes)
signals the circadian system to start shutting down melatonin production
and prepare for activity mode. The decreasing melatonin from the slowly
increasing light will naturally and gradually pull you out of sleep without
the violent stimulus of an alarm clock. You can always set the alarm as a
backup, but you will only rarely need it when using the dawn simulator.
Philips makes a great dawn simulator.

• Get as much bright natural light as possible in the first hours after
waking up. After gently transitioning to the waking state with the
dawn simulator, continue to get exposure to bright natural spectrum
light. Ideally this “natural” light would be the sun, but realistically
many of us will need to resort to artificial sources of light that mimic
the broad spectrum light of the sun. The most practical way to do
this in the morning is to buy light bulbs that emit a substantial
amount of “blue spectrum” light.

Many of these light bulbs are advertised as “natural” light on the

package and are rated with a scale called Correlated Color Temperature
(CCT). The CCT scale relates to the color of light produced and is
measured in units of Kelvin (K). Low CCT lights emit more yellow and
orange light (longer wavelengths) and high CCT bulbs emit more blue light
(shorter wavelengths). Look for light bulbs that are rated in the high CCT
range, between 5000K and 6500K on the CCT scale for use in the
morning. CCT in these ranges has a substantial amount of blue light in the
spectrum and is the most similar to natural sunlight.

The left picture shows a low CCT and high CCT bulb next to each other. You
can’t tell which is which just by looking at them. The picture on the right
shows the bulbs in identical fixtures. You can tell the difference when the
lights are on in the picture on the right. The high CCT bulb is on the far right
and the light emitted is “whiter” (representing more blue light in the
spectrum) compared to the light on the left that looks yellow in comparison.

Install 5000-6500K CCT bulbs in areas of your home where you spend
the most time in the morning getting ready for work—the bathroom,
bedroom, and kitchen.

You can find these compact fluorescent light bulbs at most large home
improvement stores and online as well. The blue light emitted from these
bulbs is enough to provide a strong signal to the circadian system to start
activity mode.
 STRONG MEDICINE TACTICS:
Install light bulbs with a CCT between 5000-6500K in areas of your
home where you spend the most time getting ready for work in the
morning to maximize your blue light exposure after waking.

RESEARCH UPDATE:
Recent research has shown that exposure to light with high blue
spectrum content in the first few hours after waking increases
alertness, decreases feelings of fatigue, increases brain function for
problem solving, and enhances productivity at work.

This will help synchronize your initial waking time with the start of the
circadian activity mode.

Using high-range CCT artificial light just after waking is especially

important if...

• You do not have time to spend outdoors in the morning sunlight.

• You need to wake up before the sun rises.
• You live in a region predominated by gray skies and rain with little
sunshine.
• You work indoors.
 Giving a strong signal to start the circadian activity mode with blue
spectrum light will ensure that your waking time is supported by the
master clock and organ clocks, optimizing mind and body functions for the
demands of the day. This simple intervention will ensure your circadian
system issues you an adenosine “gold card” to prevent fatigue during your
waking hours.

As your waking time draws to an end, we have to give an equally strong

signal to start the circadian regeneration mode and prepare for sleep. The
strategies to synchronize entering regeneration mode with your planned
bedtime are the opposite from the morning strategy. We need to eliminate
blue spectrum light exposure.

• Eliminate exposure to blue spectrum light 2-3 hours prior to your

planned bedtime. You can still use artificial light after the sun goes
down, but the type of light used is crucial to prevent circadian
disruption. Recall that it will take about 2-3 hours after the last blue
spectrum light exposure for melatonin levels to start to rise, signaling
the start of regeneration mode. If you can synchronize the start of
melatonin production with your planned sleep time, your transition
into a deep recuperative sleep will be effortless.

The easiest way to avoid blue spectrum light but still have artificial
light for evening activities is to use compact fluorescent light bulbs
that are yellow/orange in color. These bulbs are traditionally sold as
“bug lights” in home improvement stores. The yellow/orange bulbs
should be installed in the areas of your home where you spend most
of your late evening hours.

Approximately 2-3 hours before you plan to sleep, turn off all the
light sources except for the yellow/orange “bug lights.” This will
allow you to continue evening activity without disrupting melatonin
production. By the time you get ready to sleep, melatonin production
and the beginning of regeneration mode will have started. Sleep
should come much easier.
SCIENCE TRIVIA
Yellow “bug lights” block most of the blue spectrum in visible light. Bug
lights do not repel insects as many people believe, they just do not
attract bugs. Many insects are very receptive to short wavelength light
(blue spectrum) and use it as a navigational aid. If they detect blue
spectrum artificial light at night they are drawn to it. They will not
detect the light from the yellow bulbs because most of the blue
spectrum has been blocked.

STRONG MEDICINE TACTICS:

Install yellow/orange light bulbs (“bug lights”) in areas of your home
where you spend the most time in the late evening to eliminate blue
light spectrum exposure 2-3 hours before planned sleep time.

QUICK TIP:
Many people spend a significant amount of time in some areas of the
house in both the morning and the evening (kitchen, bathroom, etc.).
Many of these “dual use” areas have more than one light source. Take
advantage of this and install the high CCT natural light in one source for
morning use, and the “bug lights” in another source. This way you can
 use certain light switches for the morning to get blue light exposure
and the other switches for turning on the “bug lights” in the evening to
avoid blue light exposure before bedtime.

• Use amber-tinted glasses to eliminate blue light exposure from

computer monitors or TV screens. Modern computer and television
screens emit LED-generated light with a substantial amount of blue
light in the spectrum. Staring at these screens until bedtime will
ensure that your circadian rhythm is disrupted by delaying melatonin
production and regeneration mode. There are blue light filters you
can purchase for television and computer screens but a simpler
option is just to wear amber-tinted glasses to block the blue spectrum
light.

The glasses are a great option for people with family members or
roommates that will not support the use of the “bug lights” at night. Just
put the glasses on 2-3 hours before your planned bedtime to ensure
melatonin production happens on schedule.

Amber-tinted glasses-an inexpensive circadian solution

The amber-tinted glasses are also very valuable for nighttime shift
workers who have to drive home as the sun is coming up. The glasses will
block the blue spectrum part of the morning sunlight and prepare you for
sleep when you arrive home. More on this use to come...
 STRONG MEDICINE TACTICS:
Wear glasses with amber-tinted lenses to block blue spectrum light
from televisions and computer screens at night. The glasses are also
valuable to shiftworkers.

• Ensure your bedroom environment is optimum for sleep. These

interventions are crucial for ensuring a night of regenerative sleep.
Your sleep environment should be similar to a cave.
— Keep the bedroom cool (usually between 65-72 degrees depending
on individual preference). Part of the regeneration mode is a slow
fall in body temperature as the night progresses. A cool room
encourages this natural fall in body temperature.
— Keep the bedroom dark. Use “blackout” curtains to block outside
light from neighbors’ porch lights and streetlights. You can buy
blackout curtains at most major retailers. Cover any light-emitting
electronic devices as well.
— Move televisions out of the bedroom. Bedrooms should be
dedicated to sleeping. If this is not an option, make sure you wear
the amber glasses while watching TV before bed.

STRONG MEDICINE TACTICS:

Make your nighttime sleep environment “cave-like” to ensure
uninterrupted regenerative sleep.
 These relatively simple interventions strategically using light to train
your circadian system are extremely effective. They all have been tested in
research settings with positive results. Although light is the most powerful
“trainer” of your circadian system, exercise can have dramatic effects as
well as long as it is properly timed.
EXERCISE AND THE CIRCADIAN SYSTEM
Your muscles, heart, liver, and adipose tissue are all directly involved in
supporting exercise. Each has its own organ clock governing function
during activity and regeneration modes. Obviously, exercise should take
place in the activity mode of the circadian cycle, since the body is not
optimally primed for exercise during regeneration mode. Most people do
not wake up in the middle of their sleep to exercise, but many do perform
exercise near the transition zones between activity mode and regeneration
mode which can be problematic.

The benefits of regular exercise can be obtained anytime during the

activity mode of the circadian system. Exercise timing falls more to
individual preference and schedule requirements. There are two general
guidelines to follow:

• Ensure that your body and brain have received a strong signal to
enter activity mode before exercising first thing in the morning. Use
the early morning light exposure strategies discussed previously to
ensure your circadian clocks are set to activity mode before starting
exercise.

• Avoid exercise 2-3 hours before planned bedtime. Exercise during this
time acts much like blue light and can delay the onset of melatonin
production and delaying entry into regeneration mode.

STRONG MEDICINE TACTICS:

Perform exercise consistently at the same time of the day. This will
train your clocks to anticipate physical activity, and prepare your body
to optimally support exercise.
RESEARCH UPDATE:
Recent research has shown that muscle is able to generate the most
force near the end of activity mode. Late afternoon or early evening
exercise may be the natural time in the circadian cycle for peak
performance.

This does not mean that exercise at different times of the day is less
effective in promoting favorable adaptive gains in strength and fitness.
The muscle clock can be “entrained” to anticipate exercise at different
times during the activity mode if you consistently train at the same
time of day.

Consistency in training time seems to be the best way to ensure that

your system is prepared for exercise, whether your training sessions are
in the morning, lunchtime, afternoon, or evening.

COACH’S CORNER:
If you are a competitive athlete and have an upcoming event, adjust
your daily training time to the event’s time. If your competitive event is
at 4PM, you should adjust your daily training time to as close to 4PM as
possible, allowing your body clocks to support maximal performance at
that time.
 While exercising within 2-3 hours of planned sleep will delay entry into
regeneration mode, an exercise session 4-6 hours before sleep (late
afternoon/early evening) will have the opposite effect on the circadian
system. Research has shown that late afternoon/early evening exercise can
actually help stimulate melatonin production and the beginning of
regeneration mode.

Scheduling exercise 4-6 hours before planned sleep and avoiding blue
light exposure will send a strong signal to enter regeneration mode, greatly
aiding your transition to recuperative sleep.

STRONG MEDICINE TACTICS:

Exercise 4-6 hours before planned sleep time to aid in priming
melatonin production and the onset of regeneration mode.

The sleep enhancing effects of exercising 4-6 hours before planned

bedtime is the only reason to advocate a specific time for exercise. If your
schedule will allow for it, this is a pretty good reason to switch over to late
afternoon or early evening exercise.

MELATONIN SUPPLEMENTATION?
Recently there has been a substantial amount of research on melatonin
supplementation and chronic disease. In some scenarios, supplementing
melatonin may show some benefit, but the Strong Medicine approach is to
support the body’s own production of melatonin with the proper
environmental cues—light, exercise, etc.

Most melatonin supplement dosage is well beyond what the body will
produce naturally and may cause problems by inhibiting the body’s natural
production of melatonin with long-term use. The other problem with
melatonin supplementation is that it has a very short half-life in the body.
The melatonin only lasts for about 20-40 minutes in the bloodstream
before it is metabolized and eliminated.

The pineal gland in the brain constantly produces new melatonin during
the night so this is not an issue the during regeneration phase. However, a
single supplement will only last for 20-40 minutes. You would have to take
melatonin approximately every 30 minutes to mimic the pineal gland’s
natural production during sleep. Supporting the natural cycle of melatonin
production through the right environmental signals such as light and
exercise is a much better solution to circadian problems.
MELATONIN SUPPLEMENTS AND JET LAG
Temporary use of melatonin can be useful for adjusting to rapid time
changes from jet travel. Taking a low dose (usually 0.3 mg) of
melatonin before bedtime after arriving in a new time zone may help
you fall asleep for the first couple of nights as your circadian system
adjusts.

RESEARCH UPDATE:
A longer acting melatonin supplement is currently being researched for
use with the elderly and those with Alzheimer’s. As we age, melatonin
production declines. There may be some benefit to using a long-acting
melatonin formulation to counteract the declining melatonin
production to help restore normal sleep for the elderly. Use of
melatonin for Alzheimer’s (AD) patients is also an active area of
research as AD also decreases melatonin production.
SHIFT WORKER CASE STUDY
The circadian disruption from nightshift work is very difficult to correct
since the schedule is completely at odds with the natural cycle of light and
dark that entrains the human circadian rhythm. With careful planning and
smart use of light exposure strategies it is possible to improve the quality
of life—and likely the long-term health—of the nightshift worker. One
possible strategy:

• Get blue spectrum light exposure upon waking and if possible, during
the first couple hours of work. Some corporations have installed high
CCT (more blue spectrum) lighting during night shifts to increase
alertness and enhance productivity. If you are able to change the
lighting in your work area yourself to this type of light, do it. There
portable blue light emitters are available that can be powered by a
USB port on your computer and can be mounted on your monitor or
laptop.

• Make sure your eating cycles correspond to your waking time. Eat
when you get up for work, eat “lunch” mid-shift at work, and eat a
meal when you get home in the morning. This will help keep your
organ clocks working with your master clock.

• When driving home after the end of your shift, wear amber-tinted
glasses to block the blue spectrum light from the rising sun. Keep the
glasses on after work to block the blue spectrum light from outside
and from lighting inside the home. A nightshift worker has to be a
little more aggressive with their time spent wearing amber glasses
because they are working against daylight permeating everything.

• Ensure that no sunlight intrudes into your bedroom from outside.

You will have to be extremely diligent about blocking the sun from
your room which may require covering your windows with opaque
material in addition to using blackout curtains. This is where shift
workers often fall short in their attempts to sleep—even a little
 outside sunlight in the bedroom will stop melatonin production and
bring them out of sleep.

A similar strategy to the one outlined above was recently used in a

research study with small groups of shift workers such as nurses and police
officers. The results showed improved quality and duration of sleep time,
and improved alertness and productivity. Much more research needs to be
done in this area but the initial results are promising. These strategies are
worth trying if you are a nightshift worker struggling with sleep.
CONCLUSION
Circadian disruption is widespread in modern society. Artificial light
pollutes the total darkness that once existed during the night. Not all sleep
disorders are primarily circadian problems, obstructive sleep apnea and
anxiety are conditions that result in fragmented sleep without circadian
disruption. However, it is very likely that optimizing your circadian
rhythm will make treating these sleep problems easier.

Losing weight using the Strong Medicine Tactics in the obesity chapter
will certainly help obstructive sleep apnea, and interventions from the
chronic stress chapter will go a long way towards squashing anxiety. The
integrative approach to chronic disease in this book will have crossover
effects, often improving seemingly unrelated conditions. The mind and
body are not a collection of separate organ systems; everything works
together in harmony when everything is functioning correctly. This chapter
hopefully illustrated the importance of the circadian system as a master
conductor which ensures the synergy of the entire flesh machine.
Incorporating the strategies in this section will go a long way towards
helping you improve your overall health and prevent chronic disease.

By using the Strong Medicine Defensive Tactics in this section, you can
reestablish the synchrony of your internal clocks with your waking and
sleeping times—and master your circadian system. The “Thief in the
Night” will no longer steal the restorative sleep so crucial for your health.
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 PART III

BATTLE PLAN
“The best defense is a good offense.”
—Jack Dempsey
You now have the latest intelligence on the on the
inner workings of the enemy—and defensive tactics
at your disposal to repel the advances of the
Pentaverate. It is time to put your training into
action by formulating your individual battle plan.
Before you move your troops to the front line, we
will give you some training in battle strategy.

In Part III you will develop a foundation in Strong Medicine physical

training, learn the importance of food quality, and strategies for the
optimum feeding of the flesh machine. You will put together an
individualized plan for lifestyle change using your previous training
and defensive tactics, and finally track your progress with analytics
(“stuff you can measure”). Put your pieces on the board and we will
show you how to place the Pentaverate in checkmate with a
devastating offensive strategy.

I. Strong Medicine Physical Training II. Strong Medicine

Nutrition: Individualized Strategies III. Putting It All Together
IV. Analytics: “Stuff You Can Measure”
BATTLE PLAN I
PHYSICAL TRAINING: UNLOCKING
YOUR BODY’S POTENTIAL
STRONG MEDICINE PHYSICAL TRAINING
Regular, mindful, intense physical training is central to the Strong
Medicine transformational plan. The body and mind need physical stress
to thrive, and the absence of regular exercise results in physical and mental
deterioration over time. The necessity of physical stress through exercise is
supported by the health benefits shown by scientific research.

• Exercise slows the aging process.

• Exercise protects us from bone and muscle wasting (osteoporosis and
sarcopenia).
• Exercise dramatically increases insulin sensitivity, protecting us from
diabetes and obesity.
• Exercise strengthens the heart and prevents heart attacks and stroke.
• Exercise rebuilds the stressed brain, making us resilient against
chronic stress.
• Exercise protects us from neurodegenerative diseases such as
Alzheimer’s Dementia.
• Exercise helps us build a strong immune system and recover from
illness faster.
• Exercise makes us more physically resilient, preventing injury and
allowing for faster recovery after injury.
• Exercise helps reset a broken circadian rhythm.

Without exercise and its protective benefits in your daily life, the aging
process is accelerated and you are vulnerable to disease and injury.
 In the terms of hormesis, inactivity represents an inadequate “dose” of
exercise and physical stress. We are going to show you how to train
smartly and effectively to maximize your health benefits by staying in the
“green zone” of the proper dose of exercise. We will also keep you out of
the “overdose” zone that so many people fall victim to if they’re following
a regular high volume “boot camp beat down” program.

The Strong Medicine physical training program does not require gym
memberships, huge time investments, or fancy equipment. We are going to
strip things down to the basics and give you a foundation for a lifetime of
health and fitness.

Inactivity is the fifth member of the

“Pentaverate,” the cabal of chronic
preventable disease. Like the other four
members, inactivity results in chronic
inflammation and oxidative stress.

We can break this link to chronic disease with

a scientifically-based training program,
informed by an elite-level coach’s years of
experience.

We will start with a primer on progressive resistance training—a true

fountain of youth—then present a scientific approach to cardiovascular
training. These exercise defensive tactics are the equivalent of a tactical
nuclear weapon against the Pentaverate. This is high-yield training for your
war against chronic disease and a keystone for achieving your genetic
potential.

We are only going to cover a few critical exercises to build a progressive

resistance training foundation. You may add other exercises to create your
own individualized program, but these core movements should be the
pillars of your program:

• The Squat
• The Deadlift
• The Bench Press and Military Press
 • The Row
• Abdominal Training
PHYSICAL TRAINING I
STRONG MEDICINE RESISTANCE
TRAINING: INTRODUCTION
USE IT OR LOSE IT
In a fundamental sense, muscle and strength follow a “use it or lose it”
scenario—but that would imply that the aging population (over 60) “had
it” to begin with—yet flaccidity is epidemic in most of the Western
population long before the sixth decade is reached.

A cursory glance at traditional hunter-gatherer cultures (the few still in

existence) reveals that their senior citizens are muscular, ripped and
functional. They always had “it” and never lost “it.” They were lean with
functional muscularity in their youth, maintained their physique through
mid-life and retained it in late life. The elders in tribal cultures are active,
fit, disease-free and exhibit the lean muscle mass that twenty-year-olds of
modern society would envy.

Their secret is simple; they maintained their primitive diets, eating the
food-fuels they were designed to use. They inherited excellent genetics and
attained a miraculous degree of functional fitness in their youth. They
never stopped using their bodies in intense and prolonged ways, and as a
result their flesh-and-blood machinery retained a magnificent readiness.
Instead of driving carts around a golf course, these senior citizens lift,
carry, run, jump, and hunt.

Compare this to the classical ‘civilized man’ born in a controlled

environment, and who has never attained fitness. Fueled by artificial
‘foods’—just like running a race car on cheap kerosene instead of nitro-
methane—this ‘civilized man’ has never exerted himself in the slightest.
With no muscle tone or strength gained earlier in life, physical
functionality continues to diminish from an ever-increasing lack of late life
activity. The end result is a pathetic, weakened creature unwilling, unable
and incapable of being functionally mobile. Weak flaccid muscles grow
weaker, bones which have never been stressed become lighter than air.
Further immobility is compounded with fragility. Next they might fall
down—if they are lucky, they’ll avoid shattering a hip as fragile as a glass
figurine on concrete—at best they will have fallen and are incapable of
standing back up.
 We have all seen the commercial with the pathetic plaintive cries of the
elderly person helpless on the floor after a fall. The advertisers are saying,
if you are old you need their “alert system” so you can be safe and secure
in your own home. The not-so-subtle underlying message is that this
situation is inevitable for everyone in the last decades of life. But, this
could be your fate if you succumb to sarcopenia and osteoporosis in your
“experienced” years.

We are seeing sarcopenia at younger and younger ages in modern

society. It’s caused by a lack of resistance-based activity in an increasingly
sedentary population.
SARCOPENIA
Sarcopenia literally means “loss of skeletal muscle mass”—and the
resulting loss of strength—as we age. You may think it is natural and
expected for everyone to lose muscle as we age. Yet, we can do plenty to
slow the decline of muscle-mass through the expert use of resistance
training. Sadly, the majority of us are needlessly sarcopenic.

• The rate of muscle loss in adults is 1-2% every year after age 50.
• Strength loss after age 60 is 3% every year.
• The healthcare cost of sarcopenia is 18 billion dollars every year.
• Sarcopenia has been associated with increased risk of death.

MUSCLE MASS MAINTENANCE IS CRUCIAL FOR HEALTH.

• Retaining muscle mass and strength keeps a person biologically
young, regardless of their chronological age. Many adherents to
resistance training are able to retain lean muscle mass and
tremendous strength late into their 70s and 80s. Many 50 year olds
have a body significantly more capable and functional than sedentary
25 year old men and women.

• Maintaining muscle mass is the best defense against insulin resistance

and diabetes. Muscle is the largest insulin sensitive organ in the body.
The loss of muscle mass (sarcopenia) disrupts the body’s ability to
handle glucose effectively. Loss of muscle mass has been shown to be
an extremely strong predictor of the development of insulin
resistance and diabetes.

• Progressive resistance training is hugely beneficial in treatment and

prevention of sarcopenia. Clinical studies repeatedly show the benefit
of progressive resistance training in treatment and prevention of
sarcopenia. Impressive improvements in strength are routine; power
is gained from specific workout protocols. Strong Medicine protocols
can increase power, strength, and can stop sarcopenia in its tracks.
OSTEOPOROSIS
Our bones are the body’s central support structures which allow us to
function upright against gravity. Our muscles can only exert force when
they are attached to our bones, so maintaining a robust skeletal system is
of upmost importance—particularly as we age. Osteoporosis is the
thinning of bone tissue as mineral content decreases. The body constantly
builds new bone while reabsorbing old bone. Osteoporosis and osteopenia
(the early stages of osteoporosis), occur when bone break-down exceeds
bone construction.

Osteoporosis is rampant in women after

menopause. One out of five women over 50
have some degree of osteoporosis. Half of
women over the age of 50 will suffer a hip,
wrist, or spine fracture in their lifetime. Men
get osteoporosis later in life than women, but
are still at risk. There are many contributors to
the development of osteoporosis, but inactivity
—specifically lack of resistance training—is the
primary factor that enables osteoporosis to take
root.

If we view osteoporosis through our “first principles” lens, bone

physiology is simple—bones respond favorably to systemic, prolonged and
consistent resistance training by becoming thicker, denser, and more
resistant to breaking, chipping or cracking. Bone subjected to weight
training grows dense and strong.

The age-defying benefits of resistance training do not require a

complicated approach. The Strong Medicine approach uses simple
stripped-down strength training protocols accessible to everyone.
KEY POINT:
If you want to age successfully, prevent life altering fractures, and stave
off insulin resistance and diabetes, then resistance training is not
optional.
DOING FEWER THINGS BETTER
Long before the current economic crisis forced fitness-minded
individuals to reexamine and reduce their fitness spending, barebones
approaches were prophetically championed by retro experts. These men
insisted that modern fitness—fancy health clubs, ineffectual personal
trainers, expensive exercise machines, elaborate supplements and miracle
fat burners—was bogus, false and not nearly as productive as the old-
school methods first used in the 1950s.

This back to basics approach is always a tough sell, especially during

good economic times. But now, people are taking a second look at
minimalistic training methods.

• The most result-producing methods of progressive resistance training

use free-weights—barbells, dumbbells, and kettlebells. The goal of
resistance training is to build and strengthen the 600-plus muscles in
the human body. Compound multi-joint exercises using barbells and
dumbbells cause groups of muscles to work together in synchrony to
stimulate muscle fibers in a way unobtainable using resistance
machines.

• Exercise machines that mimic free-weight movements are

demonstrably inferior since they eliminate the “third dimension of
tension.” Free-weight exercises require activation of the muscle
stabilizers to control side-to-side movement. Free-weight exercises
always result in more muscle fiber stimulation (the goal of resistance
training) than resistance machines mimicking free-weight exercises.
Free-weight exercises also translate better to real-life movements such
as lifting, carrying, pushing and pulling.
MAKING LIGHT WEIGHTS HEAVY
Although one of us is a top powerlifting coach, we are not here to make
you a powerlifter. You do not need to fear getting crushed under a heavy
barbell or otherwise injuring yourself with heavy weights with the Strong
Medicine approach. Our techniques use relatively light weights to
maximum benefit by “making light weights heavy.” This will protect you
from injury while you make transformative gains in strength and function.
There is no need to fear free-weights.

The Strong Medicine program is truly strength training for anyone. It

doesn’t matter if you are very experienced or have never performed a squat
in your life. We will build you from the ground up with technique,
strength, and confidence.

You will learn free-weight lifting techniques step-by-step from a master

coach with 50 years of experience. The squat, deadlift, bench press,
overhead press, and the “statue row” will be the pillars of the program.
Even if you are experienced with the lifts, you will improve your technique
and maximize your strength gains. We will also show you how to
maximally train the abdominal muscles without ever doing a sit-up or
crunch.
PHYSICAL TRAINING II
KING SQUAT

“KING SQUAT”
Why is the squat the king of all progressive
resistance exercises? When it comes to building leg
power, proper upright squats performed with a
perpendicular torso and significant weight is
unsurpassable. Properly performed, full, deep squats
stimulate more muscles than any other single
progressive resistance exercise.

No one does proper full squats anymore for

numerous reasons. “Experts’’ of every kind have Friends don’t
either condemned full squats as dangerous—or let friends squat high.
worse, they teach some perverse technical abomination instead of the
productive classic deep squat. Our core technique for all squat variations—
front squats, back squats, kettlebell squats, or squats with no weight—is
identical. The hardcore squatter’s motto is, “Shallow squats are worthless
squats. Friends don’t let friends squat high.”
 SOME TRAINERS AND MEDICAL
PROFESSIONALS WILL SAY, “DEEP SQUATS
ARE BAD FOR THE KNEES.”
My response—after watching them demonstrate
a squat—is, “The way YOU squat is bad for the
knees.”

A deep squat with the correct biomechanics (body

positioning) is far from “bad for the knees.” The
forces on the knee joint in a proper deep squat are
significantly less than in partial or parallel squats.

The damaging forces in question are joint shear

and compression stress. Compression stress is the stress on the knee
from force pushing the knee cap backwards onto the knee joint. Joint
shear is a force attempting to move the upper leg bone (femur) either
backwards or forwards over the tibia (a lower leg bone).

Many trainers will tell you not to squat below parallel. This is bad advice
since the greatest compression stress on the knee occurs at parallel
(90 degrees). These trainers want you to stop your squat then exert
more force to stand up from the point of maximum compressive force
on the knee joint. This makes NO sense.

Also, most people squat by initiating the movement from the knees
first, shooting the shins way out in front of the feet. This knee poison
puts huge joint shearing forces on the knees.

Force measurements of the deep squat with vertical shin position

show less compression stress and less joint shear than the “safe”
parallel or partial squat.

The deep squat is not only safe for knees, but may actually help
strengthen the knee joint and make it more resilient in daily physical
activities and sports. Olympic weightlifters routinely go into ultra-deep
squat positions with heavy loads and have one of the lowest rates of knee
injuries in any sport. This is a proven fact.

We have taken countless clients who previously avoided squats because

they “hurt their knees” and have helped them perform full depth, pain-free
squats in a matter of minutes.
MAKING LIGHT SQUATS HEAVY
No other progressive resistance exercise triggers the primal “fight or
flight” psychological response to the same degree as limit squats. Limit
squatting unleashes tremendous hormonal benefits. We seek ways in which
to increase squatting’s degree of difficulty. Why would we want to
exponentially increase the difficulty of the world’s most excruciating
exercise? Why are we requiring butt-to-heels depth on every rep of every
set—with a purposeful pause at the bottom of each super-deep rep?
Because this will strengthen the squatter over the entire range of motion
(ROM). This will simultaneously maximize muscle growth and
exponentially increase our brute power. Strict attention to technique will
limit the amount of weight we’re able to handle—we will reap maximum
physiological results by lifting a minimum amount of weight.

The Strong Medicine squat technique makes light weights heavy by

achieving an ultra-deep squat depth and pausing at the bottom of the rep
before ascending.

• The ultra-deep squat involves starting the upward movement from a

compromised position—as far as leverage allows and the optimum
length the muscle will stretch. There is no need to load up on the
weight. The ability to get a potent neurological stimulus (our goal
with strength training) from relatively light weight, has many
advantages. You can generate much more strength (technically,
torque) in a curl when your elbow is flexed to 90 degrees than when
it is fully extended. The ultra-deep squat puts you at a leverage and
muscle length disadvantage, requiring much more effort from the
nervous system to drive you out of the bottom. This allows us to use
light weights and still trigger the adaptive response. Light weight also
decreases load on the spine, making our squat safer for those with a
history of back injuries.

• The pause at the bottom of the squat makes light weights heavy by
taking away an important advantage—the stretch shortening cycle
(SSC). This a reflex similar to the one produced when a doctor hits
 your patellar tendon with a reflex hammer. The SSC is most active in
plyometric exercises, but research has shown that it is also significant
in normal-speed squats. The lowering portion of a normal speed
squat increasingly stretches the leg muscles. This stretch primes them
for greater activation, and adds to the force used when ascending
from the squat. Think of it as a “turbo boost” from the bottom of
the squat. But, there is only a very short window for taking
advantage of this SSC reflex. Our insistence on a one second pause at
the bottom of the squat takes away this “turbo boost” reflex.

COACH’S CORNER:
When we champion maximum range-of-motion squats, we are
accused of resistance training malpractice. Delicate people claim
squatting that deep will blow out knees and cause the deep squatter to
become permanently confined to a wheelchair. Despite being called
out on it, and despite the lack of deep-squat cripples or blown knee
victims, the seriousness of the accusation has gained traction in the
wider athletic training community who largely believe super deep
squats are dangerous.

Meanwhile, trainees who squat super deep using precise techniques

develop injury-proof knees and astounding muscle and strength
results.
BASIC SQUAT MECHANICS DESCENT

BASIC SQUAT MECHANICS ASCENT

SQUAT PROGRESSION 1: THE BODYWEIGHT
SQUAT
1. The bodyweight squat is the key squat progression, the foundation
on which all subsequent squat variations are built. Learn it, master
it.
2. Start with a shoulder-width stance, and toes slightly turned
outwards.
3. Sit back and down while keeping your shins vertical. Do not let the
knees shoot forward.
4. Keep your weight balanced mid-foot; do not shift forward or
backwards.
5. Imagine a stake driven through the mid-foot to keep you rooted
into the floor.
6. On ALL squat variations, the knees are FORCED out to the sides
(laterally) during descent and ascent.
7. Inhale into the lower belly as you descend.
8. Knees should stay over the ankles as much as possible, and not
shoot out in front of the toes.
9. Sink all the way to the bottom, going as far as you can while
maintaining correct form.
10. In the bottom position, exhale; relax and sink further, losing all
tension. (Only do this with bodyweight or light loads).
11. After a one second pause, using diaphragm breathing, inhale to
ascend while pushing your gut out against your thighs.
12. For heavier loads, use this alternate technique: inhale, sink to the
bottom, maintain tension and pause for one second. Exhale at the
top of the ascent.
13. When ascending DO NOT let the tailbone shoot up first! The
tailbone and upper body should move as one unit during ascent.
“Grind” out of the bottom position.
14. Perform three sets of 10 reps before moving up to loaded squat
variations. Stop immediately if your technique breaks down.

“GRIND” THE SQUAT

After sinking as low as possible while maintaining a bolt-upright torso,
the squatter pauses a beat before ascending. How someone rises from
a paused, upright, ultra-deep squat determines the amount of benefit
he or she will derive.

Never let the tailbone “shoot upward” when the ascent begins from
the bottom of the squat. Fight this natural inclination to “make the
move easier” on the legs. When the tailbone shoots upward, allowing
the legs to extend, they’re put in a much more favorable position to
push. But, it’s a devil’s bargain—allowing the tailbone to shoot up
causes your weight (or bodyweight) to shift forward, in front of the feet.
Now the spinal column must be hoisted erect, using the hip-hinge and
a few tortured vertebra on the verge of ruptuing.

Instead, we should “grind” out of the bottom, embracing the sticking

point and slowly pushing through it with perfect technique, the
tailbone and upper body rising as one unit.

A purposefully slowed “grind” speed is an expression of low-end

torque. The actual speed of the grind rep is not—and should never be
—radically slowed down. Slow rep proponents continually make this
fatal mistake. Grind speed is purposely slow, just barely slow enough.

We “make light weights heavy” by adding “intensity boosters” to full

range-of-motion squats. We add pauses at grind rep speed to create
the ultimate excruciating exercise. Repeatedly grinding full ROM
paused squats optimally trains proper technique.
THE BODYWEIGHT SQUAT

Side view of squat descending sequence

Front view of squat ascending sequence

SQUAT PROGRESSION 2: THE GOBLET SQUAT

The second squat progression, uses added weight held with both hands
out front like a goblet. Otherwise, it is performed exactly like the
bodyweight squat.

The added weight in front acts as a counterbalance to make sitting

backward in the squat feel more stable.
1. Hold a single appropriately-sized kettlebell or dumbbell at chest
height with both hands.
2. Start with a shoulder width stance, toes slightly turned outwards.
3. Sit back and down while keeping your shins vertical. Do not let the
knees shoot forward.
4. Keep your weight balanced mid-foot; do not shift forward or
backwards.
5. Inhale into your lower belly as you descend.
6. Force your knees out to the sides (laterally) during descent and
ascent.
7. Knees should stay over ankles as much as possible, they should not
shoot out in front of the toes.
8. Sink all the way to the bottom, or as far as you can descend while
maintaining correct form.
9. In the bottom position, exhale then relax and sink further, losing all
tension. Only perform this step with bodyweight or light loads.
10. After a one second pause, using diaphragm breathing inhale to
ascend while pushing your gut out against your thighs.
11. For heavier loads, use this alternate technique: inhale then sink to
bottom while maintaining tension. Pause for one second. Exhale at
the top of the ascent.
12. When ascending, DO NOT let the tailbone shoot up first! The
tailbone and upper body should move as one unit during ascent.
“Grind” out of the bottom position.
13. Follow the sets and reps of your current program. Stop
immediately if your technique breaks down.
THE GOBLET SQUAT

Goblet squat descending sequence: note that the

knees are forced out to the sides as he initiates the
movement from the hips, sinking back and down. The
spine stays straight into the bottom position. He will
pause for one second at the bottom position and then
ascend with his tailbone and upper body moving
together.

SQUAT PROGRESSION 3: THE

FRONT SQUAT
The third squat progression, uses added weight in each hand, held at
shoulder level. Otherwise, it is performed exactly like the bodyweight
squat.
The added weight held at shoulder level makes the abdominal muscles
The added weight held at shoulder level makes the abdominal muscles
work hard to maintain a stable upright posture.
1. Hold a single appropriately-sized kettlebell or dumbbell in each
hand at shoulder level. Arms are kept tight against your ribs.
2. Start with a shoulder width stance, and your toes slightly turned
outwards.
3. Sit back and down while keeping your shins vertical. Do not let your
knees shoot forward.
4. Keep your weight balanced mid-foot; do not shift forward or
backwards.
5. Inhale into your lower belly as you descend.
6. FORCE your knees out to the sides (laterally) during descent and
ascent.
7. Your knees should stay over your ankles as much as possible, they
should not shoot out in front of your toes.
8. Sink all the way to the bottom, or as far as you can descend while
maintaining correct form.
9. In the bottom position, exhale then relax and sink further, losing all
tension. Only perform this step with bodyweight or light loads.
10. After a one second pause, using diaphragm breathing inhale to
ascend, pushing your gut out against your thighs.
11. For heavier loads use this alternate technique: inhale then sink to
the bottom while maintaining tension. Pause for one second.
Exhale at the top of the ascent.
12. When ascending, DO NOT let the tailbone shoot up first! The
tailbone and upper body should move as one unit during the
ascent. “Grind” out of the bottom position while keeping an
upright posture.
13. Follow the sets and reps of your current program. Stop
immediately if your technique breaks down.
THE FRONT SQUAT

Front squat: the higher center of gravity of the weight makes for a increased
challenge for the core to maintain a straight spine during the movement.

HELP FOR BEGINNERS WITH KNEES THAT

SHOOT FORWARD
Newcomers to the squat often struggle to start their descent with a hip
hinge. Instead, they will immediately shoot their knees forward to squat,
putting significant shearing forces on the knees. People with this motor
pattern avoid squatting because it hurts their knees—and no doubt it does!

The most direct way to stop the “shooting knee” pattern is to position
the lower body so that shooting the knees forward is almost impossible.
This will force the correct pattern of beginning a squat with a hip hinge.
Simply place the forefoot on a 1-2 inch board as shown below.

Practice with the board until the hip hinge feels natural, then remove the
board and start training.

Knees shooting forward is poor squat form and bad for the knees.
Placing the board under the feet does not allow for the knees to come
forward, and helps train starting the squat movement from the hips.

KNEE COLLAPSE?
Knees collapsing inward (called “valgus collapse” in medical
terminology) during the squat is the most common fault seen in those who
include the squat in their training. It is an easy trap to fall into, especially
as loads increase, but it is relatively easy to fix. We will provide a minimal
force to push the knees inward, using physiotherapist Gray Cook’s idea of
“feeding the mistake.” We can use a simple Theraband to provide the
force. The nervous system will respond to the inward force by reacting
against it with the natural reflexive response of forcing the knees outward
—which is what we want. This technique is good for correcting beginners,
and also useful for priming the nervous system of experienced trainees for
correct movement before a squat workout.
The arrows show the valgus (inward) collapse of the knees.
Adding the band cues the nervous system to resist the inward collapse,
correcting the knee position.
THE ASSISTED SQUAT
If you have not squatted deeply since childhood, and are having
difficulty getting started with the bodyweight squat, begin with our multi-
phase assisted squat progression.

PHASE I: THE SHORTENED REP-STROKE SQUAT

We will use proper technique for partial squats. Establish an initial rep
stroke depth that is comfortable, and adjust a seat to this level. Work up to
one set of 10 perfect reps, lightly touching the seat, not bouncing, and
standing back up. Sit back and down, inhaling on the descent, exhaling on
the ascent. When you can perform a perfect set of 10 reps, add a second
set. Finally, in a few sessions or few weeks, add a third set. When you are
capable of three sets of ten reps, lower the seat FOUR inches. Start from
the beginning with one set of 10 reps and repeat the process above until
you can perform 3x10 at this height.

After you have lowered the seat height over time and are now capable of
squatting 3x10 to parallel, we will begin squat school, phase II.

PHASE II: THE DOORWAY/POLE SQUAT

Stand facing a doorjamb or pole and grab the support at waist height.
Now squat down and back, allowing your arms to pull on the
doorway/pole as you descend. Inhale until you reach parallel. Now exhale,
relax any leg tension, and allow the weight of your torso to push your hips
to the lowest possible position. Use your arms to offset your bodyweight
and to keep your torso upright (critically important). Inhale and stand up,
using only your legs to lift your torso. Pull upward with your arms as
necessary to stand up while maintaining perfect technique. Pulling with
your arms will take weight off of the torso as needed, helping you to push
though the squat sticking point. You are self-assisting a forced rep.
Using a pole for assisted squatting instead of a door jam (phase II). Anything
stable you can grab with your hands will do. The phase III assisted squat will
use a towel or rope to increase instability and thus difficulty.

PHASE III: TOWEL OR ROPE SQUAT

Loop a rope or towel over the top of a chin-up bar or other sturdy
overhead anchor-point. Grab one end of the rope or towel in each hand,
then lower yourself down into a perfectly ultra-deep full squat. Pull on the
rope or towel to lighten the load as you descend, then pull on the rope or
towel as much as needed when standing back up.

We can learn perfect squatting by self-assisting—reducing the amount of

weight lifted—with the rope or towel. When we learn squatting from
absolute weakness, we will develop a series of bad habits when “sneaking”
through sticking points. Gains in strength and hypertrophy lie in battling
through sticking points—not developing questionable techniques that
allow us to avoid them.
GRADUATION
Once you have increased your basic leg strength and are able to perform
three sets of ten reps of ultra-deep bodyweight squats with correct
technique, you are ready to work with dumbbells or kettlebells for the
weighted squat.

STRONG MEDICINE TACTICS:

Use the squat as one of the foundations of your resistance training
program.
PHYSICAL TRAINING III
THE DEADLIFT = THE HEALTHLIFT

THE CROWN PRINCE OF THE

POSTERIOR
The squat is the undisputed king of resistance exercises, but the deadlift
certainly has a place in the royal family. Many would argue that the
deadlift is a stiff competitor with the squat for the overall title of the “king
of exercises.” That is debatable, but the “Crown Prince” is surely eyeing
Dad’s throne.

The proper deadlift is the undisputed prince of the posterior chain—the

back and gluteal muscles.

No other progressive resistance exercise adds strength and muscle to the

back (traps, upper lats, lower lats, erectors, rhomboids, teres, and rear
deltoids) and your gluteal muscles than a perfectly executed deadlift.
 Like Bubba Gump’s endless shrimp possibilities, there are a seemingly
infinite number of deadlift variations. Deadlifts can be performed while
standing on a plate or box of varying heights for different results. Box
deadlifts are also much more difficult at the start. Stiff-leg deadlifts can be
done “Chaillet Style”, the lifter drags a super heavy barbell up the thighs.
A lighter and more precise “bodybuilder stiff-leg” deadlift requires that the
lifter purposefully allows the barbell to swing away from their body, this
subtly shifts the muscular stress from the erectors to the hamstrings. You
can do speed deadlifts or halting deadlifts. You can even incorporate
partial rep deadlifts using a power rack.

Other options include ultra-wide-stance sumo deadlifts, and various

“double overhand” deadlifts to build an eagle talon grip. You can also use
straps to allow for overloading the back muscles. There are enough
legitimate deadlift variations to keep a serious trainee very occupied for the
rest of his natural life.
 THE HEALTH LIFT
From a medical perspective, no other exercise translates better to
protecting the back and preventing injuries during daily activities than
the deadlift. Regular deadlifters are never in the doctor’s office with
back pain complaints; the deadlift has made their backs virtually
indestructible when faced with the physical trials of work and home.
This may sound contrary to the idea many people have of the deadlift
being “bad for the back.” With a properly executed deadlift, nothing
could be further from the truth. The deadlift can even be restorative for
a previously injured back.

WHY THE SUMO DEADLIFT IS ALL WE NEED

For our purposes, the only deadlift variation we need is the “sumo-style”
deadlift. It is the easiest to teach, to perform, best translates to daily
activities. It is also safer for the beginner while still providing plenty of
challenge for the experienced lifter.

“One technique, deeply ingrained, is ten times better than

ten superficial techniques.”
—Bruce Lee

In a perfect world, we could effortlessly teach athletes the sumo and

conventional-style deadlift with equal ease and effect. 50 years of
experimentation tells us something quite different. If an individual takes
the time and effort to learn our particular upright posture squat technique,
learning the sumo deadlift will be as easy and natural as taking a walk.

The conventional deadlift is a sophisticated exercise that requires

accurate positioning and the discipline to maintain the strict, straight,
upward pull. The conventional deadlift has many more opportunities for
breaking form. Repeatedly breaking technique to skirt a sticking point is
shortsighted—both immediately and ultimately detrimental. Over time,
bad habits become ingrained and almost impossible to break or correct.

The conventional deadlifter can find a lot of ways to work around or

completely avoid sticking points. Resorting to these shortcuts is not clever
or advisable. Elite trainers and master deadlifters understand that the
essence of deadlifting (and of resistance training) is to find and embrace the
resistance. These elite purposefully power through the sticking point,
pushing or pulling with all their might straight ahead with no variation—
and fail wherever they may fail.

The maximum muscle and strength gains are born from the struggle of
these barely completed reps. We should live to struggle through the
sticking point instead of trying to find clever—and ultimately shortsighted
—ways to slip by the resistance. Those who truly understand seek
muscular conflict will regularly and routinely push up to (and past)
momentary capacity.

How a trainee deals with the sticking points and the struggle associated
with effective resistance training will ultimately determine the degree of his
success. We define successful progressive resistance training in two ways—
a radical increase in raw strength with a radical increase in lean muscle
mass. Nothing more, nothing less. Acquiring these two attributes is
profound.

WHY THE SUMO DEADLIFT?

Experience has repeatedly shown that teaching proper sumo deadlift is
far easier than teaching the conventional deadlift. First, there is a lot of
technical similarity between a correct squat and a proper sumo
deadlift. Think of the sumo deadlift as a “reverse squat” as there are far
more similarities than differences.

The perfect sumo deadlift is similar to a partial rep squat—only instead

of the weight being on your clavicles (as in a front squat) or on your
back (back squat) the weight is in front, hanging down from your hands.

Using an upright torso style for a sumo deadlift puts the emphasis on
Using an upright torso style for a sumo deadlift puts the emphasis on
leg power. Those with weak legs will try to neutralize their relative lack
of leg strength by compensating with high hips to start the lift. The
lifter will invariably end up struggling to force their out-of-position
torso into the final lockout.
THE SUMO DEADLIFT
1. Grip a barbell, kettlebell(s), or dumbbell (around one end) and
assume the start position.
2. Feet should be wider than shoulder width, with the torso as vertical
as possible.
3. Tense the upper back, attempting to pull the shoulder blades
together. Tense the gluteal muscles, lower back, and thighs, then take
a big breath into the bottom of the belly.
4. Smoothly bring the weight off the floor with your legs. Do not jerk
the weight.
5. The tailbone and upper body rise together, initially maintaining an
upright torso. Do not let the tailbone shoot up first!
6. The reverse hip hinge powered by the gluteal muscles finishes the
lift. The lower back and torso must be locked into one unit.
7. Maintain muscle tension at the top (the standing portion of the lift)
during exhalation.
8. Inhale into the belly and start to lower the weight using the reverse
squat technique—squatting down and back while maintaining an
upright torso.
9. Lower the weight in a controlled grind speed and gently place it on
the ground with minimal noise. This controlled lowering technique is
an exercise unto itself with profound benefits.
10. If you are performing multiple reps, do not lose tension as the
weight touches the floor. Break the weight off the floor (#4) and start
another rep.

The Strong Medicine Robots demonstrate optimal sumo start position.

Now, simply push your thighs downward.
Your leg and torso length will determine
how vertical your torso will be at the start.
The robots have long legs which
necessitate a more inclined torso. Try to
achieve a spine position as vertical as your
anatomy will allow. A wider stance will
enable a more vertical torso.

Sumo Deadlift starting position.

DEADLIFT TACTICS
EMBRACE THE HARD START.
Our deadlifts have a signature technique rooted in structural
architecture, physics and safety. The idea is to never lose tension once
the deadlift set starts. Do not let the weight “settle” on the floor
between reps, this prevents a loss of body tension. We want to create
maximum body tension at the start of the first rep of the first deadlift
set, and never lose that tension for an instant. Optimally, the weight
will lightly touch the floor between reps.

BRAKING THE “NEGATIVE”.

As the barbell approaches the floor between reps, the muscular brakes
are applied with increasing tension, like a car approaching a brick wall.
Slowing the weight down causes a new level of muscle fiber
stimulation, maximally stimulating the back, glutes, upper thighs, and
hamstrings. The braking effect enables the lifter to exert maximum
control at the “turn-around” where descent becomes ascent. Slow,
slower, slowest—lightly touch the weight to the platform and begin the
next rep.
NO SHORTCUTS.
If the legs are not strong enough to break the weight from the floor
while maintaining the proper start position, then go back and work on
squats until your legs are strong enough to deadlift. Stop playing to
your biases and strengths—correct your weaknesses. Those who think
the hip-hinge trumps the legs are missing the point. The question is not
whether the hip-hinge trumps leg power or if the legs are better than
strength from the hip-hinge. The Taoist answer is, ‘Not one, not the
other, both!’ The optimal deadlift technique uses both the legs and
hip-hinge.
EMBRACE THE STICKING POINT...
In the sumo deadlift, as long as the torso is held
erect and only leg power is used to break the bar
from the floor, there is no opportunity to avoid a
sumo sticking point. Bouncing reps are not allowed.
To reduce momentum, we use heavy breaking on
the eccentric movement and accelerate during the
concentric pull.

In the sumo, the sticking point occurs when

breaking the barbell from the floor. The first six
inches of a sumo pull is 100% leg power. To keep
the sumo deadlift simple, and to increase the amount of weight you’re
able to lift, increase your squat and leg power.

Once the bar approaches the knees, the lift is as good as done. The
upright torso allows for a perfect, straight-line pull. The pull becomes
easier the closer you are to the lockout. A limit set of deadlifts activates
every muscle on the human body to some degree.

EDDIE PENGELLY: SUBLIME

SUMO
Note the wide stance allowing a near vertical
torso. The vertical torso requires almost 100%
leg power to break the weight from the floor.
Once off the floor, the hips and back can finish
the lift.

SINGLE DUMBELL/KETTLEBELL SUMO DEADLIFT

Sumo Deadlift side view with single kettlebell: from the
starting position, the tailbone and upper body ascend
together (arrows) as the legs break the weight from the
floor at grind speed. As the weight passes the knees the
hips extend to an upright position to finish the lift.
Reverse the sequence to bring the weight down slowly
enough so there is minimal sound when the weight
touches the floor.
DOUBLE KETTLEBELL SUMO DEADLIFT

Sumo Deadlift front view with double kettlebells: The technique is identical
to the single kettlebell lift except for a wider stance. Double kettlebells allows
for heavier loads as you get stronger.
Start position for the Sumo Deadlift with a barbell: the stance width is wide
enough so that your arms can be positioned inside of you knees. You can
alternate grip position with your hands (shown here) or put both hands in a
pronated (palm down grip).

Sumo Deadlift with a barbell: the technique remains the same with the
tailbone and upper body ascending together as the legs break the weight
from the floor at grind speed. As the weight passes the knees the hips extend
in a reverse hip hinge to an upright position to finish the lift. Reverse the
in a reverse hip hinge to an upright position to finish the lift. Reverse the
sequence to bring the weight down slowly enough so there is minimal sound
when the weight touches the floor.

To the trained eye, a perfect deadlift—sumo or conventional—is every

bit as beautiful and technically intricate as a golf swing, a tennis serve, or a
baseball pitcher’s windup. Careers are built on coaching the raw mechanics
of athletic swings and throws. Every pro baseball team has a batting coach;
every NFL team has a quarterback coach who drills quarterbacks on an
ideal technical template for throwing and releasing a football. Definable
coaching specialists and technical experts exist for improving raw athletic
mechanics in every sport—a quicker release for a young NFL quarterback,
a faster bat speed for a pro baseball power hitter, a more refined power
serve for a grand prix tennis player, or a better golf swing for a PGA
circuit pro.

Sadly, in the deadlift, there’s no equivalent—anybody can claim to be a

deadlift expert and “teach” deadlift technique. It seems every self-
proclaimed deadlift expert is blissfully ignorant of deadlift technique, and
prefers to lecture about sets, reps and frequency. Or, worse yet, they will
teach some sort of “spinal cracker” deadlift technique that works well
initially, quickly plateaus, and ultimately runs a high risk of spinal column
injury. Bad deadlift technique forces a poorly positioned spinal column to
straighten for the lock out on a limit deadlift rep. Proper deadlift technique
keeps the spinal discs stacked as the lifter pulls the bar straight up.

BUILT-IN SUMO SAFETY”

We insist on breaking the weight from the floor with leg power first
then finishing with the hip hinge not just for strength, but for safety.

Breaking the weight from the floor with the hip hinge with high hips
and an inclined torso at the starting position, puts significant shearing
stresses on the lower back. The upright, more vertical torso position we
require stacks the vertebrae of the back, and minimizes stress on your
spine.
 It’s less likely with our more vertical torso position for the lower back to
“round” (a common cause of back injury) when fatigued under load.

COMMON FLAWS IN FORM

1. THE HYPEREXTENDED SPINE
This back position is called “hyper-lordosis” in medical terminology. It
happens when the upper torso becomes unlocked from the lower body
during the initial part of the lift. This occurs when the legs are not strong
enough to break the weigh from the floor. The upper part of the torso will
change position to become more upright without the legs moving. This
puts the entire initial load on the back, and places the spine in a bad
position.

Reduce the amount of weight and concentrate on

keeping the lower back and upper torso locked
together. The rule—if the legs do not move, the
upper body does not move. Use a weight that will
allow you to break the weight off the floor using
only your legs.

Here the trainee’s upper body rises before her

tailbone at the start of the lift causing hyperextension
(backward bend) of the spine. This form error usually
means the weight is too heavy and the legs are not
strong enough to break the weight from the floor. Lighten the load in this
case so that the tailbone and upper body can rise in unison, maintaining a
straight spine during the lift.

2. ROUNDING THE BACK DURING DESCENT

Avoid the temptation to bend forward while descending with the
barbell. Using a precise and slow lowering technique will maximize the
strength and muscle building attributes associated with the heavy
eccentric/negative phase of the deadlift rep.

Maintain an upright posture during descent, similar to a reverse squat.

Rounding the back during the descent of a deadlift is asking for a ruptured
disc. The deadlift should look exactly the same during the ascent and
 descent. If we took pictures of a lifter during the
upwards and downwards parts of the lift, they
should be identical.

Poor descending technique with the Sumo Deadlift:

the trainee lets her back bend forward (flexion)
instead of maintaining the neutral spine position as
she lowers the weight. This is usually a sign of fatigue
and is a sure way to injure your back.

The sumo deadlift is a required part of your

resistance training program. It will protect your back from injury and
forestall the hands of time by potently preventing sarcopenia and
osteoporosis.
STRONG MEDICINE TACTICS:
Implement the Sumo Deadlift as part of the foundation of your
resistance training program.
PHYSICAL TRAINING IV
BENCH PRESS AND OVERHEAD PRESS

When it comes to building front torso muscles, no other progressive

resistance exercise comes close to duplicating the results from proper,
repeated and intense flat bench pressing. You might think lying flat on a
bench and pressing a barbell or pair of dumbbells to arms’ length would be
the simplest task imaginable. But, we are confronted by a myriad of
choices...

What technical pathway will we use for the lowering phase? Where will
we touch on the chest? Will we pause the rep, or touch-and-go? If we
pause, for how long?

Will we push on a straight or curved arc path?

The trajectory and speed of the bar’s path during the lowering and
raising phases dramatically affects muscular targeting, and overall
effectiveness of the exercise. We need to consider these things before every
set. Become conscious and attuned to what you are doing during every rep
of every set.
BENCH PRESS TECHNIQUES, TACTICS
AND TOOLS
We want to make the bench press maximally difficult, while the rest of
the fitness world wants to make their bench presses easier with half-reps,
machine pressing, reps bounced off the chest, or raising the butt off the
bench at the sticking point. These are ego-inflating techniques that degrade
strength and hinder results.

Anyone who consciously or unconsciously makes their bench presses

easier is defeating the purpose of resistance training. They don’t
understand why they are lifting weights! Our mission is to resurrect the
ancient tactics used by champion bench pressers, men who sought ways to
increase the difficulty when they benched. Difficultly in resistance training
is the pathway of progress. Making resistance training easier makes
resistance training less effective.

Our goal is not to present a comprehensive

set of bench press techniques and variations.
We will provide our strategy on sets, reps,
frequency and workout duration. The goal is
to produce dramatic increases in lean muscle
mass and equally dramatic increases in pure
pushing power. A universe of pushing
possibilities exist within the tight confines of
flat benching. But, we will focus on a single
variation, and hone the dumbbell bench
press to perfection.
LEARN TO LOVE DUMBBELLS
Elite trainers love the cumbersome and awkward nature of the unwieldy
dumbbell. In the right hands and used the right way, dumbbells are
unrivaled for stimulating the pecs, shoulders and triceps. Dumbbells cause
muscle stabilizers to fire to a higher degree than two-handed barbell work,
or any of the resistance machines that mimic the bench press.

We will pair the dumbbell’s inherent instability (an advantage) with our
intensity-enhancing techniques. In our first dumbbell variation, pause with
the dumbbells at the bottom of the rep, then actually release the tension in
the chest and arm muscles with an exhalation. This relaxation tactic is
considered heretical by the resistance-training mainstream. After the pause,
re-engage the stretched, relaxed pecs, inhale and use a purposefully slow
speed on the concentric (push) phase to increase the difficulty of the rep.
All of our subsequent bench press variations are constructed based on our
ultra-basic dumbbell techniques.

DUMBBELL BENCH PRESS TECHNIQUE:

RELAX, PAUSE, GRIND
The most difficult bench press technique you will probably encounter is
a limit set of ultra-deep, relaxed, paused, dumbbell bench presses
performed with a purposeful “grind” (slightly slowed) rep speed. Mastery
of the paused dumbbell bench using grind speed is our very own version of
bench press boot camp—a bench press version of SEAL BUDs Hell Week.
Once you have paid your dues with long and prolonged bouts of paused
dumbbell bench presses, everything else seems like a walk in the park.
DUMBBELL BENCH PRESS TECHNIQUE
1. Select two dumbbells and sit on the end of the exercise bench with
both dumbbells. The handles should be vertical with the plates in
your lap.
2. Lie back and simultaneously turn the handles outward. You are now
lying on the bench with the dumbbells in the bench press start
position.
3. Exhale and allow the dumbbells to sink. Maintain control, even
though the pecs and shoulders are relaxed, the grip stays tight. The
dumbbells are now in push position.
4. Relax, feel the dumbbells stretch the pecs and shoulders
downward. Perform this “pre-stretch” at the start of every single
rep.
5. We have maximally inhaled and are full of air at the same instant
the dumbbells touch the chest at the bottom of the descent. Then,
we exhale, relax, and stretch.
6. After allowing the bells to stretch downward, consciously re-engage
the pecs, delts, and triceps. Shift from stretching and relaxation
into pushing and contracting.
7. When it is time to push, inhale mightily and push upward. The rep
speed is not fast or super slow—but it is consciously slowed.
8. This consciously-slowed rep speed is called “grind.” We grind the
dumbbells to a “hard” (full-and-complete) lockout. We
synchronize our exhalation to end at lockout.
9. This unorthodox strategy accomplishes two monumental tasks: it
ingrains perfect technique and isolates/stimulates the maximum
number of muscle fibers.
10. This fundamental bench press technique succeeds in making light
weights heavy, and stays true to our overall philosophy.
11. All subsequent bench press variations spring from this pause-relax-
and-grind technique. After practicing this technique, all other
forms of benching are easy.

Dumbbell Bench Press set up position.

Dumbbell Bench Press start position (top view and floor level).
Dumbbell Bench Press: start from relaxed bottom position, produce tension,
press at grind speed to top lockout, descend slowly, pause at the bottom,
repeat…
DUMBBELL BENCH PHASE II: BEYOND
PAUSE, RELAX, GRIND
Our bench press theme is the pause-relax-and-grind dumbbell technique.
As we introduce each subsequent new bench press variation, it will be
easier than its predecessor. This the natural order of proper progressive
resistance training. Human nature is to jump ahead to the sexier bench
press variations without mastering the basic theme.

This is a big mistake. How can we develop a deep understanding of any

variations without first mastering the theme?

The first step—which includes all the physiological benefits of bench

press expertise—is to master the dumbbell bench press with the pause-
stretch-relax-in-the-bottom-position technique, then using the grind speed
to push the dumbbells to lockout.

All subsequent bench press and barbell variations are built on this core
technique. Do not skip ahead before mastering the “pause-relax-and-
grind” style. Without mastering this technique, the trainee cannot
appreciate the “easing effect” as they master each subsequent bench press
variation.

We adhere to an overarching philosophy of using ultra-strict, ultra-

simplistic, but sophisticated techniques to make light weights heavy. By
design, any bench press techniques after the pause-relax-and-grind
approach with dumbbells will seem light and easy by comparison.
ADVANCING THE DUMBBELL BENCH
PRESS
After mastering the core technique, we can proceed with the next two
dumbbell variations:
1. Pause at the bottom like before, but instead of pushing with a slow
“grind” speed, push the dumbbells up explosively.

Compared to the excruciatingly slow pause-relax-and-grind technique,

dumbbell bench presses with an explosive push seem easy by
comparison.
2. The second variation eliminates the pause. Lower the dumbbells to
the bottom position, then immediately push them up explosively.
This is the “touch and go” variation.

The second variation (touch-and-go) allows for maximal loads. Strong

Medicine trainees coming from the hell of pause-and-relax grind
benching to touch-and-go explosive dumbbell bench press technique
will feel as though they are cheating. Now we can choose to use a
barbell—or not.
THE OVERHEAD DUMBBELL PRESS
The ability to push in the vertical plane is important in daily life. The
overhead dumbbell press will train this ability, giving you specific strength
that not many people possess. While big bench press numbers are
impressive, overhead pressing arguably translates better to real-life applied
strength. In our opinion, “How much can you press?” should be the
benchmark question for upper body strength, not, “How much can you
bench?”.

COILED ENERGY: FROM BOTTOM TO TOP

The perfect press starts with the lower body, not the upper body. You
must have a strong, steady foundation. A flaccid lower body during the
press is a very serious “energy leak”. Energy which could help push the
weight overhead is lost to an unstable lower body if improper technique is
used. Your press should start by tensing the entire lower body, as if you
are compressing a coiled spring.

COACH’S CORNER:
A successful standing overhead dumbbell press depends on a super
stable push platform. The thighs and legs are maximally contracted,
glutes are clenched, and there is tremendous tension in the mid and
upper back.
THE OVERHEAD PRESS
Dumbbells and kettlebells are the ultimate tools for overhead pressing.
You can press one are at a time, or both at once. We will be using two
dumbbells or kettlebells for the double arm press.
1. Grab a set of appropriately sized dumbbells or kettlebells. Be
conservative and err on side of “too light” if you are in doubt.
2. Position the bells in the clean position at shoulder height.
3. Clench your calves, thighs, glutes, and abdominal muscles
maximally before pressing. This is the start position.
4. Press the bells explosively overhead to full elbow lockout.
5. Pause with the bells overhead while maintaining maximal tension
throughout your body.
6. As you lower the bells slowly, build even more tension in your
body. You are compressing the coiled spring. Do not let gravity
take control of the bells in an uncontrolled drop. The negative
(lowering) part of this exercise is just as important as the push
upwards.
7. The coiled spring tension generated will prepare you for the next
rep. Pause briefly at the bottom then explosively push the bells
upward again to lockout.
8. Repeat until the desired number of repetitions are completed.
Dumbbell Overhead Press: start the press from a strong base with legs and
glutes contracted. Build tension (coiled spring) during the descent to power
the explosive push on the next repetition.

The dumbbell bench press and overhead press are the pinnacle of upper
body pushing movements. After you have developed good technique in
both, you can move forward in your training. With every push, we need a
pull to maintain balance. For our purposes, the row is the best option for
an upper body pulling exercise.
STRONG MEDICINE TACTICS:
Use the dumbbell bench press as one of the foundations of your
resistance training program.

STRONG MEDICINE TACTICS:

Implement the overhead press as one of the foundations of your
resistance training program.
PHYSICAL TRAINING V
THE ROW

When selecting an appropriate pulling exercise, the choices are extremely

limited. The elite choose from chin-ups and pull-ups done with various set
and rep combinations. For those able to perform them, proper chin-ups or
pull-ups from a dead-hang stretch to chin-over-bar is unparalleled for
activating, building, and strengthening every muscle of the back. But, few
have the requisite strength-to-bodyweight ratio needed to perform this
difficult exercise.

Chin-ups and pull-ups are difficult because we are forced to handle

100% of our bodyweight—and most people are not that strong. There are
clever gym machines for assisted chin-ups and pull-ups with
counterweighted knee platforms that push upwards—but how many of us
have access to such a marvelous device? We are forced to look around for
exercise alternatives.

After experimenting with different back exercises, one that seems to fit
all the criteria as a successful chin-up/pull-up replacement is the “frozen
statue row.” But, before we can do the “frozen statue row” (FSR), we will
start with the single arm row to build a foundation of perfect technique
before advancing.
The Chin-up: works the back like nothing else.

COACH’S CORNER:
We realize that a row pulls in the horizontal plane while a chin-up pulls
in a vertical plane. While the row is not a true substitute, it works for us
because it is the direct opposite of a dumbbell bench press. The row
will help us build symmetry by offsetting the horizontal push of the
bench press with a horizontal pull.

PHASE I: THE SINGLE ARM SUPPORTED ROW

1. Use a dumbbell that is lighter than you think you need, and put it
next to the bench.
2. Grab one end of the bench with your left hand and place your left
knee and shin on the bench. The left side of your body is now
supported on the bench.
3. Bring your right leg directly out from the bench and plant your right
foot with a stance wider than shoulder width. You now have 3
points of support—your left hand, left knee/shin, and your right
foot.
4. Keep this position. Reach down and grab the dumbbell with your
right hand. Now raise your right shoulder (keeping your arm
hanging straight down) until it is level with your left shoulder. Let
the weight of the dumbbell stretch your back muscles but do not
let your shoulder drop. Your spine should be straight (do not
“hunch” your back). This is the starting position.
5. First, retracting shoulder blade (scapula) towards your spine. Your
elbow should not bend at this point. The dumbbell will start to rise
as you move your shoulder blade towards the spine (imagine trying
to pinch something between your shoulder blade and your spine).
Do not jerk the weight up from the starting position, move at a
slow “grind” speed.
6. Direct your elbow up towards the ceiling. It will naturally bend when
you do this, but we are not curling the dumbbell. Bring the elbow
up as high as possible but do not let the front of your right shoulder
rise much above the level of your left shoulder. This mistake results
in twisting the spine and poor technique.
7. Briefly pause at the top position and lower the dumbbell with a slow
“grind” speed back to the start position.
8. After completing your reps, switch to the other side and repeat the
above steps.
Single Arm Supported Row: the shoulders stay level and the forearm pulling
the weight stays vertical. The elbow is directed toward the ceiling in a vertical
line.

THE “FROZEN STATUE” ROW

The single arm dumbbell row performed at grind speed with a pause
truly makes light weights heavy. You can build incredibly strong and dense
lats, rhomboids, lower trapezius, and posterior deltoids with this technique
while using minimal weight.

After several months of training, you can progress to the double

dumbbell row, the “frozen statue” row (FSR).
 EXERCISE SAFETY
Do not attempt the “frozen statue” row until you have developed the
requisite posterior chain (back, glutes, hamstring) strength and postural
stability from training the sumo deadlift and squat with perfect
technique for several months. The postural demands from this exercise
could result in back injury if you are insufficiently prepared.

The FSR involves holding your body in a static position “like a statue.”
Instead of using a bench for support as in the single arm row, the “frozen”
position is the base of support for the double dumbbell row. Holding this
base of support adds a significant level of difficulty and a much higher
stimulation of the central nervous system. Stabilizing this position while
just holding dumbbells is a workout in itself. Rowing the dumbbells from
this position is maximally stimulating for the adaptive response we want
from our resistance training.

WHY MOST FREE-WEIGHT ROWS ARE

WORTHLESS
The classical barbell row and all its variations are often fundamentally
flawed in their execution.

The problems are numerous:

• Stances tend to be too narrow—widen your stance to at least
shoulder width.
• The spine is often bent, make sure to maintain a neutral spine
position without bending the back.
• Most rowers jolt the weight upward to start the movement. The
latissimus (lats) muscles are not engaged (and not exercised) by
 jerking the weight at the start. This is also very bad for the spine, and
places significant, abrupt shearing forces on your vertebrae.
• Lifters make most of these “mistakes” on purpose and are driven by
ego. These technical errors allow for heavier weights to be “rowed.”
Moving the weight in this manner is not a row and misses the
muscles we want to exercise. These attempts to impress others are
just a setup for injury.

Heavy weight is not needed for maximum benefits from a correctly

performed row.

PHASE II: THE “FROZEN STATUE” ROW

1. Grab a pair of dumbbells that are lighter than you think you need
and hold them at your sides while standing erect.
2. Move your feet at least shoulder width apart.
3. While maintaining a flat, neutral spine, hinge
at the hips and lower the angle of your
torso until it is almost parallel to the floor.
We avoided this high hip position with the
deadlift, but the lighter weights used for the
FSR, ensures that the stress on the spine is
safe and manageable as long as the spine
remains locked in to a neutral position. The
dumbbells will hang relatively close to the
floor at this point. This is the starting “frozen statue” position.
4. Hold this position as you begin the row. If initiating the row causes
you to break the “frozen statue” position, the weight is too heavy.
5. The first movement is retracting your shoulder blades (scapula)
towards your spine. Your elbows should not bend at this point. The
dumbbells will start to rise just from moving your shoulder blades
towards the spine (imagine trying to pinch something between
 your shoulder blades and your spine). Do not jerk the weights up
from the starting position, move at a slow “grind” speed.
6. Point your elbows up towards the ceiling. They will naturally bend
when you do this, but do not curl the dumbbell. Bring the elbows
up as high as possible while keeping yourself locked in the “frozen
statue” position with a flat, neutral spine. Keep squeezing your
shoulder blades together.
7. Pause at the top position briefly and lower the dumbbells with a
slow “grind” speed back to the start position.
8. Start another repetition and repeat until your set is complete.

Frozen Statue Row: the spine remains flat (almost parallel to the floor) during
the lift. The elbows are directed in a vertical line toward the ceiling with the
forearms remaining perpendicular to the floor. (Note that the trainee has a
hyperextended (bent back) neck in the start position but fixes it during the lift
itself).
 SIMPLE IS AS SIMPLE DOES
Many people have a hard time making the mind/muscle connection
with the main muscles we’re trying to target—the lats. Here is a bit of
muscle trivia I heard eons ago: the lats are the least used muscles on
the human body. Because of this, they are the easiest muscles to
strengthen and grow—assuming the smart trainee uses techniques
that actually stimulate the lats to a significant degree.

The muscle elite had a saying, “Show me a man with great lats, and I’ll
show you a man with sub-par biceps; show me a man with outstanding
biceps and I’ll show you a man with terrible lats.” In other words, if you
can “arm pull” your rows by activating the biceps, you are not using
your lats. We must concentrate on pulling our rows with the muscles of
the back. Become a dumbbell row technician and really learn, hone
and develop your technique over time.

You have now learned the five core exercises which form the Strong
Medicine resistance training foundation. But no resistance training
program is complete without mentioning abdominal training.

We will show you how to develop rock hard abdominal muscles without
ever doing a sit-up or crunches. Before you think this sounds like a
television infomercial, read on.

STRONG MEDICINE TACTICS:

Incorporate the row as one of the foundations of your resistance
training program.
PHYSICAL TRAINING VI
STRONG MEDICINE ABS

We all want a hard, chiseled abdominal region—a “six-pack” to show

off. There are literally hundreds of abdominal training videos that promise
to give you the coveted six-pack. The truth is, only proper nutrition and
lifestyle management (good sleep, stress control) will give you six-pack abs,
not endless crunches and sit-up variations.

SIT-UPS ARE A BAD IDEA...

Not only will you fail to achieve the “six-pack” look from sit-ups, they
may lead to injury. Most sit-up variations involve anchoring the feet and
significantly engaging your hip flexors (psoas) to achieve the sit-up
movement. This is a problem for a couple of reasons...

• The abdominal muscles are not optimally activated or strengthened

since the hip flexors are doing most of the work.

• High activation of the psoas (a major hip flexor) puts major

compressive forces on the spine. A look at the psoas anatomy
explains why. According to Dr. Stuart McGill, a leading spine
biomechanics expert, the average sit-up generates about 730 lbs. of
compression on the spine with every repetition. This amount of
 compression is known to lead to disc injuries over time. Doing
hundreds of sit-ups will not do your back any favors.

SIT-UPS ARE LOW BACK “POISON”

As Dr. McGill has studied in his spine biomechanics laboratory, sit-ups
put a huge compressive load on the spine. To make matters worse, this
large compressive force is applied when the lower back is in a flexed
position.

According to Dr. McGill’s research, the best way to herniate a disc is

with high compressive forces and repeated flexion, which exactly
describes a sit-up!
 Many clinicians are still telling their back pain patients to do sit-ups to
strengthen their abdominals. But, situps are the exact opposite of
what you should do for a healthy back.

The abdominal muscles’ function is to stabilize the spine during activities

such as lifting, carrying, pushing, and pulling. We need to train them as
they were meant to function, instead of isolating them with exercises such
as sit-ups and crunches.

If you have progressed to the dumbbell front squat,

you will recognize the inherent difficulty in
maintaining a neutral spine position while holding
the weights at shoulder level during the squat. You
should feel your abdominal muscles struggling to
maintain an upright spine position while you are
squatting.

The abdominal muscles are meant to stabilize the

spine during activity. So, this is how we will train the
abdominals.

ABDOMINAL TRAINING PHASE I: THE BASIC

PLANK
A properly performed plank fits the bill for a great abdominal exercise
that works the abs with the rest of the body and strengthens their
function as a spine stabilizer. The Strong Medicine plank can seriously
test your resolve. There will be no doubt that your abdominal muscles
are working.
1. Find a relatively level space on the ground; use a mat if needed. Put
your forearms on the ground with your elbows directly underneath
your shoulders. Your forearms should be shoulder width apart on
the ground. You are in a kneeling position at this point.
2. Keeping your forearms in place, come off of your knees and
straighten your legs. Now, only your forearms and the balls of your
feet are touching the ground. Your feet are positioned next to each
other.
3. Flatten your back (no sag in the middle), then tighten your glutes
and your thigh muscles. Do not look up; keep your eyes and head
downward.
4. Push your heels away from you while keeping the balls of your feet
planted (you will feel a stretch in your calf muscles). This is the
starting position.
5. To begin your repetition, push your forearms and elbows down into
the ground while simultaneously “pulling” them toward your feet.
Your forearms and elbows will not move from their position. This
“down and backwards” force is isometric, like pushing against a
wall.
6. At first, try to hold this position with the “down and back force” on
the forearms and elbows for 10 seconds per repetition. Work your
way up to sustained 30-second holds.

The Plank (phase 1): the spine remains

neutral and the entire body is under
tension. Push the heels backwards
while you press your forearms down
and back.

ABDOMINAL TRAINING PHASE II: THE HIGH

PLANK
Once you can hold the basic plank for several sets of 30-second holds,
move up to the high plank. This variation is exactly like the basic plank
except that you are on your hands instead of your forearms.
 1. Find a relatively level space on the ground; use a mat if needed. Put
your hands on the ground directly underneath your shoulders with
your fingers facing foreword. Your hands should be shoulder width
apart on the ground. You are in a kneeling position at this point.
2. Keeping your hands in place, come off of your knees and straighten
your legs. Now, only your hands and the balls of your feet are
touching the ground. Your feet are positioned next to each other.
3. Flatten your back (no sag in the middle), then tighten your glutes
and your thigh muscles. Do not look up; keep your eyes and head
downward.
4. Push your heels away from you while keeping the balls of your feet
planted (you will feel a stretch in your calf muscles). This is the
starting position.
5. To begin your repetition, push your hands down into the ground
while simultaneously “pulling” your hands toward your feet. Your
hands will not move from their position. The “down and
backwards” force you are using is isometric, like pushing against a
wall.
6. At first, try to hold this position with the “down and back force” on
the hands for 10 seconds per repetition. Work your way up to
sustained 30-second holds.

The High Plank (phase II): this variation

uses the same technique as the plank but
from the hands instead of the forearms.
Push the heels backwards while you press
your hands down and back. The One-
hand Plank (phase III) will use the same
technique but holding one hand out in front of your body reaching toward
the wall in front of you.
ABDOMINAL TRAINING PHASE III: THE ONE
HAND PLANK
Once you can hold the high plank for several sets of 30-second holds,
move up to the one hand plank. This variation is exactly like the high
plank except you use only one hand for support. This adds an extra
layer of challenging instability.
1. Find a relatively level space on the ground; use a mat if needed. Put
your hands on the ground directly underneath your shoulders with
your fingers facing foreword. Your hands should be shoulder width
apart on the ground. You are in a kneeling position at this point.
2. Keeping your hands in place, come off of your knees and straighten
your legs. Now, only your hands and the balls of your feet are
touching the ground. Your feet are positioned about shoulder
width apart. You will need a wider base of support from your feet
at first.
3. Flatten your back (no sag in the middle), then tighten your glutes
and your thigh muscles. Do not look up; keep your eyes and head
downward.
4. Push your heels away from you while keeping the balls of your feet
planted (you will feel a stretch in your calf muscles). This is the
starting position.
5. To begin your repetition, lift one hand off of the ground and hold it
out in front of you. Generate the same isometric “down and back”
force with the hand on the ground. Try to hold this position for 5
seconds. Keep your shoulders level with each other with no
twisting of the spine.
6. After holding the one hand position for 5 seconds, switch hands
and lift the opposite hand up in front of you. Continue to switch
hands every 5 seconds for the duration of the repetition (10-30
seconds).
“ANTI-ROTATION”
The one hand plank is more difficult since the abdominals not only
stabilize the spine from flexing or extending (in the sagittal plane), but
also must stabilize the spine against rotation (in the transverse plane).

This stabilization against rotation (Dr. McGill calls it “anti-rotation”) is

an extremely important function of our abdominal muscles. Anti-
rotation is trained with the one hand plank by keeping the shoulders
level during the hand switch.

ABDOMINAL TRAINING PHASE IV: THE PLANK

ROW
Once you have worked up to several sets of 30-second sustained one
hand planks, you are ready for the plank row. This exercise is a huge
challenge to the stabilizing function of the abdominal muscles. You will
definitely feel it.
1. Find a relatively level space on the ground; use a mat if needed.
Grab two light dumbbells and place them in front of you, parallel
to the long axis of your body (see photo). Instead of placing your
hands on the ground, you will grab the dumbbells firmly and use
them as your front base of support. Be sure that the dumbbells are
directly below your shoulders.
2. Keeping your hands in place on the dumbbells, come off of your
knees and straighten your legs. At this point only the dumbbells
and the balls of your feet are touching the ground. Your feet are
positioned about shoulder width apart (or greater if needed).
3. Flatten your back (no sag in the middle), then tighten your glutes
and your thigh muscles. Do not look up; keep your eyes and head
downward.
 4. Push your heels away from you while keeping the balls of your feet
planted. This is the starting position.
5. To begin your repetition, lift one dumbbell off of the ground with
the identical technique used in the previous section for the single
arm row. Lift the dumbbell at grind speed and pause at the top.
While one arm is rowing, generate the isometric “down and back”
force with the hand grasping the dumbbell on the ground. Keep
your shoulders level with each other and do not twist your spine
during the row. Do not allow your back to bow or sag.
6. Row on alternate sides for up 2-10 repetitions per side.

The Plank Row (phase IV): the starting position (not shown)
is a plank position on top of dumbbells or kettlebells.
Shoulders remain level and the supporting hand pushes the
dumbbell or kettlebell into the floor keeping the wrist
straight. Use the same rowing technique you learned
previously leading with the elbow directed toward the
ceiling. Notice that he has a wider foot position for stability.

SAFETY TIP:
Make sure you use hexagonal style dumbbells or kettlebells with a large
flat bottom for this exercise. A rounded bottom surface on dumbbells
or kettlebells will not work, and will put you at risk for injury.
 Phases I-IV of Strong Medicine abdominal training will progressively
work the abdominals as they are meant to work in daily life. This
progression will also help your deadlift and squat since both lifts
require significant stabilization of the spine.

The deadlift and squat by themselves are already training the

stabilizing function of the abdominal muscles.

There are many excellent ways to train the abdominals as stabilizers

(including the “anti-rotation” function). The progression covered here
only scratches the surface.

Stop training the abdominals in isolation with back-busting sit-ups and

crunches. The Strong Medicine abdominal training program will give
you a six-pack (if your nutrition and lifestyle are locked on) and a
bullet-proof back.

STRONG MEDICINE TACTICS:

Use Strong Medicine abdominal training to build an iron core and
prevent back injuries.

The last six sections have been a primer on Strong Medicine resistance
training. These exercises should form the foundation of your weight
training. Feel free to add exercises to this foundation to suit your
individual needs and goals. We will now transition to cardiovascular
training for both the beginner and the experienced trainee.
PHYSICAL TRAINING VII
STRONG MEDICINE BASIC CARDIO

High Intensity Interval Training (HIIT) is the preferred way to maximize

the adaptive response of the body and lose fat in the shortest amount of
time exercising.

But, not everyone is ready for HIIT from both a fitness and
psychological perspective. The effort and high target heart rates of HIIT
can be overwhelming and intimidating to the new trainee. For an obese or
diabetic trainee, making monumental changes in nutrition while starting an
intensive exercise program at the same time is often too much to handle at
once.

We have created a Basic Cardio “ramp-up” for those in the above

categories, or who are new to training and are substantially deconditioned.
The Basic Cardio program can be progressed to subsequent advanced
training using Strong Medicine tactics.
PREPARATION
All you need to start is a basic heart rate monitor and your calculated
theoretical maximum heart rate (HRmax). You will use your HRmax to
plan your basic cardio training “ramp-up.”
MAXIMUM HEART RATE CALCULATION
REVIEW
For men: 208 - (0.7 X Age) = HRmax
For women: 206 - (0.88 X Age) = HR max
Example 1: Chris is 43 and wants to calculate his maximum heart rate.
He will multiply his age (43) by 0.7, which equals 30.1. He will then
subtract 30.1 from 208 to get 177.9 (we’ll round to 178). Chris’s HRmax
is about 178 beats per minute.

Example 2: Carrie is 46 years old. To calculate her HRmax, we would

multiply her age (46) by 0.88 to get 40.5. We then subtract 40.5 from
206 to get 165.5 (we’ll round up to 166). Carrie’s HRmax is 166 beats
per minute.
 At this stage, our preferred cardio method is outdoor “power walking.”
This is purposeful walking at a pace that will bring your heart rate up to a
predetermined level. It is not a leisurely stroll chatting with friends. Train
outdoors exclusively as long as your environment is safe. Outdoor training
has added benefits (stress relief, etc.) that slogging away on a treadmill will
not provide.

The following is a sample 10-week basic cardio “ramp-up” using the heart
rate monitor and a waist to height ratio to track your progress. (Find directions
for calculating your waist-height ratio in the “Stuff You Can Measure” section
at the end of the book.) Carrie, a 46 year old female, is our example. Her
HRmax was previously calculated to be 166 beats per minute (bpm). We will
calculate her weekly target heart rate as a percentage of her HRmax of 166
(bpm).

The goal of Strong Medicine Basic Cardio training is to help someone start an
exercise program from the beginning very slowly at a low intensity and
volume.

They will steadily increase both volume and intensity over 10 weeks and will
be well prepared for the full Strong Medicine physical training program.

Carrie calculated her By week 5, Carrie is By the tenth week,

week 1 target heart power walking 5 Carrie’s waist size
rate of 91 bpm by times a week for 20 has decreased
taking her HRmax of minutes per session. significantly. She is
She is keeping her wearing clothes 2
 166 and multiplying it target heart rate as sizes smaller than
by 0.55 (55%). close to 112 bpm as when she started.
possible during the She is exercising at a
166 X 0.55 = 91 bpm. entire session. relative high
She will keep her intensity (80% of
heart rate at this level We have steadily HRmax) every day
for the duration of her increased both the of the week for 35
session. volume and minutes per session.
intensity of her
She will do 3 sessions workouts over the She is ready to
during week 1 for 8 past 5 weeks. She move on to Strong
minutes per session. has already seen the Medicine High
benefits with a Intensity Cardio.
decreasing waist-
height ratio.

Use Strong Medicine Basic Cardio as an “on-ramp” to your fitness

program. You can also use power-walking as an active recovery
exercise instead of a complete rest day. Basic cardio can also be used
any time you feel your stress cup is near overflowing and high intensity
exercise may be too much that day.

STRONG MEDICINE TACTICS:

Build your cardiovascular training foundation with Strong Medicine
Basic Cardio.

Now that you have a cardio training foundation, we will progress to the
more advanced high intensity interval training to work the cardiovascular
system to its fullest capacity. This will provide increased health benefits
and accelerated fat burning.
PHYSICAL TRAINING VIII
STRONG MEDICINE HIGH INTENSITY CARDIO

Most official physical activity guidelines from exercise and public health
authorities recommend “at least 150 minutes per week of moderate to
vigorous aerobic exercise.” For many people, fitting this much exercise
into their hectic schedules means at least 30 minutes of mind-numbing
monotony on a treadmill, bike, or elliptical machine 5 days each week.

It is no wonder that over 50% of those who start a new exercise

program will not continue with it for even 6 months. The most common
excuse for not exercising is a lack of time. Also, a half hour of moderate-
intensity exercise on a machine is just plain boring. The boredom factor is
a big part of exercise non-adherence.

Strong Medicine addresses the time and boredom problems with our
advanced cardio program centered on High Intensity Interval Training
(HIIT). This type of exercise uses very brief periods of very high
effort/intensity separated by periods of rest/recovery. HIIT protocols allow
you to get all of health and fitness benefits of sustained moderate exercise
(though HIIT is superior is some aspects) in a short amount of time. HIIT
not only cuts down on the time needed for an effective exercise session, but
it also only requires you to do cardio 3 days per week, instead of 5 days or
more with traditional moderate intensity cardio.

Recent medical research supports the use of HIIT as a superior form of

exercise for people with heart disease, diabetes, high blood pressure,
and obesity.
• A single session of HIIT improves blood glucose control in diabetics
and non-diabetics for 1-3 days after the exercise session.
• For people with heart disease, HIIT results in better heart health
improvements as compared to moderate intensity exercise, even
when the amount of calories burned are the same.
• HIIT was superior to moderate intensity exercise for improving heart
and blood vessel function in heart failure patients.
• HIIT is more effective than moderate intensity exercise for
controlling and preventing high blood pressure.
• HIIT is far superior to moderate intensity exercise for reducing body
fat, especially around the belly.

The secret to the effectiveness of HIIT is the high intensity. HIIT

protocols require you to push your heart rate up to 90% (or more) of your
maximum heart rate for brief periods of time. The small amount of time
spent at these high heart rates produces incredible beneficial adaptations in
the body that moderate intensity exercise cannot touch.
MAXIMUM HEART RATE CALCULATION
REVIEW
For men: 208 - (0.7 X Age) = HRmax
For women: 206 - (0.88 X Age) = HR max
Example 1: Chris is 43 and wants to calculate his maximum heart rate.
He will multiply his age (43) by 0.7, which equals 30.1. He will then
subtract 30.1 from 208 to get 177.9 (we’ll round to 178). Chris’s HRmax
is about 178 beats per minute.

Example 2: Carrie is 46 years old. To calculate her HRmax, we would

multiply her age (46) by 0.88 to get 40.5. We then subtract 40.5 from
206 to get 165.5 (we’ll round up to 166). Carrie’s HRmax is 166 beats
per minute.

KEY POINT:
High Intensity Interval Training (HIIT) involves periods of high intensity
exercise separated by rest and recovery periods.
HIGH INTENSITY INTERVAL TRAINING
PROTOCOL
The HIIT protocol involves pushing your heart rate to approximately
90% of your maximum heart rate for short periods of time with rest
breaks in between. Let’s use Carrie as an example:

Carrie has already calculated her HRmax at 166 beats per minute. She
will multiply her HRmax by 0.9 (90%) to get about 149 beats per
minute.
166 X 0.9 = 149 beats per minute. This is her target heart
rate.
1. She will put on her heart rate monitor and choose a cardio machine
(a bike, elliptical, treadmill, stair climber, etc.).
2. She will warm up her muscles at a slow pace for 2-3 minutes.
3. She will then exercise hard enough to get her heart rate up to her
149bpm target, for a total exercise time of 60 seconds.
4. After the 60-second exercise interval, she will rest for 60 seconds
(or pedal/walk very slowly).
5. After the 60-second rest period, she will start another 60-second
exercise interval at the target heart rate of 149 beats per minute.
6. Carrie will repeat this for a total of 10 60-second exercise intervals,
then cool down for 2-3 minutes after finishing.
7. The basic HIIT protocol has been used in many research studies and
works great for weight loss and reversing diabetes.
 IMPORTANT MEDICAL REMINDER:
As we discussed in the obesity chapter, it is extremely important that
you speak with your doctor first before starting a protocol like HIIT. This
is especially true if you have previously had a heart attack or chest pain
with physical exertion. If you fall into these categories, you MUST get
approval from your physician first for safety reasons. There are plenty
of other exercise routines that you can do safely and will still be
beneficial.

HIIT is highly beneficial, but make sure your heart can tolerate high
intensity exercise before you begin.

You can use the HIIT protocol with a variety of different exercises. You
can even set up your HIIT session with alternating exercise types after
every 60-second interval. For example, rowing for the first interval, cycling
on the second interval, elliptical on the third.

There is something very primal about pushing your cardiovascular

system to 90% (or higher) of your maximum heart rate. It is hard to get
bored or preoccupied with worry or rumination when you are exercising at
this level. The stress relieving effects and endorphin (feel-good brain
chemicals) rush are second to none with these protocols.

HOW MUCH IS TOO MUCH?

There are circumstances when the basic HIIT protocol is too much of a
good thing. A night of bad sleep or an exceedingly stressful day at work
may not leave room in your stress cup for the demands of the basic HIIT
protocol. How can we make sure to get the optimum (hormetic) dose of
exercise on any given day?
We want to be in the “green zone” with exercise intensity, the “hormetic
dose.”

We do not want to under-train and miss the benefits of the adaptive

response to exercise, and we certainly do not want to overtrain and overfill
the stress cup.

To address this problem we have devised an alternate HIIT protocol that

automatically takes into account the “fullness” of your stress cup on any
given day, and ensures that you get the right “dose” of exercise. It also
automatically adjusts for fitness levels, and will not overtrain the novice
while still giving the veteran trainee all that he or she can handle. We call it
the “Burst Cardio” protocol.

BURST CARDIO—INDIVIDUALIZED HIIT

“Burst Cardio” is a 20 minute protocol for getting the most out of your
workout without overfilling your stress cup.

A 20 minute Burst Cardio session:

• Burst up to 90-95% of your predicted max heart rate (HRmax), then
stop as soon as you reach it.
• 90% HRmax is the requirement, 95% is the goal.
• Recover until your heart rate slows to 70% of HRmax.
 • Burst again up to 90-95% of your
HRmax.
• Repeat the burst cycle until 20
minutes have elapsed.

Using a heart rate monitor with

Strong Medicine “Burst Cardio” will
ensure you don’t overfill your stress
cup.

On a day when stress is low and you feel rested, you will have a
relatively low sympathetic (flight or fight) nervous system drive. Once you
“burst” up to 90-95% of HRmax you will recover to 70% of HRmax
relatively quickly. This quick recovery will allow you to do more cycles up
to your 90-95% HRmax in the 20 minute time period.

There is plenty of room in the stress cup for high intensity exercise
when overall stress is low. The sympathetic (flight or fight) nervous
 system will have relatively low overall sensitivity, allowing for quick
heart rate recovery. More “burst cycles” can be completed in that 20
minute session. You will be able to do more work in the session
without overflowing the stress cup.

On a day when your overall stress is high, your sympathetic nervous

system will be sensitive to further “threats,” including exercise. Once you
burst up to 90-95% of heart rate max, it will take longer for you to
recover to 70% HRmax because the nervous system is overactive from
work stress, poor sleep, etc. Longer recovery times mean you will not be
able to do as many cycles of the burst protocol in the 20 minute workout.
More time will be spent in the recovery period.
 High stress at work, a bad diet, and poor sleep have filled most of your
stress cup today. Using the Burst Protocol with a heart rate monitor will
protect you from overfilling the cup. You will need longer recovery
times for your heart rate to drop back down to 70% HRmax, which will
ensure that your body is gets the rest it needs between “bursts” on a
stressful day.

THE BUILT-IN SAFETY SYSTEM

Using the heart rate monitor allows you to plug into the state of your
nervous system, and ensure you get adequate rest between bursts. On low
stress days, your fast heart rate recovery may allow you to get 10 burst
cycles in 20 minutes. On high stress days, your slower heart rate recovery
may only allow for 4-5 burst cycles.

Getting only 4-5 burst cycles on a high stress day is a good thing. You
are listening to your nervous system by monitoring recovery and not
overtraining (overfilling the stress cup). Remember that consistently
overfilling the stress cup leads to chronic inflammation, oxidative stress,
and chronic disease.

KEY POINT:
Using the heart rate monitor with the burst protocol is a built in safety
system that allows you to get the most out of your workout on any
given day. It automatically adjusts the protocol to the other stresses in
your life and your fitness level.

Individual heart rate recovery also allows a very fit person to train with
a beginner. The person with a high fitness level will be able to do more
intervals because their recovery time will be much shorter than the
beginner’s. Their well-conditioned heart and nervous system will require a
higher relative intensity to reach their target heart rate. The beginner will
shoot up to their target heart rate relatively quickly, but will take
considerably more time to recover than the fit person. The beginner will do
fewer total intervals in during the 20 minute session by design. Monitoring
heart rate will ensure both get exactly the right amount of exercise to
trigger beneficial adaptations without overtraining. As the beginner
becomes more fit, they will recover faster and be able to increase their
number of intervals in 20 minutes.

You can use any modality or tool for your burst cardio protocol:

• Running

• Elliptical or stair stepper

• Biking

• Cross country skiing (or simulation)

• Burpees, medicine ball slams, kettlebell swings, or any other

bodyweight circuit training exercise.

We prefer “4-limb” cardio that activates arms and legs at the same time.
Cross country skiing, rowing, and many bodyweight circuits work well. Be
creative with your choice of exercises for your intervals and mix it up.

We will look a little deeper into the Burst Cardio protocol, and see it in
action. We will also show you how use it to fine-tune your nervous system,
and as a potent tool for stress relief.

Take a look at the graphic on the next page. There are some important
things to note on the two profiled workouts.

• The recovery periods get longer as the workout progresses. The

recovery interval needed between exercise periods automatically
adjusts itself as you become more fatigued during the workout. Your
nervous system is dictating how much recovery
 time you need, instead of using a set interval as
in the basic HIIT protocol.

• When your “stress cup level” is low (as in

workout #1), you can spend more time in the
higher intensity heart rate zones because you can
perform more exercise intervals in the 20
minutes. Although workout #1 and #2 were
performed by the same person in the same week,
you could easily imagine the data from workout
#2 being generated from a beginner or deconditioned trainee.

• It is easy to see how much a night of bad sleep—or anything else that
fills the stress cup—has an impact on your nervous system. You
would never know this unless you were monitoring your heart rate.
This is the built in safety system that prevents overtraining and
allostatic overload (an overflowing stress cup).

• During the recovery periods, you never drop below the 70%
moderate intensity level. You are still burning significant calories
during the recovery intervals.

BURST CARDIO: FURTHER ANALYSIS

Chris uses the Polar® Beat application for iPhone or Android, and the
Polar® Flow website to track workout data. Both are free and highly
recommended. All you need is a Bluetooth heart rate monitor. The
following graphics have been taken from actual workout data from his
Polar® Flow account.

The following are examples of the Burst

Cardio protocol in action with data from
Chris’s actual workouts. At the time, Chris
was 43 years old. His HRmax was
calculated at 178 bpm, putting his 90-95% target heart rate range between
approximately 160 and 169 bpm (0.95 X 178 = 169 and 0.90 X 178 =
160). His 70% HRmax is about 125 bpm (0.70 X 178 = 124.6).
WORKOUT #1:
Chris was able to do 6 total intervals in 20 minutes, with relatively quick
recovery times between intervals. Notice the proportion of time spent in the
higher intensity “zones” (zones 4 and 5) is relatively high in this workout.

WORKOUT #2:
This workout was 5 days after the first workout above and took place after a
night of bad sleep. Notice that Chris was only able to do 4 intervals in the 20
minute workout with long recovery periods needed to get back down to
70%. Also notice the time spent in zones 4 and 5 is relatively low compared
to workout #1.

TRAINING THE RECOVERY, BALANCING

YOUR FITNESS
The Burst Cardio protocol also allows us to do something almost never
discussed in modern fitness—using the recovery period as a trainable event.
Modern society is hyper-competitive, always looking to achieve higher
levels of performance in the speed of our cars, our computers, and
certainly our workouts. This is why “boot camp beat-down” fitness
programs are really popular. In Chinese philosophy, we are too much in
the “yang” direction without the balance of “yin.”

The time it takes to recover from the “burst” up to 90-95% of max

heart rate down to the 70% level will vary depending on your fitness and
stress levels. We can actively train during the recovery time with the
mindfulness breathing techniques and biofeedback we learned in the
chronic stress chapter.

• Once you have hit 90-95% of your maximum heart rate with the first
interval, stand in a relaxed posture and start the breathing exercises.
We are calming the sympathetic (flight or fight) nervous system in a
mindful manner to reduce our heart rate.

• Watch your heart rate monitor display as you breathe, using it as a

biofeedback device. Follow your heart rate as it slows, slowing your
breathing and releasing muscle tension. Follow your heart rate down
to 70% then start your next interval.

Using this technique for training your recovery, you will be able to bring
your heart rate down faster between intervals and ultimately complete
more total intervals in your 20-minute burst protocol. Referring again to
Chinese philosophy, we are balancing the interval training (yang) by
actively enhancing the recovery (yin). In Western scientific terms, we are
balancing the sympathetic nervous system stimulus of the exercise interval
by training the parasympathetic nervous system during the recovery
period.

Training the recovery has carryover effects into our daily life. Being able
to quiet your mind and focus your breathing during recovery from a high
intensity exercise interval (often in the midst of the noise and distraction of
a busy gym) is a very valuable health-enhancing skill.

Imagine the benefits of training to be calm in the middle of the “storms”

of your daily life. This is another approach—built in to your workout—to
help master your stress/threat system
and reduce the effects of chronic
stress.
AN ADAPTABLE SYSTEM
The burst cardio system also takes into account the type of exercise you
are performing in your interval. Heavy kettlebell swings will take more of
a toll on your nervous system than the elliptical machine. It will take
longer to recover from the kettlebell swing interval than the elliptical
machine interval. It is no problem to mix different exercises as your
nervous system will adjust automatically for the proper recovery time
between exercises. This is important since most injuries happen when the
nervous system is fatigued and exercise form breaks down. The protocol
will help prevent injury from poor form due to nervous system fatigue.

KEY POINT:
Most injuries happen in a state of nervous system fatigue. The Burst
Cardio protocol will help prevent injury by monitoring the state of the
nervous system with the heart rate.

The total time of the burst cardio protocol can be adjusted if you are
really feeling run down, have limited time, or have performed intense
strength training directly before your cardio session. Burst cardio sessions
of 10 minutes are still highly effective in the right circumstances. You can
use this protocol in your home, the gym, or ideally immersed in a natural
setting.
TRAINING TIP:
If you are having difficulty achieving at least 90% HRmax during your
intervals, find another exercise. You may have become too efficient at
a single exercise (i.e. elliptical) and your nervous system has adapted.
Mix up your exercises!

TRAINING TIP:
HIIT has been shown to significantly improve performance capacity in
endurance athletes like marathon runners, cyclists, and triathletes.
Research has shown that endurance athletes were able to cut as much
as 25% of their regular training and replace it with HIIT protocols
without losing any performance capability during competition. This is a
great way to cut down on training volume and potentially prevent
overuse injuries for competitors in endurance-based sports.

A trail run in the woods is an ideal way to do the Strong Medicine burst
cardio protocol.
Burst interval: pushing up to 90-95% of HRmax.
Burst recovery: mindful breathing and biofeedback down to 70% of HRmax.

The Strong Medicine burst cardio protocol will give you the health
benefits of HIIT with an extra built in safety system to prevent
overtraining and injury. We are now going to show you how to program
your exercise sessions weekly, combining strength training and cardio for
an individualized template of physical transformation.
STRONG MEDICINE TACTICS:
Implement Strong Medicine “Burst Cardio” to supercharge your
metabolism, enhance fat burning, sensitize insulin, and train your
recovery without overfilling your stress cup.
PHYSICAL TRAINING IX
EXERCISE PROGRAMMING

TRANSFORMATIONAL FITNESS

“Eventually, after all the books are read and all the thoughts
are thought, it becomes time to actually train—what to do:
how to do it.”
—Marty Gallagher

We need a transformational template and we need to structure our lives

to “make room” for fitness. Once we have the game plan and have set
aside training time, it is time for the rubber to meet the road for some
actual training. Training is split into two generalized disciplines: resistance
training and cardiovascular training. The idea is to mix and meld these two
training disciplines to elicit specific physiological effects. There are
enumerable variations within each discipline.

We won’t throw you into the deep end of the pool—most professional
fitness trainers require new trainees to engage in drills past the limits of
their capacity. It is cruel and counterproductive to make an untrained
person—who has done nothing more strenuous than walk to the
refrigerator for decades—suddenly and immediately begin high-impact
jogging at a pace past their capacity on day one.

Our approach eases the trainee into our methodology: we establish

initial performance benchmarks and improve upon the previous week’s
performance, in some way each week. By asking slightly more of ourselves
each week we continually trigger the adaptive response and the extremely
beneficial hormonal tsunami that accompanies it. We want to safely and
consistently exceed our best efforts—that is where the progress lies.

DAY ONE, WEEK ONE, SESSION ONE

We will assume you have spent the time to develop your technique for
the five core exercises—the squat, deadlift, bench press, overhead press,
and the row—before launching into a formal program. Once you have
done your homework with the lifts, you can start training.

TACTICAL TEMPLATE: WEEKLY TRAINING REGIMEN

DAY RESISTANCE TRAINING CARDIO

Monday Superset of Squat with Power-walk or
overhead press Rest
Tuesday None Burst Cardio
session 10-20
minutes
Wednesday Superset of Dumbbell Power-walk or
Bench Press with Row Rest
Thursday None Power-walk or
Burst Cardio
Friday None None
Saturday Sumo Deadlift Power-walk or
 Rest
Sunday none Burst Cardio
session 10-20
minutes

Using the Tactical Template as a guide, the following is a six-week plan

for progressing the exercises from week to week.

Use the Tactical Template to determine what exercises you will do on

specific days of the week, and use the weekly progression charts to
determine how you are doing the specific exercise as it relates to sets, reps,
time, and intensity.

WHAT IS A SUPERSET?
A superset consists of two exercises performed one after another
without pause. For example, on Monday we will alternate or ‘superset’
ultra-deep squats with overhead dumbbell presses. First perform a
technically perfect set of ultra-deep paused squats. Upon completion
of the squats, walk to the dumbbell station, pull the dumbbells to your
shoulders and complete the press reps, then rest.

The athlete will perform the pattern three times in succession—squat,

press, rest, squat, press, rest, squat, rest, press. This strategy is used
again on Wednesday alternating the dumbbell flat bench press with
the statue row—bench, row, rest, bench, row, rest, bench, row, rest.

The superset alternating exercise strategy is a major time saver. The

trick is to pair up “non-conflicting” exercises. For example, you would
never pair up, or superset overhead presses with bench presses
because these two exercises use many of the same muscles. We would
never superset or alternate deadlifts and squats as they also use many
of the same muscles.

How long should you rest between supersets? Wait until your
breathing normalizes then hit it again.
WEEK 1
Exercise Sets/Reps/time/intensity

Squat Bodyweight, 3 sets, 8 reps

Overhead Press 3 sets, 8 reps (enough weight so 8 reps is

hard)

Dumbbell Bench 3 sets, 8 reps (enough weight so 8 reps is

Press hard)

Row 3 sets, 8 reps (enough weight so 8 reps is

hard)

Sumo Deadlift 3 sets, 6 reps (enough weight so 6 reps is

 hard)

Power Walk 15 minutes at 60% HRmax

Burst Cardio 10 minutes with exercise(s) of choice

Example: Using the Tactical Template, our workout on Monday of Week 1

would be: supersets of bodyweight squat and overhead presses, for 3
supersets of 8 reps per exercise. You could power walk for 15 minutes (60%
HRmax) after lifting or skip the power walk and rest.after lifting or skip the
power walk and rest.

WEEK 2
Exercise Sets/Reps/time/intensity

Squat Bodyweight, 3 sets, 10 reps

Overhead Press 3 sets, 10 reps (maintain poundage from last

week)

Dumbbell Bench 3 sets, 10 reps (maintain poundage from las

Press week)

Row 3 sets, 10 reps (maintain poundage from last

week)

Sumo Deadlift 3 sets, 10 reps (maintain poundage from last

week)

Power Walk 25 minutes at 65% HRmax

Burst Cardio 11 minutes with exercise(s) of choice

Example: Using the Tactical Template, our workout on Tuesday of Week 2

would be: no resistance training today, perform an 11 minute Burst Cardio
session.

WEEK 3
Exercise Sets/Reps/time/intensity

Squat Goblet Squat, 3 sets, 6 reps (enough weight

that 6 reps is hard)

Overhead Press 3 sets, 6 reps (use 5 lbs heavier dumbbells

than last week)

Dumbbell 3 sets, 6 reps (use 5 lbs heavier dumbbells

BenchPress than last week)

Row 3 sets, 6 reps (use 5 lbs heavier dumbbells

than last week)

Sumo Deadlift 3 sets, 6 reps (use 10 lbs heavier than last

week)

Power Walk 30 minutes at 68% HRmax

Burst Cardio 12 minutes with exercise(s) of choice

Example: Using the Tactical Template, our exercise on Wednesday of Week

3 would be: supersets of dumbbell bench presses and rows for 3 supersets of
6 reps per exercise, using dumbbells 5 lbs. heavier than last week. After lifting,
you could power walk for 30 minutes (at 68% HRmax) or rest.

WEEK 4
Exercise Sets/Reps/time/intensity
 Squat Front Squat, 3 sets, 10 reps (enough weight
that 10 reps is hard)

Overhead Press 3 sets, 8 reps (maintain poundage from last

week)

Dumbbell Bench 3 sets, 8 reps (maintain poundage from last

Press week)

Row 3 sets, 8 reps (maintain poundage from last

week)

Sumo Deadlift 3 sets, 8 reps (maintain poundage from last

week)

Power Walk 30 minutes at 70% HRmax

Burst Cardio 13 minutes with exercise(s) of choice

Example: Using the Tactical Template, our workout on Thursday of Week 4

would be: no resistance training today, power walk for 30 minutes (at 70%
HRmax) or choose a 13 minute Burst Cardio session.

WEEK 5
Exercise Sets/Reps/time/intensity

Squat Front Squat, 3 sets, 6 reps (use dumbbells

5lbs heavier)

Overhead Press 3 sets, 10 reps (maintain poundage from last

week)

Dumbbell Bench 3 sets, 10 reps (maintain poundage from last

Press week)
 Row 3 sets, 10 reps (maintain poundage from last
week)

Sumo Deadlift 3 sets, 10 reps (maintain poundage from last

week)

Power Walk 30 minutes at 73% HRmax

Burst Cardio 14 minutes with exercise(s) of choice

Example: Using the Tactical Template, our workout on Friday of Week 5

would be: No training. A complete rest day.

WEEK 6
Exercise Sets/Reps/time/intensity

Squat Front Squat, 3 sets, 8 reps (maintain

poundage from last week)

Overhead Press 3 sets, 6 reps (use dumbbells 5 lbs heavier

than last week)

Dumbbell Bench 3 sets, 6 reps (use dumbbells 5 lbs heavier

Press than last week)

Row 3 sets, 6 reps (use dumbbells 5 lbs heavier

than last week)

Sumo Deadlift 3 sets, 6 reps (use 10 lbs heavier than last

week)

Power Walk 30 minutes at 73% HRmax

Burst Cardio 14 minutes with exercise(s) of choice

Example: Using the Tactical Template, our workout on Saturday of Week 6
would be: sumo deadlift, 3 sets of 6 reps using weights 10 lbs. heavier than
in week 5. After the weight training, power walk for 30 minutes (at 73%
HRmax) or rest.

ADVANCED PROGRAMMING: SEASONAL

“PRIMORDIAL CYCLING”
Elite athletes know that the optimal length of time to peak the human
body for athletic competition is twelve weeks. This is empirically-based
experiential knowledge based on 70 years of observation and preparation.
Elite athletes and coaches at the highest levels try to avoid preconceptions.
Preconceptions interfere with the perception of reality.

• The fundamentalist has a set of frozen, fossilized beliefs and will

reverse engineer an elaborate rationale to justify their belief system.
The fundamentalist rejects new input and knowledge as it could
potentially threaten or undermine their beliefs.

• The scientist continually expands his knowledge, and seeks new data.
Without clinging to beliefs, the human performance scientist has
loyalty to one master—tangible, measurable, physiological results.

Empirical science has formulated a loose consensus for the optimal time
period of a serious fitness effort. All this assumes the athlete has a goal—
by definition, all athletes have a goal—to improve performance within
their sport. We have learned through hard-earned gym wisdom that twelve
weeks (84 days, three months) is an optimal length of time for building
muscle mass, power, strength, conditioning, leanness, stamina and
endurance.
PRIMAL CORRELATIONS
We think it is no accident that the optimal length of time to peaking
human performance is three months is one season. Summer, winter, spring
and fall are three month chunks. Primal hunter-gatherers migrated with
animal herds for hundreds of thousands of years. Widespread agriculture
was only implemented about 10,000 years ago, a mere blip compared to
the total time we have been on this planet.

Prior to agriculture, we spent our time foraging and following migrating

herds of animals for protein sources. Walking, moving, running, chasing,
being chased, living on pristine animals, supplemented with whatever wild
fruits, roots, and vegetables could be found. Humans were parasites living
off of massive migrating herds of animals.

In temperate regions to a great degree, and all geographic regions to a

lesser degree, each passing season caused humans to adjust to nature’s
whims. Even in a desert, a summer drought can wreak havoc on all living
things. By all accounts, these primal hunter-gatherers, would physically
wipe the floor with modern man. The primal ancients were far leaner,
more muscular, had greater endurance, no cardiovascular or insulin-related
maladies, and no cancer or obesity. These people continually adjusted their
lives, based on nature, the seasons, and their impact on the herd.

The animal herd sustained them. In a time of drought, if the herd

suffered, then humans suffered. Optimally, the herd moved south as cold
weather set in. The migration reached the southernmost point as spring
gave way to summer. With the onset of the warm months, the herd moved
north until fall gave way to winter and the cycle repeated. Indigenous
tribes worldwide were synced up to the weather-induced migratory habits
of animals.

Flashing forward to the present day, is it any surprise that modern elite
strength athletes have discovered that a three-month training cycle is
optimal? Once we understand and embrace this idea, the next logical step
is to sync a transformational goal with the seasonal cycle of 12 weeks. It
would make sense to meld seasonally appropriate training and eating in an
attempt to reconnect with our primal encoding.

Winter: the best time for goals of gaining muscle mass and strength.
What better time than the dead of winter for hardcore, barebones, ultra-
heavy strength training when the thick soups, root vegetables, and heavy
rich foods taste better. Add some muscle mass and add 20% to your
strength during winter’s 12-weeks.

Spring: when the magnificence of the true spring arrives, shift

physiological gears. After a winter strength training cycle, shift to more
volume, more sessions, less weight, and more cardio. Shift to seasonally
appropriate lighter meals with more carbohydrates.
 Summer: as the deep summer takes root, we want to become maximally
lean. During the summer heat, our activities peak, our appetite is low and
we want the lightest proteins, more salads, fruits, vegetables and less food
volume. Weight training becomes high-rep, high-volume, and high-
frequency. We will do a lot of cardio with plenty of moving and sweating.

Fall: with the onset of true fall, we will add more substance to our
weight training. Richer, more savory foods suddenly taste delicious as the
weather becomes colder. The fall phase peaks over the holidays—we want
to be maximally large and lean heading into the almost hibernation-like
strength-training winter phase.

Give seasonal training a try to see how it works for you. It makes sense
from a “first principles” perspective and also aligns with our “feed your
activity” concept.
CONCLUSION
We have presented a template for training that
incorporates foundational resistance training with
proper doses of cardiovascular training. This is a
template that may be especially useful to the
beginner but it remains only a template. Use it as
a starting point. Entire books have been written
on exercise modes and periodized training, and
deeper coverage of these topics is well beyond the
scope of Strong Medicine.

We have given you a foundation of ideal

techniques and tactics for resistance training that can be progressed as you
advance. This is a rock solid program to begin your fight against inactivity,
the fifth member of the Pentaverate.

Inactivity is no match for Strong Medicine physical training.

“MILITARY INTELLIGENCE” (REFERENCES):
Adams OP. The impact of brief high-intensity exercise on blood glucose levels. Diabetes Metab
Syndr Obes 6 (2013): 113-122.

Bird SR, & Hawley JA. Exercise and type 2 diabetes: new prescription for an old problem.
Maturitas 72 (2012): 311-316.

Burd NA, et al. Muscle time under tension during resistance exercise stimulates differential muscle
protein sub-fractional synthetic responses in men. J Physiol 590 (2012): 351-362.

Ciolac EG. High-intensity interval training and hypertension: maximizing the benefits of exercise?
Am J Cardiovasc Dis 2 (2012): 102-110.

Gibala MJ, et al. Physiological adaptations to low-volume, high-intensity interval training in health
and disease. J Physiol 590 (2012): 1077-1084.

Gillen JB, et al. Acute high-intensity interval exercise reduces the postprandial glucose response and
prevalence of hypergly-caemia in patients with type 2 diabetes. Diabetes Obes Metab 14 (2012):
575-577.

Hartmann H, et al. Analysis of the load on the knee joint and vertebral column with changes in
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Hawley JA, & Gibala MJ. What’s new since Hippocrates? Preventing type 2 diabetes by physical
exercise and diet. Diabetologia 55 (2012): 535-539.

Larsen I, et al. High-and moderate-intensity aerobic exercise and excess post-exercise oxygen
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Li G, & He H. Hormesis, allostatic buffering capacity and physiological mechanism of physical

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Little JP, et al. Low-volume high-intensity interval training reduces hyperglycemia and increases
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1554-1560.

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McGill S. Low Back Disorders, Second Edition. Human Kinetics (2004).

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Molmen-Hansen HE, et al. Aerobic interval training reduces blood pressure and improves
myocardial function in hypertensive patients. Eur J Prev Cardiol 19 (2012): 151-160.

O’Donovan, G, et al. Changes in cardiorespiratory fitness and coronary heart disease risk factors
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98 (2005): 1619-1625.

Rehn TA, et al. Increasing physical activity of high intensity to reduce the prevalence of chronic
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Rognmo O, et al. High intensity aerobic interval exercise is superior to moderate intensity exercise
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Tjonna AE, et al. Aerobic interval training versus continuous moderate exercise as a treatment for
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Tjonna AE, et al. Aerobic interval training reduces cardiovascular risk factors more than a
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Trapp EG, et al. The effects of high-intensity intermittent exercise training on fat loss and fasting
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Whyte LJ, et al. Effects of single bout of very high-intensity exercise on metabolic health biomarkers
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3094.
BATTLE PLAN III
PUTTING IT ALL TOGETHER

“Though no one can go back and make a brand new start, anyone can
start from now and make a brand new ending.”
—Carl Bard

“If you always put limits on everything you do, physical or anything
else, it will spread into your work and into your life. There are no
limits. There are only plateaus, and you must not stay there, you
must go beyond them.”
—Bruce Lee
PUTTING IT ALL TOGETHER I
LIFESTYLE CHANGE: “THE NECK OF
ROY BUCHANAN’S GUITAR”

The authors are both musicians; Chris is a

guitarist and Marty a jazz pianist. Many of
our conversations together center on our
mutual love for music and musicians.
Sometimes there are some universal truths that
can be applied to health and fitness lurking
beneath our shared anecdotes. Marty’s tale of
the guitar neck of Roy Buchanan is one of
Underground guitar
these...
legend-Roy Buchanan
I was always struck by the modesty of Roy Buchanan’s guitar gear. His
beat-to-hell scarred-wood Telecaster was as plain as an Amish farmer.
When he had a few beers and was feeling good and relaxed, he was
incredible. His playing was extremely subtle with lots of soaring, sustained
anthem-like riffs. Roy was majestic, elegant, loud, and crystal clear. His
patented “ghost tones” and effortless three-octave speed runs were all done
with the greatest of ease, as he exhibited ho-hum nonchalance that added
to the effect. He was a relaxed, laid back, rural dude creating amazing
music with effortless pyrotechnics.

I once watched Roy from a front table, stage left, from a distance of
perhaps 15 feet. He rolled into an extended arpeggio with his pick-holding
right hand tracing a perfect oval on the six strings; touching each string at
precisely the right instant in time over and over, creating a cascade of
crystalline glass notes, all perfectly timed. I imagined if he had a piece of
chalk in his hand instead of a guitar pick, and a blackboard instead of a
guitar, the result would be a series of perfectly drawn ovals.

Often, Roy would turn his back to the crowd as he played. Early on I
noticed the back of the neck of his Telecaster was rubbed raw in a one-
inch wide pathway up the exact center. Over the years, this path had been
worn away as a direct result of nothing more than Roy’s palm repeatedly
passing lightly up and down the neck. He would move his hand with great
smoothness, gentleness, and dexterity—he used the lightest of touches. I
wondered how many passes up and down the neck of Roy Buchanan’s
guitar it took to wear off that varnished finish?

Undoubtedly, hundreds of thousands of ever-so-light palm passes were

needed to wear off the factory varnish—perhaps a million hand passes
were needed. There is a great lesson to be learned: virtuosity comes with a
price, and lifestyle change doesn’t happen overnight. While Buchanan was
certainly gifted, the more he practiced, the more gifted he became. When
talent collides with a serious time investment, and you add in patience and
a single-minded dedication to a craft, the results are astounding.

Physiological quantum leaps happen in direct proportion to the amount

of quality time invested in lifestyle change. Roy didn’t baby himself; he
immersed himself. In your own more limited and modest way, you too
should seek to emulate Roy’s dedication to his art. Train smart, train
intense, eat right, and rest big. Do copious amounts of healthy outdoor
cardio training to keep the internal plumbing working at peak efficiency.
Let’s follow Roy’s example and put in the work.
 When all the elements are in place and executed in that consistent,
balanced fashion for weeks on end, synergy occurs and results accelerate.
Our system relies on the expert use of basic tools with simplistic and
effective methods—with periods of enforced rest and the support of
nutrient-dense and seasonally appropriate food.

Transformation is achieved by implementing a bare bones basic strategy

in a systematic fashion. We need to understand the simple core themes,
plan how to weave minimalistic new activities into our lifestyle and reality.
You must incorporate “the process” within the time constraints of your
life. This takes planning, patience, and persistence, but is achievable for all.

We are not here to be your personal cheerleaders; you only need to

supply the motivation and we’ll take you the rest of the way.
PUTTING IT ALL TOGETHER II
STRONG MEDICINE LIFESTYLE CHANGE
—STRATEGIC PLANNING

PUMMEL THE “PENTAVERATE”

Circadian disruption, chronic stress, obesity, gut
inflammation and inactivity are the enemy. They are
the prime sources of chronic oxidative stress and
inflammation—the real underlying causes of chronic
disease.

The effects of each of these sources add up to cause the preventable

diseases listed in the black box. To achieve optimal health of your mind
and body, you will have to implement the Strong Medicine tactics from
each chapter to attack each enemy.
 Any of the 5 sources left unchecked will overflow your stress cup
(allostatic overload), and over time result in destruction of your health.

Keep reading and we will show you how to strategically plan your own
assault on chronic disease, achieving victory with optimal health.

The Strong Medicine Defensive Tactics will break the links of the
Pentaverate, and prevent the chronic inflammation and oxidative stress that
lead to disease. Start by assessing which member(s) of the Pentaverate is(are)
most problematic for you.

STEP 1: SELF ASSESSMENT

As Sun Tzu said in the Art of War, “If you know the
enemy and know yourself, you need not fear the
result of a hundred battles.” As a result of your hard
training, you now know the enemy. It is time to take
a look at the current state of your mind-body and
your environment.

Decide which members of the “Pentaverate of

Pestilence” are your biggest enemies in your own private war against
poor health. For some, circadian disruption and the poor sleep that
accompanies it is the biggest obstacle. Chronic stress affects most of us
and most likely is a problem for you as well. Do you have recurrent
digestive problems or gastrointestinal issues? Are you overweight,
diabetic, or have the activity level of a three-toed sloth? You get the
idea.

It is crucial that you do this self-assessment and be honest with

yourself. Once you have identified which members of the
“Pentaverate” are most problematic, you can formulate an initial
assault plan.

STEP 2: TARGETED ASSAULT

Once you have identified which enemy is your biggest obstacle to
health, pick a few Strong Medicine Defensive Tactics from that section.
If you are overweight or diabetic, pick a couple of tactics in the Obesity
section. If poor sleep is your biggest issue, start with tactics from the
Circadian Disruption Section.

Implement these tactics in your daily life to start your targeted assault
on your selected “enemy.” Only implement the amount of defensive
tactics that you can handle at once. Change itself (even positive
change) is inherently stressful. Many new trainees are super-motivated
at first and charge the enemy lines with all of their guns blazing, trying
to change too much too soon. These trainees inevitably fail to truly
incorporate the defensive tactics into their lifestyle change.

Stick with a few of the defensive tactics and incorporate them

consistently until they no longer feel like stressful changes, but
become part of your normal routine.

STEP 3: REASSESS THE

BATTLEFIELD
Once you have had an initial successful assault on
your enemy, go back to STEP 1 and reassess the
battlefield. Try to identify the next enemy that
represents the biggest obstacle to achieving your
health and fitness goals.

Do not hurry and try to conquer the enemy in one massive assault by
attacking all of your obstacles at once. This is what happens to millions
of people every year around January when they try to “fix” themselves
as part of a New Year’s resolution. By mid-February they realize they
have tried to make too many changes at once. Their battle plan
collapses and they lose the ground they have gained, allowing the
enemy to advance again—lost weight is gained back, and their gym
memberships go unused. This pattern repeats itself the following
January. No true progress is ever made.

Our slow and methodical approach will ensure that you truly make
lasting lifestyle changes which can be built upon. By the time next year
rolls around, you will be leaner, healthier, and more fit, instead of
starting from square one. If it takes you several years to achieve
complete victory over your enemy, so be it. This is how wars are won,
battle by battle. Instant gratification with quick weight loss plans and
“Hollywood” exercise programs will fail and have no place in true
lifestyle change.
 IT’S ALL CONNECTED...
Using the Strong Medicine battle plan, assaulting one member of the
“Pentaverate” often causes collateral damage to the others.
 Over time you will assimilate the Strong Medicine Defensive Tactics into
your lifestyle. You will truly be on your way to becoming a Strong
Medicine Warrior ready to recruit new trainees for the war against chronic
disease.
 For those of you who like to track your accomplishments and enjoy goal
setting we have created a Strong Medicine “rank structure.” The rank
structure makes use of a point system; you will progress to a higher “rank”
as you accumulate a defined number of points.

STRONG MEDICINE TACTICS: “GOLD” = 15 POINTS

STRONG MEDICINE TACTICS: “SILVER” = 10 POINTS

STRONG MEDICINE TACTICS: “BRONZE” = 5 POINTS

Points will be awarded for every Strong Medicine Defensive Tactic you
incorporate successfully into your lifestyle. If you have used a defensive
tactic consistently for 90 days, it is safe to say it is part of your lifestyle and
you may claim the points.
 Some of the tactics will not apply to your situation (i.e. tactics for
trainees with cancer). Do not concern yourself with missing possible points
from these tactics as the rank progression in the Strong Medicine will
account for the “special population” tactics (such as cancer) in the point
ranges.

You can promote yourself to the next rank once you have achieved the
requisite points for each (note that you can also be “demoted” to a lesser
rank if you lose enough points by “falling off the wagon” if you stop
consistently using a previously incorporated defensive tactic).

Use of the rank structure is not required, but can be motivating for many
trainees. It will keep you honest by forcing you to periodically assess your
progress.

As we move up the ranks, it will be beneficial to have other measures of

our progress besides points. We want to see the beneficial changes that
accompany promotions in the Strong Medicine rank structure. The
following section on Analytics will cover “stuff you can measure” for
tracking the physical, physiologic, and metabolic changes in your flesh
machine as you progress through your battle plan.

There are countless metrics we can measure as potential markers of

health (biomarkers). We have picked the four biomarkers we find to be the
most useful and meaningful for tracking physical improvement during
lifestyle change.
BATTLE PLAN IV
ANALYTICS: “STUFF YOU CAN
MEASURE”

“Not everything that can be counted counts, and not everything that
counts can be counted.”
—Albert Einstein
STUFF YOU CAN MEASURE:
INTRODUCTION
BIOMARKERS AND THE “HOLY GRAIL”
OF CORRELATION AND CAUSATION

The conceptual framework of the “stress cup”—using the concepts of

hormesis and allostatic load to inform your daily health and wellness
decision making—makes sense on an intellectual level. But, many of us
would like some way to measure our self-experiments in lifestyle
management as we wage our war against chronic disease.

In this section, we will cover some of these measurements, known as

“biomarkers.” They can be measured with procedures like blood work and
heart monitoring.

CORRELATION ≠ CAUSATION
 Keep in mind that many of these biomarkers only correlate with health
and disease. This means that they do not necessarily cause health or
disease, but are associated with it.

In the first section discussing cholesterol and lipoproteins, we’ll see that
small-dense LDL and oxidized LDL measured from our blood in a
laboratory test are associated with an increased risk of heart disease—but
higher LDL hasn’t been proven to cause heart disease. In other words,
when heart disease is present, this type of LDL seems to be around more,
but we haven’t fully determined exactly how it causes heart disease
(although there are some strong theories).

Correlations from things we can measure to disease can lead us astray if

we are not very careful. This is especially true with observational studies as
we discussed in the nutrition section very early in the book.

Here is an example of jumping to the wrong conclusion based on

correlations found in observational studies:

100,000 people filled out questionnaires regarding their lifestyle (food

and activity) and any diseases that they may have. We analyze the
questionnaires and find that the people who drank the most coffee had the
highest rate of lung cancer. From the data we see that coffee drinking is
correlated with having lung cancer. The media gets wind of our early study
results and releases a story saying that drinking coffee will give you lung
cancer. This scenario isn’t that far-fetched as we see stories every day in the
news media about red meat, eggs, and saturated fat all stemming from
observational studies.

After coffee sales start drop as a result of the news media releasing their
“coffee=lung cancer” story, we realize that we forgot to ask about smoking
in our questionnaire. When we re-analyze the data, we find a very strong
correlation with cigarette smoking and lung cancer. It also turned out that
the coffee drinkers in our study were also more likely to smoke.
 Coffee drinking was correlated with lung cancer, but was not the cause
of lung cancer seen in our observational study. Smoking, a known cause of
lung cancer (proven with actual laboratory studies), was not accounted for
in our original study. In the study results, smoking is a confounder.

Coffee drinkers were more likely to smoke, and smokers are more likely
to get lung cancer. Coffee was correlated with lung cancer because of the
relation of coffee drinking to smoking in our study, not because coffee
causes lung cancer.

The hard part with any observational study is controlling confounders.

Researchers try to think of all the other possible things in the environment
that could have an effect on a correlation with an exposure (coffee) and the
disease (lung cancer). It is impossible to control for all confounders—
which is why observational studies should primarily be used to form
hypotheses for future studies when a correlation is found.

Finding a correlation with coffee drinking and lung cancer doesn’t make
much sense from what we know about the mechanism of lung cancer.
There isn’t a plausible mechanism for coffee to cause lung cancer. The
researchers could have used the correlation of coffee and lung cancer to
generate a hypothesis that they could test further, but certainly should
never draw any conclusions that coffee causes lung cancer. Unfortunately,
this happens very often, and the news media does all of us a real disservice
by generating sensational headlines. This leads to further confusion among
the general public. Invariably, another observational study will come out
the following month showing an opposite correlation.
 We are spending time talking about this because many of the biomarkers
we will discuss have correlations with disease. Some have stronger
correlations than others, and some have been studied enough to approach
showing that they contribute to a cause for the disease.

We have to use biomarkers as “engine warning lights” (a car analogy)

that we may be going the wrong direction with our lifestyle choices, but
the biomarkers themselves may not be a cause of disease.

The “witch scene” from the classic movie, Monty Python and the Holy
Grail is a great example of how correlation can go wrong with disastrous
consequences.

The scene starts with the villagers trying to decide if a woman is a witch,
and Sir Bedevere and King Arthur come in to “school” them on correlation
and causation...

BEDEVERE: Quiet, quiet. Quiet! There are ways

of telling whether she is a witch.
CROWD: Are there? What are they?
BEDEVERE: Tell me, what do you do with
witches?
VILLAGER #2: Burn!
CROWD: Burn, burn them up!
BEDEVERE: And what do you burn apart from
witches?
VILLAGER #1: More witches!
VILLAGER #2: Wood!
BEDEVERE: So, why do witches burn? [pause]
VILLAGER #3: B--... ‘cause they’re made of
wood...?
BEDEVERE: Good!
CROWD: Oh yeah, yeah...
BEDEVERE: So, how do we tell whether she is made of wood?
VILLAGER #1: Build a bridge out of her.
BEDEVERE: Ah, but can you not also build bridges out of stone?
VILLAGER #2: Oh, yeah.
BEDEVERE: Does wood sink in water?
VILLAGER #1: No, no.
VILLAGER #2: It floats! It floats!
VILLAGER #1: Throw her into the pond!
CROWD: The pond!
BEDEVERE: What also floats in water?
VILLAGER #1: Bread!
VILLAGER #2: Apples!
VILLAGER #3: Very small rocks!
VILLAGER #1: Cider!
VILLAGER #2: Great gravy!
VILLAGER #1: Cherries!
VILLAGER #2: Mud!
VILLAGER #3: Churches—churches!
VILLAGER #2: Lead—lead!
ARTHUR: A duck.
CROWD: Oooh.
BEDEVERE: Exactly! So, logically...,
VILLAGER #1: If... she.. weighs the same as a duck, she’s made of wood.
BEDEVERE: And therefore—?
VILLAGER #1: A witch!
CROWD: A witch!
BEDEVERE: We shall use my larger scales!

DON’T GET NEUROTIC

The best way to use the biomarkers covered below is to periodically
monitor them so you can correlate the results with “how you are feeling”.
If your periodic testing shows “bad” results, and you have gained fat mass
and generally feel lousy, it stands to reason in this case the tests are
reinforcing the conclusion that you are on the road to poor health. Those
of you who have type-A personalities and/or obsessive “tendencies” could
easily fall into the trap of stressing over this testing, or testing too
frequently. The idea behind using these biomarkers is to hone your
intuitive sense of your body’s state, day-to-day. Ideally, as you dial-in the
ability to “listen” to your body, you will need to use the biomarker testing
less and less.
 We’ll discuss in detail the background and rationale for measuring the
following biomarkers. These sections are very technical, but are necessarily
so for understanding what you are measuring and its significance—along
with each biomarker’s limitations. Here’s what will be covered:

I. Lipid Panel (AKA Cholesterol)

II. Physical Measurements

III. Markers of Inflammation

IV. Heart Rate Variability

We’ll start by measuring cholesterol, which shouldn’t be controversial if

you understand the science. Unfortunately, a great deal of
misunderstanding and outright misinformation surrounds cholesterol in
general, not to mention the blood testing of “cholesterol.” Hopefully we
can clear things up a bit before we come to the conclusion that cholesterol
is “a witch.”
STUFF YOU CAN MEASURE I
CHOLESTEROL: WHAT ARE WE
MEASURING?

“Saturated fat and cholesterol in the diet are not the cause of
coronary heart disease. That myth is the greatest ‘scientific’
deception of the century, and perhaps any century.”
—George V. Mann, M.D.
SCIENTISTS AS HERETICS
Dr. Mann was one of the co-directors of the Framingham Heart Study,
and spent his career attempting to determine risk factors for heart disease.
His contention that cholesterol (and saturated fat) from the diet was not a
contributor to heart disease was very controversial to say the least. As a
society, we have been completely “brainwashed” by constant messages
about the evils of cholesterol, that statements such as Dr. Mann’s are like
going against gospel.

Cholesterol has been demonized more even than saturated fat in the past
50 years. The marketing of “low cholesterol” foods and anti-cholesterol
public health messaging has been so effective that to even suggest taking a
second critical look at the basis for these recommendations puts us at risk
of being labeled “medical heretics”. The anti-cholesterol movement has
approached a level of religious fervor. As with saturated fat in the nutrition
section, let’s take a step back, look at the science, and make informed
opinions regarding cholesterol.

WHAT IS CHOLESTEROL?
Before we discuss measuring cholesterol as a biomarker, it is crucial to
understand the biochemistry and physiology of cholesterol and
lipoproteins (more on this in a bit). Only with this foundation will you be
able to make sense of the laboratory testing and make informed decisions
about your health.
CHOLESTEROL
This is what the fuss is all about......

Cholesterol is an absolutely ESSENTIAL compound for normal brain

and body function. Here are a few of its uses:

• Proper cell membrane function. Cholesterol is a stabilizing structure

and an antioxidant in the cell membranes (remember our lipid
peroxidation discussion) that can stop membrane-damaging free
radical chain reactions.

A piece of cell membrane in cross-section, showing

the double layer of fats called phospholipids, and
cholesterol in the roles of membrane stabilizers and
antioxidants. Without cholesterol to stabilize the
membrane surrounding the cell, our cells would need a cell wall like plants
have, and would be susceptible to damage by oxidation.

• Cholesterol is necessary for effective nerve cell communication—it is

an integral part of the nerve “insulation” called myelin. Myelin is
wrapped around the axon “transmitters” on nerve cells, similar to
the insulation/coating on electrical wiring. It ensures that nerve
signals can be carried quickly and efficiently from one nerve cell to
another.
In fact, cholesterol has been found to be the “rate-limiting step” in the
formation of myelin in the brain and nerves outside the brain. In other
words, the speed of myelin production depends on a steady supply of
cholesterol. It is therefore no surprise that cholesterol is crucial for the
developing brain during childhood, and for slowing the rate of the
degeneration of brain connections in old age. Recent studies have shown
that as people approach old age, those with the highest cholesterol have
been shown to live the longest.

• Cholesterol is the molecular building block for the making many

important hormones, including cortisol, aldosterone, progesterone,
 testosterone, estrogens, and vitamin D.

• Cholesterol is the molecular building block for making many

important hormones, including cortisol, aldosterone, progesterone,
testosterone, estrogens, and vitamin D.

A simplified pathway showing some of the important hormones made from

cholesterol. The hormones testosterone and estrogen have obvious
importance to us. Aldosterone is involved in maintaining electrolyte balance
in the kidneys and cortisol is a critical hormone involved in the stress
in the kidneys and cortisol is a critical hormone involved in the stress
response.

• Cholesterol is also the building block for bile salts, crucial for
digestion and absorption of dietary fats (and fat soluble vitamins, A,
D, E, and K).

• Cholesterol is present in significant amounts in human breast milk—a

vital component for infant brain development.

Because of cholesterol’s very important functions, your body has a

system to keep levels adequate for these vital functions. Because of this
system, you can’t significantly alter cholesterol levels by changing dietary
intake.

CAN YOU CHANGE CHOLESTEROL LEVELS IN

YOUR BLOOD BY CHANGING HOW MUCH
CHOLESTEROL YOU EAT?
Research has shown that most people can only change their blood
levels of cholesterol about 5% in either direction by changing how
much cholesterol they eat in their diets. When you do get a small
increase in cholesterol in your blood from increased dietary
cholesterol, there also is an increase in HDL associated cholesterol, and
more of the large buoyant-type of LDL cholesterol carriers. (More
about this later, but both are good things!)

Changing how much cholesterol you eat (despite what you may have
heard) does not alter blood levels of cholesterol much for most people.
The small change that may happen doesn’t affect your risk for heart
disease, according to recent scientific studies.

If you take in less cholesterol than your body needs in the diet, the body
will produce more. If you take in more cholesterol in the diet, the body will
produce less. The bottom line is that your body knows what it is doing
with cholesterol (even if you or your doctors don’t).
 Based on the above information, it would follow from a “first
principles” perspective that artificially lowering cholesterol levels with
pharmacology may have unintended consequences.

We are seeing more of these unintended consequences in some of the

side effects recently observed by artificially lowering cholesterol levels
using drugs.

• Memory loss (cholesterol is needed for proper nerve functioning in

the brain)

• Muscle damage (thought to be due to depletion of CoQ10, a crucial

antioxidant which shares part of the same pathway as cholesterol for
its synthesis)

• Erectile dysfunction (possibly due to low testosterone from depleted

cholesterol, testosterone’s building block)

QUICK MEDICAL NOTE:

There are certainly some individuals who can benefit from cholesterol
lowering medication, such as males who have already had a heart
attack. Most of us can change our “lipid profiles” in the right direction
with proper nutrition, lifestyle, and exercise—without any of the side
effects listed above.

Current science is starting to catch up with the “first principles,” even

though many in the scientific and medical community can’t seem to let go
of the idea that cholesterol itself is the problem. The current science points
to problems arising from lipoproteins, the carriers of fat and cholesterol.
KEY POINT:
As we will soon show you, cholesterol itself does not lead to heart
disease, but certain types of cholesterol carriers that are thought to be
problematic.
LIPOPROTEINS 101
Fat and cholesterol transport (carrier) molecules—lipoproteins—come in
a variety of “flavors” and have very different functions. An important idea
to keep in mind is that recent research has shown that it is the amount and
type of dietary carbohydrate which is one of the biggest factors in how
lipoproteins can “go bad”—not dietary cholesterol or saturated fat. This
overview is very simplified, but hopefully the message is clear.

The major classes of lipoproteins are: chylomicrons, VLDL, LDL, and

HDL. You may have heard about a couple of these lipoprotein “carriers”
of fat and cholesterol while talking with your doctor. The message we will
keep repeating is that none of these are cholesterol, they are carriers of
cholesterol!

TYPES OF LIPOPROTEINS (CARRIERS)

CHYLOMICRONS
Chylomicrons are the primary form of lipoprotein that transport dietary
lipids (i.e. the fat that you eat).

• Triglycerides (fat) from the diet associated with chylomicrons are

transported through the lymph system first before they enter the
bloodstream (except for short chain and medium chain fats). This
prevents a large amount of lipids from rapidly entering the
bloodstream.

• Tissues with a high need for triglycerides (skeletal and cardiac muscle
for energy, adipose tissue for storage) have an enzyme called
lipoprotein lipase in nearby blood vessels. This enzyme separates the
dietary triglycerides from the chylomicrons to allow the cell to use
the fat (for energy or structural requirements).

The picture above depicts the basic structure of a lipoprotein particle in

cross-section. The actual particle is a 3 dimensional sphere. The
phospholipids lining the outside have 2 tails (in black) each composed
of an unsaturated fatty acid. These unsaturated fats with double bonds
are susceptible to oxidation (from our discussion of fats in Nutrition
 are susceptible to oxidation (from our discussion of fats in Nutrition
101).
The apolipoprotein part of the particle (in red) is the protein responsible
for recognition by various receptors. The type of apolipoprotein
present on the particle is the “calling card” that distinguishes LDL, HDL,
and chylomicrons. Free cholesterol (yellow) is present in the
phospholipid membrane, helping to give it structural support and to act
as an antioxidant. The inner core consists of the fats called triglycerides
(in green) and cholesterol esters (yellow outlined in orange).
The core contains the “cargo” of cholesterol and triglycerides, which is
delivered to the various cells of the body for use. Cholesterol esters are
made of cholesterol with a “tail” consisting of various types of fatty
acids.

VERY LOW DENSITY LIPOPROTEIN (VLDL)

• VLDLs are produced and released by the liver.

• VLDLs carry internally produced fat and cholesterol. Very low

density lipoproteins carry the triglycerides produced from excess
glucose when the liver “glycogen tank” is full. They are also the
initial carrier for cholesterol produced in the liver that is needed by
tissues for the crucial functions cholesterol provides (mentioned
above).

• VLDLs also interact with lipoprotein lipase, an enzyme that releases

fat from the VLDL carrier for storage in fat cells or utilization by
other tissues for energy or structural uses.

• After much of the triglyceride has been removed, the VLDL is

transformed into a relatively cholesterol-rich LDL.

LOW DENSITY LIPOPROTEIN (LDL)

LDL is the carrier unfortunately known as “bad cholesterol”. It is
neither cholesterol nor always bad. Its function is to carry cholesterol from
the liver to supply the body’s various cells with needed cholesterol. This
cholesterol is then used by the cells to perform the essential functions listed
above. Under normal circumstances, the LDL travels through the blood
vessels and “docks” with an LDL receptor at its delivery site. You can
think of LDL as a commuter bus that arrives at a station (the LDL
receptor) and drops off its cargo of cholesterol.

KEY POINT:
LDL is not cholesterol, despite being called “bad cholesterol.”
Cholesterol is cholesterol regardless of what carries it. LDL is a
cholesterol carrier.

As always, the “devil is in the details”. It turns out that the LDL carrier
exists in subclasses according to size: small-dense LDL (sdLDL), and large-
buoyant LDL (lbLDL). The latest science shows that these subclasses may
act VERY differently in contributing to heart and vascular disease, and the
amounts of each can be largely influenced by diet. Much more on this
soon.

HIGH DENSITY LIPOPROTEIN (HDL)

Known as “good cholesterol”, even though it also is NOT cholesterol,
but another cholesterol carrier. In basic terms, this carrier takes the excess
cholesterol not used by tissues, and carries it back to the liver.
 KEY POINT:
HDL is not cholesterol despite being called “good cholesterol.”
Cholesterol is cholesterol regardless of what carries it. HDL is another
cholesterol carrier.

SMALL-DENSE LDL AND LARGE-BUOYANT LDL

We just introduced the idea that the LDL carrier has size “subclasses”.
The differences between the two main subclasses of large buoyant LDL
and small dense LDL are much more than just size—they act very
differently in the body for the development of heart disease.

Both types of LDL carry cholesterol. The cholesterol they carry is

identical, but the carriers themselves are different. Just as you are the same
person whether you travel by bus or by taxi.

The different types of LDL, small-dense and large-buoyant are formed

from VLDL. Genetic factors determine the ratio of lbLDL to sdLDL
someone has, but what we eat is a huge player in how much of each will be
formed.

The key point to understand is that the cells in your body need
cholesterol and the liver makes the lipoprotein carriers which deliver the
amount of cholesterol the body needs at any one time. Large-buoyant LDL
carries more cholesterol than a small-dense LDL carrier, so it takes fewer
large-buoyant LDL particles to carry the same amount of cholesterol. If
you are making small-dense LDL particles, you need more of them to carry
enough cholesterol to meet the body’s demands. This has extremely
important health consequences as we will see shortly.
 Put simply, think of large buoyant LDL as a commuter bus that can
carry many “passengers” (cholesterol) and small dense LDL as a taxi that
can carry far fewer “passengers” (cholesterol).

The following section will use the “commuter bus” and “taxi” analogy
to show you how the different types of lipoproteins are formed. Once you
understand this, you will better understand the lab tests your doctor draws
to look at your cholesterol levels.

CHOLESTEROL “TRANSPORTATION”
To briefly review, lipoproteins are the carriers of fat (triglycerides) and
cholesterol:

• Chylomicrons are the carriers that transport the fat and cholesterol
that you get directly from food when you eat.

• VLDL and LDL are the carriers that transport the fat (triglycerides)
and cholesterol made or processed in the liver.

• LDL is the primary transporter of cholesterol from the liver to the

rest of the body.

• HDL is the carrier that takes any excess cholesterol from the body
and transports it back to the liver for “recycling.”

The process starts when VLDLs are made in the liver and “packed” with
triglycerides (fats) and cholesterol. The amount of triglycerides in each
VLDL depends on your diet and your “metabolic health.”

A quick review of STEP 6 in the Diabesity Intervention section will

remind you that excess glucose and fructose in the diet will be made into
triglycerides (fat) by the liver. Also remember from the Diabesity section
that if you have insulin resistance or diabetes, the fat cells are not doing
their storage job well and are releasing triglycerides to be processed back in
the liver. Both excess sugar in the diet and insulin resistance will cause
more triglycerides to be either created or processed by the liver (usually
both are happening). These triglycerides are packaged into the VLDL
carriers by the liver, in the hope that they can be delivered to muscle or fat
cells for use or storage. The liver is trying to get the triglycerides out of the
liver so they don’t build up and become toxic (as in forming a “fatty
liver”).
VLDL packed with triglycerides with a small amount of cholesterol.

If there are high amounts of triglycerides from excess dietary sugar and/or
insulin resistance, the “packaging” process will load the VLDL with
triglycerides, without much room left for shipping out the cholesterol to the
body.
VLDL with more cholesterol as “cargo” and fewer triglycerides.
A healthy person who doesn’t eat excess sugar or have insulin resistance will
not have an excess of triglycerides created in the liver. When the VLDL is
made to transport triglycerides and cholesterol out to the body, there is more
room to “package” cholesterol in the VLDL because there are not as many
triglycerides around.

The VLDL will leave the liver and travel to deliver the triglyceride cargo
first to muscle or fat cells for energy use or storage. Once the triglyceride
cargo is offloaded, the VLDL undergoes processing and is transformed
into a LDL. The LDL is left with a cargo of cholesterol to deliver to the
body.

The type of LDL formed depends on how much triglyceride content was
present in the original VLDL.

• A VLDL that was “stuffed” with triglycerides will be transformed

into a small dense LDL after the triglyceride cargo is dropped off.
The resulting small dense LDL has relatively little cholesterol cargo,
because there wasn’t much room for cholesterol in the original
triglyceride-packed VLDL.
 • A VLDL with a “normal” amount of triglycerides and more
cholesterol, will be transformed into a large-buoyant LDL once the
triglyceride cargo is dropped off. The large-buoyant LDL has more
cholesterol cargo because there was more room for cholesterol in the
original VLDL.

LARGE-BUOYANT LDL (LBLDL)

Large-buoyant LDL formed from normal VLDL carry a relatively large
amount of cholesterol cargo on each “particle” of lbLDL. These
particles travel to the cells in your body that need cholesterol and drop
off their “cargo”.
 When the lbLDL arrives at a cell to drop off cholesterol, it pulls up to a
designated “station” (like a bus pulling up to a bus station). The
“station” is an LDL receptor. The lbLDL particle “docks” with the LDL
receptor to drop off the cargo of cholesterol. This is what LDL particles
are supposed to do as a transporter of cholesterol.

The larger lbLDL particles are also less prone to damage from free
radicals and can stay in the bloodstream longer without becoming
oxidized.

The lbLDL is like a commuter bus with cholesterol as passengers. A bus

is large, sturdy, less prone to damage, and also less likely to be in an
accident while traveling—much like an lbLDL particle.

The large-buoyant LDL “Commuter Bus” packed with cholesterol.

INNOCENT BYSTANDER?
The cholesterol theory of heart disease started early in the 20th century
after cholesterol was found in the walls of the arteries from people who
had recently died from heart attacks. This finding started the demonization
of cholesterol as a cause of heart disease, especially in the last 50 years.

Recent science has shown that cholesterol itself that is not leading to the
buildup of plaques and narrowing of the arteries, but the lipoprotein
carriers, especially the small-dense LDL we just described.

SMALL-DENSE LDL (SDLDL)

 The small-dense LDL particles formed from triglyceride-packed VLDL
don’t act like the large-buoyant LDL. First, they are only transporting a
small amount of cholesterol, so it takes more of them to carry the
same amount of cholesterol “passengers” than the large-buoyant LDL.

Small-dense LDL particles (sdLDL) are also more susceptible to

damage by free radicals, which turns them into a highly reactive and
dangerous particle called “oxidized LDL” (oxLDL).

Small-dense LDL particles are also more likely not to arrive at the
designated “stations” (LDL receptors) to deliver their cholesterol cargo.
They are more likely to get in “accidents”—stuck in the walls of your
arteries.

To summarize, the sdLDL is a particle that can’t carry much cholesterol,

is susceptible to damage by free radicals, and gets into “accidents” by
crashing into the walls of your arteries. They are also not reliable for
arriving at the designated dropoff stations for cholesterol.

The small-dense LDL “taxi” with little cholesterol.

Early studies showed that cholesterol is present in “artery clogging”

plaques, and that continues to be true. We now know that cholesterol was
more of an innocent bystander, carried into the walls of the arteries by the
lipoprotein carriers, especially small dense LDL.

Blaming cholesterol for causing artery plaques is like blaming the fare-
paying taxi passenger for an accident on the interstate. The passenger
(cholesterol) was just riding in the taxi, and had nothing to do with the
accident. The faulty logic would be: we found the passenger at the scene of
the accident, so they must be responsible for the damage.
 It obviously makes no sense to leap to the conclusion of blaming the
passenger, so why are we doing it with cholesterol?

The large-buoyant LDL (lbLDL) are operating as they should, transporting

large amounts of cholesterol from the liver, through the bloodstream to their
designated “stations” (LDL receptors) on the various cells in the body that
need cholesterol for the vital functions we discussed at the beginning of this
section.

Large-buoyant LDL—for the most part—don’t cause problems by crashing

and lodging themselves into the sides of the artery walls. Many medical
providers and public health entities continue to refer to the cholesterol
carried by LDL particles in general as “bad cholesterol.” The lbLDL is
unfortunately lumped in as “bad cholesterol,” even though your doctor does
not measure what types of LDL particles you have; they only measure the
cholesterol passengers. We will discuss this much more very soon.

This is a “cross-section” of an artery. Imagine looking at your artery as you

would the end of a garden hose. You can see the lumen where the blood
travels has no narrowing or “blockages”. The healthy cholesterol transport
system of mostly lbLDL is operating correctly
and not causing problems.

The small-dense LDL particles (sdLDL) are very prone to cause serious
problems in the walls of your arteries while carrying their “cargo” of
cholesterol along with them. The sdLDL can bind with the artery walls in
places that they are not supposed to bind. These are unap-proved stops in
their journey to deliver cholesterol. Instead of stopping at designated dropoff
stations (LDL receptors) for their cholesterol passengers, sdLDL particles are
prone to “crash” into the walls of the arteries, damaging the cells lining the
arteries (endothelial cells).
Once the sdLDL particle penetrates the endothelial cells lining the artery wall,
and move into the muscular layer of the artery, they are readily oxidized by
free radicals. Now the sdLDL is a highly reactive oxidized LDL (much like a car
on fire after crashing into the guard rail). The immune system goes on high
alert. Cells of the “innate guardian” immune system, known as macrophages,
respond to the scene of the accident, much like police do in an automobile
accident on the interstate. These macrophages “know” that the sdLDL
particle (with cholesterol passengers) is not supposed to be inside the artery
wall. To protect the body from this reactive oxidized sdLDL, the macrophages
engulf the sdLDL particle. The macrophages that engulf the sdLDL particles
turn into foam cells.
The body recruits more of the immune system to wall the area off, turning
the area into an atheroma. This atheroma bulges up through the artery wall
from the inside and leads to the narrowing of the arteries in heart disease.
Looking at the cross-section of the artery
again, the atheroma described below has
narrowed the area in the artery where blood
flows (lumen). Also note that the area of the
atheroma is highly inflamed. This is how
sdLDL in particular, contributes to heart
disease. Imagine this process in the very
small blood vessels supplying your heart. Over time the narrowing will
become worse, leading to a heart attack.
TESTING CHOLESTEROL
When my doctor tests my cholesterol, what are we testing?

The typical lipid panel (cholesterol test) reports HDL cholesterol, VLDL,
triglycerides (TG), total cholesterol, and LDL cholesterol. The VLDL,
LDL, and HDL numbers represent the amount of cholesterol associated
with these lipoproteins.

In other words, we are measuring the amount of cholesterol

“passengers” that are riding on each of the different carrier lipoproteins.

KEY POINT:
Conventional cholesterol laboratory tests only measure the amount of
cholesterol (passengers) associated with each type of lipoprotein
carrier.

These values tell us very little about the number and size of the
lipoproteins themselves. Additionally, the value measured for LDL-
associated cholesterol is not even a direct measurement, it is calculated by
a mathematical formula known as the Friedewald equation.

The Friedewald equation gives us only an estimate of the passengers

(cholesterol) being carried by LDL particles.
 THE FRIEDEWALD EQUATION
To estimate the amount of cholesterol associated with your LDL
particles, the following equation is used:
LDL cholesterol = total cholesterol - HDL cholesterol -
triglycerides/5

Again, the LDL cholesterol tests are measuring cholesterol “riding” on

LDL carriers, and do not tell us how many LDL carriers are present or
what type of LDL is present. Both of these missing pieces of information
are extremely important to predict your risk of developing heart and
vascular disease.

Conventional cholesterol testing is

measuring…

cholesterol passengers…

and is not measuring lipoprotein carriers.

Knowing your particle number and particle size is important because

recent research shows that both are more predictive of developing heart
disease than just measuring the amount of cholesterol passengers
associated with the LDL particles. To illustrate why this makes sense, let’s
create a scenario.

“PATIENT A”
 Patient A goes to his doctor and has a cholesterol test. His results show a
(calculated) LDL cholesterol of 150 mg/dl. His doctor is concerned and
says it is too high. He is told to reduce the amount of cholesterol he is
eating in his diet—this advice continues to be given despite the science!
After arguing with his doctor, he is given a second test that evaluates his
LDL particle size and number. The results show a relatively low actual
LDL particle (carrier) number, and mostly large-buoyant LDL particles
(mostly “buses”).

Patient A has mostly “commuter buses” carrying his cargo of 150 mg/dl
of cholesterol, and the actual number of the buses was normal when
checked, but he was given advice to lower his cholesterol based only on the
initial blood test showing 150 mg/dl of cholesterol “passengers.” Patient A
has a relatively low heart attack risk with our information on particle
number and size, despite his “high” initial cholesterol test.

“PATIENT B”
Patient B comes in the following day for his annual check up. He gets his
cholesterol test and it shows an LDL (calculated) cholesterol level of 125
mg/dl. His doctor tells him his “bad cholesterol” level is pretty good, but a
little on the high side, and tells him he should watch how much cholesterol
he eats. One month later, Patient B has a minor heart attack and was
found to have blockages in the small arteries of his heart. He gets a stent
placed and the cardiologist caring for him in the hospital also orders an
LDL particle size and particle number test.
 The test results show a higher than normal particle number and mostly
small-dense LDL particles (mostly “taxis”). Patient B is mystified and tells
the cardiologist that his “bad cholesterol” was normal on a checkup 1
month ago. The cardiologist explains that although the amount of
cholesterol “passengers” counted was normal, they are being carried on a
high number of small-dense particles, known to correlate strongly with
heart disease.

You can see how Patient A could have a larger amount of cholesterol
“passengers” carried in his large-buoyant LDL commuter buses, than
Patient B. but have a fewer number of particles (he has a fewer number of
“buses” than Patient B has “taxis”). Unfortunately, Patient B had a larger
number of LDL particles overall, and most were of the small-dense type
associated with heart and vascular disease. Because the small-dense
particles carry less cholesterol per particle, the standard cholesterol test
came back as normal because it was just counting the passengers.

Patient A had more passengers overall, but less LDL particles, because
his large-buoyant LDL particles can carry more passengers. The large-
buoyant LDL particles are also less likely to cause problems in the walls of
his arteries. His “high bad cholesterol” in this case was not a risk to his
heart health.

The different scenarios of Patient A and Patient B show some of the

problems with relying solely on conventional cholesterol testing when
figuring your risk for heart disease. However, the conventional lipid panel
is far from useless. We will show you how to gather some very valuable
information from this test outside of the LDL cholesterol amount. First,
let’s discuss particle size in a bit more depth.
WHAT AFFECTS MY LDL PARTICLE SIZE?
While genetic factors certainly predispose some people to have more
small-dense LDL, nutrition plays a larger role for most people in
determining how much large-buoyant vs. small-dense LDL they have.

KEY POINT:
Genetics contribute, but nutrition plays the largest role in determining
LDL particle size.

We already discussed the role of nutrition in particle size previously, but

it bears repeating:

Forming small-dense LDL particles happens from the following diet and
lifestyle factors:

• Consistently eating more sugar and starch than your body can handle
leads to more triglycerides made from the excess sugar.

• Insulin resistance from inflammation and oxidative stress (diabetes,

obesity, poor sleep, gut inflammation, chronic stress) can lead to
decreased fat storage in fat cells (they are already stuffed full with
fat). The excess comes to the liver for processing.

• The liver deals with the triglycerides (fat) from both of these sources
and packages the triglycerides into VLDL. These VLDL are stuffed
with triglycerides, and have little room for cholesterol.

• A small-dense LDL is formed after the triglyceride-stuffed VLDL

drops off the triglycerides.
 You can see that excess starch and sugar coupled with insulin resistance
is primarily responsible for formation of small-dense LDL.

If you are already insulin resistant, and eat a diet heavy in starch and
sugar, the fat in the diet will contribute to formation of small-dense LDL
by increasing triglycerides further. However, fat in the diet is not the
specific underlying problem as many would have you think. The problem
is fat eaten with sugar and starch in an insulin resistant state.

TECHNICAL NOTE:
The type of fat that you eat is also very important. High amounts of
omega-6 PUFA in vegetable oils from fast food and processed food
will increase inflammation, oxidative stress, and worsen insulin
resistance.

As insulin resistance becomes worse, it will decrease carbohydrate

tolerance, resulting in more triglycerides produced and processed by
the liver—leading to more sdLDL.

The sdLDL that is formed is more prone to oxidation as some of the

omega-6 PUFA will be incorporated into the sdLDL particle.

Notice that cholesterol in the diet does not lead to small-dense

LDL. Reducing cholesterol in the diet only causes the body to
produce more cholesterol “from scratch” as needed.
Forming large-buoyant LDL particles happens when you are insulin
sensitive and don’t eat more starchy carbohydrate and sugar than your
body can handle. The liver does not have to produce triglycerides from
excess sugar and starch, and the fat cells are able to store triglycerides so
the liver does not have to process them.

• With fewer triglycerides for the liver to package in VLDL, a “normal”

VLDL is formed with more room for cholesterol “passengers.”

• After the small amount of triglycerides is dropped off, the VLDL is

transformed into a large-buoyant LDL.

• Not eating high amounts of pro-inflammatory omega 6 PUFA will

also help reduce inflammation, reduce oxidative stress, and help
maintain insulin sensitivity leading to fewer triglycerides and more
lbLDL.

TECHNICAL NOTE:
Eating more dietary cholesterol causes your body to produce less
cholesterol. Any short-term small increase in cholesterol in the body
from eating more cholesterol will cause a small short-term increase in
large-buoyant LDL, not small-dense LDL.

Most dietary saturated fat has the same effect of a short-term small
increase in large-buoyant LDL. Saturated fat and cholesterol in
the diet also increase the amount of HDL, the cholesterol
scavenger (known as “good cholesterol”). The only saturated fat
to avoid is the pro-inflammatory palmitic acid that we have
discussed extensively in previous sections.

IS STANDARD CHOLESTEROL TESTING

USELESS?
 There is some very useful information in a standard cholesterol test
(commonly called a lipid panel), without resorting to testing for particle
size and particle number.
I. It is generally accepted that higher HDL-associated cholesterol levels
are correlated (remember correlation vs. causation) with a lower risk
of heart disease. A high HDL-associated cholesterol value says that
HDL is doing a good job of carrying excess cholesterol back to the
liver. As cholesterol itself is not causing vascular disease, it is unclear
what the actual mechanism resulting in decreased risk may be, but it is
an active area of research. There is not much more we can say about
HDL, except that higher levels generally show lower risk of heart
disease.

KEY POINT:
High HDL-associated cholesterol is well correlated with a lower risk of
heart and vascular disease.

II. High triglycerides are well correlated with a higher risk of heart
disease. The medical community generally used to ignore the
triglyceride level on laboratory tests unless it was very high. We have
established a pretty strong mechanism showing how high triglycerides
lead to the formation of small-dense LDL—a strong risk factor for
heart disease. As we have repeatedly discussed, high triglycerides are
associated with obesity, diabetes, and fatty liver disease, which are all
inflammatory diseases. We also know that heart disease is primarily an
inflammatory disease and is accelerated by obesity and diabetes. More
medical providers are paying closer attention to triglyceride levels for
this reason.
III. A pattern usually seen on standard lipid panels is high triglycerides
with low HDL. It is also common to have low triglycerides associated
with high HDL levels. Recent science has shown that the
HDL/triglyceride ratio is a better predictor of risk of heart disease and
diabetes than standard LDL cholesterol levels:

• High HDL and low triglycerides = LOW RISK

• Low HDL and high triglycerides = HIGH RISK

IV. There is also a pattern seen with the HDL/triglyceride ratio and LDL
particle size:

WHAT NUMBERS ARE “GOOD” ON THE

STANDARD LIPID PANEL?
First remember that any lab values on cholesterol testing are only
correlated with health and disease. Remember to use them as “engine
warning lights” and make sure they are viewed in the context of any other
risk factors for heart disease you may have. Family history of heart disease,
high blood pressure, obesity, diabetes, and smoking all are well-known risk
factors for heart and vascular disease. The lipid panel (cholesterol and
triglycerides) is just another piece of the puzzle.

We have just spent a great deal of time showing the differences between
large-buoyant and small-dense LDL, especially sdLDL’s proposed
contribution to heart and vascular disease. Keep in mind that all the risk
factors listed above contribute to the development and progression of heart
and vascular disease, and the underlying main mechanisms of disease are
chronic inflammation and oxidative stress.

“Bad” lipid profiles such as the pattern of low HDL, high triglycerides,
and small-dense LDL are usually seen in the setting of inflammatory
conditions such as diabetes, obesity, and high blood pressure. Most people
with heart disease have most of the risk factors present at the same time,
not just unfavorable lipid panel values in isolation. “Fixing” obesity and
diabetes lowers inflammation and oxidative stress, and often “fixes” high
blood pressure and abnormal lipid panels, changing small-dense LDL to
large-buoyant LDL without directly “treating” cholesterol.

The purpose of this long-winded discussion is to emphasize that we

shouldn’t be looking at any of these laboratory tests in isolation, without
taking other factors into account. We should also avoid the habit of
“treating” laboratory values, instead we need to treat the person, and often
the lab values “fix” themselves. Use the lipid panel as one of the measures
to gauge your progress in your pursuit of health. All this being said, below
are some suggested targets for the traditional lipid panel:

PATTERN A (FAVORABLE)
• Triglycerides 100 mg/dl or less
• HDL 60 mg/dl or greater
• LDL-associated cholesterol may vary, but this
pattern is generally associated with large-
buoyant LDL particles

Note that the triglyceride target is set at 100 mg/dl or less. Most tests
set “normal” at less than 150 mg/dl. My bias is to set the target a bit
lower for triglycerides. I don’t consider 150 mg/dl to be “metabolically
healthy.”

PATTERN B (UNFAVORABLE)
• Triglycerides 150 mg/dl or greater
• HDL 40 mg/dl or less
• LDL-associated cholesterol may vary (can be
“normal”), but this pattern is generally associated
with small-dense LDL particles
TECHNICAL NOTE & RESEARCH UPDATE :
Tests to measure LDL particle size are currently available but
sometimes don’t give consistent results. The tests will likely become
more reliable as technology improves, so ask your doctor which test is
currently the most reliable if you want to test particle size directly
(especially if you are considering starting medication).

The NMR test for particle number is currently the most reliable and can
be very useful if you are trying to sort out a confusing lipid panel, and
are trying to make a decision about starting medication.

Current science shows that the total LDL particle number (not LDL
cholesterol number) has the best correlation with heart disease. A
high LDL particle number is often associated with small-dense
particle size (but not always).
IT GETS MORE COMPLICATED .......
Believe it or not, the topic of cholesterol and lipoproteins is even more
complicated. No wonder people are confused! Here are some highlights for
those who want to dig deeper:

• Lipoproteins such as LDL are involved in the immune response to

bacterial invasion, and are elevated when we have to fight off an
infection. If your blood work is done during this time, your numbers
may be abnormal.

• The amount of LDL receptors (“stations”) can change in response to

various situations. For instance, thyroid hormone controls how much
LDL receptor is made. If you have low thyroid function
(hypothyroidism), you will have low LDL receptors. Low LDL
receptors can cause some major problems:
— The lipoproteins need to “dock” with the LDL receptors
(“stations”) to offload their cholesterol cargo for the cells to use.
— If there are not enough LDL receptors (“stations” to drop off
passengers), the normal sized large-buoyant LDLs stay in the
bloodstream longer.
— The longer the LDLs stay in the bloodstream, the more susceptible
they are to oxidation (even large-buoyant LDL). You can think of
this as a ship in the water too long. Even the hulls of the best-
made ships will rust if they are in the water for long enough.
— “Fixing” a poorly functioning thyroid can “fix” your cholesterol
and lipoprotein problem by making more “stations”(LDL
receptors) for LDL particle “docking.”

• Statin-type cholesterol drugs don’t change the proportion of small-

dense LDL; they theoretically may even make the proportion worse.
This may be because one effect of statins is to cause cells to make
more LDL receptor. This is good for the large-buoyant LDL, but
remember that small-dense LDLs don’t bind well to normal LDL
receptor “stations.” This will preferentially leave more small-dense
LDL in circulation—and small-dense particles are more easily
 oxidized! There are plenty of people having heart attacks with
“normal” cholesterol while taking statins. This may be why.*

*A recent article by a group of researchers addressed the observations

that statin-type drugs make the proportion of small-dense LDL greater
during cholesterol lowering therapy. While it is true that the clinical
significance of the higher small-dense LDL proportion with statin
therapy is somewhat uncertain, there is strong biological plausibility to
support the altered proportion of small-dense LDL may indeed be
problematic.

The point of this technical note is that the researchers authoring the
article in question dismissed the increase in proportion of small-dense
LDL with statin therapy as a potentially problematic finding. Of
particular interest is that ALL of the authors of this paper had strong
ties to the pharmaceutical companies that make statin drugs. Several
of the authors are even employees of the pharmaceutical companies,
making their opinions/findings subject to massive potential conflict
of interest. This type of conflict of interest in cholesterol research is
unfortunately far from rare.

• The amount of oxidative stress and inflammation produced from

processed food, environmental pollution, and metabolic derangement
(diabetes) contributes to how fast LDL is oxidized in the
bloodstream.

• Small-dense LDLs carry a relatively low amount of cholesterol with

each sdLDL particle. Remember that cholesterol itself is an
antioxidant, and the low amount of cholesterol may be a reason for
the increased oxidation rate of sdLDL.

The subject of lipoprotein and cholesterol is complex enough even at this

level to make your head swim when wondering how to really interpret
your lab values. The bottom line is that laboratory values for cholesterol
and lipoproteins only correlate with health and disease. Although we are
getting a pretty good idea that oxidized lipoprotein particles and their
interaction with our immune system play a MAJOR role is the
development of heart disease, they still just represent a strong correlation
with the disease process. We still can’t definitively call what we measure in
blood work causative. There are so many other factors in play and context
is extremely important.

SUMMARY, TAKE HOME MESSAGES,

CONSIDERATIONS
1. High triglycerides and low HDL usually indicate an unfavorable
metabolic state and can be greatly modified by diet.

2. High triglycerides and low HDL are often associated with small-
dense LDL, which is more susceptible to oxidation and formation of
atherosclerotic plaques. High triglycerides and low HDL are strong
predictors of insulin resistance and diabetes.

3. Very high overall cholesterol numbers on a lipid profile (high total

cholesterol and high LDL—even high HDL) can be due to several
underlying issues which need to be addressed:

• Poor thyroid function: treat the thyroid and cholesterol numbers will
likely improve.

• Recent infection: lipoproteins are involved in the immune response to

invading bacteria.

• An underlying genetic abnormality resulting in poor LDL receptor

function. This is called familial hypercholesterolemia. Be sure to
discuss this possibility with your doctor, especially if there is a family
history of the condition.

• Very high cholesterol levels are often associated with an LDL receptor
dysfunction and should be approached cautiously. Remember that
even large-buoyant LDLs left in circulation too long are susceptible
to oxidation.
 4. Look for number patterns moving in the right direction, and don’t
get too hung up on the specific numbers themselves. For instance,
triglycerides decreasing below 100 with increasing HDL is generally
a good sign. Don’t wring your hands over whether a triglyceride
value of 70 is better than 80.

5. Current science shows that total LDL particle number (not LDL
cholesterol number) has the best correlation with heart disease.
High LDL particle number is usually associated with small-dense
particle size (but not always). High total LDL particle numbers may
require statin use while the underlying cause (genetic, thyroid, etc.)
is being determined.

6. Dietary cholesterol (and most saturated fat) has very little to do

with heart disease risk. Altering how much you eat either way does
little to change blood cholesterol levels. Maybe Dr. Mann isn’t such
a heretic after all.

7. Laboratory values of lipoproteins and cholesterol are correlates of

disease or health. Remember to use them as “engine warning
lights”. The body is INCREDIBLY complex and we haven’t
completely figured out all of the moving parts.

Hopefully this section at least gives you the knowledge to clear up

misconceptions and misinformation, and can help you make a more
informed decision regarding your health. If you are still somewhat
confused, you are not alone. As science advances, we will get a clearer
picture of the role lipoproteins and cholesterol play in our health. If all we
have done is to stop you from saying “good cholesterol” and “bad
cholesterol,” then it has all been worth it!
STUFF YOU CAN MEASURE II
PHYSICAL MEASUREMENTS

AN UNHEALTHY OBSESSION WITH WEIGHT

In popular culture, measuring lifestyle change success has focused on

“weight loss” as measured on the scale. People often brag about how much
weight they have lost in short amounts of time on the latest fad diets.
Rapid weight loss often comes with radical caloric restriction, and as
discussed previously, a significant amount of the weight is lost from
valuable muscle mass.

But, it is not just popular culture that is centered on weight as a

measurement of health. The scientific and medical communities have long
used the Body Mass Index (BMI) as a health marker. The BMI formula
incorporates height along with weight and is the method currently used to
determine if someone is “normal,” “overweight,” or “obese.” Recent
science has shown that BMI may not be the best marker to gauge body fat
and health.

The problem with using BMI is that it does not adequately account for
muscle mass.
 • People with large amounts of muscle mass can be classified as
“overweight” even though their body fat percentage is low. Many
athletes’ BMIs categorize them as “overweight” when it is obvious by
looking at their lean bodies that they are far from overweight or
unhealthy.

• People with very low muscle mass (not a good thing) are categorized
by BMI as “normal” even though they have a significant amount of
body fat and may even have a metabolic disease such as insulin
resistance or diabetes.

“NORMAL WEIGHT OBESITY”

Using the weight-focused BMI has given us a new classification of
unhealthy people—normal weight obese. These people have a “normal”
BMI, but also have a high amount of body fat as compared to their muscle
mass. They often carry this excess body fat around their midsection
(central obesity). Recall from the Obesity chapter that this type of body fat
is highly inflammatory and certainly far from healthy even though their
weight is considered “normal.”
GET RID OF YOUR SCALE
Weighing yourself to gauge progress with lifestyle changes is not a
scientific way to measure health benefits. It also creates a source of stress
and can become neurotic. Body weight can fluctuate on a day to day basis,
primarily due to shifts in fluid gain and loss, not body fat loss. We have
seen many frustrated and stressed dieters weighing themselves daily and
not understanding how they gained two pounds overnight. They respond
by restricting calories further or crushing themselves in the gym based
solely on what they saw on the scale that morning.

This practice is not good for mental health and

contributes to creating an unhealthy relationship
with food and exercise. This is a huge factor in the
long-term failure of dieting and can create the
vicious cycle of weight gain, weight loss, rebound
weight gain, and the demoralization that goes with
it. The diet industry is invested in continuing this
futile cycle and reinforces the message of “weight
loss” in their advertising. Stop falling victim to obsessive weighing and put
your scale out with the other garbage.

We need another simple but scientifically sound measurement to

monitor our progress that does not focus on the unreliable measurement of
body weight. We want a measurement that correlates well with health. The
waist to height ratio is such a measurement.

THE WAIST TO HEIGHT RATIO (WHR)

The waist to height ratio (WHR) is a simple formula that is easily
calculated.

1) Measure the circumference of your waist at the level of the

umbilicus (belly button). You can use inches or centimeters as long
as you are consistent when you measure your height.
 2) Measure your height (most of us know this
already).

3) Divide your waist measurement by your

height measurement. The result is your waist
to height ratio (WHR).

WAIST TO HEIGHT RATIO (WHR) EXAMPLE

CALCULATION
RecUsing one of the author’s (Chris) measurements, the WHR is
calculated as follows:
• Chris’s waist measurement (circumference) at the level of the
umbilicus (belly button) is 32 inches.
• Chris’s height is 69 inches (5 feet 9 inches).
• To find the WHR, we divide 32 by 69.
• 32/69= 0.46
Chris’s waist to height ratio (WHR) is 0.46

We want to keep our WHR below 0.5 for optimum health and to
avoid chronic diseases.
WHRs above 0.5 have been correlated with the following diseases:

• Diabetes
• High blood pressure
• Heart disease
• High triglycerides from metabolic syndrome

These are the same diseases associated with the chronic inflammation
and oxidative stress from obesity.
 KEY POINT:
Keep your waist to height ratio (WHR) below 0.5 to prevent
development of chronic diseases such as diabetes, heart disease, and
high blood pressure.

It is important to note that many people at risk for these diseases may
be classified as healthy if we used the weight-based BMI for screening.
The “normal weight obese” person would be classified as healthy by
the BMI, but would be correctly identified as unhealthy by the WHR.
Using only the BMI would miss people at risk for the above diseases.

Most of us strive for a healthy, lean physical appearance—even if we are

not particularly concerned about our health. Most people would not
approach a prospective mate and say, “Sure you look really fit, but I will
have to pick you up to make sure you don’t weigh too much.” This
scenario sounds ridiculous but isn’t that the message we are sending by
being preoccupied by weight? A lean, well-muscled person is healthy and
attractive regardless of what the scale shows.

The WHR is the best measure of how healthy you are and how your
clothes will fit. Developing lean muscle mass is also the best prevention
from chronic disease and accelerating aging. Lean mass will increase body
weight. Here are a couple of scenarios to illustrate the advantages of using
WHR over scale weight:

SCENARIO 1: JILL
Jill started at 5’6 inches tall, 180 lbs., and had a 38” waist. Jill went on a
calorie restricted crash diet and monitored her weight loss with a scale.
At the end of 4 months her results were:
• Weight dropped from 180 lbs. to 150 lbs. (30 lbs. lost)
• Waist circumference dropped from 38” to 34”.
• BMI dropped from 29 (overweight) to 24.2 (normal).
• WHR dropped from 0.58 to 0.52.

SCENARIO 2: KATHERINE
Katherine started with identical proportions to Jill at 5’6 inches tall, 180
lbs., and a 38” waist. Katherine started lifestyle change using Strong
Medicine tactics. At the end of 4 months her results were:
• Weight dropped from 180 lbs. to 155 lbs. (25 lbs. lost)
• Waist circumference dropped from 38” to 31”
• BMI dropped from 29 (overweight) to 25.0 (overweight).
• WHR dropped from 0.58 to 0.47.
SCENARIO ANALYSIS
If you look just at weight loss, it would seem that Jill’s crash diet was
more effective that Katherine’s Strong Medicine approach. After all, Jill
lost 5 more pounds than Katherine, right? If we followed BMI as a
measure of progress, Jill went from overweight to normal while Katherine
was still technically classified as overweight at the end of 4 months.

If we look beyond weight loss, we see that Jill only lost 4 inches off of
her waist circumference while Katherine dropped 7 inches. Jill finished her
4 months of dieting with a WHR still above 0.5 and still at risk for chronic
disease. Katherine’s WHR dropped into the healthy range at 0.47.
Katherine is also leaner and able to wear smaller sized clothes than Jill
despite less total weight loss. What gives here? Jill lost more weight so why
isn’t she leaner than Katherine?

Jill went on a calorie restricted crash diet with inadequate food to fuel
her activity. As far as her brain was concerned, her reduced food intake
was a threat and the threat response system was initiated to prevent
starvation. High levels of cortisol from the stress-threat system
cannibalized muscle mass to produce glucose to feed the brain during
starvation mode. The high cortisol levels made body fat loss around her
belly very slow. Upon further investigation, it was found that of the 30
pound weight loss, 10 pounds were lost from muscle and only 20 pounds
were lost as fat.

Katherine followed Strong Medicine tactics and fed her activity levels.
The emphasis on food quality helped restore her hunger communication
system in her brain. She spontaneously ate enough calories to fuel her
activity without sending a threat message to the brain, preventing high
cortisol levels. She also followed the Strong Medicine exercise plan and
added 5 pounds of muscle in 4 months (while Jill lost 10 lbs. of muscle
starving herself). Further investigation showed that Katherine lost 30
pounds of fat. Despite losing less overall weight than Jill, Katherine lost
10 pounds more fat and added muscle mass. Katherine also looks leaner
and more physically fit even though she weighs 5 pounds more than Jill.
She also now wears clothes 2 sizes smaller than Jill.

From these scenarios you can see how following weight (and BMI) can
be a poor measure of progress with lifestyle change and can even lead you
astray. The WHR is a much better measure of improvement both inside
your body from a health perspective, and outside from an aesthetic sense.
As you make your journey through lifestyle change using Strong Medicine
tactics, heed the two take-home messages from this section.

TAKE HOME MESSAGE:

1) Keep your waist circumference less than half of your height.
2) Throw your scale away and replace it with a tape measure!
STUFF YOU CAN MEASURE III
MARKERS OF INFLAMMATION

Long-term low level inflammation and

oxidative stress are the underlying causes of
preventable chronic diseases as we have
discussed throughout this book.

C-REACTIVE PROTEIN
(CRP)
Laboratory tests to reliably measure chronic oxidative stress are not
readily available in the clinic setting at this time, but there is a good
marker for chronic inflammation. This “marker of inflammation” is called
C-reactive Protein (CRP).

CRP is a protein produced by the liver in response to inflammation.

Doctors classify CRP within a group of proteins called acute phase
reactants. The acute phase reactant proteins are produced during periods
of high levels of inflammation as part of a defense response to stresses such
as injury—especially invading bacteria.
 Recall from Basic Training that immune cells produce chemicals called
cytokines to carry the inflammatory message throughout the body to
stimulate wound healing after an injury, or to repel the attack of foreign
bacteria. When the liver detects cytokines produced by immune cells, it
starts making acute phase reactants such as C-reactive protein to aid in
defense of the body.

TECHNICAL NOTE:
There are many potential markers of inflammation that are currently
being studied for use as predictors of risk of chronic inflammatory
diseases such as heart disease and diabetes. CRP has been shown to be
the most predictive and the only one we recommend following to
track your progress if you are engaged in lifestyle change to treat or
prevent diabetes, obesity, or heart disease.

Modern medicine has used the fact that CRP levels are elevated during
inflammation, and physicians can routinely measure it with blood tests. In
the clinic, CRP can be used to help differentiate bacterial and viral
infections. We will use CRP to help identify the low level chronic
inflammation that is a risk factor for numerous preventable diseases.
Indeed, CRP has been shown to be highly predictive as a marker for the
development of diabetes and heart disease, and CRP is consistently
elevated in obesity.
 KEY POINT:
Elevated CRP is highly predictive for developing type II diabetes and
heart disease. CRP is also elevated in obesity.

CRP AND RISK OF HEART DISEASE

Elevated C-reactive protein has been found to be a better predictor of
developing heart disease in the future than LDL cholesterol levels or
high blood pressure.

The National Academy of Clinical Biochemistry Laboratory Medicine

recently found that CRP was the only biomarker that met criteria for
use in the prevention of heart disease.

HIGH SENSITIVITY C-REACTIVE PROTEIN

(HSCRP)
When CRP was first used as a laboratory test for inflammation, the
technology to measure low levels of CRP was not available. Since chronic
inflammation is usually present at very low levels, we needed to develop
testing that could accurately measure low levels of CRP. This was
accomplished with the development of the high sensitivity C-reactive
protein (hsCRP) test. Now we are able to measure the very low levels of
CRP that accompany chronic inflammation.
Each member of the Pentaverate produces low level chronic inflammation,
so it is no surprise that elevated levels of hsCRP have been found with each
one.

CRP IS NONSPECIFIC
The often cited “drawback” of using hsCRP is that it is a nonspecific
marker for inflammation. That means that it can be elevated by anything
that increases the inflammatory response by the immune system. The test
may not be useful for doctors trying to diagnose a specific disease. For the
Strong Medicine trainee using hsCRP to monitor progress in reducing the
sources of chronic inflammation leading to preventable disease, the
nonspecificity of hsCRP is a strength.

Circadian disruption, chronic stress, obesity, gut inflammation, and

inactivity all produce low levels of inflammation and will elevate hsCRP.

The nonspecific nature of hsCRP elevation from any source of low level
inflammation means we can follow hsCRP levels as a marker of progress
as we attack each member of the Pentaverate.

KEY POINT:
The nonspecific nature of hsCRP elevation with any source of low level
inflammation means we can follow hsCRP levels as a marker of
progress as we attack each member of the Pentaverate.

WHAT IS A GOOD LEVEL OF HSCRP?

Most of the research with hsCRP has studied the correlation of hsCRP
levels with the risk of heart disease. These levels are shown in the table
below:

hsCRP level Risk for Heart Disease

Less than 1.0 mg/L LOW

1.0 to 3.0 mg/L INTERMEDIATE

Greater than 3.0 mg/L HIGH

The Strong Medicine trainee’s goal is to keep hsCRP below 1.0 mg/L.
KEY POINT:
The goal is to keep hsCRP levels below 1.0 mg/L as you are tracking
your progress in the battle against the Pentaverate.

TECHNICAL NOTE:
Increased hsCRP above 1.0 mg/L will also increase risk for developing
other preventable chronic diseases such as diabetes, high blood
pressure, and cancer but the actual correlated levels of hsCRP and risk
for these diseases are not as well characterized as it is for heart disease.

QUICK MEDICAL NOTE:

Since CRP is a nonspecific marker for inflammation, people with
inflammatory diseases such as rheumatoid arthritis or active cancer will
have elevated CRP far above the normal levels.

Active infections or injury will also cause very high levels of CRP. If any
of these situations applies to you, measurement of hsCRP to monitor
risk for chronic diseases will not be useful.
 risk for chronic diseases will not be useful.

High sensitivity C-reactive protein can be a useful part of the “Stuff You
Can Measure” to monitor your progress in your personal battle to prevent
chronic disease.

• Correcting circadian disruption and getting regenerative sleep will

lower hsCRP levels.

• Controlling chronic stress with brain training will diminish your

hsCRP.

• Reducing body fat and insulin resistance through the 8-step program
will minimize hsCRP levels.

• Stopping gut inflammation will bring down high hsCRP.

• Exercise crushes inactivity-induced inflammation and brings down

hsCRP levels as well.

As part of your Strong Medicine battle plan, work with your doctor to
get a hsCRP blood test (along with a lipid panel) at your regular preventive
checkup.
STUFF YOU CAN MEASURE IV
HEART RATE VARIABILITY

If you had to pick just one single biomarker of health to measure, heart
rate variability (HRV) would be the one. HRV is your “desert island”
biomarker.

In our opinion, HRV deserves this exalted status because it is the best
window to view the day to day status of your stress cup.

REVIEW OF HEART RATE

VARIABILITY (HRV)
We discussed HRV briefly in the Chronic Stress chapter
along with the subject of biofeedback. HRV in simplistic
terms is the natural variation of the length of time between
each heartbeat. Heart rate is controlled by the two branches
of the autonomic nervous system (ANS), specifically the
sympathetic “flight or fight” nervous system (SNS), and the
parasympathetic “rest and digest” nervous system (PNS).
Go back and review your Basic Training on the Stress-Threat system if you
need a refresher on this topic.

The “flight or fight” sympathetic nervous system (SNS) causes the heart
rate to speed up in response to any threat. It also causes the heart to beat
with a machine-like regularity, with minimal variation of the time between
each heartbeat.

The SNS (flight or fight) causes heart rate to increase, and for the heart to
beat with precise regularity—very little variation in time between each
heartbeat. This regularity is shown by the nearly identical lengths of the red
arrows above. These arrows show that the time between each heartbeat is
the same. This is called LOW heart rate variability (Low HRV).

When the “flight or fight” SNS is dominant, heart rate variability (HRV)
is LOW. There are no health consequences to having periodic SNS
dominance, such as while actively exercising or responding to an
emergency. The health consequences show themselves when the SNS
remains dominant most of the time due to chronic stress and diseases.

The “rest and digest” parasympathetic nervous system (PNS) slows

down the heart after a threat has passed. For most of the time, the PNS
should be the active system controlling how the heart beats. A healthy
heart controlled by a relaxed (PNS dominant) nervous system shows
differing times between each heartbeat.

The PNS (rest and digest) causes the heart rate to decrease after the threat
has passed (or exercise is completed) and for the heart to beat with a
variation of time between each heartbeat. This variation is shown by the
different lengths of the green arrows above. These arrows show the time
between each heart beat is different, with arrows having darker shades of
green correlating with increased time between heart beats and lighter green
arrows for shorter times between beats. This variation in time between beats
is called HIGH heart rate variability (High HRV).

HRV AS A WINDOW INTO YOUR “STRESS

CUP”
Chronic stress, poor fitness, poor sleep, and a broken metabolism are all
sensed as “threats” by the brain. In response to these daily threats, the
“flight or fight” sympathetic nervous system is always on. The low level of
“flight or flight” in which many of us live our daily lives causes chronic
inflammation and oxidative stress. The always-on “flight or fight” system
overfills our stress cup on a daily basis leaving the brain and body fighting
a losing battle to adapt.

Measuring heart rate variability (HRV) lets us see the current state of
our autonomic nervous system—is it dominated by the “flight or fight”
SNS, or by the “rest and digest” PNS? For optimum health, we want PNS
dominance most of the time.

Most of the Strong Medicine defensive tactics in this book

have the ultimate effect of maximizing PNS dominance, and
turning down the level of the “flight or fight” SNS.
We can track our autonomic nervous system status over time as we
incorporate Strong Medicine defensive tactics to measure our progress.

• Low HRV corresponds to dominance of our nervous system by the

“flight or fight” SNS. This is not a good sign. We are moving in the
wrong direction for our health, and low HRV indicates that our
“stress cup” has been overflowing.

• High HRV corresponds to dominance by the “rest and digest” PNS.

This is the natural state of the flesh machine and leads to optimum
health. High HRV is a good sign that we are currently within the
limits of our “stress cup”.
 We used a variation of this idea in the high intensity “burst cardio”
protocol when we measured heart rate recovery after exercise, even though
we were not measuring HRV.
HRV AND HEALTH
Our view that HRV is a window into the “stress cup” is supported by
recent scientific research. Recall from Basic Training that we presented
allostasis and allostatic overload (the state of your “stress cup”) as a way
of looking at chronic disease as a whole. Current research shows that
allostatic overload (overflowing the “stress cup”) has been associated with
obesity, diabetes, heart disease, high blood pressure, anxiety, and
depression. The same diseases are also associated with low HRV.

HRV is emerging as a predictive marker for the development of chronic

disease (and of health).

• Low HRV has been shown to predict the development of high blood
pressure.

• Low HRV predicts poor glucose tolerance and insulin resistance seen
in diabetes.

• Low HRV predicts development of heart disease better than most

other risk factors such as high blood pressure and lipid testing.

• High HRV predicts longevity. The longest lived people have the
highest HRV into old age.

• Exercise is the most powerful stimulus to raise HRV (as long as you
do not overfill your “stress cup” by overtraining).

The overarching concept that links low HRV to poor health is chronic
activation of the stress-threat system.
 The stressed-out brain constantly activates the threat system which keeps
the “flight or fight” sympathetic nervous system (SNS) turned on. This
creates dominance of the SNS and reduces HRV. This is why low HRV is
associated with so many diseases, and is present even before the diseases
become clinically apparent (before they can be detected by your doctor). In
this way, HRV is the “canary in the coal mine” for heading down the road
to poor health. As you learned in Basic Training, both external and
internal “threats” activate the stress-threat system.
 • An internal threat of swollen fat cells in obesity causes inflammation.
Inflammation activates the stress-threat system and lowers HRV.

• An external threat—a stressful work environment—will activate the

stress-threat system, decreasing HRV.

• An internal threat of bacterial infection or injury will lower HRV in

the short-term for these types of threats.

• An external threat of processed food will cause inflammation and

oxidative stress. The stress-threat system is activated as the free
radicals from processed food overwhelm the ADS “bouncers.” This
causes low HRV and predicts the development of a broken
metabolism.

• An internal threat of rumination and worry causing chronic

psychological stress will lower HRV because of the “ramped-up”
flight or fight system.

• An external threat of consistent overtraining from “boot camp beat

down” exercise programs is a threat to the body causing reduced
HRV.

• Chronic stress is a threat that leads to anxiety and depression. People

with anxiety and depression have low HRV.

• An internal threat of inadequate sleep and disruption of the circadian

rhythm is a huge threat to the brain. It also results in low HRV.
 HRV AND CIRCADIAN RHYTHM
HRV follows a natural circadian rhythm with increased HRV during
regeneration mode. This makes sense, as increased HRV is associated
with the dominance of the “rest and digest” parasympathetic system.

An overflowing “stress cup” results in loss of the high HRV during the
night and leads to poor recovery and regeneration. Loss of high HRV at
night also predicts development of diabetes.

You can see why HRV is potentially a very good measurement for
assessing the state of your “stress cup” and overall health. There are some
scientists who even think that measuring HRV should be done in the clinic
as part of a preventive checkup to help predict development of disease.
You doctor could potentially use HRV to measure both physical and
psychological wellness, something that blood tests cannot capture. As a
Strong Medicine trainee, you know that the physical and psychological are
one, linked by the mind-body.
MEASURING HEART RATE VARIABILITY
Not so long ago, measuring HRV required specialized equipment costing
tens of thousands of dollars and was beyond the reach of the average
person. Now we can get fairly accurate measurements of HRV with a
smart phone and a chest strap heart rate monitor.

Calculation of HRV is fairly complex and requires some relatively

sophisticated mathematics. Modern smart phone applications read the
heart beat input from the chest strap and do the calculations for us. The
result is a HRV score that is scaled from 0-100. Higher scores correlate
with high HRV.

High HRV scores usually correlate with a healthy state of the nervous
system and low levels indicate activation of the stress-threat system. The
higher your HRV score, the more you are in a parasympathetic nervous
system (PNS) dominant state—a good thing. The lower your HRV score,
the more you are dominated by the “flight or fight” sympathetic nervous
system (SNS) which indicates an overflowing “stress cup”.
FOLLOWING YOUR HRV SCORE
The HRV score is a very individual measure and should not be
compared with scores from other people. But, higher HRV scores are often
found in physically fit, healthy people. The idea is to get a baseline score to
evaluate the current state of your health and fitness, then follow it as you
incorporate defensive tactics from the Strong Medicine program. Your
overall HRV scores will slowly improve as you reduce your stress, get
better sleep, clean up your nutrition, lose body fat, and get regular
exercise.

It is important to note that your HRV will fluctuate day to day

depending on your current situation. A night of bad sleep, increased stress,
overdoing your exercise, or a particularly bad couple of days of “dietary
indiscretion” will cause your scores to drop temporarily.

WHEN AND HOW TO MEASURE?

Ideally, HRV measurement should be done at the same time every day
and while attempting to reproduce the same method of measurement as
closely as possible. We prefer to measure HRV immediately after waking
in the morning while still in bed. This way the time of day is the same (and
accounts for circadian changes in HRV) and the body position during
measurement is the same. HRV is very sensitive to changes in your
environment. We also like waking measurements because the various
stresses of the upcoming day have not yet affected your body and brain,
giving a measurement that has fewer variables to affect it.

You can use these measurements to make lifestyle decisions—especially

regarding exercise—and avoid overfilling your “stress cup”.
USING HRV TO PLAN ACTIVITY
To illustrate the use of a daily HRV score, let us construct a hypothetical
case.

HRV CASE REVIEW:

Chris is a 44 year old male with no chronic diseases and a relatively
high level of fitness. His HRV scores usually fall in the range of 80 to
85.

He normally exercises three to four times per week and generally gets
good sleep. Chris wakes up after a restless night of sleep due to an
upper respiratory infection. His HRV score (usually in the 80s) is 68
that morning. His exercise schedule had a planned squat workout that
evening. Chris comes home after work (an unusually stressful work day)
and performs his squat workout with a 10 minute burst cardio protocol
afterwards.

The next morning his HRV is down to 58. He feels exhausted and the
upper respiratory infection is worse.

Chris had a drop in his usual HRV score of at least 12 points after a
night of bad sleep due to an illness. Instead of modifying his workout plan,
he continued with his planned workout of squats and a burst protocol that
put a high amount of stress on his body. This caused an already mostly full
“stress cup” (from poor sleep and illness) to overflow. We saw the results
of Chris not heeding his falling HRV score the next day with a further 10
point drop in HRV. He should have altered his workout plan that day to
be either a rest day, or at most a short walk instead of the taxing squat
workout. He is now at risk for the relatively minor upper respiratory
infection to become much worse due to his immune system becoming
suppressed from an overfilled “stress cup”.

If he would have taken a rest day on the morning of the HRV score of
68, he would have recovered. Most likely, he would have had a higher
score the next day and been able to do his squat workout without
overfilling his “stress cup”.
 GUIDELINES
There are no hard and fast rules for responding to a falling HRV score,
but we do have some suggestions.
• If your score drops 10 points or more, consider taking a rest day from
exercise and add a brain training session.
• If you score drops for two consecutive days, you really need to pay
attention to what could be causing the drop. Sleep is the usual
culprit for this so prioritize getting regenerative sleep that night
(using tactics from the Circadian Disruption chapter) and certainly
forget about any heavy physical training.

Following your HRV can be very powerful for making sure you do not
overtrain. You can also use it to see the impact of various Strong Medicine
defensive tactics. If Chris would have replaced the planned squat workout
that day with a 30 minute session of mindfulness breathing practice, his
HRV score the next day would likely have been back up in the 80-85 range
instead of 58 and feeling sick and exhausted.

You can use a falling score as motivation to incorporate an appropriate

defensive tactic that day to bring you back from an overflowing “stress
cup”. A dropping HRV score might motivate you to pay more attention to
your sleep that night, clean up your diet, or engage in some brain training.
HRV EQUIPMENT
As technology advances, there will be more options available to perform
daily HRV monitoring at home. There are currently some good products
available. To get you started, here are two systems we have personally used
(we have no financial or personal relationships with either developer):

• SweetBeat™ by SweetWater Health. This is a smartphone application

that is low priced and is reliable for measuring HRV. It requires a
Bluetooth heart rate monitor strap such as the Polar® H7. It has
other features related to food sensitivity and weight loss that we have
not used or evaluated, so we cannot comment on these features.

• BioForce HRV. This is a HRV measurement package developed by

top MMA (mixed martial arts) trainer Joel Jamieson. This product is
a bit more pricey but comes with an excellent guide on using HRV
with physical training. The BioForce HRV uses a smartphone
application and a Bluetooth heart rate monitor chest strap. It also
has a good website to track your measurements. Chris used this
product for 3 months and found it reliable for tracking HRV and to
plan his training. Special Note: The accompanying manual has
extensive technical information on HRV and allostasis (much to our
surprise and pleasure). From reading the manual, it is obvious that
Mr. Jamieson is extremely well versed on allostasis, allostatic load,
and has applied the concepts very well to training high-end athletes.
Highly recommended.
CONCLUSION
HRV measurement truly is a window to the state of your nervous system
and your “stress cup”. This is one of the most powerful and relevant
biomarkers in this Analytics section. We strongly suggest you consider
routinely checking your HRV to keep your “stress cup” from overflowing.
Managing your “stress cup” effectively will have downstream benefits and
HRV is currently the best way to keep an eye on it.

By successfully managing your “stress cup” with HRV, you will likely
see the other three biomarkers in this section improve as well. This is truly
your “desert island” biomarker.

This also marks the end of the Stuff You Can Measure (Analytics)
section. Use these biomarkers appropriately, remembering the difference
between correlation and causation. Also, do not get neurotic when
measuring these biomarkers and turn them into sources of stress.

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DOC’S REFLECTION
Strong Medicine is a reflection of everything I wanted to say when my
patients asked me “What can I do to get healthier?” There were only so
many preventative recommendations I could impart to them in a 30 minute
appointment.

The idea for this book started as a series of in-depth informational

handouts that I could give my patients for “homework” reading between
office visits on topics such as nutrition, stress relief, exercise, sleep habits,
etc.

I researched the handouts by combing the scientific literature for the

latest up-to-date information that would support my recommendations.
After compiling dozens of handouts, I realized that I had the skeletal
framework for a book. The project took on a life of its own, growing far
beyond the original scope.

Originally projected to take a month or so, this small project became a

two year obsession that eventually became Strong Medicine. It spanned life
events such as leaving the military, finding a new job, and relocating to a
new state.

This book was truly a labor of love fueled by a passion for science,
medicine, and the need to contribute something meaningful to public
health. I have always been frustrated when hearing flawed
recommendations for health promotion and prevention that lacked any
scientific foundation. I found myself ranting about this fact with increasing
frequency.

Strong Medicine was cathartic for me. I finally put my own cards on the
table and did something instead of continuing to complain about the
inadequacies of conventional recommendations for disease prevention.
Through Strong Medicine, I offer solutions instead of complaints and
criticisms.
 So many of our friends and family members are afflicted by chronic
preventable disease and desperately want effective solutions that they can
implement. We live in the information age, and in the face of so much
conflicting information it is difficult to find the needle in the proverbial
haystack. My hope is for this book to give people the foundational
knowledge to sift through the haystack of misinformation and find their
“needle.”

After reading countless scientific research articles on seemingly disparate

subjects, I felt the best course of action was to start with the basic
processes that are the sources of chronic disease and build a prescriptive
framework around them.

Looking at the proposed mechanisms, it became obvious that sleep,

nutrition, physical activity (or a lack thereof), stress, and obesity all
contributed to a variety of chronic diseases. There was an underreported,
underlying commonality that linked these maladies.

Chronic inflammation and oxidative stress were the underlying

mechanisms that tied together the many causes of chronic disease.
Allostatic overload, the “Stress Cup,” was the overarching concept that
showed how chronic stress, gut inflammation, circadian disruption,
obesity, and inactivity all join hands to promote long-term inflammation
and oxidative stress, the precursors to chronic disease.

The irony of writing a book on wellness, while

working at a full time medical practice, was that I
consistently overflowed my own stress cup. I was more
stressed and sick than I had ever been in my life! I
certainly was a case study and proof of concept of
allostatic overload! Hypocrisy abounded for two years
while writing this book as I gave advice to my patients
on stress relief while being the perfect illustration of the
overflowing stress cup. I am sure I lost several layers off
my telomeres. After the book was complete, my road
back to health put into play the concepts outlined in this book: “Physician
Heal Thyself!”
 The goal of Strong Medicine was to explain difficult concepts of human
biochemistry, physiology, and pathology in a way the lay-person could
comprehend. These interlinking, interrelated concepts would create a
foundation of knowledge that could empower normal people to make
beneficial lifestyle decisions.

I wanted to demystify chronic disease by opening the “black box” of the

flesh machine for all to see. One goal was to help people understand the
effects of their lifestyle choices and the scientific foundations for our
prevention recommendations.

I continue to hold strongly to the notion that when people understand

and can visualize what is going on inside the body and brain as a result
their lifestyle decisions, it becomes easier to become motivated and
implement sustainable change. Ignorance is truly bliss, and once the veil of
the unknown and unseeable is lifted by knowledge, your bad habits
become harder to ignore. When bad habits are transformed into good
habits, the resulting positive impact on the body creates enthusiastic
momentum.

The military theme of this book was comfortable to me since I spent

thirteen years of my life serving our country in the military—in both the
Army and Navy. More importantly, I used the military theme to portray
the true peril of our current public health crises. If you do not believe we
are in a war against preventable disease, you are choosing to live with your
head in the sand.

Is it not shocking that reliable prognosticators indicate that the current

generation will be the first in modern history projected to live shorter lives
than their parents or grandparents?

Why is this? What has bought about this horrific situation and is it
preventable? Optimum health is difficult and near impossible to attain
while existing in our modern environment. To acquire optimal health
requires knowledge, diligence, planning and methodical application.

We no longer live in the pristine environments of our distant ancestors,

but can certainly learn a lot from them. They “exercised” intensely, got
lots of cardio and ate pure, natural food. That template works in our
present time quite nicely. However modern problems require modern
solutions.

We need to jettison dogmatic and unyielding paradigms—is it impolite

to note that they don’t work? Strong Medicine seeks to approach the
battle against chronic disease and the search for optimal health with a
combination of the wisdom and practices of our ancestors and advances of
modern science.

Strong Medicine will empower those that truly are motivated. If you
have the motivation, we have shown you the game plan. If you have had
enough and are “sick and tired of being sick and tired” then put into play
the very real and very concrete steps we outlined. We told you why
something is the way it is, then related how to improve it. Every one of us
can achieve our health goals, but there are no shortcuts.

COACH’S CONCLUSIONS
What is the “take away” message of this book? Self-empowerment.

There is really should be no more confusion on your part regarding what

you need to do to renovate your body and your life. You have a
transformational roadmap. You supply the requisite mental motivation
and disciplined application of our battle-tested methodology. It works
every single time it is enacted fully and completely.

Our systematic and appropriate strategies for exercise and nutrition are
not the ever popular, one-size-fits-all mainstream health and fitness
strategies. Our strategies are elite athlete practices, diluted and made user-
friendly, pared down without losing the core essence that makes them
effective.

You can now create customized training templates that fit your lifestyle
and time constraints. We have made provisions for the out-of-shape to
gradually adapt to our fitness practices and procedures. Unlike the
Sergeant Fury boot camp types, we don’t throw you into the proverbial
deep end of the fitness pool in the first minute of your first session. We
teach you how to swim first.

We have established parallel strategies in related disciplines. By enacting

these strategies simultaneously, we have engineered a physical
transformation and psychological recalibration. Someone undergoing a
profound physical transformation also undergoes a profound psychological
transformation.

Oscar Wilde once noted, “Perception is everything.” He was right about

everything and this observation about how we see ourselves and our
surroundings is no exception. While a negative self-perception is a psychic
boat anchor hung around one’s neck, convert that negative perception into
a positive perception—complete with some very real detoxification and
high intensity, endorphin-releasing exercise—and a man or woman is
reborn physically and psychologically.

I have facilitated hundreds of dramatic physical transformations, and

one of the defining characteristics of true transformation is self
redefinition. We enable people to reinvent themselves. Camille Paglia once
described bodybuilding (the combination of nutrition and exercise to
reengineer and reconfigure the human body) as “a struggle against
nature.” Indeed, rather than be swept away by life and force of habit, the
individual can seize control of their life. They can fight against
“inevitability” and the idea of settling for whatever life hands them. We
are either compliant with our seemingly preordained fate or we fight.

We who choose to embrace the fight understand that life itself is a

struggle and embrace it. Compliant living is mere existing. We want more
—we want to improve our quality of life by methodically engaging in our
parallel disciplines. Over time our practices will transform us, and we will
attain and maintain vibrant muscular health and virility.

We subscribe to old school methods, rooted in intensity, sweat, and

common sense. We believe in the idea of doing fewer things better; we will
detoxify ourselves by practicing power nutrition and gourmet organic
eating. Using powerhouse nutrients, we can expertly prepare meals we
look forward to eating. We combine power nutrition with power training.
 Everything you need to engineer your very own radical physical
transformation is contained within the two covers of this transformation
manual. This book is meant to be a workbook—so put our ideas into play
and breathe life into the strategies we have shared with you. Try to avoid
the cafeteria syndrome of cherry-picking our methodology. Avoid the
temptation to only embrace the aspects of our system that appeal to your
preconceptions and prejudices. Don’t reject parts of this holistic system
that you deem unpleasant, stupid or ill-informed.

Our strategies are purposefully interrelated. Break them apart and the
results will be substandard. There is a tangible physical synergy when all
the aspects are practiced systematically and simultaneously. If you come to
love this vibrant way of living, then transformation is no longer a question
of “if” but “when.”
ABOUT THE AUTHORS

CHRISTOPHER G. HARDY, D.O., MPH, CSCS

Dr. Chris Hardy is emerging as a leader in public
health, merging his expertise in nutrition, strength and
conditioning, and in clinical and preventive medicine
into a comprehensive approach to treat chronic disease.

Dr. Hardy has a diverse background, including 13

years active military service in both the U.S. Army and
U.S. Navy. He is a previous graduate of the Naval
Diving and Salvage Training Center and Underwater
Construction Basic Course, going on to serve as a military deep sea diver.
He left the military the first time after four years of service to start his
higher education.

Dr. Hardy is a graduate of Old Dominion University, earning a bachelor

of science in biochemistry. He went on to medical school at WVSOM in
Lewisburg WV, graduating as a Doctor of Osteopathic Medicine.

After medical school and internship, Dr. Hardy reentered the military as
a Navy physician, serving aboard the USS WASP (LHD-1) as medical
officer and joining the ship on deployment in support of Operation
Enduring Freedom. He then served another operational tour as a medical
officer before attending Johns Hopkins University for medical specialty
training.

Dr. Hardy completed his specialty training in Occupational and

Environmental Medicine at the Johns Hopkins School of Public Health
where he served as Chief Resident, also earning a Master of Public Health
degree with a concentration in toxicology.

Dr. Hardy is Board Certified in Occupational and Environmental

Medicine under the American College of Preventive Medicine. He has also
completed formal training in medical acupuncture and is a Certified
Strength and Conditioning Specialist by the NSCA. He is currently enrolled
in the Fellowship in Integrative Medicine at the University of Arizona.

Chris lives in Everett Washington and is passionate about guitars,

mountain biking, and health and wellness. He is still active as a trainer and
gives nutrition lectures around the local community. He is married to his
talented wife Carrie, a former biochemist and current student in
Naturopathic Medicine at Bastyr University. His daughter Anna is a
graduate student in Geophysics at Virginia Tech University.
ABOUT THE AUTHORS
MARTY GALLAGHER
Marty Gallagher has been involved in high-level athletics for over 50
years. He captured his first national title and set his first national records
as a 17-year old teenage Olympic weightlifter in 1967. In May of 2013 he
set his most recent national records as a 64-year old powerlifter. He won
the 1992 IPF world masters powerlifting title and has taken silver and
bronze medals in world championships. He is a six-time national
champion masters powerlifter.

As a coach he guided Team USA to the IPF world

team title in 1991 and coached Black’s gym to five
national powerlifting team titles. He was mentored by
the 1st world powerlifting champion Hugh “Huge”
Cassidy and Gallagher in turn mentored hall-of-fame
powerlifting world dominator “Captain” Kirk
Karwoski. Gallagher competition coached Ed “King”
Coan, the world’s greatest powerlifter, along with iron
immortals Doug Furnas, Lamar Gant and Mark
Chaillet. Marty works with the military elite spec ops
fighters (in this country and abroad) along with governmental special units
within various agencies.

As a writer Gallagher is widely read and considered one of the finest

writers operating within the health, nutrition, bodybuilding, strength and
athletic training genre. He has had over 1,000 articles published since
1978, including 232 weekly ‘ask the expert’ fitness columns for the
Washington Post.com and 89 articles published during a ten year
relationship with Muscle & Fitness and Flex magazine. Gallagher’s
biographic on Ed Coan was called, “the greatest powerlifting book ever
written,” by the late Joe Weider. Rock star Henry Rollins called the Coan
book, “Awesome!” Dr. Jeff Everson described Gallagher’s Magnus opus,
The Purposeful Primitive “A literary masterpiece.” Gallagher lives in rural
Pennsylvania.
INDEX

Note: Entries in this index, carried over verbatim from the print edition of
this title, are unlikely to correspond to the pagination of any given e-book
reader. However, entries in this index, and other terms, are easily located
by using the search feature of your e-book reader.
A
AA. See Arachidonic acid Abdominal muscles, 413
Abdominal obesity. See Visceral obesity Abdominal training, 419
and anti-rotation, 416
basic plank, 414
high plank, 415
one hand plank, 416
plank row, 417–418
sit-ups
as low back “poison,” 413
problems caused by, 412–413
variations, 412
Accelerated aging. See also Premature aging and chronic stress and AGEs, 244
chronic stress, 285
and exercise, 362
obesity and chronic insulin
resistance, 197–198
and processed food, 246
sleep problems, 334
ACTH. See Adrenocorticotropic hormone Actin and myosin, 62
AD. See Alzheimer’s disease Adaptive immune system, 8–9, 128
Adaptive response
and oxidative stress, 23–24
triggering, 24
Adenosine, in brain, 325
Adenosine triphosphate, 325, 326
as energy currency, 98
production of, 104
Adipocytes. See Fat cells Adiponectin functions of, 176
production and inflammatory
cytokines, 182
release, 209
Adrenal glands, 35
Adrenalin, 33
Adrenocorticotropic hormone, 143
ADS. See Antioxidant defense system Advanced glycation end-products, 201
“dock” with RAGE, 244
and elevated sugar levels, 244
in food, 245
formation of, 244
inflammation and oxidative
stress by, 101, 244, 246–247
Aerobic exercise recommendation, 249–250
AGE. See Advanced glycation end-products Age and protein intake, link between, 65–66
ALA. See Alpha linolenic acid Alcohol consumption and fatty liver disease, 58
Algae, 83–84
Allergies, 91
Allium sativum, 462
Allostasis, 12, 206
definition of, 39
endorphin release, 40
vs. hormesis, 40
responses in environmental stress, 40
Allostatic load, 206
harmful effects of, 41–42, 45
measuring markers of, 43
and obesity, 179
Allostatic overload. See Allostatic load Alpha linolenic acid, 80, 89–90, 459
Alzheimer’s disease, 202, 353
Amber-tinted glasses, 350
Amino acids
essential, 63
side groups of
chemical properties of, 61
non-polar, 61
polar, 62
structure of, 60
Amygdala, 275, 277, 278
Anaerobic glycolysis, 103–104
Animal-based foods, 63
and AGE formation, 245
nutrient density of, 64
Animal Factory, 456
Animal foods, fat in, 455
ANS. See Autonomic nervous system Antibiotics
and dysbiosis, 155–157
from environmental sources, 157
IBD risk with, 156
Antibodies, 9
Antigens, adaptive immune response to, 8–9
Anti-inflammatory response, 9
Anti-nutrients, 160
Antioxidant defense system, 338
and free radicals, balance
between, 11–13
functions of, 10
plant-based foods, 236
Antioxidant supplements, 23
Anti-rotation and abdominal training, 416
Apolipoprotein, 515
Arachidonic acid, 86
Aromatase, 195
Assisted squat
doorway/pole squat, 381
shortened rep-stroke squat, 380
towel or rope squat, 381–382
Asthma, 91
Astrocytes, 141
Atheroma, 523, 524
ATP. See Adenosine triphosphate Auto-antibodies, 163
Autoimmune disease, 129
chronic stress, 285
genetically predisposed to, 132
sleep problems, 334
Autoimmunity
definition of, 9, 128
factor required for, 129
in tissue types, 128
Autonomic nervous system
functions of, 33
parts of
enteric nervous system, 34
parasympathetic nervous system, 33
sympathetic nervous system, 33
Autoxidation, 79
Axons, neighboring nerve cells, 269
Axon transmitter, synapse of, 270
B
Bagels, metabolic response to glucose production, 107
insulin release, 107–109
reactive hypoglycemia, 109
Basic cardio “ramp-up,” 420–422
Basic plank abdominal training, 414
Basic training, foundations of, 2
B-cells, 8, 128
BDNF. See Brain derived neurotrophic factor Bedroom environment, 350
Beef pot roast, 487
Belly breathing, 297
Bench press technique, 396
dumbbell, 397
advancing, 401
overhead, 402–404
“pause-relax-and-grind”
style, 398–400
physiological benefits of, 401
Beta-cell failure, 189
Biofeedback technique, for stress reduction, 301–303
HeartMath, 303
heart rate variability, 302
monitoring muscle tension and skin conductance, 302
muscle tension, 302
real-time information, 302
BioForce HRV, 554
Biological vs. chronological age, 198
Biomarkers
cholesterol, 509–534
correlations with health and disease, 504–508
as engine warning lights, 506
heart rate variability and, 546–553
of inflammation, 541–545
physical measurements of, 535–545
Blood sugar control, stepwise approach to, 260–261
adequate sleep, 258–259
avoiding HFCS, 242–247
gluten-containing products, avoiding, 229
insulin sensitivity with exercise, 249–258
plant-based foods, 234–241
antioxidant defense with, 236
 fermentable fiber content, 235–236
fermentation by gut bacteria, 234
legumes, 237
polyphenol content, 239–240
sulforaphane content, 237–239
and whole wheat, 235
processed seed oils, avoiding, 229–232
omega-6 PUFA, 230
for salad dressing, 231–232
protein consumption, 232–233
starch/glucose tolerance determination, 222–227
stress reduction techniques, 259
Blood sugar level. See also Blood sugar control, stepwise approach to person with normal insulin
sensitivity, 224, 225
pharmaceuticals to control, 227
unprocessed whole grains and, 226–227
BLT. See Bright light therapy Blue light signals, brain, 330
BMI. See Body mass index Body
affects brain, 288
anti-inflammatory/calming effects, 296
composition and gut health, 166
union of mind, 268
Body mass index, 173, 535–536
problem with, 536
weight-focused, 536
Body-scan technique, 299
Bodyweight squat, 372–373
Box deadlift, 384
Brain, 288
axon-dendrite, transmitter-receiver, 271
changing, 268
first principles perspective, 281
survival advantage, 283
chased by bears, 274
as energy and glucose hog, 99–100
epigenetic changes, 285
“fight-or-flight” response, 31
functions of, 30
and gut, 125
hypothalamus, 313, 314
ketones as energy source, 116
and mental health, 285
negativity bias, 282
response to stress, 143
threats, 275
Brain-based threat response system “fight or flight” system. See “Fight or flight” system primitive
and modern threats, 32
Brain derived neurotrophic factor, 303, 304
Brain training, 307
Brain Training Triumvirate, 308
Brain-train mind method, 293
“Brain wasting,” 201
“Branched-chain” amino acids, 62
Breast cancers, 195
Breastfeeding, 147
Breathing belly, 297
exhalation time, 296
inhalation time, 296
sympathetic nervous system, 295
Bright light therapy, 341
Broccoli sprouts, 237–239
Buddha’s Brain, 300
Buddhist meditation practices, 294
Bug lights, 350
“Burst Cardio” protocol, 428– 429, 432–435
Butyric acid (butyrate), 70, 234
C
Caffeine, 334, 345
Caloric restriction diet, 474–476
Calories calculation, 207
and hunger communication system, 220
Cancer cells, phenomenon of, 193
Cancers
characteristics of, 192–193
chronic stress, 285
dependent on glucose, 193–195
link with obesity and chronic insulin resistance, 192–196
sensitive to estrogen, 195
sleep problems, 334
trigger for, 193, 196
uncontrolled cell growth, 193
Capsaicinoids, 463
Capsicum annum, 463–464
Carbohydrates, 55
fiber, 59
health effects of, 119
misconception about, 119
starches, 57
sugar, 56–57
fructose, 57
glucose, 56–57
sucrose, 58
Carbohydrate tolerance, 465–468
low carb eating, 466–468
LSS eating pattern, 466–468
overview, 465
Cardio training foundation, 420–422
Cardiovascular training, 250, 363, 436, 444
Carrot noodles, 485
Cayenne, 463–464
CCT. See Correlated color temperature CD. See Clostridium difficile CDC. See Centers for Disease
Control Celiac disease, 129
Centers for Disease Control
exercise recommendation
“moderate intensity” aerobic, 249–251
“steady-state” exercise, 252
“vigorous intensity,” 251–252
Chain reactions of free radicals, 11
Chin-ups, 405–406
Chipotle butternut squash soup, 480
Cholesterol, 509–534
in artery clogging plaques, 521
building block for bile salts, 512
for cell communication, 511
cell membrane function of, 510
chemical structure of, 510
for developing brain during childhood, 511
dietary, 455
in human breast milk, 512
lipoproteins, 514–517
as molecular building block for hormones, 511–512
standard lipid panel, 529–531
testing of, 524–527
transportation, 517–524
Cholesterol esters, 515
Cholesterol levels, in blood, 513
Chronic disease, 45
Chronic inflammation, 129, 164, 221
causes of, 125
and chronic preventable disease, 14–15
definition of, 9
of gut, 123
sources of, 14
outside “environment,” 15
Chronic intestinal permeability, 130–131, 164
Chronic preventable diseases, 14
Chronic stress and threat response, 32
Chronobiology, 342
Chronological vs. biological age, 198
Chylomicrons, 514
transport of fat and cholesterol, 516
Cinnamomum spp, 463
Cinnamon, 463
Circadian disruption. See Sleep problems, circadian disruption Circadian rhythm, 312, 500
CLA. See Conjugated linoleic acid Clostridium difficile, 155
Coconut oil, 71, 72, 232
Coffee drinking
correlation with lung cancer, 505–506
relation to smoking, 506
Colonocytes, 59
Color additives, 219
Combination antibiotic therapy, 156
Complimentary proteins, 64
Compound multi-joint exercises, 367
Confounders, 51
Conjugated linoleic acid, 95
Conventional vs. organic produce, 461
Cooking
methods and AGEs, 245
strategy, 49–491, 490–491
Correlated color temperature, 347, 348
Corticotropin releasing hormone, 143
Cortisol, 274
Cortisol receptor resistance, 286, 287
C-reactive protein, 541–542
high sensitivity, 544–545
nonspecific, 544
and risk of heart disease, 542
CRH. See Corticotropin releasing hormone CRP. See C-reactive protein Culinary consensus, 447–
464
deadly meat, 455–456
food quality
demand for, 456
for omnivore, 449–455
for vegetarian, 457–460
herbs and spices, 461–464
cayenne, 463–464
cinnamon, 463
five health-promoting, 464
garlic, 462
ginger, 462
turmeric, 463
local food and, 449
Curcuma longa, 463
Curcumin, 463
Cytokines, 8, 9, 177–178, 182, 184
D
Dawn simulator, 346
Deadlift, 383
“bodybuilder stiff-leg,” 384
box. See Box deadlift
common flaws in, 393–394
conventional, 384
stiff-leg. See Stiff-leg deadlift sumo. See Sumo deadlift
tactics, 388
variations, 384
Deep squat, 369, 371
Defensive tactics, 2–3
Dementia, 202
Dendrites, neighboring nerve cells, 269
Depression
and chronic stress, 285
and sleep problems, 334
Descartes, Rene, 267
DGLA. See Dihomogamma linolenic acid DHA. See Docosahexaenoic acid Diabesity, 180
Diabetes. See also Blood sugar control, stepwise approach to; Type 1 diabetes; Type 2 diabetes
causes of, 53
and chronic stress, 285
and depression, 288
muscle mass maintenance as
defense against, 365
nutrition and exercise, 340
and “prediabetes,” laboratory
tests for
charts, 205
fasting blood sugar, 203–204
HbA1c test, 203
OGTT, 204
risk for developing, 206
and sleep problems, 334
Diabetics, whole grains for, 226–227
Dietary cholesterol, 455
Dietary sources
arachidonic acid, 86
gamma linolenic acid, 86
linoleic acid, 86
Diets, 21
and epigenetic changes, 18
 and epigenetic changes, 18
failure in long-term, 50, 54
Digestion, 222
Digestive tract messengers, 215
and satiety, 214–215
Dihomogamma linolenic acid, 90
DNA
damage by free radicals, 10
discovery of, 16
mutation, 20
Docosahexaenoic acid, 82, 89–90
Dopamine release, 217
Double bonds, 79
Dumbbell bench press technique, 397
advancing, 401
overhead, 402–404
“pause-relax-and-grind” style, 398–400
Dysbiosis causes of antibiotic use, 155–156
LPS levels, 154
processed foods, 152–153
sanitized food supply, 155
definition of, 149–150
dietary source of, 155
diseases and disorders associated with, 151
E
Eastern meditation tactics, 293
E. coli O157:H7, 455
Edison, Thomas, 329
EGCs. See Enteric glial cells Egg scramble, 478
Eicosanoids, 87
Eicosapentaenoic acid, 82, 89–90
Elaidic acid, 93
Elite athletes, 442
Endometrial cancer, 195
Endorphin release and allostasis, 40
Endorphins, 140
Endotoxemia, 154
Endotoxin, 154
Energy drinks, 247–248
Energy generation
from fat catabolism, 105
from glucose catabolism, 103–104
ENS. See Enteric nervous system Enteric glial cells, 141
Enteric nervous system, 34
and brain, similarity between, 141
components of, 141
enteric glial cells, 141
gut-brain axis
stress reduction, 143
two-way communication network, 142
vagus nerve, 142
neurotransmitters, 141
response to stress, 143
as “second brain,” 34
Environment, 18
Environmental challenge. See Environmental stresses
Environmental signals
changes in epigenome, 20
epigenetic system response to, 17–18
for health, 21
Environmental stresses
adaptations/responses in, 40
adaptations through allostasis in, 40
dosage of, 23
 dosage of, 23
dose of food and exercise, 26–27
and hormetic window, 27
importance of, 22–23
Environmental stressors, 21
Environmental stress sensor, 241
EPA. See Eicosapentaenoic acid Epigenetics, 21, 202, 284
case study, 19
definition of, 16
of fetus, 20
response to environmental signals, 17–18
Epigenome, 20
and environmental stressors, 21
Epinephrine. See Adrenalin Epithelial cell barrier, 126
Essential amino acids, 63
Essential amino acids deficiency, 457
Essential fatty acids, 80–81
Excess fat, 190–191
Exercise, 21, 24, 351–352. See also Progressive resistance training benefits of regular, 351
CDC recommendation for, 249–250
defensive tactics, 363
and epigenetic changes, 18
health benefits of, 361–362
and hormesis, 26–27
and insulin sensitivity, 249–258
HIIT. See High intensity interval training “moderate intensity” aerobic, 249–251
“steady-state,” 252
“vigorous intensity,” 251–252
reasons for avoiding, 250
recommendations, fundamental flaws in, 48
for reducing obesity and chronic stress, 500
scheduling, 352
sleep enhancing, 352
and “stress cup,” 42–43
timing, 351
Exercise intensity
definition of, 250
and HRmax, 250–252
Exhalation time, 296
Exorphins, 140
F
“Fad diets,” 49
“Fast pathway,” 33
Fast pathway and HPA axis, 35
Fat cells
adiponectin release, 209
definition of, 174
as energy storage facilities, 102, 177
functions of, 174
metamorphosis of, 175, 177–179
bloated adipocyte, 177
cytokine release, 177–178
obesity-related inflammation, 178–179
Fat loss, stepwise approach to, 260–261
adequate sleep, 258–259
avoiding HFCS, 242–247
gluten-containing products, avoiding, 229
insulin sensitivity with exercise, 249–258
plant-based foods, 234–241
antioxidant defense with, 236
fermentable fiber content, 235–236
fermentation by gut bacteria, 234
legumes, 237
polyphenol content, 239–240
sulforaphane content, 237–239
and whole wheat, 235
processed seed oils, avoiding, 229–232
omega-6 PUFA, 230
for salad dressing, 231–232
protein consumption, 232–233
starch/glucose tolerance determination, 222–227
stress reduction techniques, 259
Fats, 55
in animal foods, 455
breakdown, 187
burning for energy, 119
functions of, 67
glucagon stimulating burning of, 113
and glucose, balance between use of, 102–103
glucose conversion into, 102
metabolism, 102
as primary energy source, 101
saturated. See Saturated fat (triglyceride) catabolism, 105
Fatty acids
carbon chain double bond
 carbon chain double bond
configurations, 92–93
carbon chain of, 69
Fatty liver, 58
Fatty liver disease, 58
Feeding, for training and activity, 470–476
caloric restriction diet, 474–476
in high intensity interval training, 472–473
low carb diet, 474–476
LSS eating pattern, 475
in non-training days, 470–471
carbohydrates as fermentable fiber, 470
fat intake from protein sources, 471
25-30 grams of high quality protein, 471
sugary fruit and starchy food intake, 471
in training days, 471–474
“Feel-good” satisfaction response, 216–217
Fermentable fiber
and gut health, 153
health benefits of, 235
and non-fermentable fiber, 60
in plant-based foods, 235–236
sources of, 235–236
Fermentation, 59
definition of, 157
product of, 158
Fermented foods and probiotics, 157–158
Fetus, epigenetics of, 20
Fiber, 59
health benefits of, 60
in whole wheat, 235
“Fight-or-flight” response, 31, 40
“Fight or flight” system, 297, 338
components of autonomic nervous system. See Autonomic nervous system hypothalamic-
pituitary-adrenal axis. See Hypothalamic-pituitary-adrenal axis conditions triggering, 38
decreases activation of, 303
health effects of, 37
sympathetic nervous, 162
yin/yang concept, 36
Fish oil capsules, 90
Flavor additives, 219
Flaxseed, 80
Flesh machine, 314
Foam cells, 523
Foie gras, 58
Food, 53. See also Diets and exercise, 26–27
and nutrition, 25
Food and Drug Administration, 93
Food label, 86
trans fats, 93
Food processing and gluten-related diseases, 135–136
Food quality
demand for, 456
for omnivore, 449–455
for vegetarian, 457–460
Formula feeding, 147
Free radicals
and ADS, balance between, 11
chain reactions, 11
DNA damage by, 10
“importing,” 13
and premature aging, 197–198
unpaired electron of, 10
and unsaturated fatty acid, 79
Free-weight exercises, 367
Free-weight lifting techniques, 367
“Frozen statue” row, 408–411
Fructose, 57
and AGE, 244
chemical structure of, 56
in energy drinks, 248
in fruit drinks, 248
in fruit juices, 248
in fruits, 242
intake and fatty liver disease, 58
in soft drinks, 247
“Fruit-flavored” drinks, 247–248
Fruit juices, 248
FSR. See “Frozen statue” row
G
Gamma linolenic acid, 86
Garlic, 462
Gastrointestinal problems, 140
Genes
collections of DNA, 16
definition of, 17
expression and environment, 15
functions of, 16
mutations, 17
“turning off,” 17–18
“turning on,” 17–18
Genetic variations, 16
Genome, 146
definition of, 17
GH. See Growth hormone Ginger, 462
GLA. See Gamma linolenic acid Gliadins and glutenins, 134
Glucagon
functions of, 111–112
release, 111
stimulating fat burning, 112–113
Gluconeogenesis, 100, 188
Glucoraphanin, 238
Glucose
as brain fuel, 99–100
chemical structure of, 56
connected in chains, 57
conversion into fat, 102
in energy drinks, 248
and fat, balance between use
of, 102–103
in fruit drinks, 248
in fruit juices, 248
and insulin, controlling interaction between, 101
metabolism, 101
anaerobic glycolysis, 103
production of, 188
in soft drinks, 247
tolerance, 222
Glucose meter, 222
Gluten-containing products
health consequences for, 140
 health consequences for, 140
Gluten free diet, 124
for type 1 diabetes, 165–166
Gluten-free processed products, 229
Gluten-related diseases
celiac disease, 135
autoimmune and inflammatory disorders IN, 137–138
causes of, 136–137
diagnosis of, 138
microvilli destruction, 139
prevalence of, 136
food processing impact on, 135
gluten sensitivity, 135
and celiac disease, difference between, 139
symptoms of, 139
and metabolic disorders, 136
spectrum of, 135
Good nutrition, 49
Google, 294
Grain-based fibers, 60
Grains
genetic modification of, 136
Gram-negative bacteria, 154
Groupthink, 52–53
Growth hormone
functions of, 116
release during sleep, 116
signals for release of, 115
Gut
bacteria species, 145
and brain, 125
chronic inflammation of, 123, 125
as first barrier, 125
intestinal lumen, 125
nutrient absorption, 125
response to stress, 143
villi, 125
Gut bacteria
and auto-antibodies, 163
beneficial
African children, 155
European children, 155
fiber transformation by, 157
health benefits of, 148
opportunistic pathogens and, balance between, 148, 150
signaling Treg cells formation, 149
in traditional fermented foods, 157–158
 in traditional fermented foods, 157–158
diversity of, 145
and enteric nervous system, 162
imbalance, correcting, 147
in infants, factors influencing, 146–147
influence on hormones, 163
influence on mood and behavior, 161–163
microbiome, 146
restoring “balance” in, 161
and Treg cells, 149
Gut-Brain axis, 307
Gut health
and body composition, 166
and fermentable fiber, 153
Gut immune system, 125
adaptive immune system. See
Adaptive immune system
as first line of defense, 126–127
innate immune system. See
Innate immune system
members of, 127
stimulation of, 123
T-regulatory cells. See Treg cells Gut inflammation, 164
and chronic disease, 144
Gut inflammation, triggers for, 133
dysbiosis, 145
gluten
and gluten-related diseases. See Gluten-related diseases prolamin protein, 134
toxic components of, 134
variance among responses to, 135
stress and intestinal permeability, 141–144
H
HDL. See High density lipoprotein HDL/triglyceride ratio, 101
Health
and lacto-fermenting bacteria, 160–161
and muscle mass maintenance, 365–366
Heart and vascular disease risk, 196
Heart disease, chronic stress, 285
HeartMath, 303
Heart rate variability, 302, 546–554
and circadian rhythm, 550
equipment, 553–554
exercise and, 549
and health, 548–551
high, 547, 548
high/low, 302
low, 547, 548
measurement of, 551–553
for plan activity, 552–553
review of, 546–547
scores, 551–553
stress-threat system and, 550
Heart/vascular disease, sleep problems, 334
Heat (Calor), 7
Heme iron, 459
Herbs and spices, 461–464
cayenne, 463–464
cinnamon, 463
five health-promoting, 464
garlic, 462
ginger, 462
turmeric, 463
High blood pressure, sleep problems, 334
High carbohydrate meals (bagels), metabolic response to glucose production, 107
insulin release, 107–109
reactive hypoglycemia, 109
High-density carbohydrate foods and dysbiosis, 152
High density lipoprotein, 516
High-fructose corn syrup, 242 and AGEs, 244
bad press on, 242–243
comparison with table sugar, 243
consumption by average
American, 243
 American, 243
and NAFLD, 58
High intensity interval training, 252–258, 420
benefits of, 253, 425
glucose transporters, 255–256
increased insulin sensitivity, 257–258
muscle glucose storage, 254–255
built-in safety system, 430–431
“Burst Cardio,” 428–429, 432–435
for diabetes and prediabetes, 257–258
effectiveness of, 425
effort and high target heart
rates of, 420
example of, 426
with exercise types, 427
feeding for training and activity in, 472–473
and glucose levels, 472–473
and hormetic dose, 427–428
HRmax calculation, 425, 428–429
preparation, 420–421
for short periods of time, 252–253, 424
and stress cup, 427–429
High plank abdominal training, 415
High sensitivity C-reactive protein, 543, 544–545
in chronic disease, 545
level of, 544–545
nonspecific CRP, 544
High temperature cooking and AGE, 245
HIIT. See High intensity interval training Hippocampus, 276, 278
stress, 275
Hormesis, 12, 21, 362
adverse and beneficial effects, 28–29
vs. allostasis, 40
concept of, 25–27
definition of, 23
food and nutrition, 25
graph of, 26, 27
Hormetic zone, 26–28
Hormones
cortisol, 35
epinephrine and norepinephrine, 35
Hormone sensitive lipase, 113
HPA axis. See Hypothalamic-Pituitary-Adrenal axis; Hypothalamic-pituitary-adrenal axis HRmax.
SeeMaximum heart rate HRV. See Heart rate variability HRV score, 552–553
hsCRP. See High sensitivity C-reactive protein HSL. See Hormone sensitive lipase Human genome,
17
Hunger, 208
Hunger communication system, 209
gut-brain axis and satiety signal digestive tract signaling messengers, 214–215
protein, 215–216
leptin, 209
communicating with brain, 210
functions of, 210–212
and hypothalamus, 210
in obese people, 211–212
resistance, 211, 213
palatable foods and reward
center, 216–217
and restricting calories, 220
signal to stop eating, 210–213
Hunger drive, 208–209
Hunter-gatherer cultures, 364
Hydrogenation, 94
Hyperextended spine, 393–394
Hyper-lordosis, 393
Hyperplasia, 179
Hypertrophy, 179
Hypothalamic-pituitary-adrenal axis adrenal glands, 35
diabetics experience chronic
activation, 288
fast pathway, 274
fast pathway and, 35
health effects of, 37
hormones
cortisol, 35, 37
epinephrine and norepinephrine, 35
hypothalamus, 34
pituitary gland, 34
slow pathway, 274
slow pathway and, 35
stop, stress response, 284
stressed-out brain, 280
stress response, 273, 275, 276, 278
sympathetic nervous system’s threat-stress response system, 288
Hypothalamus, 34, 100
I
IBS. See Irritable bowel syndrome Ice cream and cake, metabolic response to fat storage, 118–119
insulin release, 118
IEL. See Intraepithelial lymphocytes IGT test. See Individual glucose tolerance test Immune system,
8, 13
adaptive. See Adaptive immune system early development of, 147
inflammatory response, 9
innate. See Innate immune system Individual glucose tolerance test, 226–227, 465
Inflammation, 6, 285
acute and chronic, 9, 87
acute, basic process of, 8
beneficial effects of, 12–13
benefits of, 12
cardinal signs of, 7–8
insulin sensitivity loss by, 181–183
long-term, 14
and omega-3 PUFA, 87–88
and oxidative stress
by AGE, 101
allostatic overload by, 42
stimulating threat response, 38
trans fatty acids linked with, 92–93
primary generator of, 8
short-term increases in, 13–14
Inflammation markers, 541–545
C-reactive protein, 541–542
high sensitivity C-reactive protein, 543, 544–545
Inflammatory cytokines
and insulin receptor, 181–182
oxidative stress triggering, 184
Inflammatory response
by cells, 8
palmitic acid triggering, 76
Inhalation, sympathetic nervous system, 295
Inhalation time, 296
Innate immune system, 8, 127
Insulin
functions of, 107–108
glucose and fat for energy, 103
health effects of, 119
misconception about, 119
Insulin/glucagon ratio, 114
Insulin receptor
resistant, 183
sensitive, 182
short-circuited, 181–182
Insulin resistance, 110, 188
causes of, 187, 222
chronic, consequences of
accelerated aging, 197–198
“brain wasting,” 201
cancer risk, 192–196
excess fat, 190–191
fat breakdown, 187
gluconeogenesis, 188
heart and vascular disease risk, 196
high insulin levels, 188
high palmitate levels, 190–191
muscle wasting, 189
definition of, 187
inflammation reduction and, 500
from inside, 186
muscle mass maintenance as defense against, 365
Insulin-resistant obese
restricting starchy carbohydrates and sugars in, 228
Insulin sensitivity
and blood sugar levels, 222
of cell, 110
definition of, 109–110
and exercise, 249–258
HIIT. See High intensity interval training “moderate intensity” aerobic, 249–251
“steady-state,” 252
“vigorous intensity,” 251–252
loss by inflammation and oxidative stress, 181–183
Internal timekeeper, 313–319
adrenal gland’s clock, 316
fat clock, 317
gut clock, 317
heart clock, 316
immune clock, 317
kidney clock, 317
liver clock, 316
muscle clock, 317
pancreas clock, 316
Intestinal barrier
as first line of defense, 125–127
Intestinal permeability, 127
and autoimmunity, 129
consequences of, 129–131
short term increases in, 133
 short term increases in, 133
Intestinal tract. See Gut Intraepithelial lymphocytes, 139
IP. See Intestinal permeability Iron deficiency, 459–460
Irritable bowel syndrome, 139
K
Ketogenic diets, 201
Ketones, 116
Kidney dysfunction and protein intake, 66
Knees
collapsing inward, 379–380
shooting forward, 378–379
Krebs cycle, 104
L
LA, 89–90
Lactic acid, 103
Lacto-fermentation, 158–159
Lacto-fermented fruits and vegetables anti-inflammatory effects of, 161
health benefits of, 160
Lacto-fermenting bacteria and health, 160–161
LAN. See Light at night Large-buoyant LDL, 517, 519, 520, 522
particles, formation of, 529
Lauric acid (laurate), 71
LBLDL. See Large-buoyant LDL
LDL. See Low density lipoprotein LDL particle number, 534
LDL receptors, 532–533
LED-generated light, 349
Legume preparation, for toxicity, 458
Legumes, 237
Lifestyle change, 54, 494–502
defensive tactics in, 497–502
neck of Roy Buchanan’s guitar, case study, 494–495
strategic planning, 496–502
Light at night, 331
asleep, 332–333
chronotherapy, 333
circadian disruption, 333–334
exposure, 332
poor sleep, 333
caffeine, 334
space at night, 331
Light pollution, 331
Light squat, 370–371
Linoleic acid, 80, 86, 230
Lipid peroxidation, 79
Lipid peroxide, 79
Lipopolysaccharide, 154
Lipoproteins, 514
chylomicrons, 514
high density, 516
low density, 516
structure of, 515
types of, 514–517
 structure of, 515
types of, 514–517
very low density, 516
Liver cancers, 192
Liver metabolism, 100
Local food, 449
Long-chain fatty acids
long chain omega-3 fats, 459
and metabolism, 72
Long-chain saturated fat
palmitic acid, 73
stearic acid, 75
Long-term eating signal, 214
Low carb diet, 466–468, 474–476
Low density lipoprotein, 516
Friedewald equation for, 525
in immune response, 532
large-bouyant, 519
oxidized, 523
particle number, 534
particle size, 527–529
small-dense, 519
transport of fat and cholesterol, 517–519
Low starch/high protein meal, metabolic response to carbohydrate component, 111
fat burning, 112–113
glucagon release, 111–112
insulin release, 112
Low starch/sugar (LSS) eating pattern, 466–468, 475
LPS. See Lipopolysaccharide
M
Macronutrient ratio, 25
Macronutrients
biochemistry perspective, 55
carbohydrates. See Carbohydrates fat. See Fat
protein. See Protein
Macrophages, 177, 523
Malnutrition and hormesis, 26–27
Margarine, 94
Mast cells, 143
Master clock
cortisol levels, 318
hormone levels, 318
in hypothalamus, 319–320
leptin levels, 318
malfunctioning, 335–337
blood sugar, 336
diabetes, 336, 339–340
diabetes, loss of insulin, 337
disrupt sleep, 336
fatty liver disease, 336
heart, 336
heart disease, 337
inflammation, chronic, 337
insulin resistance, 336
poor athletic performance, 337
sleep, 339–340
stroke, 337
melatonin levels, 318
Maximum heart rate, 250–251
definition of, 250
determination of, 250–251, 420–421
Maxwell’s Equations, 51
MBSR. See Mindfulness-based stress reduction MCTs. See Medium-chain triglycerides Medicine,
future of, 45
Meditation tactics
biofeedback technique, for stress reduction, 301–303
HeartMath, 303
heart rate variability, 302
monitoring muscle tension and skin conductance, 302
real-time information, 302
eastern/western high technology, 293–294
exercise, 303–305
 exercise, 303–305
interventions, 294
mindfulness practice, 294
body-scan, 299–301
mindful breathing, 295–298
Medium-chain fatty acids lauric acid, 71
and metabolism, 72
Medium-chain triglycerides, 232, 471
Melatonin
benefits, 338
connection, 338–339
gateway hormone for regeneration mode, 321
natural light’s effects, 330
supplementation, 353
temporary use of, 353
Mental challenges, 271
Mental defect, physical brain changes, 285
Mental health and brain changes, 285
Metabolic response to food intake, 106
high carbohydrate meals (bagels)
glucose production, 107
insulin release, 107–109
reactive hypoglycemia, 109
ice cream and cake
fat storage, 118–119
insulin release, 118
low starch/high protein meal
carbohydrate component, 111
fat burning, 112–113
glucagon release, 111–112
insulin release, 112
during sleep
GH release, 115–116
ketone production, 116
liver gluconeogenesis, 116–117
Metabolism, 95
fat, 101–103
gluconeogenesis, 100
glucose, 99–101
lean and athletic youngster, 99
liver, 100
mitochondria, 103
muscle, 101
obese person, 99
Metformin, 188, 227
Methylmercury (MeHg) in fish, 453–454
Mexican chicken with sautéed kale, 481
Mind, 31
Mindfulness-based stress reduction, 300
Mindfulness training, 294–301
Mind, union of body, 268
Misinformation, 53
Mitochondria
as energy factories, 103
fat catabolism, 105
glucose catabolism, 104
oxidative stress in, 183, 185–186
Mitohormesis, 200
“Moderate intensity” exercise definition of, 250
HRmax of, 251
Modern and primitive threats, 31–32
“Moist” cooking methods, 245
Molecular mimicry, 163
Monosaccharide, 56
Monounsaturated fatty acid
characteristics of, 78
chemical bonds, 77
health effects of, 78, 80
liquid at room temperature, 78
oleic acid, 78
Monty Python and the Holy Grail, 506
Mother’s womb and epigenetic changes, 20
MUFA. See Monounsaturated fatty acid Muscle building, dietary signal for, 65
Muscle cannibalism, 100
Muscle mass and strength
retaining, 365–366
“use it or lose it” scenario, 364
Muscle mass maintenance and health, 365–366
Muscles
glucose storage by, 101
primary energy source of, 101
Muscle tension, 301, 302
Muscle wasting, 189
Mutations
definition of, 16
of genes, 17
Myelin, 269
Myostatin, 189–190
N
NAFLD. See Non-alcoholic fatty liver disease National Sleep Foundation, 259, 344
“Nature vs. nurture” environment argument, 20
Negativity bias
brain reacts, 282
first principles perspective, 283
Nerve cells
connections, 271
dendrite receivers, 279
drawing of, 269
glial cells, 268
prefrontal cortex, 279
signal direction, 270
Nervous system and long-term stress, 286
Neuroplasticity
brain’s ability to physically
change, 268
definition of, 269
Nightshift work, 354
Nightshift worker, 342, 343
Nitrogen balance
concept, 64
positive/negative, 65
Non-alcoholic fatty liver disease, 58, 242
Non-rapid eye movement sleep, 322, 324
light sleep stage, 345
slow wave sleep, 340
Non-training days, feeding in, 470–471
carbohydrates as fermentable fiber, 470
fat intake from protein sources, 471
25-30 grams of high quality protein, 471
sugary fruit and starchy food intake, 471
Norepinephrine, 33
Nourishing Traditions, 460
NREM. See Non-rapid eye movement sleep Nutrient timing around exercise, 468
Nutrition, 48
and food, 25
recommendations
fundamental flaws in, 48, 50
observational results to make, 52
Nutrition research and practice, problems with first principles, 50
groupthink, 52–53
groupthink, 52–53
reductionism, 52
study design, 51
O
Obesity, 170. See also Fat loss, stepwise approach to causes of, 53
chronic diseases linked to, 172
and chronic stress, 285
consequences of
accelerated aging, 197–198
“brain wasting,” 201
cancer risk, 192–196
excess fat, 190–191
fat breakdown, 187
gluconeogenesis, 188
heart and vascular disease risk, 196
high insulin levels, 188
high palmitate levels, 190–191
muscle wasting, 189
definition of, 179
insulin resistance caused by, 181–183
elevated stress levels, 183
short-circuited insulin receptor, 181
prevalence of, 172
reward system of brain in, 217–218
and sleep problems, 334
and stop eating signal, 218
and type 2 diabetes, 180
Obesity-related disease, cost of, 172
Observational data, 51–52
Observational studies, 52
Occupational and Environmental Medicine, 342
OEM. See Occupational and Environmental Medicine Official recommendations, 53
OGTT. See Oral glucose tolerance test Oily (or fatty) fish, 83
Okinawan diets, 119
Oleic acid, 93
Omega-3 fatty acids
alpha linolenic acid, 82
docosahexaenoic acid, 82
eicosapentaenoic acid, 82
food sources of, 83–84
health effects of, 82–83
omega-3 and omega-6 conversion pathways, 89–90
and omega-6 fatty acids, balancing, 87–88, 91
structure of, 81
supplementation, 90–91
Omega-6 fatty acids balanced dietary intake of, 85–86
dihomogamma linolenic acid, 90
food sources of, 85
harmful effects of, 88
health effects of, 85
and omega-3 fatty acids, balancing, 87–88, 91
vs. omega-3 PUFAs, 85
structure of, 84
supplementation, 90–91
Omega-6 PUFA
biologically important, 86
inflammation and oxidative stress by, 230
in vegetable and seed oils, 231
Omega-6 to omega-3 ratio, unbalanced, 91
One hand plank abdominal training, 416
Open-Focus Brain, 299
Opportunistic pathogen, 148
CD overgrowth, 155
overgrowth as threat to body, 162
Oral glucose tolerance test, 223, 225
Organic vs. conventional produce, 461
Osteoporosis, 366
Outdoor “power walking,” 421
Overhead dumbbell bench press technique, 402–404
Over-nutrition, 25, 26–27
Overtraining, 26–27
Oxidation reactions, 10
Oxidative stress, 6, 221, 285
and adaptive response, 23–24
and ADS, 10–12
balance between free radicals and ADS, 11
beneficial effects of, 12–13
and chronic preventable disease, 14–15
definition of, 10
delicate balance of, 12–13
importance of, 12
insulin sensitivity loss by, 181–183
long-term, 14
in mitochondria, 183, 185–186
primary generator of, 8
short-term increases in, 13–14
sources of, 14
outside “environment,” 15
unsaturated fats and, 79
Oxygen free radical. See Reactive oxygen species
P
Pain (Dolor), 7, 8
Palatable foods and reward system, 216–217
Palmitic acid (palmitate), 73, 190
alarm system activated by, 191
obesity and chronic insulin resistance, 190–191
scientific studies on, 76–77
triggering inflammatory response, 76
Pancreas, 188
beta-cell failure in, 189
Paracelsus, 23
Parasympathetic activity, 143 Parasympathetic nervous system, 33, 296
and SNS, interaction between, 35
parasympathetic nervous system anti-inflammatory actions, 33, 37
“rest and digest” system, 33
Pastured pork chili, 483
Pentaverate, 362, 496–502
PFC. See Prefrontal cortex PHA. See Phytohemagglutinin Phospholipids, 515
Photo-oxidation, 79
Physical functionality
of ‘civilized man,’ 365
of tribal, 364
Physically rebuilding, 298
Physical mindfulness, 305
Physical stress and exercise, 361–362
Phytate, 459–460
Phytohemagglutinin, 458
Pituitary gland, 34
Plank row, 417–418
Plant-based chemicals and health polyphenols, 239–240
sulforaphane, 237–239
Plant-based proteins, 63–64
PNS. See Parasympathetic nervous system Poison, 23
Polyphenols, 24, 239–240
Polysaccharides, 57
Polyunsaturated fatty acid, 80–81
Preconceptions, 442
Prediabetes
laboratory tests for
charts, 205
fasting blood sugar, 203–204
hemoglobin A1c (HbA1c) test, 203
Oral Glucose Tolerance Test (OGTT), 204
self-monitoring program, 225
Prednisone, 36
Prefrontal cortex, 276, 278
stress, 275
Pregnancy, epigenetic changes during, 20
Premature aging and chronic stress, 197–198, 288–289
Primal correlations, 442–444
Primitive and modern threats, 31–32
Probiotics
definition of, 157
effect on anxiety and mood, 162
and fermented foods, 157–158
Processed foods, 53
and accelerated aging, 246
and AGEs, 245
and dysbiosis, link between, 152–153
omega-6 fatty acids in, 85–86, 88, 90
palatability and reward, 219
processed grain-based carbohydrate foods and dysbiosis, 152–153
Processed seed and vegetable oils, 229
inflammation and oxidative stress with, 229
omega-6 PUFA, 230
omega-6 PUFA content, 230
omega-6 PUFA content of, 231
Progressive resistance training, 366. See also Exercise for building front torso muscles
bench press. See Bench press deadlift. See Deadlift primer on, 363
result-producing methods of, 367
row. See Row
squat. See Squat
Prolamins, 134
Protein berry breakfast shake, 490
Protein food, quality of, 63–64
Protein intake
dependence on age and physical activity, 65–66
and kidney dysfunction, 66
reasons for increased, 66
recommendation for minimum daily, 64–65
Proteins, 55
chemical properties, 61
 chemical properties, 61
composition of, 60
consumption, “rule of thumb” estimates for, 232–233
formation of, 16
functions of, 17, 62, 232
metabolic effects, 66
and satiety, 215–216
structure of, 61
Pseudomembranous colitis, 155
Psychological stress, chronic, 265
Psychological stress duration and intensity, 271
PUFA. See Polyunsaturated fatty acid Pulled pork wraps with mango Jalapeño relish, 488
Pulling exercises, 405
Pull-ups, 405
R
RAGE. See Receptor for advanced glycation end-products Randle Cycle, 102
Rapid eye-movement sleep, 323, 324, 325
Reactive hypoglycemia, 109
Reactive oxygen species
definition of, 10
formation of, 10
Receptor for advanced glycation end-products, 244
Recipes, 477
beef pot roast, 487
carrot noodles, 485
chipotle butternut squash
soup, 480
cooking strategy, 49–491
egg scramble, 478
Mexican chicken with sautéed kale, 481
pastured pork chili, 483
protein berry breakfast shake, 490
pulled pork wraps with mango Jalapeño relish, 488
roasted chicken with roasted celery root, 486
salmon with carrot noodles, 484
spicy burger with jicama chips, 479
spicy chicken soup, 482
steak and potatoes, 489
Red blood cells, 101
Redness (Rubor), 7, 8
Reductionist nutritionism, 52
REM. See Rapid eye-movement sleep Resistance training, 63, 250, 436, 444
benefits of, 366
goal of, 367
and protein intake, 65–66
Reward system of brain
in obese individuals, 217–218
palatable foods stimulating, 216–217
processed food and palatability, 219
“stop eating” signal, 218
sugar and HFCS stimulating, 247
Roasted chicken with roasted celery root, 486
ROS. See Reactive oxygen species Row, 405
“frozen statue,” 408–411
single arm supported, 407–408
“Runners high” sensation, 40
S
Salad dressing, olive/coconut oil for, 231–232
Salmon with carrot noodles, 484
Sanitized food supply and dysbiosis, 155
Sarcopenia, 65–66
causes of, 365
definition of, 365
Satiety, 66
definition of, 214
and digestive tract messengers, 214–215
and proteins, 215–216
Saturated fat
butyric acid (butyrate), 70
carbon chain of, 68–69
classification of
by chain length, 70
definition of, 68
lauric acid, 69
lauric acid (laurate), 71
misconception about, 67–68, 76–77
palmitic acid (palmitate), 73
resistant to free radicals, 68
structure of, 68
SCFA. See Short-chain fatty acids SDLDL. See Small-dense LDL
Seasonal “primordial cycling,” 442
Sedentary/low activity and hormesis, 26–27
Sedentary vegetarian, 64
Selenium, 453–454
Short-chain (SC) fats, 148
Short-chain fatty acids, 153
Short-term eating signal, 214
Sit-ups
as low back “poison,” 413
problems caused by, 412–413
variations, 412
Skeletal muscle, glucose storage by, 101
Skin conductance biofeedback, 301
Sleep deprivation, 27
health consequences of, 258–259
Sleep problems, circadian disruption, 312
amber-tinted glasses, 349–350
 amber-tinted glasses, 349–350
bedroom environment, 350
brain/body, effects, 340–341
caffeine, 345
chronic disruption, 334
correlated color temperature, 347, 348
credit-limit, 326, 327
dawn simulator, 346
eliminate exposure to blue spectrum light, 348
exercise, 351–352
internal timekeeper, 313–319
adrenal gland’s clock, 316
fat clock, 317
gut clock, 317
heart clock, 316
immune clock, 317
kidney clock, 317
liver clock, 316
muscle clock, 317
pancreas clock, 316
light at night, 331, 333–334
asleep, 332–333
exposure, 332
light pollution, 331
malfunctioning master clock, 335–337
blood sugar, 336
diabetes, 336, 339–340
diabetes, loss of insulin, 337
disrupt sleep, 336
fatty liver disease, 336
heart, 336
heart disease, 337
inflammation, chronic, 337
insulin resistance, 336
poor athletic performance, 337
sleep, 339–340
stroke, 337
master clock
cortisol levels, 318
hormone levels, 318
in hypothalamus, 319–320
leptin levels, 318
melatonin levels, 318
melatonin
connection, 338–339
gateway hormone for regeneration mode, 321
natural light’s effects, 330
supplementation, 353
National Sleep Foundation, 344
natural light, 346
in night, 312
 in night, 312
non-rapid eye movement sleep, 322
rapid eye-movement sleep, 323, 325
shift work, 342–343, 354
sleep drive
adenosine gold card, 327
chemical system, 325–326
circadian systems, 328
gray card, 327
slow wave sleep, 323
waking and sleeping schedule, 345
Slow pathway and HPA axis, 35
Slow wave sleep, 323
Small-dense LDL, 517, 521, 522, 533
Small-dense LDL particles, 521
SNS. See Sympathetic nervous system “Soda addictions,” 247
Soft drinks, 247
Spices. See Herbs and spices Spicy burger with jicama chips, 479
Spicy chicken soup, 482
Sprouting, 460
Squat
assisted. See Assisted squat bodyweight, 372–373
deep, 369, 371
grind, 373–374
health benefits of, 368
knees collapsing inward during, 379–3, 379–380
knees shooting forward, 378–379
light, 370–371
limit, 370
mechanics descent, basic, 371–372
pause at bottom of, 370
progression, 372–373
bodyweight squat, 372–374
front squat, 377–378
goblet squat, 375–376
ultra-deep, 370, 373
variations, 368
SSC. See Stretch shortening cycle Starch, 57, 222–224
Steak and potatoes, 489
Stearic acid (stearate), 75
Stiff-leg deadlift, 384
“Stop eating” signal, 218
Stress, 22, 31
brain response to, 143
gut inflammation from, 144
gut response to, 143
Stress, chronic, 265, 266, 271
brain
rewiring of, 273
transmitter-receiver connections, 272, 279
and brain training, 307
health-damaging and age-accelerating aspects, 289
physical changes, 279–281
higher threat perceptions, 279
non-threatening stimuli, 279
PFC and hippocampus functioning, 279
and premature aging, 288–289
and resistance, 287
rewires threat-stress circuitry, 278–280
self-treatment approaches, 285
structural and functional changes in the brain, 306
“Stress cup,” 206
concept of, 41
definition of, 38
lack of exercise and, 42–43
overflowing, 42
super-sizing, 44
use in daily life, 45
Stressed-out brain, 280
Stress reduction techniques, 44, 259–260
biofeedback, 301–303
HeartMath, 303
heart rate variability, 302
monitoring muscle tension and skin conductance, 302
muscle tension, 302
real-time information, 302
Stress-related behaviors, 289
Stress response
amygdala, 275
changing, 281
early life experiences, 284–285
high intensity. See Stress, chronic hippocampus, 275
HPA axis, 275
isolated, short-term, 271
nerves of steel/courageous/crazy, 283
prefrontal cortex (PFC), 275
rumination, 289
stop, 284
turned on, 284
Stress/threat system. See “Fight or flight” system Stretch shortening cycle, 370
Strong Medicine Defensive Tactics, 355
Sucrose, 56, 58
Sugar. See also Specific types cravings, 100
in energy drinks, 248
in fruit drinks, 248
in fruit juices, 248
in soft drinks, 247
Sulforaphane, 237–239
Sumo deadlift, 384–387
with barbell, 392
built-in sumo safety, 393
double kettlebell, 391
health benefits of, 384–385
hyperextended spine with, 393–394
poor descending technique with, 394
procedure, 386
single kettlebell, 390
starting position, 387
and sticking point, 389
sublime, 389
tactics, 388
Superset, 438
Supplement industry, 158
SweetBeat™, 553
Swelling (Tumor), 7, 8
SWS. See Slow wave sleep Sympathetic nervous system, 273, 295
functions of, 33
inflammation and oxidative stress by, 37
and PNS, interaction between, 35
short-term activation of, 286
Systemic inflammation, 136
T
Table sugar. See Sucrose Tai chi, 305
T-cells, 128
functions of, 8, 9
T1D. See Type 1 diabetes T2D. See Type 2 diabetes Telomeres, 197–199
TFA. See Trans fatty acids The Open-Focus Brain, 300
Threats, 38
to modern man, 31
to primitive man, 31
Three-dimensional proteins, 61–62
Tight junctions, 126
failure of, 129–130
TJ. See Tight junctions Training days, feeding in, 471–474
Trans fatty acids
double bond configuration, 92
as foreign invaders, 92
Transformational fitness template importance of, 436
seasonal “primordial cycling,” 442and superset, 438
weekly training regimen, 437, 439–441
Treg cells, 9, 128, 130–131
and gut bacteria, 149
T-regulatory cells. See Treg cells Triglycerides, 74, 242, 514–515, 531
medium-chain, 72
“Turbo boost” reflex, 370
Turmeric, 463
Type 1 diabetes
definition of, 124
and gluten free diet, 165–166
treatment of, 227
Type 2 diabetes
economic cost of, 180
fatty liver disease, obesity and LPS, link between, 154
medication for, 227
prevalence of, 180–181
and resistant insulin receptor, 182
restricting starchy carbohydrates and sugars in, 228
risk factor for, 181
Type 3 diabetes, 201
U
Ultra-deep squat, 370, 373
Under-nutrition, 25
Unhealthy obsession with weight, 535–540
Unsaturated fatty acid
double bonds, 79
and free radicals, 79
oxidation of double bonds in, 94
Unsaturated vegetable oils, hydrogenation of, 94
US Department of Agriculture organics, 448
V
Vaccenic acid, 95
Vagus nerve stimulation, 162
Vegetable shortenings, 94
Vegetarians, EPA and DHA needs of, 90
Very low density lipoprotein, 516
with more cholesterol as “cargo,” 518
normal, 519
packed with triglycerides, 518
transport of fat and cholesterol, 517–519
triglyceride-packed, 519
“Vigorous intensity,” 250
Visceral obesity, 178
Vitamin B-12 deficiency, 457
VLDL. See Very low density lipoprotein
W
Waist to height ratio, 535–540
“Warburg Effect,” 193
Weight, unhealthy obsession with Body Mass Index, 535–536
normal weight obesity, 536
scenario analysis for, 539–540
waist to height ratio, 535–540
Western diets
and dysbiosis, link between, 152–153
habits, 54
Western high technology, 293
Whole grains for diabetics, 226–227
Whole wheat, fiber in, 235
Y
Yin/yang concept, 36
Z
Zietgebers, 319
Zinc deficiency, 459–460
Zingiber officinale, 462
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