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Healing From

COVID Vaccine Side Effects


A Guide to Selecting Nutritional Support

August 10, 2022


Minor corrections on November 4, 2022

by Chris Masterjohn, PhD

COVID vaccines have been used all over the world. In the United States alone, 1,371,474
adverse events have been reported, with 56,021 listed as leading to permanent disability and
29,981 listed as leading to death. Not all of these reports represent cause-and-effect
relationships, and the purpose of this guide is not to provide a risk assessment that quantifies
the relative safety of different vaccines. Rather, the purpose of this guide is to help those who
believe they are suffering from post-vaccine side effects heal from them.

In the vaccine adverse event reporting system (VAERS), adverse event reports resemble
long-COVID in having high rates of fatigue, headache, trouble breathing, and coughing. They
differ in having far fewer reports of the loss of taste and smell, or mild cognitive impairment.
They stand out as having an entirely unique effect on women’s menstrual cycles, having a much
greater impact on heart inflammation and blood pressure, and leading to a far higher incidence
of debilitating neurological disorders. Published case reports support these disorders including
multiple sclerosis, generalized demyelination, aneurysmal subarachnoid hemorrhage, various
neuropathies, postural orthostatic tachycardia syndrome (POTS), and various types of neuralgia
and myelitis.

React19.org is a community of patients, researchers, and clinicians attempting to understand


and heal post-COVID vaccine side effects. I have no relation with this organization, and they
have not reviewed this protocol. In a React19 survey collecting responses from September,
2021, through March, 2022, the ten most common complaints were fatigue, exercise
intolerance, brain fog, heart palpitations, muscle weakness, tingling or numbness in the
extremities, dizziness, muscle aches, sleep disturbances, and joint pain.

Not far behind were shortness of breath, elevated heart rate, insomnia, nerve pain, headaches,
muscle twitching, feeling off balance or in motion while at rest, memory loss, tinnitus, severe
anxiety, visual disturbances, and abdominal pain. Hair loss was much more commonly reported
than in VAERS.

Unfortunately, only 30.5% of respondents reported that they were improving.

Copyright © Chris Masterjohn, 2022. All rights reserved. Not for distribution. Do not store this in the files of a public web site.
This guide is for educational purposes only and does not constitute medical or nutritional advice. Do not use these strategies as a
substitute for medical advice or treatment.
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This guide is for those who believe they could use more scientific guidance or new ideas to
improve faster, or to obtain improvement that has so far proved elusive.

Since there is very little research on post-COVID vaccine side effects and since there is a
general reluctance to acknowledge them, this guide is necessarily based on scientific best
guesses, and not validated treatments. Please always listen to your body, discuss what you
experience with your doctor, and when you’ve had enough experience with the protocol herein,
provide feedback using the protocol feedback survey. Be especially careful to review any
exercise or fasting protocol with your doctor before undertaking it. If anything causes you
adverse effects, stop it, and discuss it with your doctor, and let me know in a comment on
Substack.

This is not a promise of a cure. It is merely a contribution to the existing discussion on how to
better understand these side effects and heal from them. I hope with all my heart you find this a
valuable contribution to your healing journey.

Disclaimer
I have a PhD in Nutritional Sciences and my expertise is in performing and evaluating nutritional research.
I am not a medical doctor. This guide is meant for educational purposes only, and does not constitute
medical or nutritional advice or act as a substitute for seeking such advice from a qualified health
professional. It is not to be used to diagnose or treat any disease. Reading this guide does not establish a
doctor-patient, coach-client, or any other type of relationship between us, and you use anything learned
from this protocol at your own risk. In using this protocol, you agree to not hold me liable for any
consequences of what you learn. Please discuss everything herein with a caring health professional
before putting any of it into practice.

In order to make this guide easier to read, I have used a conversational tone in many places with
personal pronouns, such as “I” and “you.” This is meant only to make it more pleasant to read, and is not
meant to imply that the guide constitutes any form of advice, whether personal or general.

Copyright © Chris Masterjohn, 2022. All rights reserved. Not for distribution. Do not store this in the files of a public web site.
This guide is for educational purposes only and does not constitute medical or nutritional advice. Do not use these strategies as a
substitute for medical advice or treatment.
2
Table of Contents
The Protocol………………………………………………….…..3

The Science Behind This Protocol……………………………19

Staying in Touch and a Final Note…………………………….63

Appendix 1: Tissue-Specific Symptoms of Amyloidosis…….64

Appendix 2: How to Get Enough of Everything………………65

References……………………………………………………….66

The Big Picture


While this protocol emphasizes nutritional support for healing, it is important to remember that
good sleep, rest, healthy stress management, rich social connections, an enjoyable life, a
positive outlook, a sense of purpose, sunshine, fresh air, and exercise are all important to
staying healthy. When it comes to nutrition, any nutritional deficiency can hurt our health. To
make sure no stone goes unturned, please see Appendix 2: How to Get Enough of Everything
to make sure you are implementing this protocol against a background of a healthy and well
balanced diet.

The Protocol
To make this protocol easier to follow, all of the practical stuff is on top. The scientific justification
for each part of the protocol can be found in “The Science Behind This Protocol.”

While my analysis found that lipid nanoparticles are of toxicity concern at the doses used, my
comparison and contrast of the adverse effects of the natural virus with the vaccines, and of the
vaccines with each other, strongly supports spike protein toxicity and spike protein-generated
autoimmunity as the driver of most long-lasting adverse effects. This protocol therefore focuses
on these as the core issues.

The central thesis of this protocol is that not everyone suffering from post-COVID vaccine side
effects has the same problem. This is mainly because the spike protein is not distributed
through tissues in the same way in everyone, and because immune reactions to the spike
protein are not all the same. Therefore, there are multiple problems going on that are affecting
different people differently.

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This guide is for educational purposes only and does not constitute medical or nutritional advice. Do not use these strategies as a
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Often, the symptoms of different problems overlap. That is why labwork is essential to the
protocol.

The first task is to institute the Base Protocol, which is for everyone.

The second task is to run labwork to help classify yourself along four different axes:

● The Immunosuppressed Type vs the Autoimmune Type


● The Hyperpermeable Type vs the Hypertension Type
● The Clotting Type vs the Bleeding Type
● The presence or absence of the Leaky Membrane Type

Then, you will use your types to put together a unique protocol tailored specifically to your own
set of symptoms and lab results to best promote healing within your own body.

I recommend reading the entire protocol before you start, that way you know what is coming
ahead and why you are doing each step.

The Protocol | Table of Contents

Step 1: The Base Protocol……..……..……..……..……..……..……..……..4


Step 2: Labwork, The First Round…..……..……..……..……..……..………5
Step 3: Define Your Types…..……..……..……..……..……..……………….6
Step 4: Address Any Vitamin or Mineral Imbalances..……..……………….9
Step 5: Design Your Personal Protocol…..……..……..……..……………..11
Following Up……..……..……..……..……..……..……..………………….…18

Step 1: The Base Protocol


Vitamins A and D: 10,000 IU each, as retinol or retinyl palmitate, and as vitamin D3. Cod liver
oil may be used to supply all or a portion of the target. Liver is very rich in vitamin A. If you eat
liver, count each ounce as 5,000 IU of vitamin A.

Vitamins A and D synergistically support immune function. They increase the defense against
toxic things that do not belong in the body – like the COVID vaccine spike protein – while also
cooling down the flame of autoimmunity. They should always be taken with a meal, preferably a
big one that contains fat.

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This guide is for educational purposes only and does not constitute medical or nutritional advice. Do not use these strategies as a
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Vitamins A and D should be balanced with 200 micrograms per day of vitamin K2, preferably as
a mix of MK-7 and MK-4, and 20 IU of vitamin E as alpha-tocopherol (preferably with a
background of naturally occurring mixed tocopherols and tocotrienols). This helps make sure
there are no imbalances between the fat-soluble vitamins.

Omega-3 Fatty Acids: Either one or two servings of fatty fish per week, or cod liver oil or fish
oil that provides at least 300 milligrams of DHA per day. If you use cod liver oil, count its A and
D toward the target above.

Omega-3 fatty acids, particularly DHA, are involved in the resolution of inflammation.
Over-the-counter anti-inflammatories and even many herbs interfere with the inflammatory
process, but DHA does not. DHA provides a smooth transition away from inflammation as soon
as the body decides it is ready.

Step 2: Labwork, The First Round


To reduce variability and lab interferences, I recommend cutting out any biotin supplements with
doses greater than 300 micrograms for four days before any labwork; not taking any
supplements on the evening prior; and on the morning of, fasting from both food and
supplements.

Plasma Amino Acids: This can be ordered from major laboratories, and can also be found as
part of a bigger profile in functional medicine laboratories, such as the Genova NutrEval or
Metabolomix+. This looks for signs of suppressed T cells that would compromise your clearance
of the spike protein.

Labcorp ANA Profile 12: This first tests for anti-nuclear antibodies, which are usually high in
autoimmunity. If they are positive, it tests the twelve most common autoantibodies to help further
clarify the nature of the autoimmunity.

Angiotensin II: This test is especially important to understanding the cause of post-vaccine
blood pressure rises. However, it is also used to assess the probability that you need to follow
the hyperpermeability protocol, regardless of your blood pressure.

D-Dimer: This is a sign you have excess clotting going on.

Prothrombin Time: This is a sign you have deficient clotting.

Complete Metabolic Panel: This is used to look for signs your electrolytes are being messed
with. They are likely off if you are a “leaky membrane” type.

Quest Diagnostics Calcium, Total, RBCs: Elevated red blood cell calcium is a more
conclusive sign you are a “leaky membrane” type.

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5
Urine pH: This is tested at home, either with a pH meter, or with pH strips in the 3-5 and 5-8
ranges. It provides more insight into leaky membranes and electrolyte disturbances.

Serum Vitamin A: This may be used to revise your dose of vitamin A.

25(OH)D: This may be used to revise your dose of vitamin D.

Plasma Selenium: Your selenium level must be known before supplementing or altering your
diet around this mineral, and it could be extremely important to autoimmunity and
hyperpermeability.

Plasma Zinc: A minority of side effects may be due to inflammation hurting zinc status.

Serum Copper: Zinc supplementation can hurt copper status, and copper deficiency can hurt
iron handling. Copper itself is important to neurological and mood health.

Iron Panel (Serum Iron, TIBC, UIBC, Iron Saturation %), Ferritin, Transferrin: Some side
effects, especially hair loss, may be due to inflammation causing mishandling of iron.

CBC With Differential/Platelet: This helps better clarify iron handling.

Step 3: Define Your Types


Define yourself on all four axes. If nothing within that axis describes you, make a note of it. You
should have three or four “types” at the end, or in substitution of a type, a note that nothing on
that axis applies to you.

Axis 1: Immunotypes
If plasma arginine and tryptophan are toward the bottom of the normal range or below it, and
there is no other obvious explanation – such as you haven’t been eating protein and all of your
amino acids are low across the board – you are an Immunosuppressed Type. This makes it
more likely you have spike protein persisting in your body and causing toxicity.

If the ANA is positive, you are an Autoimmune Type. This makes it more likely you have an
immune reaction to the spike protein that is hurting your own body. This may be especially
important to neurological disorders and blood pressure.

If both are true, you are a Mixed Immunotype.

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This guide is for educational purposes only and does not constitute medical or nutritional advice. Do not use these strategies as a
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6
Axis 2: Hyperpermeable vs Hypertension

If your blood pressure is high and angiotensin II is high, you are a Hypertension Type.

The Hyperpermeable Type is not easily detected with lab work and needs to looked for using
symptoms:

● If you have a persistent fever over weeks or months, especially if it is combined with low
blood pressure, cardiac dysfunction, shortness of breath, and diarrhea, or you have
been diagnosed with multisystem inflammatory syndrome, then you are definitely
hyperpermeable type. If you have a persistent fever, please seek medical attention.

● If you have edema (swelling) of any tissues, any symptoms of pneumonia, or new-onset
eczema that gets worse with exposure to soap, these are strong indications you are a
hyperpermeable type.

● The following are less obvious but possible signs of this type: insomnia, anxiety,
palpitations, tingling and numbness, elevated heart rate, new-onset food allergies that
are very broad in their scope, or headaches.

Make an executive decision about whether you fit into the hyperpermeable type category.

If you are unsure based on symptoms alone, elevated angiotensin II would suggest you are not
in the hyperpermeable category.

If your hyperpermeability symptoms are strong and you also have elevated angiotensin II and
high blood pressure, you are a Mixed Hypertension/Hyperpermeable Type.

Axis 3: Clotting vs Bleeding

This type is defined exclusively on labwork, and not on whether you have bruises, nosebleeds
or bleeding gums.

If your D-Dimer is elevated, you are a Clotting Type.

This may explain fatigue, brain fog, weakness, headaches, dizziness, shortness of breath,
visual disturbances, nose bleeds, bleeding gums, heavy menstrual periods, and bruising.

If your prothrombin time is elevated, you are a Bleeding Type. This is not expected. If you are
in fact a bleeding type, do followup testing for protein induced by vitamin K absence or
antagonism (PIVKA). If it is elevated, add 200 micrograms of vitamin K1 to the vitamin K2
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This guide is for educational purposes only and does not constitute medical or nutritional advice. Do not use these strategies as a
substitute for medical advice or treatment.
7
already in the Base Protocol, and add additional leafy greens to your diet on a daily basis. If
PIVKA is not elevated, follow up with your doctor or a hematologist to find alternative causes. If
you find none, review the signs of amyloidosis in Appendix 1 and make a decision with your
doctor whether the symptoms are debilitating or concerning enough to warrant a biopsy to look
for amyloid plaques. If you find anything in this pursuit please let me know in the protocol
feedback survey.

Axis 4: The Leaky Membrane Type

If Quest Diagnostics Calcium, Total, RBCs shows elevated RBC calcium, you are a Leaky
Membrane Type.

You can be even more confident in this if you see any abnormalities in your sodium, potassium,
or total CO2 on the complete metabolic panel.

You can also be more confident in it if you test your urine pH upon waking and after meals and
find that it is consistently or erratically below 6.0 or above 7.2 throughout the day after eating
your first meal, or if it is below 5.0 upon waking.

If you suffer from muscle twitching or cramping, play around with different electrolytes. For
example, if your urine pH is low, try ¼ teaspoon or ½ teaspoon of baking soda. Try bringing your
dietary food-based potassium to five grams a day (use food, not supplements). Try salting your
food, drinking salted lemon water, or using LMNT. See if 300 or 400 milligrams of calcium or
magnesium citrate help. If your twitching is electrolyte-responsive, this is another hint you could
be a Leaky Membrane Type.

The most important finding is the RBC calcium, and without it, the other findings are less
certain.

This could explain fatigue, exercise intolerance, brain fog, heart palpitations, muscle weakness,
tingling or numbness in the extremities,or muscle twitching or cramping, and could make a
contribution to severe neurological disorders.

Save Your Types


Make a note of your type on each axis. You will put it to work in Step 5. First, however, it is time
to fix any nutritional imbalances uncovered by the labwork.

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This guide is for educational purposes only and does not constitute medical or nutritional advice. Do not use these strategies as a
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Step 4: Address Any Vitamin or Mineral Imbalances
It is incredibly important to fix any nutrient deficiencies or imbalances found before attempting
other parts of the protocol, especially the Fasting-Feeding Reset.

Vitamins A and D
Serum vitamin A should be maintained in the upper half of the normal range, and 25(OH)D
should be maintained in the 50-60 ng/mL range.

If serum vitamin A is above the top of the normal range, cut the dose in half. Eliminate the
vitamin A if serum levels are high and you newly develop nausea, vomiting, and headache, hair
loss, or scaling or chapped skin.

If the ANA Profile 12 is normal, and the 25(OH)D is above 70 ng/mL, cut the dose in half. If the
ANA Profile 12 shows autoimmunity, allow the 25(OH)D to remain high, but followup by
measuring serum and urine calcium, and cut back on the vitamin D if these are elevated.

Eliminate the vitamin D if serum calcium is elevated alongside 25(OH)D.

Maintaining proper status of vitamins A and D is especially important for clearing the spike
proteins and cooling autoimmunity.

Plasma Selenium
Plasma selenium should be 100-140 ng/mL. If it is below this range, supplement 100
micrograms per day as selenomethionine. If it is above this range, cut out all selenium
supplements and Brazil nuts, and aim for it to fall into the range over time.

This is especially important for hyperpermeability and autoimmunity.

Zinc

If plasma zinc is below the 90-120 microgram per deciliter range, supplement with 15 milligrams
four times a day, either on an empty stomach (at least 3 hours after the last meal and 1 hour
before the next meal) or with a meal that does not contain any coffee, whole grains, nuts, seeds,
or legumes. Be careful that this could cause deficiencies of copper and iron if you are not also
managing their status.

This is needed to support all of the functions of vitamins A and D, as well as most hormones,
and is especially likely to help with sore throat and diarrhea.

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Copper

If serum copper is in the bottom third of the normal range or below, supplement with 4 capsules
of Mitosynergy Mitoactivator Extra Strength per day, or one of the following: 8 ounces of liver per
week; two ounces per day of spirulina, shiitake mushrooms, or sesame seeds; or 3-4 ounces of
chocolate per day.

This is most likely to help with fatigue, trouble breathing, brain fog, memory or attention
problems, or hair loss. It also may help normalize any abnormalities in the iron bloodwork or
the white blood cell counts on the CBC.

Iron

Take the serum iron on the iron panel, and divide it by the transferrin measured separately,
and multiply this value by 70.9%. This is the transferrin saturation. The transferrin saturation
should be close in value to the iron saturation percentage from the iron panel. If it is not, it is
probably because albumin levels are altered, which can be measured separately. If they are in
close agreement, transferrin can be dropped from followup testing and the iron saturation can
be used. If they are not in agreement, use the transferrin saturation.

If transferrin saturation is below 30%, especially if hemoglobin, RBC, or hematocrit levels on


the CBC are low, this indicates functional iron deficiency. If ferritin is also low, this is likely a
case of frank iron deficiency. If ferritin is high, this is likely a case of anemia of chronic
disease. In either case, 18 milligrams per day iron bisglycinate should be used until the
transferrin saturation is brought into the 30-40% range and all of the anemia-related markers on
the CBC are normalized. This should ideally be taken with a meal rich in animal protein but
devoid of plants and egg whites.

Iron deficiency that proves resistant to supplementation might respond better to a strict
carnivore diet based on red meat and clams. If iron deficiency is still resistant to this and ferritin
is high, it is probably because hepcidin is persistently elevated, probably driven by high
interleukin-6 (IL-6). Fasting could be tried to liberate iron from ferritin. Other treatments could be
tried to lower IL-6 and hepcidin, such as two scoops of whey protein to provide iron-saturated
lactoferrin, 1000 milligrams per day of curcumin, or 1000 milligrams once or twice per day of
black seed oil. If this fails, iron infusion could be tried under medical supervision.

If the transferrin saturation is considerably above 40%, and the ferritin is high, and the
CBC is normal, this may be a case of iron overload. This interpretation is strengthened if the
skin color, if altered at all, is darker rather than paler; if muscle pain is a dominant symptom and
is accompanied by joint pain; and if iron supplementation worsens symptoms. In this case,
phlebotomy (blood donation, lab testing, or isolated phlebotomy for iron removal) can be tried.

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This guide is for educational purposes only and does not constitute medical or nutritional advice. Do not use these strategies as a
substitute for medical advice or treatment.
10
If the transferrin saturation is considerably above 40%, and the ferritin is high, and the
CBC presents obvious anemia (e.g., low red blood cells, hemoglobin, and hematocrit) and
other causes of anemia have been ruled out (e.g. zinc, copper, riboflavin, iodine, hypothyroidism
vitamin B6, vitamin C, vitamin A, vitamin E, selenium, folate, vitamin B12, genetic blood
disorders, etc), it may make sense to seek erythropoietin treatment under medical supervision.

Normalizing iron and anemia markers is most likely to help with fatigue, trouble breathing,
brain fog, memory or attention problems, or hair loss.

Step 5: Design Your Personal Protocol


Next you use your types from Step 3 to define your personal protocol. Take notes on your
phone, computer, or a piece of paper, and use this algorithm to choose which sub-protocols to
add to the Base Protocol:

● Immunosuppressed Types will use the T Cell Rejuvenation Protocol. Mixed


Immunotypes are given a variation of this.
● Autoimmune and Mixed Immunotypes will order the Autoimmune Nutritional
Bloodwork. Only after both the initial bloodwork and the autoimmune blood work has
been fully normalized will they then move on to the Immunological Variation of the
Fasting-Refeeding Reset.
● Hypertension Types can move on immediately to the Hypertension Protocol, in
addition to everything they are doing for their immunological type. Mixed
Hypertension/Hyperpermeable Types will not follow the Hypertension Protocol.
● Hyperpermeable Types and Mixed Hypertension/Hyperpermeable Types can move
on immediately to the Hyperpermeability Protocol, in addition to everything they are
doing for their immunotype.
● Leaky Membrane Types should first make sure they have resolved any abnormalities in
their initial blood work and then move on to the Cellular and Mitochondrial Variation of
the Fasting-Refeeding Reset. Those with neurological disorders regardless of their
type on this axis should also do the Fasting-Feeding Reset and should add the extra
suggestions in the Neurological Variation.

T Cell Rejuvenation Protocol

This is to be used by all Immunosuppressed Types. Those who suffer from herpes flareups
should omit the arginine and tryptophan. A variation for Mixed Immunotypes is discussed
below.

L-Arginine: 1.5 grams of L-arginine taken twice a day, for a total of 3 grams per day, with a full
glass of water on an empty stomach or before (but not during or after) a meal.

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This guide is for educational purposes only and does not constitute medical or nutritional advice. Do not use these strategies as a
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11
Caution: Omit arginine if you suffer from flareups of a herpes infection.

L-Tryptophan: 1.5 grams L-tryptophan taken twice a day, for a total of 3 grams per day, with a
full glass of water on an empty stomach or before (but not during or after) a meal.

Caution: Omit tryptophan if you suffer from flareups of a herpes infection.

N-acetylcysteine (NAC): 2 grams of NAC taken every 3 waking hours five times a day, with a
full glass of water on an empty stomach or before (but not during or after) a meal.

Glycine: 2.5 grams of glycine taken three times a day, with a full glass of water on an empty
stomach or before (but not during or after) a meal.

Alternatives to each 2.5-gram dose of glycine include 7.5 grams of collagen or gelatin, or
three-quarters cup of a well-gelled bone broth or a commercial bone broth that has been
standardized to contain 10 grams of protein per cup.

Caution: Some people may experience increased oxalate production with collagen, gelatin, or
bone broth, which could worsen the risk of kidney stones in vulnerable people. The best
defense against this is to make sure you are consuming 3 milligrams of vitamin B6 for every 100
grams of total protein (including the collagen). See “Appendix 2: How to Get Enough of
Everything” section for optimizing vitamin B6 using diet, or consider supplementing with 25
milligrams of vitamin B6 as pyridoxal 5’-phosphate once per week while using this approach.

Run a second amino acids test in 3 months. If things all look normal, you can reduce the doses
of these amino acids gradually over a week, and if you still feel good, move on from this
protocol. Do not start the Fasting-Refeeding Reset until you graduate from this protocol. Run the
followup labwork earlier if you are eager to try the Reset.

Mixed Immunotypes should try the above protocol at half the doses listed for a week and note
carefully whether symptoms improve, stay the same, or worsen. If they are improving or staying
the same, the full protocol should be used. If they stay the same, the full protocol should be
given a test run for three weeks and adopted if it leads to improvement. If they worsen, the
protocol should be stopped, and the vitamins A and D should be given more time to improve the
regulation of the immune system. After three months, if repeat labwork shows the pattern
persisting, the half-protocol can be tried again.

Autoimmune Nutritional Bloodwork


Autoimmune Types and Mixed Immunotypes should order this additional bloodwork, as it
uncovers deficiencies of nutrients involved in protecting against oxidative stress, which is a
major cause of the tissue damage that can light the flame of autoimmunity. Resolve anything on
this labwork before proceeding to the Fasting-Refeeding Reset.
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12
This includes the following labwork:

● Plasma vitamin E
● Lipid panel with cholesterol and triglycerides
● Plasma vitamin C
● Labcorp whole blood manganese or Quest RBC manganese
● LabCorp whole blood glutathione.

To reduce variability and lab interferences, I recommend cutting out any biotin supplements with
doses greater than 300 micrograms for four days before any labwork; not taking any
supplements on the evening prior; and on the morning of, fasting from both food and
supplements.

Plasma vitamin E should be in the normal range. However, if cholesterol or triglycerides are
substantially outside the normal range, they could be throwing the vitamin E measurement off.
For example, if one of those measurements is twice the top of the normal range, cut your
vitamin E measurement in half and see if it is still normal. If that adjustment makes it low, you
may need more vitamin E. Supplement with anywhere from 20-145 IU of alpha-tocopherol,
preferably on a background of mixed tocopherols and tocotrienols, until your vitamin E
measurements are normal.

Plasma vitamin C should be 45-90 uM (0.8-1.6 mg/dL). If it is low, supplement with 200 mg
vitamin C, preferably from a whole-food source, twice a day. Raise the dose over time if needed,
but this will be plenty for most people.

Whole blood or RBC manganese should be in the middle third of the normal range. Supplement
with 3 milligrams per day if it is lower than that.

Whole blood glutathione should be in the upper third of the normal range.

The shortcut to boosting glutathione is to supplement with 500-1500 milligrams of reduced


glutathione one to three times a day, on an empty stomach with a full glass of water or before a
meal but not during a meal. However, if you are a Mixed Immunotype and following the T Cell
Rejuvenation Protocol, the NAC and glycine are likely to improve your glutathione status over
time. Retest it in followup labwork and don’t worry about it now.

With that said, consider the following as extra ways to boost glutathione status.

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This guide is for educational purposes only and does not constitute medical or nutritional advice. Do not use these strategies as a
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13
These Glutathione-Boosting Behaviors May Help

These are a list of strategies to make sure you produce your own glutathione and maintain
healthy levels of it that go beyond the supplements listed above:

● Make sure to consume at least one gram of protein per kilogram of bodyweight or at
least a half gram of protein per pound of bodyweight.
● Keep diabetes well treated, and reverse type 2 diabetes if possible, and reverse any
signs of emerging pre-diabetes.
● Keep any thyroid, adrenal, or other metabolic disorder well treated.
● Eat a diet that keeps postprandial blood sugar under 140 mg/dL (7.7 mmol/L). Within
that constraint, eat freely of whole fruit and unrefined sweeteners, but use moderation
and steer very far away from 42% of calories coming from simple sugar. Within these
constraints, any increase in carbohydrate is likely to improve glutathione status by
increasing insulin.
● Don’t start a new milk habit while sick. If you use dairy products habitually, however, no
need to stop.
● Eat a diet very rich in low-sugar fruits, vegetables, herbs, and spices.

Hypertension Protocol
If you are a Hypertension Type, the following will help decrease your levels of angiotensin II
and lower your blood pressure. Do not follow this (specifically, do not add the fully cooked natto)
if you are a Mixed Hypertension/Hyperpermeable Type, until you finish resolving all
hyperpermeability symptoms with the Hyperpermeability Protocol below.

● Make sure to consume 1200 milligrams of calcium per day, preferably from whole
foods and spread evenly across meals. If needed, use a calcium citrate supplement.
● Eliminate all store-bought processed foods, including bread and cheese. Make these at
home if you want to eat them.
● Either eat 50-100 grams of fully cooked natto per day, or empty one capsule of 2000
FU (100 mg) nattokinase on top of your food before cooking and fully cook the
contents of the capsule. Raw natto, and uncooked nattokinase, will not lower
angiotensin II. Whether you use the food or the encapsulated enzyme, it must be fully
cooked through to at least 250 degrees Fahrenheit (121 Celsius) to work.

Hyperpermeability Protocol
Hyperpermeable Types and Mixed Hyperpermeable/Hypertension Types who are following
the T Cell Rejuvenation Protocol do not need glutathione support. Those who are not
following that protocol should take 1500 milligrams reduced glutathione three times a day,

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14
with a full glass of water, on an empty stomach, or before but not during a meal. Test one 500
milligram capsule first to make sure you respond well to it.

Hyperpermeable and Mixed Types should also try the following:

● Avoid sauna and uncomfortable heat exposure.

● Avoid ice baths and extreme cold exposure.

● Spend as much time outdoors in the sunlight as possible, with unprotected skin exposed
to the sun for at least part of it, but be extremely careful not to burn, to avoid any
sun-induced flushing of the skin, and to avoid feeling overheated. Start small, increase
gently, and try to emphasize the morning and evening when the sun isn’t too strong.

● Spend most of your time in a comfortably cool environment. Consider using mattress
coolers or cooling headbands such as those made by ChiliSleep.

● Review the These Glutathione-Boosting Behaviors May Help section to put them into
practice.

Clotting Protocol
Clotting types should supplement with 2000 FU (100 milligrams) nattokinase per day. If using a
higher dose, space the doses out every four hours. However, do not do this without letting your
doctor know, as it is important to make sure you don’t develop the opposite problem, a bleeding
disorder. In contrast to the Hypertension Protocol, the nattokinase must not be cooked with
food. 50-100 grams of raw natto may be substituted and it must be raw.

If you are also a Hypertension Type, combine both protocols so that you are using both cooked
and raw natto or both cooked and raw nattokinase.

The Fasting-Refeeding Reset

This reset is used by Autoimmune Types after they have normalized all their initial and
autoimmune labwork, Leaky Membrane Types and those with neurological disorders after
they have normalized all their initial labwork. Specific variations for these types are suggested at
the end. If you are an Immunosuppressed Type, you should run a second amino acids test
showing the original abnormalities have been resolved before starting the reset.

Caution: Always clear any fasting regimen or any exercise protocol with your doctor before
starting.

Caution: Children and pregnant or nursing mothers should not use the fasting protocol.
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15
First, choose an existing fasting program to adopt. If you are new to fasting and want to just get
your feet wet, try Valter Longo’s Fasting-Mimicking Diet. If you want to try something a little
more ambitious, try eating a “one meal a day” plan two or three times a week. You can even
incorporate longer multi-day fasts, but spend time reading about these and joining a community
first, as detailed guidance for fasting is beyond the scope of this protocol.

This reset starts with your choice of a fasting protocol, and then modifies it as follows:

● Make sure you put every bit as much emphasis on the refeeding phase as the fasting
phase. The fasting phase cleans house. The refeeding phase is where healing takes
place.

● During fasting periods, do at least 60-90 minutes of steady-paced, non-interval “zone 2”


cardio with no breaks. It is incredibly important to realize that if you suffer from exercise
intolerance, a zone 2 workout may simply be a gentle walk. This has to be adapted to
your abilities. The simple way to know you are in a zone 2 workout is if you find it
annoying but still possible to hold a conversation throughout the workout. Similarly, if you
are on the phone with someone, they can tell by your voice and your breathing that you
are working out. The more sophisticated way is to buy a lactate meter. Measure lactate
(with very clean hands!) before and after the workout. You want to stay beneath 2
millimoles per liter, but your workout should bring you to 0.3-0.5 millimoles per liter
above your baseline.

Emphasize rest during refeeding periods. The zone 2 workouts should be done 3-5
times per week, on average. If you are using a one meal a day plan, do them in the
fasted state and rest during your feeding period. If using multiple days per week of
fasting, do the workouts on the fasting days and rest on the refeeding days. If you are
not fasting often enough or in a pattern that allows 3-5 of these workouts during the
fasting periods, add additional workouts to feeding periods, but do them in the morning
before you eat.

● Take 1000 milligrams of resveratrol twice a day, 12 hours apart, on fasting days.

● When refeeding, eat a diet that has at least one third of the plate devoted to animal
protein, that provides at least 0.5 and ideally 1 gram of protein per pound of bodyweight
(multiply by 2.2 if you measure your weight in kilograms), that has whole-food starches
and/or fruits at every meal, and that provides enough calories that you regain any weight
you lost in the fasting phase. This is not a weight loss diet. Healing depends on proper
refeeding!

● When refeeding, do not take resveratrol.

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16
● Supplement with 150 milligrams of nicotinamide riboside per day during the refeeding
phase. You may increase this if you feel it benefits you, but be conservative. Take with a
meal.

● Supplement with 1600 milligrams per day of S-adenosylmethionine (SAMe), spread as


evenly as possible across meals, during the refeeding phase. Take before the meal with
a glass of water.

● Take 3 grams of L-arginine a day, preferably spread across two meals. Take with a full
glass of water before the meal.

● Take 9 grams of L-leucine a day, preferably spread across two or three meals. Take with
a full glass of water before the meal.
● This leucine will increase your need for biotin by 180 micrograms per day. See
“Appendix 2: How to Get Enough of Everything” for optimizing biotin with diet (the extra
180 micrograms listed here is over and above what that section says you otherwise
need), or supplement 5 milligrams (5,000 micrograms) of biotin once a week with a
meal. Make sure to stop the biotin at least four days before any labwork.

Combine the SAMe, arginine, and leucine for convenience.

Try this as often as it seems to help. Be gentle and gradual, listen to your body, discuss with
your doctor, but make it a lifestyle if it works.

Implement these variations according to your type:

The Immunological Reset

This uses the Fasting-Feeding Reset as described above. Just emphasize getting into it a little
faster and deeper if all your nutritional bloodwork looks good, because fasting has particularly
well supported promise as an immunological reset for adults.

The Cellular and Mitochondrial Reset

This uses the Fasting-Feeding Reset as described above, but emphasizes extreme caution that
if you are suffering from mitochondrial dysfunction the fasting portion may make you feel worse.

If you find that it is too much for you, focus on getting 4-5 60-minute zone 2 workouts per week.
Remember that a zone 2 workout may be a light walk for some people with health problems.
Calibrate the zone carefully. Do them in the morning before you eat, and rest once you’ve eaten.

One other suggestion for Leaky Membrane Types regardless of your participation in the
Fasting-Feeding Reset: avoid cold showers, ice baths, and other extreme cold exposure until
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17
you feel better. It could temporarily increase the leakiness of mitochondrial membranes and
potentially worsen the problem while healing.

The Neurological Reset

The neurological reset uses the Fasting-Feeding Reset as described above, with the following
additions:

● Add 1200 milligrams alpha-GPC a day during the refeeding phase. Use two 400
milligram doses at breakfast and the third 400 milligram dose at lunch.
● Use 240 milligrams of ginkgo biloba per day during the refeeding phase at breakfast.
● Experiment with increasing the amount of omega-3s in the Base Protocol to see if higher
doses help. Go slow and do not keep increasing if there is no benefit. Five grams per
day of total omega-3s is the maximum.

Following Up for Everyone


Followup labwork should be done by everyone quarterly, and should include everything that was
abnormal in the original labwork, as well as bloodwork for vitamins A and D to make sure no
toxicities develop.

If the algorithm did not direct you to the Fasting-Refeeding Reset, take some time to graduate
from the path it directed you on, and then feel free to join the Fasting-Feeding Reset when you
are done and feel you could use more healing.

Once you have enough experience with this protocol to provide feedback, please provide it
using the protocol feedback survey.

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This guide is for educational purposes only and does not constitute medical or nutritional advice. Do not use these strategies as a
substitute for medical advice or treatment.
18
The Science Behind This Protocol
Side effects to COVID vaccines could be driven by toxicity of the spike protein, toxicity of the
delivery vehicles or minor ingredients, or dysfunctional immune responses to any of these.

One set of clues we can use to tease out these hypotheses is to consider the differences
between the virus and the vaccines, and to similarly consider the differences between the
different vaccine technologies. If side effects are shared across them all, they are most likely
driven by what they share in common. If the side effects profiles differ among them, the
differences in side effects may be explained by the differences in their components and in how
they are distributed within the body.

The Science |Table of Contents

Components of the Natural Virus……..……..……..……..……..……..……..…….19


Components of the Vaccines……..……..……..……..……..……..……..………….20
Toxicity of the Vaccine Components…..……..……..……..……..………………….25
Immune Reactions to the Virus and the Vaccines..……..……..…………………..37
Comparing and Contrasting Adverse Effects of Vaccines vs Natural Infection….39
Comparing and Contrasting Adverse Effects of Different Vaccine Types………..46
What is Driving Vaccine Side Effects?…..……..……..……..……..……..…………51
How Do We Heal From Vaccine Side Effects?..……..……..……..……..…………52

Components of the Natural Virus


SARS-CoV-2, the virus that causes COVID-19 (hereafter called “COVID” and “the COVID virus”)
is a coronavirus. Coronaviruses are named after the Latin word corona meaning “crown”
because under electron microscopy the projections on their surface appear as a halo
reminiscent of a solar corona, which is the outermost layer of a star’s atmosphere. The virus has
a lipid envelope and a protein coat known as a nucleocapsid that it uses to transport the RNA
contained in its core. The RNA codes for numerous proteins the virus needs to replicate with the
help of human cellular machinery. Among these is the RNA for the spike protein, the most
important protein we need to understand for the disease process of the virus, and the only
protein we really need to understand when looking at the vaccines.

The spike protein is a spike-shaped protein that sticks out from the viral membrane and is
responsible for its ability to bind to, fuse with, and enter human cells. It does this by binding to
ACE2, a zinc-dependent enzyme on the surface of human cells.1 The normal function of this
enzyme is to convert angiotensin II to angiotensin(1-7). These are two compounds that regulate

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19
blood pressure and other aspects of physiology. ACE2 under normal circumstances is serving to
keep our blood pressure from raising too much by making this conversion.

The spike protein sees ACE2 as a “recpetor.”2 It first binds to ACE2, and this associates it with
the cell surface. Then, a human enzyme called “furin” splits the spike protein into two subunits,
one called S1 and the other called S2. Furin is not the only enzyme that does this, but it is
extremely ubiquitously expressed throughout human tissues, and because such a ubiquitous
enzyme can make this cleavage, the virus can be expansively broad in the number of tissues it
can infect. Thus, this cleavage site is named the “furin cleavage site” after the human enzyme.
Once the furin cleavage has taken place, a second cleavage breaks the S2 subunit into S2’ (“S2
prime”) and the “fusion peptide.” The spike protein then undergoes a change from a “prefusion”
state to a “postfusion” state that involves bending over backwards in a “jacknife” maneuver to
stick the fusion peptide in the membrane and fuse the two membranes together. Then, the virus
enters the cell.

Some, or perhaps much, of the free subunits can be shed into the circulation and go anywhere
once this happens. This is most often discussed for the S1 subunit and is called “S1 shedding.”

Note that the significance for the virus of the prefusion-postfusion transition is that this is
involved in entering the cell. However, vaccine manufacturers have an entirely different interest
in this transition: during it, sugars move from the inside of the spike protein’s three-dimensional
shape to the outside. This can block the immune system from recognizing it and make it less
stimulatory to the immune system; that is, less “immunogenic.” To lock it into the most
immunogenic shape, most vaccine spike proteins have been “prefusion stabilized.”

Components of the Vaccines

Spike Protein and Its mRNA and DNA


The mRNA (Moderna and Pfizer) and adenoviral vectored (Johnson and Johnson, hereafter
“J&J,” and AstraZeneca) vaccines all code for the spike protein with only one or two
modifications to the final protein, but substantial modifications to the underlying mRNA and
DNA. In the case of mRNA, which is easily attacked by the immune system when outside cells
and is normally degraded after a moderate amount of time within cells, the changes help the
mRNA evade the immune system and last longer. The adenoviral vectored vaccines deliver
DNA rather than mRNA. For both the mRNA and the DNA, the changes are made to make them
be expressed into protein at a higher rate.3–5

The much more recently authorized Novavax vaccine uses direct injection of the spike protein
into humans, rather than the DNA or mRNA that codes for the spike protein. Nevertheless,
because the protein is manufactured by inserting its DNA into a virus that infects insect cells,
the DNA used in production has been modified to be highly expressed in insect cells.6

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20
The Pfizer,7 Moderna,8 and AstraZeneca9 vaccines all retain the natural furin cleavage site,
while the J&J and Novavax vaccines have had it removed.6,9 The J&J and Novavax may be less
likely to shed the subunits into circulation than the others because of this. However, other
enzymes besides furin can split apart the spike protein. In fact, it was recently discovered that
neutrophils can digest spike protein into 98 different peptide fragments, three of which are
particularly toxic.10 So it may be that some tissues but not others have high rates of subunit
shedding and that neutrophils would be entirely capable of digesting it into further fragments.
The subunits and the neutrophil-digested fragments could then travel anywhere throughout the
body.

All but the Astrazeneca have been “prefusion stabilized.”11,12 This is meant to make them more
immunogenic. This should not impact spike protein toxicity. It would if the vaccine spikes were
delivered as viruses. While the adenoviral vectored vaccines are technically delivered as
viruses, they don’t have membranes that can fuse with human membranes, and they don’t carry
spike protein on their surfaces. Thus, any restriction the prefusion stabilization imposes on the
fusion peptide is irrelevant.

In terms of the actual biological activity of the spike protein, it should be nearly identical between
the virus and the vaccines. This was a major goal of vaccine development, and was supported
in the developmental research by showing that the vaccine spike proteins bind to ACE2 like the
natural virus does. In fact, the vaccine spike proteins bind to ACE2 more strongly than the spike
protein from the natural virus.3,6,13–16

In addition to these modifications to spike proteins or their coding nucleotides, the delivery
systems of the vaccines employ different technologies, all of which are absent in the natural
virus.

Lipid Nanoparticles

The Pfizer and Moderna vaccines are both mRNA vaccines that deliver mRNA using lipid
nanoparticles. The exact structure of lipid nanoparticles17 is debated within the literature and
discussed using theoretical models. They likely are similar to the lipoproteins that carry
cholesterol and fat-soluble vitamins in our blood, but several times smaller than an LDL particle
and have their cargo arranged differently on the inside.

“Cargo” will be generally used here as the word for the contents being carried and transported
by the particles. For the vaccines, the primary cargo is the mRNA.

Lipid nanoparticles are spherical. The outside is lined with phospholipids, which are
water-soluble on the outside and fat-soluble on the inside. This allows fat-soluble things to be
carried in the water-rich blood (this is why our lipoproteins have them), and allows material with
an electric charge (such as mRNA) to stay inside the particle rather than dissolving in the blood.

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21
Cholesterol stabilizes the membrane. Blended with the phospholipids are somewhat similar
lipids bearing positive charges (cationic lipids), and others decorated with some variant of
polyethylene glycol (PEGylated lipids). Water, sucrose, and various salts keep the pH and
osmotic pressure optimized.

The mRNA is found inside the particle. Because it is negatively charged, it is stabilized by
binding to the cationic lipids. The cationic and PEGylated lipids help the particles assemble
during production. During delivery, it is thought that the PEG keeps the particle in circulation for
longer while the cationic lipids help it get released inside cells by destabilizing the membranes
of the vesicles that take them in.

Pfizer and Moderna both use lipid nanoparticles, but they use different buffers, variants of PEG,
and cationic lipids.

A Pfizer document that was originally leaked was more recently released in a Freedom of
Information Act (FOIA) request in a more detailed and formalized yet heavily redacted form.18 In
this paper, lipid nanoparticles with a radioactive tracer were injected intramuscularly into rats
and the distribution of the tracer was monitored for 48 hours. The largest concentration of the
tracer was found at the injection site, but it accumulated at high concentrations in the liver,
adrenal glands, and ovaries, at somewhat lower concentrations in the bone marrow, and at
non-zero concentrations in every single organ tested.

This study used a labeled form of cholesterol that is unable to leave cells and can be detected
based on its radioactivity. If the cells take up the particles intact, then the label would tell us
exactly which cells were first to take it up. However, as covered below, it is possible that specific
components of the particles are exchanged with lipoproteins in the blood, or selectively
harvested by some cells, all without the intact particle being taken up. It is also possible that
specific components leave cells after being taken up. This study tells us nothing about these
processes. Therefore, it does not have the last word on how the cargo is distributed.

In another Pfizer document first leaked and then later FOIA'd,19 the nanoparticles were injected
into mice using a so-called reporter gene, which expresses the protein luciferase. When
activated, luciferase glows like a firefly, and researchers can determine where the luciferase
wound up based on which part of the animal is glowing. This doesn’t tell us where the spike
protein mRNA would go, because it is possible that the mRNA cargo has some influence on the
distribution, but it gets closer than the rat study.

It doesn’t provide so much as a useful hint, however, at how long the spike mRNA lasts,
because mRNAs for different genes are widely variable in their stability. This study did make it
clear that the luciferase is found in the liver at 6 hours and disappears after 48 hours, but it
didn’t clearly report whether the signal could be found in other organs. The graphics in the
document are heavily redacted, and the images were clearly selected from among a much

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22
larger collection of pictures. For reasons I have described elsewhere, my impression is they are
hiding pictures that show a signal in the ovaries.

There is no information available on how the specific cationic and PEGylated lipids in these two
vaccines impact their distribution within the body under different physiological states. However,
other research using these vehicles suggests that they exchange contents with lipoproteins in
the blood,20 that if they are injected systemically some 60% is taken up by the liver,21 and that
enzymes such as lipoprotein lipase (LPL) may be involved in harvesting their components.22
This is in addition to their more well-accepted path of cell entry, in which they are taken up intact
through processes known as endocytosis and macropinocytosis.

If, in fact, LPL plays a role in harvesting cargo from within these particles, it has enormous
implications its biodistribution:23

● It would mean that heart, skeletal muscle, and fat are major tissues that take up the
cargo.

● It would mean that LPL-expressing macrophages would actively bring the cargo into the
lungs.

● It would allow selective uptake in the brain, kidney, mammary gland, and likely other
tissues.

● In the fed state on a high-carbohydrate diet, less would be taken up by heart, skeletal
muscle, and kidney, and more would be taken up by fat tissue and lactating mammary
glands.

● In the fasting state, after exercise, during stress, or on a ketogenic diet, much more
would be taken up into the heart and skeletal muscle.

● If fat tissue acts as a sink in some people, it could act as a release valve later on,
potentially introducing a lot of variation in the duration of the contents between people.

The interaction with lipoproteins and enzymes can lead to selective transfer of specific
components, not transfer of the entire particle. This emphasizes that there could be alternative
patterns of distribution to those shown in the Pfizer rat study. It also underscores how widely
variable the distribution could be in different people during different physiological states.

To my knowledge, biodistribution studies for the Moderna vaccine are only available in
extremely summarized format in documents produced by regulatory agencies and cannot be
analyzed in the same way the Pfizer studies were above.

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23
Further, as discussed in the “Spike Protein mRNA and DNA” section, the spike protein can be
cleaved from cell membranes and the cleavage products can be distributed throughout the
body. This is not addressed at all in any of the biodistribution experiments.

Adenoviral Vectors
Adenoviral vectors24 are based on infectious viruses known as adenoviruses, which usually
cause colds or flu-like illnesses. They are so named because they were originally isolated from
adenoids (tonsils). They consist of double-stranded DNA inside a protein coat known as a
nucleocapsid that takes a 20-faced shape known as an icosahedron. The AstraZeneca vaccine
uses a vector derived from an adenovirus that infects chimpanzees, while the J&J vaccine uses
one derived from an adenovirus that infects humans. Their surfaces are highly negatively
charged, making them attracted to anything with a positive charge. This plays a role in a
particular form of thrombosis (clotting disorder) they have been associated with, which will be
discussed further later. Because they are derived from adenoviruses, antibodies to
adenoviruses with which one has been previously infected can make them less effective.

There are a rather large collection of molecules on a cell surface that can act as receptors for
adenoviruses or vectors derived from them,25 making the potential uptake by different tissues
hard to predict but certainly very broad.

In theory, these vectors are “replication incompetent” meaning they can’t reproduce like
infection-causing viruses. However, certain cell lines used in labs allow them to replicate, so it
may be that they replicate in humans in certain cells of certain tissues under certain
conditions.26 While these vaccines contain the DNA for the spike protein and that is the main
protein expressed in the cells they enter, there is low-level expression of the other viral proteins
in these cells.

To my knowledge, biodistribution studies for the adenoviral vectored vaccines are only available
in extremely summarized format in documents produced by regulatory agencies and cannot be
analyzed in the same way the Pfizer studies were above.

Further, as discussed in the “Spike Protein mRNA and DNA” section, the spike protein can be
cleaved from cell membranes and the cleavage products can be distributed throughout the
body. This is not addressed at all in any of the biodistribution experiments.

Novavax Adjuvant
For the Novavax vaccine, a virus is engineered to express the spike protein and is used to infect
insect cells. The spike protein is harvested from insect cells and then mixed with the other
ingredients of the vaccine. As a result of the manufacturing process, each dose has traces of
insect cell proteins (less than 1 microgram), lentil lectin (less than 25 nanograms), exceedingly
trace amounts of DNA from the virus and insect cells, and various processing chemicals at
low-microgram amounts. The main ingredient besides spike protein is the adjuvant, and these
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24
two are mixed together with phospholipids, cholesterol, buffers, and emulsifiers and then
injected intramuscularly.27

The adjuvant is called Matrix-M, and is derived from a fraction of chemicals known as saponins,
from the soapbark tree. This is an evergreen tree native to Chile. In mice, subcutaneous
injection recruits cells of both the innate and adaptive immune systems to the site of injection,
while very large doses cause inflammatory cytokines to increase in the blood.28

To my knowledge, no biodistribution studies are available in any form for this vaccine, not even
summaries in the FDA documentation.

Is There Graphene Oxide in the Vaccines?

One independent analysis found graphene oxide in at least some batches of Pfizer, Moderna,
and AstraZeneca, and found its possible presence in other batches of these as well as batches
of the J&J vaccine.29 The vaccine manufacturers deny the presence of graphene oxide in their
products. Graphene oxide is used in biomedical research for potential “nanomedicine”
treatments, as biosensors, and in a variety non-biological applications.30 The paper identifying it
in vaccines needs to be replicated before we can make it a major focus of our concern, but if
there are ingredients observable in the vaccines that the manufacturers deny, this needs to be
brought to light in an air-tight manner, confirmed by multiple independent parties.

Toxicity of the Vaccine Components

The Spike Protein and Its Subunits

The Spike Protein as a Pore-Forming Toxin


As I have covered in more detail elsewhere, the whole spike protein, and to a much greater
extent its S1 and S2 subunits, appear to act as pore-forming toxins that disrupt cellular
membranes and allow charged ions to cross them more freely.31–33

It is impossible to overstate the sheer breadth of cellular and organismal dysfunction this would
be expected to create.

One of the consequences is that it allows calcium ions to enter cells more easily. Calcium ions in
the general compartment of the cell, known as the cytosol, are normally kept at vanishingly low
concentrations so that, when they enter at certain times, they can be used as an activation
signal. For example:

● Inflammatory chemicals like histamine and bradykinin act by causing calcium to enter
endothelial cells – those that line the insides of blood vessels – and epithelial cells –

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25
those that line the other internal and external surfaces of the body and its organs. Thus,
pore-forming toxins imitate inflammatory processes without the need for cytokines and
immune cells. Nevertheless, by initiating the inflammatory process, the secretion of
inflammatory cytokines and the recruitment of immune cells will inevitably follow.

● Calcium entering endothelial cells in small amounts will cause nitric oxide to be made,
and it will dilate the blood vessels and lead to healthy blood pressure. Larger amounts,
however, lead to excessive vasodilation that can cause headaches or flushing of the
skin.

● In both endothelial and epithelial cells, larger amounts of calcium flowing in will lead to
even greater amounts of nitric oxide being produced, and this will cause the barriers
between the cells to open up. In many tissues, this causes edema, or swelling. In the
lungs, such swelling is a hallmark of pneumonia. In the brain, this process opens up the
blood-brain barrier. In the gut, it causes leaky gut. On the outside of the skin, it allows
toxins and skin bacteria to get into the skin and generate local inflammation, and allows
water to leave the skin, making it dry. When it happens to multiple organs at once, it
causes multisystem inflammatory syndrome.

● Calcium entering the end of a nerve cell causes neurotransmitter release.

● Calcium entering a muscle cell causes the muscle to contract.

● Calcium entering a platelet causes the clotting process to start.

● Calcium entering the mitochondrion, the so-called “powerhouse of the cell,” acts as a
danger signal that the mitochondrion uses to initiate a programmed cell suicide.

This is just the dysfunction we would expect from one single type of ion (calcium) crossing a
membrane when it is not supposed to. We could add to this that if a pore-forming toxin messes
with sodium and potassium transport along a nerve fiber, it could stop the transmission of a
signal. But if it allows calcium to enter at the end of the fiber, it could start a signal that doesn’t
belong.

If it allows hydrogen ions to cross the inner membrane of the mitochondrion, at low levels it
would simply generate more heat; at high levels, it would crush the ability to make ATP – the
general energy currency of the cell – leading to fatigue. Worse, since ATP is what is constantly
used to power the pumping of ions across membranes, the loss of ATP would dramatically
synergize with the pore-forming toxin effect, since cells would be less able to resist the inflow of
ions by pumping them back across membranes.

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26
In neurons, this would lead to imbalances of electrolytes needed to clear glutamate from
synapses, and the resulting imbalance of glutamate and GABA could lead to seizures and
demyelinating disorders.

We can take literally any physiological process, and at the center of it, we would be describing
how, from start to finish, the ability of cell membranes to keep certain substances on one side
and others on the other side is the central theme of how the process is orchestrated.

The spike protein experiments cited above show the following effects:

● The pore-forming toxin role appears to start at concentrations at least as low as 0.1
nanomoles per liter of S1 or S2.
● Recruitment of inflammatory cells is elicited at least as low as 10 nanomoles per liter of
S1 or S2.
● Mitochondrial impairment and fragmentation occur at least as low as 50 nanomoles per
liter of S1.
● Rampant cell death occurs within 24 hours when concentrations are between 1000 and
2000 nanomoles per liter of S1.
● COVID-like illness, lung damage, and cytokine storm occur when 10 micrograms of S1
are blown into the lungs of mice.

The concentration of S1 in the plasma following Moderna injection is, on average, about 125
times lower than 0.1 nanomoles per liter, and, at maximum, 52 times lower.34 However, the
concentrations in cells have never been reported. If the subunits are slipping into cell
membranes, cell membranes could act as a sink for the subunits, keeping circulating
concentrations misleadingly low.

The best study to use for extrapolation to humans is the mouse study with 10 micrograms blown
into the lungs. The mice received 400 micrograms per kilogram bodyweight. For a 70-kilogram
standard reference man, this is the equivalent of 28 milligrams. For the average 197.9-pound
male, we get 36 milligrams. For an average adult woman weighing 166.2 pounds, we get 30
milligrams. However, standard risk assessment methodology would divide the dose by 12 to
adjust for surface area differences between mice and humans, by 10 to adjust for variation
among humans, and by 10 again for this being a short-term study.35 Dividing by 1200 would
yield doses of 2.3-3 micrograms. Since the vaccine mRNA persists in humans for at least 37
days36 I calculated elsewhere that a single shot of Moderna may yield 247-1,135 milligrams of
total spike protein, and a single shot of Pfizer may generate 75-340 milligrams. If we use the
Pfizer rat study showing 0.178% of the radiotracer in the lipid nanoparticles reached the lungs,18
we could expect anywhere from 0.13-2.0 milligrams of spike protein to reach the lungs of
humans. This is the equivalent of 130-2,000 micrograms and is in considerable excess of the
2.3-3.0 micrograms needed to warrant a safety concern.

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27
Moreover, the quantity of spike protein that reaches the lungs after vaccination is completely
unknown, as no true biodistribution studies exist, and LPL-expressing macrophages in the lungs
could selectively harvest cargo from the nanoparticles at rates that exceed those implied by the
tracer studies.

Biodistribution data for the other vaccines have not been made public. No data exist to my
knowledge on how long the adenoviral vectored DNA persists in human cells, making it much
harder to generate an estimate of the cumulative spike protein produced.

Novavax comes in two doses of 5 micrograms of spike protein each. While I am not aware of
any data on its biodistribution, this exceeds the amount needed for safety concern if half it winds
up in the lungs. While I doubt half of it winds up in the lungs, the lack of biodistribution data
warrants more caution, not less.

The Spike Protein Causes Breakdown-Resistant, Amyloid-Type Clots

Initiating blood clots is a general feature of pore-forming toxins, although some of these toxins
also destabilize clots once they are formed.37 The spike protein, however, causes blood clots
that are denser than normal clots, resistant to being broken down, and characterized by the
branched fibrils.38 These fibrils are made of fibrin, the main protein component of a blood clot.
Fibrils are nano-sized fibers, and this branched fibril structure is known as amyloid. Neutrophils
can break the spike protein into 98 fragments, three of which form amyloid fibrils on their own.10
When mixed with blood, these fragments are particularly potent at making breakdown-resistant
clots.

There are two issues here, one of amyloid clots, and the other of amyloid made from spike
protein alone. We tackle the clots first.

Formation of amyloid clots can occur in a rare genetic disorder of clotting proteins.
Beta-amyloid, a protein associated with Alzeihmer’s disease, can make fibrin clots take on an
amyloid structure and cause breakdown-resistant clots to occur in the local blood supply of the
brain. Such structures for fibrin clots have also been shown in female migraine-with-aura,
diabetes, and stroke, and other causes include bacterial components (including, but not limited
to lipopolysaccharide or LPS), oxidative stress, and high levels of free iron.39–41

Although these clots are difficult to break down, it probably just takes more enzymes and more
time. One study of acute COVID and long-COVID patients found that the amyloid-containing,
spike-induced, breakdown-resistant microclots in their blood could be dissolved with the enzyme
trypsin after two treatments.42 Spike-free blood had its clots broken down after a single trypsin
treatment. Similarly, when an Alzheimer’s-related peptide is used to make amyloid clots, this
increases the time it takes to completely dissolve the clots with enzymes by 35%.43 So, more
enzymes and more time, and the spike-containing clots do indeed get broken down, even if they
are forming amyloid fibrils.
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28
The lowest concentration used to show the amyloid clot formation is 1 nanogram per
milliliter,10,38 which is about ten times the concentration found in the blood after the Moderna
vaccine.34 The concentration needed for this might actually be vanishingly small. Other studies
have used lipopolysaccharide (LPS), a component of bacterial cell walls, to do this, and found
that it only takes one molecule of LPS to coordinate 100 million molecules of fibrin into amyloid
form.44 This is probably because blood clotting is normally an auto-catalytic process, where the
formation of a clot begets extension of the clot. If it starts out misformed, it seems to continue
misformed.

There are no studies in live animals we can use to determine what dose of spike protein is likely
to cause problems in humans, but it is likely to be exceedingly low, as supported by clotting
being elevated two months out in 25.3% of recovered COVID patients.45

Can the Spike Protein Cause Systemic Amyloidosis?

One disturbing feature mentioned in the last section is the ability of three fragments of the spike
protein created during its digestion by neutrophils to create amyloid fibrils all on their own.10
These authors noted that all common coronaviruses that infect humans have sequences that
predict amyloid formation. However, COVID vaccines are the first time we have ever injected
these proteins into people, bypassing the normal mucosal barriers.

Typical amyloid proteins make fibrils on the order of 10-20 nanometers in diameter, whereas
diabetes and other inflammatory diseases are usually accompanied by fibrin clots with fibril
diameters closer to 40 nanometers.40 The spike protein paper did not estimate the diameter,10
but when I used a ruler and the scale in the legend of their abstract graphic to estimate it, I
came up with a diameter in the 10-20 nanometer range. Thus, the amyloid formed from
neutrophil-digested spike protein resembles typical amyloid proteins more than it resembles
anomalous amyloid clots.

Could these spike-only amyloid fibrils deposit in tissues?

Many chronic diseases involve deposition of amyloid proteins in specific organs: Alzheimer’s in
many parts of the brain; Parkinson’s in a specific part of the brain where dopamine is involved in
controlling movements; or type 2 diabetes in the pancreas.40 Amyloid fibrils overlap with prion
diseases: prions are misfolded proteins that are autocatalytic, meaning they spread their own
misfoldedness to other proteins in a domino effect. Prions often form amyloid fibrils. Amyloid
proteins can also circulate systemically and deposit in many organs simultaneously. When
amyloidosis becomes systemic,46 it typically causes decreased clotting as a result of amyloid
deposits in the liver that damage the production of clotting factors. This can lead to spontaneous
bleeding, internal or external. It can cause high blood pressure when deposits are laid down in
the kidneys. If the deposits impact the nervous system, blood pressure can go up or down, but
the telltale sign is the change is caused by standing, and is therefore “postural” or “orthostatic.”
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29
Other signs of systemic amyloidosis are shortness of breath or dry cough; swelling; disturbance
in the rhythm of the heart; pain, tingling, or numbness, typically beginning in the feet or legs;
autonomic dysfunction, leading to erectile dysfunction, dysregulated urination or defecation, or
getting full without having eaten enough food; an enlarged tongue, difficulty swallowing, dry
mouth, or cramping jaws; bruising without trauma; or joint problems, including carpal tunnel.

Many of these line up with reported vaccine side effects. Others are not commonly reported, and
the decreased clotting usually found when amyloid deposits in the liver is at odds with the
tendency for COVID and COVID vaccines to both cause thrombosis, and the likelihood that the
liver is a major organ that takes up the lipid nanoparticles. Nevertheless, too little is known
about how the spike protein, its subunits, its fragments, and its amyloid fibrils distribute
throughout the body to rule it out. It may be that this happens in a certain subset of people.

The concentration of spike protein used to form amyloid fibrils is 0.1 milligrams per milliliter,10
which is one million times higher than the concentration of S1 found circulating in the blood after
the Moderna vaccine.34 Therefore, this route of inquiry needs more research to substantiate it as
a likely cause of vaccine side effects, but we should be on the lookout for any clues that arise.

Spike Protein: The Vaccine Vs. The Virus


In the “Components of the Vaccines” section, we covered why the biological activity of spike
protein from the virus or from the vaccines should be more or less identical.

The difference is in how they are distributed.

In a respiratory illness, your first line of defense is the physical barriers of your epithelial tissues,
which are designed to keep bad things out and get good things in. The second line of defense is
your mucosal immune system. This responds locally to pathogens without needing assistance
from the systemic immune system to get its job started. Some immunity preexists in the form of
innate immune cells or non-inflammatory antibodies known as IgA that happen to be generally
polyreactive (they respond to many things) or happen to be cross-reactive with the new illness
(for example, antibodies from a cold that happen to also respond somewhat to COVID). On an
as-needed basis, the mucosal immune system can develop more inflammatory responses, and
can get assistance from the systemic immune system, which can launch a whole-body
mobilization of resources.

Even when the systemic immune system has joined forces, it has as a major objective to not let
the pathogen inside the body. If a pathogen is on the surface of the skin, eyes, nose, mouth,
throat, lungs, or digestive tract, it technically is outside the body. Once it crosses the mucosa
and mounts an invasion in the blood or the internal organs nourished by the blood, things have
gotten much more serious.

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30
So, when people get a natural infection, the spike protein is definitely present in their mucosa,
but it is unlikely to penetrate that barrier except in severe cases.

By contrast, the vaccines are injected into the muscle of the shoulder. This completely bypasses
the mucous membranes and places the spike protein firmly inside the body.

This general framework is supported by studies on the blood levels of spike protein or its mRNA
in those with natural infection or vaccination.

In a small study of 64 hospitalized COVID patients, circulating viral proteins – in most patients,
including the spike protein – were found in 79% of those who were admitted into the ICU but
only 48% of those were hospitalized but never critical.47 A broader study of 104 COVID patients
included more categories of illness, but looked for viral RNA instead of viral proteins.48 The RNA
was found in the blood of 44% of those on a ventilator, 27% of those hospitalized, and 13% of
those treated as outpatients. Taken together, these studies suggest that the virus and its
proteins enter the blood primarily in severe disease, and only in a small minority of cases in mild
disease. Presumably, in those who get infected but never officially diagnosed, this happens
rarely.

In a small study of 13 patients who received the Moderna vaccine,12 of them (92.3%) had
circulating spike protein in their blood.34 The only patient who did not have any detectable spike
protein in their blood had an extremely rapid induction of high levels of anti-spike antibodies
upon vaccination. In all subjects, the spike protein was undetectable from 2 weeks after the first
dose onward. Even the second dose did not make spike protein reappear in the blood.

The authors interpreted this as the spike protein being “cleared” by the antibodies. However,
another study found that antibodies interfere with the detection of spike protein.36 This means
that the spike protein probably was never “cleared” from the blood. Rather, the rise in antibodies
made it impossible to detect.

Similarly, the single subject who had no detectable spike protein in their blood probably did have
spike protein in their blood: it just wasn’t detectable because their rapid rise in antibodies
interfered with the lab assay.

While antibodies binding to the spike protein are likely to protect it from binding to other things,
and therefore to protect it from causing harm, it doesn’t follow that because they have rendered
it undetectable that they have also rendered it harmless. They may be transiently binding to it,
grabbing it and letting it go in a back-and-forth manner. If they do this enough, they can jam up
the lab assay, but in the “letting go” phase the spike protein can still do some harm. In fact, it
could be constantly slipping from the blood into cell membranes, where it will no longer have
any chance of being detected in blood, yet actively doing the most damage.

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31
Thus, the difference between natural infection and vaccination for the spike protein is that in
natural infection it is usually isolated by the mucosal barriers, though it commonly crosses those
barriers in severe cases; with the vaccines, by contrast, systemic circulation is virtually
guaranteed.

How Long Does the Vaccine Spike Protein Stay in the Body?

Both the spike protein and its mRNA have been found in the lymph nodes of the armpits of
vaccinated individuals 60 days after vaccination.36 The S2 subunit has been found circulating on
membrane-bound vesicles that leave cells known as exosomes.49 It peaks around day 14 or
some time thereafter, and by four months it has declined from its peak but continues to persist.
No studies have adequately shown a time point after vaccination when spike protein is no
longer found.

One paper provided evidence that the mRNA from the Pfizer gene can be written into the
genome.50 I have some issues with this paper that have not been resolved, and I do not
consider it the last word on the topic by any stretch. However, it is an important finding. There is
also evidence for this with the natural virus.51

One criticism of this paper is that they did not show the DNA gets integrated into the
chromosomes. While that would make the finding even more concerning, it doesn’t matter much
to the overall point. DNA can exist as stable circular structures outside of the chromosomes and
be expressed. This DNA can even be inherited by daughter cells as parent cells divide.52–55

If the mRNA can be written into the genome in certain cells, this is equally concerning for the
adenoviral vector vaccines. Their DNA is meant to make mRNA. If the spike mRNA can be
reverse transcribed, it shouldn’t matter how it got into the cell. Furthermore, the DNA itself has
no self-destruct button. Why would it disappear after being stably expressed?

The only vaccine in our discussion that should be immune to this is the Novavax vaccine, since
it uses two doses of 5 micrograms of spike protein with no intentionally included spike DNA or
mRNA. However, there are minor traces of DNA and RNA in Novavax, so it is not inconceivable
that this process could be relevant.

One criticism of the idea of spike persistence is that none of these papers have shown
full-length spike protein on the surface of human cells lasting months. It may just be that the
spike protein is no longer produced and bits and pieces of it are flying around. The jury is out on
this, but bits and pieces are the worst part of the spike protein. As covered in the sections
above, the subunits are more toxic than the whole protein, and the amyloidogenic fragments
produced by neutrophils might be the worst.

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32
The standard view is that, once a human cell is producing spike protein, it will endure only as
long as needed to generate an immune response. Once that happens, T cells will recognize any
cell presenting spike protein on its surface and destroy it.50

According to this view, lasting side effects would be far more likely to be driven by dysfunctional
immune responses than persistent spike protein toxicity.

However, support for both of these phenomena can be found.

In a case of fulminant myocarditis emerging 24 days after the second dose of Pfizer, spike
protein was found in biopsied heart muscle, alongside T cells and neutrophils.56 This supports
persistent spike protein toxicity.

In a fatal case of COVID-like ARDS caused by the Moderna vaccine, inflammatory cells were
found but no spike protein was found in the patient’s lungs.57 However, the spike protein
produced elsewhere may have created systemic hyperinflammation, or the spike protein may
have been in the lungs earlier on but been eliminated by the inflammatory response.
Regardless, this is a case where the inflammation clearly created the fatal problem rather than
spike protein toxicity.

In a case of hepatitis following Pfizer vaccination,58 liver biopsy showed infiltration of


vaccine-induced, anti-spike, killer T cells. Spike protein was not found in his liver, probably
because it had been routed out by the T cells. The T cells had taken up permanent or
semi-permanent residence and stayed there throughout the period of observation. He only
stably improved after systemic immunosuppressive therapy. The anti-spike T cells stayed in his
liver the entire time, but lost their “killer” phenotype under immunosuppressive therapy. Loss of
the killer phenotype appeared to drive his clinical improvement. This supports the conventional
model wherein T cells kill anything expressing a spike protein, and it is their hyperactivity hurting
organ function by killing human cells.

My suspicion is that there are two major subtypes of post-COVID vaccine syndrome. In one
subset, the antibody and T cell response is inadequate to clear the spike protein; these patients
have spike protein toxicity as a dominant problem. In the second subset, antibody or T cell
responses are hyperactive. They have cleared the spike protein, but they have created
excessive tissue damage and generated an autoimmune response in the process.

Support for this general idea can be found in long-COVID patients. The most important study on
persisting antigen to date in naturally infected patients was a series of irritable bowel disease
(IBD) patients.59 46 IBD patients who had previously tested positive for COVID came in for an
endoscopy related to their IBD. The endoscopies were, on average, 7.3 months from their
positive test. 59% of the patients were in remission as far as their IBD was concerned. Although
viral RNA could not be found in their stool, it was found in biopsied gut tissue in 70% of the
patients. In all of the patients whose gut tissue tested positive for viral RNA, the gut tissue also

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33
tested positive for viral proteins. However, in no cases could replicable virus be found. In other
words, there is no chronic infection, but there is a lingering presence of bits and pieces of the
viral proteins.

Strikingly, 46% of the patients reported long-COVID symptoms and all of them showed presence
of persistent viral antigen. In trying to explain why the viral antigens persist in some but not
others, they found that low levels of anti-nucleocapsid antibodies were associated with antigen
persistence. They also noted that patients who used immunosuppressive drugs that block the
inflammatory cytokine tumor necrosis alpha (TNF-alpha) had impaired T cell responses to the
nucleocapsid protein.

Notably, these are naturally infected patients, so they have several differences with uninfected
vaccinated patients: they have nucleocapsid antigen, which is not generated by the vaccines,
but which has also been shown to be toxic in animal studies;60 and the antigen is in their gut,
which is “outside” the body on the “other” side of the mucosal barrier.

Still, it is striking that persistent long-COVID symptoms in these patients required a deficient
immune response and the persistence of toxic protein.

It is also incredibly informative that there is a relatively immunodeficient phenotype that appears
to be the primary driver of persistent viral proteins.

Presumably, in uninfected vaccinated patients, the persistence of spike protein in the body is
determined by an inadequate antibody and T cell response to it, just like in these long-COVID
patients.

One interesting finding buried in the tables of that paper and never discussed in the text is that
vaccinated people were twice as likely as unvaccinated people to have persistent viral proteins
in their gut. It may be that the vaccines mount a response so biased toward the spike protein
that they leave the nucleocapsid behind, or it may be that there are immunosuppressive effects
of the vaccines, which will be covered later.

Lipid Nanoparticles

PEG is widely used in cosmetics, many people have antibodies to it, and some people are
allergic to it. PEG and cationic lipids are both inflammatory and serve as adjuvants in the mRNA
vaccines. One study showed that the lipid nanoparticles on their own cause intense
inflammation if injected into the skin of mice. If inhaled, a sufficiently high dose will kill 100% of
mice.61 At a lower dose that only killed 20% of the mice, the surviving mice appeared to fully
recover in four to eight days. This suggests the problem is acute inflammation rather than
lasting toxicity. The inflamed tissue featured a dramatic rise in neutrophils and eosinophils.

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34
In the Pfizer rat study discussed above,18 they injected the animals with enough lipid
nanoparticles to yield the equivalent of 50 or 100 micrograms of vaccine mRNA. The high dose
was used first, then when toxicity was observed, the protocol was altered and the lower dose
was introduced. The high dose was only used in males. The low dose was used in both males
and females.

At the high dose, all the animals stopped eating and lost weight within 24 hours. By 30 hours,
three out of 21 animals were hunched over with their fur standing up straight, and remained like
that until the experiment ended at 48 hours, at which point all the animals were killed to examine
their tissues. One of them, however, was hypersensitive to noise stimulus and was killed at the
30-hour point to prevent further suffering. “Prominent lobular architecture” was found in his liver,
but they do not elaborate on this.

At the low dose, all male rats were fine.

However, one out of 21 female rats was moving less and breathing irregularly at 30 hours, and
at 48 hours was hunched over with her hair standing up straight.

There could be sex differences, but due to the difference in bodyweights between the male and
female rats, this isn’t clear. The fact that only one out of 21 female rats showed symptoms
suggests that her dose was very close to the lowest dose capable of causing those effects.
Therefore, I believe we should simply pool the male and female data with the doses adjusted to
bodyweight. The lowest dose where an adverse effect is observed is the 50 microgram female
dose, while the highest dose where no adverse effects are observed is the 50 microgram male
dose. Thus, the upper limit of safe dosing should be derived from the low male dose.

Standard risk assessment procedure calls for dividing the body weight-adjusted dose by 6 to
account for surface area differences between rats and humans, by 10 to account for variation
among humans, and by 10 to account for this being a short-term study.35 The average body
weight of the male rats was 244 grams. Dividing the dose by 600 and by bodyweight yields
0.341 micrograms per kilogram bodyweight. For the 70-kilogram “standard reference man,” the
upper limit would be 23.9 micrograms. For the average 197.9-pound male, it would be 30.7
micrograms. For an average adult woman weighing 166.2 pounds, it would be 25.8 micrograms.
Thus, the standard dose of Pfizer vaccine providing 30 micrograms of mRNA just barely falls
within a reasonable upper limit for an average-weight adult male and exceeds that limit for
leaner males and for women.

This is concerning because it doesn’t account for repeated dosing in even the two-dose “fully
vaccinated” model let alone booster shots. The European Medicines Agency estimated that half
of the lipid nanoparticles would be removed from the body in 1-2 months and 95% of them
would be removed in 4-5 months.62 Thus, the second dose in particular is raising the cumulative
exposure to lipid nanoparticles very high, as it is adding a new dose when less than half of the
first dose has been eliminated.

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35
This raises an important question: what made the rats stop eating, in some cases hunched over
with their fur standing up, made one male become hypersensitive to noise, and caused one
female to breathe irregularly? If this was acute inflammation of the type that occurred in the
mouse study, it may resolve within days rather than being related to the long-term cumulative
dose. If, however, it was a classical cumulative dose-dependent toxicity, it may play a role in
long-term vaccine side effects and imply a cumulative risk with successive booster shots.

Importantly, allergies to lipid nanoparticles would not be as strictly dose-dependent as toxicity,


so these particles are likely to cause allergic reactions in a subset of people.

Adenoviral Vectors

Adenoviral vectors are highly inflammatory adjuvants that carry a risk of adverse inflammatory
reactions, but the risk that has been most well established is their promotion of thrombosis. This
is because they are highly negatively charged, so they can bind to positively charged molecules
and generate autoimmune antibodies to them. Specifically, they can bind to and create
antibodies to platelet factor 4. This plays a role in “vaccine-induced immune thrombotic
thrombocytopenia,”63 which is discussed further in the “Comparing and Contrasting Adverse
Effects of Different Vaccine Types” section.

Graphene Oxide?
The presence of graphene oxide has been alleged by one group29 and denied by the
manufacturers. Graphene oxide is not ready for medical applications and the means of
protecting against its toxicity are poorly understood.64 It can cause thrombosis as well as
hemolysis of red blood cells. From the bloodstream, it preferentially accumulates in the liver,
spleen, and especially the lungs. In the lungs, it causes pulmonary edema and fibrosis – typical
of severe COVID pneumonia. Remarkably, it has even been shown to bind to platelet factor 4,
the same problem identified for adenoviral vectors and thought to be the cause of
vaccine-induced immune thrombotic thrombocytopenia.

Graphene oxide is mainly eliminated by macrophages, whose development is dependent on


vitamin D. The vitamin D used in this protocol may be protective, if indeed this is a real risk.

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36
Immune Reactions to the Virus and the Vaccines
A few differences in the immune response to the virus and to the various vaccines are worth
noting.

Moderna is Most Immunogenic


When comparing the four major vaccines, the greatest antibody response is for Moderna; Pfizer
is second; next is AstraZeneca; J&J has the least and most variable response, largely driven by
low responses in older people.65

When comparing Moderna, Pfizer, and J&J, Moderna has the greatest antibody durability over
time, J&J the least. Moderna stands out as having much better T cell durability than Pfizer or
J&J.66

This is important because if antibodies bind to spike protein subunits, they are the best defense
against their toxicity. If T cells eliminate infected cells, they are the best way to clear out the
production of spike protein.

If we see hints that some side effects are worse with Pfizer than Moderna, this may represent a
modestly well controlled inference that a more robust immune response helps control the side
effects.

IL-6 vs IFN-Gamma

The inflammatory cytokine interleukin-6 (IL-6) is on average nearly doubled in moderate COVID
patients and nearly quadrupled in critical patients.67 Those with mild symptoms often do not
have elevated IL-6, but those that do have a sustained rise throughout the first week of
infection.68 In severe cases that recover, IL-6 remains doubled for at least two months.69 By
contrast, IL-6 is not a dominant response to the Pfizer vaccine.70 In one study it rose on average
50% in men and 100% in women, and in some individuals can quadruple.71 However, that study
did not show the time needed for it to return to baseline. In another study, the J&J vaccine
nearly doubled IL-6, but it returned to baseline by the second day.72 Overall, the IL-6 rise seems
to be bigger on average in natural infection, and of much longer duration, when compared to the
vaccines.

On the flip side, the vaccines provoke a much stronger increase in interferon-gamma
(IFN-gamma). In response to the virus, IFN-gamma is on average increased by 11%,67 whereas
after the Pfizer vaccine it is increased 11.3-fold.70

One implication of this is that it may provide a convergence with the T cell suppression
phenotype that drives severe COVID. This is produced by myeloid derived suppressor cells

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37
(MDSCs). In natural infection, IL-6 is a driver of MDSCs, but the sharp post-vaccination rise in
IFN-gamma may represent an alternative route to activating them.73

Do MDSCs Rise After Vaccination?

In 56 healthy volunteers,70 the Pfizer vaccine did not appear to induce a rise of MDSCs,
according to the authors. However, the day after the second dose, myeloid cells rose 100-fold,
largely monocytes. They characterized this monocytic population as cells that do not occur in
natural infection and are most similar to those that increase in response to an H5N1 flu vaccine.
They looked at two markers that can be used to identify MDSCs in COVID patients – HLA-DR
and S100 – and determined that this vaccine-induced cell population neither occurs in natural
COVID infection nor represents MDSCs.

However, they did observe an increase in STAT3 – a hallmark of MDSC activation – and the
HLA-DR and S100 markers are not sufficient to determine whether cells are MDSCs.74 The most
important thing to do would be to evaluate the isolated cells for T cell suppression activity, and
they did not do this. Thus, it is quite possible that this 100-fold increased population does
represent MDSCs.

In addition, Extended Data Figure 6 from that study shows a population of cells that express the
enzyme arginase 1 increasing up to 5-fold for three days after the second dose, and in some
individuals more than 10-fold. One individual had these cells keep increasing through the end of
the study on the third week after the second dose, at which point they had risen 15-fold. These
cells have markers consistent with MDSCs, yet they are not discussed anywhere in the text of
the paper. Although they did not evaluate these cells for T-cell suppressive activity, the arginase
enzyme is a major mechanism of T cell suppression, because it is used to deplete the arginine
that T cells need for growth. Regardless of how the cells are classified, they would be expected
to suppress T cells by depleting arginine.

Therefore, it is very plausible that, in some people, the COVID vaccines are massively
increasing MDSCs, leading to T cell suppression, and that this is a major mechanism by which
spike protein would continue to be expressed in the body after months go by.

Do Autoantibodies Rise After Vaccination?

In a small study of 56 healthy volunteers,70 two subjects developed autoantibodies to


inflammatory cytokines after vaccination, but none had any that rose to clinical significance. Five
of the subjects had existing autoantibodies that did not get any worse.

This suggests that autoimmunity is not the typical response to vaccination, whereas circulating
spike protein is likely to be a nearly universal response to vaccination.

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38
However, those suffering from post-vaccine side effects are likely to be enriched with
autoimmune reactions. For example, in a React19 survey of those suffering from vaccine side
effects, 21.8% had an existing autoimmune diagnosis before being vaccinated and 13.9% had a
new autoimmune diagnosis arise.

In severe COVID infection, autoimmunity can become very broad. One individual had over 250
different autoantibodies develop.75 The breadth of autoimmunity that can develop in such cases
is not likely explained by “molecular mimicry,” where the body mistakes its own tissues for spike
protein. It is much better explained by tissue damage. The immune system looks for signs of
what is causing trouble so it can remove the problem. It looks for “danger-associated molecular
patterns'' (DAMPs) and “pathogen-associated molecular patterns (PAMPs).” Tissue damage is a
major sign that something nearby is harmful, and the immune system considers many of its
signs to be DAMPs. The immune system will look for whatever is near the damage being
caused and conclude that innocent bystanders are culprits and mount immune responses to
them.

Spike protein toxicity and autoimmunity are therefore not opposing hypotheses. Spike protein
toxicity will cause tissue damage, and this will often lead to autoimmunity.

With that said, there are cases where specific autoantibodies may be directed at spike
protein-related targets.76,77 One important class of these is anti-idiotype antibodies. If antibodies
are mounted to the spike protein, and the spike protein fits very well into the ACE2 enzyme,
then the spike protein-binding portion of the antibodies will have a very similar shape to the
spike protein-binding site of ACE2. They have to, because their shape is what allows each of
them to bind to the same part of the spike protein. If new antibodies are then mounted to those
antibodies, they will likely also react to ACE2.

Essentially, this is like making a mold of a key, and then making a key from the mold. It’s
probably going to open the same door.

This would lead to ACE2 inhibition and raise blood pressure. Something similar may happen
with another protein that the spike protein can bind to, neuropilin-1, which may play a role in
autoimmune neurological disorders.

Comparing and Contrasting Adverse Effects of Vaccines vs


Natural Infection
Comparing and contrasting the adverse effects reported for vaccines versus natural infection will
help us match differential signs and symptoms to what we expect to be the differential
mechanisms. This will help us better narrow down the mechanisms behind the signs and
symptoms, which will, in turn, help us better understand how to resolve them.

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39
The purpose of this analysis is not a relative risk assessment. Therefore, I am not attempting to
discover the true rates of any adverse effects. I assume that all of the data is seriously
hampered by reporting bias, and hope that this bias is less impactful on the patterns that
emerge among the signs and symptoms than it is on the actual rates of each sign or symptom.

All of my references to the US vaccine adverse events reporting system (VAERS) refer to data
as it existed over the first weekend of August, 2022, and are documented in this spreadsheet.

Putting aside the acute fever that can accompany illness or vaccination, fatigue and headache
are the most common symptoms reported to VAERS78 and reported in studies of
long-COVID.79,80 One way to look for a difference in overall patterns would be to compare the
adverse effects of the vaccines and of long-COVID by adjusting the rates of other effects to that
of fatigue. In all cases – vaccines and long-COVID – the rate of fatigue is roughly twice the rate
of dyspnea (trouble breathing), which is roughly twice the rate of having a cough. Surprisingly,
even though COVID infects the lungs directly and would therefore be expected to cause lasting
lung damage that the vaccines wouldn’t, these rates show the exact same pattern.

Since fatigue and dyspnea occur at roughly the same ratios, below I use either of them to
normalize the other data, since some studies of long-COVID include one but not the other.

Some adverse effects are more often reported for long-COVID than for the vaccines. In
long-COVID, smell and taste disorders are about as common as dyspnea, while in VAERS they
are six times less common than dyspnea. Hair loss and attention deficit are extremely poorly
characterized in long-COVID, but very limited evidence suggests they may occur at a similar
rate as dyspnea.80 In VAERS, hair loss is 44 times less commonly reported than dyspnea, and
attention deficit is over 100,000 times less commonly reported. Studies that have looked at
cognitive impairment alongside fatigue have suggested that in long-COVID cognitive impairment
is 69% as common as fatigue,81 while in VAERS any cognitive disorders are reported 76 times
less commonly than fatigue.

On the flip side, some adverse effects are more often reported with the vaccines. Muscle pain is
only 57% as commonly reported as dyspnea in long-COVID, but slightly more often reported
than dyspnea for the vaccines. Diarrhea is only 23% as commonly reported as dyspnea in
long-COVID, yet 48% as commonly reported in VAERS. Joint pain (arthralgia) is not well
characterized in COVID,79 but some studies suggest it occurs at 79% the rate of dyspnea,80
whereas in VAERS it is reported at 91% the rate of dyspnea.

These suggest that muscle pain is 79% more commonly reported, diarrhea twice as commonly
reported, and joint pain 15% more commonly reported in VAERS than we would expect if the
mechanisms of post-vaccine side effects and long-COVID were similar.

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40
The following differences, however, are much more dramatic:

● Hypertension is not consistently reported as an effect of long-COVID,79 but one study


suggests it happens at a rate of only 4% of dyspnea.80 Hypertension is reported at 36%
the rate of dyspnea in VAERS. That is nine times more common than we would expect
if the mechanisms of post-vaccine side effects and long-COVID were similar.

● Myocarditis is 58 times less common than fatigue post-COVID with no mention of


pericarditis,80 while in VAERS myocarditis and pericarditis are only 7 times less common
than fatigue. That makes them eight times more common than we would expect if the
mechanisms of post-vaccine side effects and long-COVID were similar.

● Long-COVID papers do not discuss menstrual changes. A prospective study showed


that COVID infection does not alter menstrual cycles while the COVID vaccines nearly
double the risk of an altered cycle.82 In VAERS, among females, menstrual changes are
reported nearly half as often as dyspnea, comprising 3% of reports among females, with
over 28,000 cases listed.

● New-onset neurological disorders or relapse of pre-existing disorders seems limited to


sparse case reports with COVID,83 in VAERS, by contrast, these disorders are reported
at 60% the rate of dyspnea, comprising 3.7% of all reports, with over 51,000 cases
listed.

In short, post-vaccine side effects overlap considerably with long-COVID, with striking parallels
in the rates of respiratory issues, but they stand out in having a lower incidence of smell and
taste disorders, a lower incidence of cognitive impairment, somewhat greater rates of muscle
pain, joint pain, and diarrhea, a unique impact on menstrual cycles, and dramatically higher
rates of hypertension, myocarditis and pericarditis, and neurological disorders.

The neurological disorders that are documented in published case reports to follow COVID
vaccines with evidence of causation include multiple sclerosis,84 generalized demyelination,85
aneurysmal subarachnoid hemorrhage,86 various neuropathies,87,88 postural orthostatic
tachycardia syndrome (POTS),89,90 and various types of neuralgia91–99 and myelitis.100–109

Mechanistic Insights
Since the commonality of the vaccines and the natural infection is the spike protein, while the
differences are that the natural infection enters the respiratory tract and the vaccines enter the
deltoid muscle, we must begin our analysis by asking whether we can easily explain this
comparison and contrast through how the spike protein would be distributed. Specifically, spike
protein should be limited to the mucous membranes in most COVID infections that are not
severe, with it especially biased toward the respiratory tract. By contrast, the vaccine spike
protein completely bypasses the mucosal barriers and can therefore more easily seep from
muscle into systemic circulation, and may sometimes be accidentally injected directly into
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41
circulation through a vein. From there, it can reach a much broader distribution of tissues, such
as the blood itself, the lungs, the gut, the heart, the ovaries, and the nervous system.

The Fatigue/Dyspnea/Cough Pattern

The fatigue:dyspnea:cough pattern in the 4:2:1 ratio is an interesting parallel between VAERS
data and long-COVID studies, yet is not replicated in any of the vaccine trials, where fatigue is
usually fairly common but dyspnea and cough are either rare or not recorded.110–113

One possibility is that the ratio in VAERS is a result of unrelated respiratory illnesses that just
happen to follow vaccination.

However, my suspicion is that the lack of parallel to the vaccine trials must be systematic bias in
the way adverse events are collected in those trials. When they are reported in these trials, they
are reported as part of the “unsolicited adverse events” that are only tracked for 28 days after
any injection, even if the trial continues for months, despite universally being used as part of the
definition of COVID. We know from the FDA’s documentation that the two-month results of the
Pfizer trial had 3,580 cases of “suspected COVID-19” based on symptoms, 95.3% of which
tested negative on PCR.114 Cough and shortness of breath are not discussed at all in the
two-month report, or the later six-month report, except to say that they were used as part of the
definition of COVID.112,115 The J&J trial included a respiratory section in its 28-day adverse
events but cough and dyspnea do not appear at all, despite being part of the COVID
definition.110 The 6-month results of the Moderna113 and AstraZeneca111 trials report cough and
dyspnea in their 28-day adverse events at extremely low rates.

Even though the standard approach of these trials was to ask the participants to self-report
COVID symptoms in order to get a PCR test, it seems that these very common COVID
symptoms – cough and dyspnea – did not make it into the reports of unsolicited adverse events.
So it seems that the self-reporting of suspected COVID may have sucked these symptoms into
itself like a vacuum. If the PCR test was positive, they became COVID symptoms. If it was
negative, they disappeared into the black hole of “suspected COVID” that, according to FDA
documentation, represented 95.3% of all such symptoms at the 2-month mark of the Pfizer trial,
but which never became part of any published trial paper.

For this reason, I am inclined to dismiss the lack of correspondence with the vaccine trials and
to take the parallel between VAERS and long-COVID seriously.

One very simple explanation for this is that the amount of spike protein that reaches the lungs
after vaccination is similar to the amount left over in long-COVID patients once the acute
infection is over. As covered in the Toxicity of the Spike Protein and Its mRNA section, it is very
reasonable to believe that the amount of spike protein reaching the lungs could have a risk of
causing acute, severe COVID-like illness in some individuals, so it is quite possible that it

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42
commonly causes mild COVID-like illness. That could explain why long-COVID patients and
vaccinated subjects both have such a strikingly similar fatigue/dyspnea/cough pattern.

The Lower Incidence of Disorders of Attention, Memory, Smell, and Taste

The vaccines seem to be less associated with attention, memory, smell, and taste disorders
compared to natural infection. Since they are much more strongly associated with severe
neurological disorders, we cannot explain this by suggesting the vaccine spike protein does not
reach the nervous system while the natural spike protein does.

Notably, the vaccines also seem to be far less often associated with hair loss than natural
infection.

However, this conflicts with a React19 survey, where 26.4% of subjects complained of hair loss
and almost half reported memory loss. This may highlight that the community of people most
motivated to find solutions to post-vaccine problems differ in certain respects from the much
larger group of people from whom VAERS reports are being generated. Or, it may represent a
bias in what medical professionals see as potentially related to the vaccines, or what the
average person is likely to tell their doctor about. On the other hand, the React19 survey is
consistent with VAERS in not showing reports of smell and taste disorders.

In my long-COVID protocol, I make the case that there is a cluster of patients with fatigue,
dyspnea, and hair loss who are suffering from functional iron deficiency, and a cluster of patients
with smell and taste disorders that are suffering from zinc deficiency. This is because
interleukin-6 drives down plasma zinc116 and leads to the storage of iron in ferritin,117 making it
unusable for biological needs. Deficiencies of iron and zinc appear to both drive ADHD in a
subset of children and adolescents.118 Deficiency of iron119 but not zinc120,121 drives cognitive
decline, including dementia. Fatigue and dyspnea upon exertion are classic signs of iron
deficiency,122 and hair loss is also documented as a sign.123,124

It seems that the broader group of VAERS reports do not show the hair loss and cognitive
decline pattern that long-COVID shows, while the React19 community is enriched with this
pattern. This is suggestive of functional iron deficiency.

Although 7.68% of people in the React19 survey reported benefiting from zinc, the zinc
deficiency pattern associated with smell and taste disorders that shows up in long-COVID
patients does not appear to be common in this group. This is consistent with the VAERS data.

Hypertension

Hypertension did not arise as a signal from the vaccine trials. However, in one study,125 about
5% of people receiving the Pfizer vaccine experienced a significant rise in blood pressure. This
is consistent with the large signal from the VAERS data.
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43
Blood pressure is a function of the volume of the blood and its viscosity, and the pressure that
exerts on the vessel wall. The vessel wall can constrict, creating more pressure, or relax,
creating less.

The rise in blood pressure is probably not related to the role of the spike protein as a
pore-forming toxin. Minor changes to the permeability of cell membranes should increase nitric
oxide signaling, which relaxes the smooth muscles that control blood vessels, causing them to
dilate, lowering the blood pressure. Major disruption of the barriers of endothelial cells should
cause blood to leak out of the vessels, lowering the blood pressure.126 Granted, we cannot rule
out disruptions to the neurological control of blood pressure or compensatory responses to the
vascular leakage, but a rise in blood pressure would not be straightforwardly predicted from this
mechanism.

In principle, thrombosis and clotting could raise blood pressure by increasing the viscosity of the
blood, but this is not very straightforward either, because, outside of extremes, an increase in
blood viscosity leads to a regulated relaxation of the blood vessels, causing blood pressure to
return to normal.127

This mechanism would also make it hard to explain why hypertension is so much more
commonly reported with the vaccines than with natural infection. D-dimer, a breakdown product
of clots that can be used as an indicator of increased clotting, is elevated in 25.3% of COVID
patients 2 months after infection.45 This is more common than the rate of dyspnea in
long-COVID. Why don’t we see commensurate increases in hypertension?

My hypothesis is that in a mild or moderate natural infection, most of the clotting is happening in
the vasculature of the lung from spike protein subunits that are shed there, or neutrophils that
metabolize them into tiny bits that create amyloid clots. It is mainly the breakdown of these clots
in the pulmonary vasculature that is feeding D-dimer into the general circulation.

By contrast, with the vaccines, not only spike protein but the mRNA needed to produce it is
entering the blood and seeding its continued production throughout the body. With whole S1
subunits in the general circulation, they can bind to ACE2, and thereby raise blood pressure. As
noted earlier, the vaccine spike proteins are actually engineered in ways that make them react
more strongly with ACE2 than natural spike protein.

I therefore favor spike protein binding to ACE2 and directly inhibiting it as the leading
explanation.

Alternatively, anti-idiotype antibodies binding to ACE2 could explain this.

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44
Myocarditis and Pericarditis

While the signal of myocarditis and pericarditis did not arise from the vaccine trials, their signals
in the post-marketing surveillance data are so strong that the FDA now includes a myocarditis
warning on the vaccine packaging. That the spike protein more easily makes it to the heart
following vaccination is a simple explanation for this relationship, and is strongly supported by
mouse experiments showing that intravenous vaccination dramatically increases the myocarditis
and pericarditis response over intramuscular vaccination.128 That is, whatever delivery route
gets more spike protein into the bloodstream will deliver more of it to the heart, and thus cause
more inflammation there. Natural infection delivers the least spike protein to the bloodstream;
intravenous injection delivers the most. Typical intramuscular injection is in the middle.

The fact that spike protein has been found in biopsied heart tissue in a case of post-vaccination
myocarditis supports its persistence in heart tissue as a cause of the myocarditis.56 The fact that
a similar pore-forming toxin from Streptococcus pneumoniae, pneumolysin, contributes to
myocarditis in animals129 supports the role for the spike protein as a pore-forming toxin in
myocarditis.

Menstrual Cycle Changes

While menstrual changes did not arise as a signal from the vaccine trials, a prospective study
has now shown that COVID vaccines double the risk of an altered cycle while natural infection
has no impact on that risk.82 The mechanisms are not clear, but the finding is reminiscent of the
early concerns when leaked Pfizer documents showed that the lipid nanoparticles accumulate in
the ovaries. This could imply the spike protein does the same. However, the prospective study
showed that the J&J vaccine is just as likely to cause this issue as the mRNA vaccines,
suggesting the delivery vehicle is not what drives the effect. Rather, this can be explained simply
by the fact that the vaccine is injected into the muscle, bypassing the mucosal barriers, and
delivering its cargo into the general circulation. Regardless of the vaccine type, intramuscular
injection allows the cargo to reach the ovaries, or perhaps another location regulating the
menstrual cycle, like the pituitary or the uterine lining.

Neurological Disorders
Early on, the AstraZeneca trials saw several cases of transverse myelitis that they dismissed as
unrelated to the vaccines,130 and the mRNA vaccine trials showed more Bell’s palsy than
placebo.113,131 There are now over 51,000 neurological disorders reported in VAERS, and, as
noted above, many case reports documenting multiple sclerosis,84 generalized demyelination,85
aneurysmal subarachnoid hemorrhage,86 various neuropathies,87,88 postural orthostatic
tachycardia syndrome (POTS),89,90 and various types of neuralgia91–99 and myelitis.100–109

A recent NIH study found that some neurological patients respond to intravenous
immunoglobulins and some to corticosteroids, and suggested that autoantibodies or T cells

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45
could be involved.132 Unfortunately, they took biopsies but did not evaluate them for the
presence of the spike protein. It is tempting to speculate that the patients who benefit most from
immunoglobulins have trouble clearing the spike protein as their dominant problem, while those
that benefit most from steroids have excessive inflammation as their dominant problem.

Regardless, the stronger association of neurological disorders with vaccines than with natural
infection is supportive of the biodistribution hypothesis: more spike protein gets into the
bloodstream with vaccines than with typical cases of natural infection, so more reaches the
nervous system to cause toxicity or immune dysregulation.

Comparing and Contrasting Adverse Effects of Different Vaccine


Types

Overall, the three major vaccines licensed in the US – Pfizer, Moderna, and J&J – have
approximately the same rate of total events per person reported in VAERS if we assume people
receive two or three doses of mRNA vaccines or one dose of J&J.

Permanent disabilities, deaths, tinnitus, allergies, and herpes-related reports have relatively little
variation across vaccines that do not rise above the background noise. Specifically, these all
have below-average coefficients of variation, which is a measure of how variable the data is
within each category for each vaccine.

The most significant difference in the side effect profile of different vaccine types identified in the
scientific literature is the association of the adenoviral vector vaccines – especially AstraZeneca
– with a specific form of thrombosis. This is “cerebral venous sinus thrombosis” especially a
subtype associated with low platelets that has been named “vaccine-induced immune
thrombotic thrombocytopenia.”63 Although this was initially associated mostly with AstraZeneca,
the appearance of a case in the J&J trial is why the trial had been paused.9

Hypotheses to explain the disproportionate share found with AstraZeneca focus on the
adenoviral vector. All of these cases show high levels of antibodies to platelet factor 4 (PF4).
PF4 normally promotes blood clotting. Yet the antibodies to it can also promote blood clotting.
Outside of this vaccine-induced subtype, this pattern is usually found in a subset of patients
undergoing treatment with the anticoagulant heparin, where heparin binds to PF4, and the
antibodies bind to the heparin-PF4 complex. PF4’s mechanism of action involves being very
positively charged. Adenoviral vectors are very negatively charged, and are adjuvants that are
designed to promote an inflammatory reaction that will immunize the host against its cargo.
Since positive and negative charges attract each other, adenoviral vectors – used in both the
AstraZeneca vaccine and the J&J vaccine – can bind to PF4 and immunize the body against it,
resulting in anti-PF4 autoimmune antibodies. The AstraZeneca vector happens to have the most
negatively charged surface, perhaps explaining why it is most strongly associated with this
syndrome.
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When looking in VAERS at this form of thrombosis – using “cerebral venous sinus thrombosis”
and "thrombosis with thrombocytopenia syndrome" – the trend confirms an increased reporting
with J&J. These only represent 4% of the total thrombosis reports, but the J&J has somewhere
between 65% and 2.5 times as many reports per person as the Pfizer vaccine. The Pfizer
vaccine has more than the Moderna, roughly in line with the total thrombosis reports described
below.

Total thrombosis reports in VAERS have a weak trend implicating the J&J vaccine but a stronger
trend favoring Moderna having the fewest reports. When considering all forms of thrombosis
together, these constitute 3% of J&J reports, 2% for Pfizer, and 1% for Moderna. When
normalizing to the number of doses administered, Moderna has the smallest share, Pfizer has
twice as many, and J&J has six times as many. When adjusting for vaccinated people, however,
the trend with J&J becomes ambiguous. If we assume each person got two mRNA shots, the
J&J has 54% more reports than Pfizer. If we assume everyone with Pfizer got a booster, this
makes the J&J look nearly identical to Pfizer. Most likely, the truth is somewhere in between.
Moderna, however, has half as many thrombosis reports as Pfizer in any of these analyses.

This might easily be explained by the stronger antibody response to Moderna binding more
spike protein and preventing it from causing clots.

In the UK Yellow Card system, the equivalent of the American VAERS, Bell’s palsy has been
reported much more often with Pfizer than with AstraZeneca. Some authors argued this
suggests it is driven by a mechanism specific to mRNA vaccines.133 On the other hand, it was
the AstraZeneca trial where transverse myelitis most clearly showed up.130 In VAERS, where
Bell’s palsy represents about 1% of total reports, it is about twice as commonly reported with
Pfizer than Moderna, but Moderna and J&J are quite similar. When all neurological disorders
are grouped together, the Pfizer/Moderna gap gets cut in half but the overall trend remains
similar. This suggests that, if anything, there may be a Pfizer-specific mechanism rather than
any relevance of mRNA versus adenoviral vector vaccines.

It is tempting to speculate that, on the one hand, the lipid nanoparticles are more effectively
taken into the brain as a result of the brain expressing lipoprotein lipase (LPL), while, on the
other hand, the greater antibody and T cell responses to Moderna cancel out this effect. Thus,
Pfizer has the worst of both worlds, delivering more to the brain but not offering any extra
protection.

In VAERS, the J&J vaccine seems to be disproportionately associated with menstrual problems.
These account for 7% of the female reports, versus 3% for the mRNA vaccines. When adjusting
for doses administered, even generously assuming everyone got three doses of the mRNA
vaccines and only one dose of the J&J, the J&J still has 63% more reports about menstrual
problems than the mRNA vaccines. The prospective study on menstrual changes found a
stronger magnitude of change for the J&J vaccine than for the mRNA vaccines but it was not

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47
statistically significant.82 Some explanations might be that adenoviruses are better delivered to
the pituitary, the ovaries, or the endometrial lining than lipid nanoparticles, that there is some
indirect influence of thrombosis, or that there is some autoimmune stimulation impacting
menstrual cycles analogous to the anti-PF4 finding. This deserves further research.

Hypertension reports are quite evenly distributed among the vaccines. They are about 2.2% of
total reports, with the J&J hitting the average almost perfectly, Pfizer falling a half percentage
point above it, and Moderna a half percentage point below it. When adjusting for people
vaccinated, assuming everyone either got two shots of mRNA vaccines or one shot of the J&J
vaccine, the J&J comes in about average, Pfizer a little above it, Moderna a little below it.
There’s a hint of fewer hypertension reports with Moderna, which does line up with Moderna
having a lower risk of thrombosis, but the lack of any signal from J&J here makes thrombosis
seem unrelated.

I believe this modestly strengthens the interpretation that hypertension is driven by ACE2
inhibition rather than by thrombosis.

The modest Moderna/Pfizer differential could be explained by the protective effects of


Moderna’s greater immunogenicity.

For myocarditis and pericarditis, Pfizer seems to have the most and the J&J vaccine seems to
have the least. As a percentage of each vaccine type’s share of reports, Pfizer is 2.2%,
Moderna is 1.1%, and J&J is 0.4%. When adjusting for doses administered, Moderna and J&J
group together with Pfizer having twice as many reports. When adjusting for people vaccinated,
however, by counting each mRNA vaccine as two doses and each J&J vaccine as one, the
original pattern reemerges. Accounting for many of the mRNA vaccines being booster doses
makes J&J look even better. Overall, Moderna seems to have 2-3 times as many reports as
J&J, and Pfizer twice as many as Moderna.

The heart is one of the three major organs that express LPL, along with skeletal muscle and
adipose tissue. The myocarditis/pericarditis pattern may be explained by heart having much
greater uptake of lipid nanoparticles, while the greater antibody and T cell response of Moderna
mitigates this.

There is a strikingly similar pattern with Creutzfeldt-Jakob Disease, a prion disorder of the brain
that sometimes involves amyloid plaques. On a per person basis, Moderna accounts for 2-3
times as many reports as J&J, and Pfizer accounts for 2.7 times as many as Moderna. With so
few cases, not much should be read into this data. Nevertheless, it is consistent with LPL
mediating greater uptake into the brain with a mitigating effect for Moderna’s greater
immunogenicity.

This particular pattern is somewhat discrepant from the pattern for total neurological disorders,
where Moderna is more in line with J&J. This might represent the heterogeneity of neurological

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48
disorders, where uptake into the brain rather than the peripheral nerves is not always relevant,
or it might represent that the greater immunogenicity of Moderna is more protective for the
majority of neurological disorders than it is for prion diseases.

Cognitive disorders are rare, only 0.17% of the reports. However, Moderna looks to have a
disproportionate share. Normalized to doses administered, it is similar to J&J and both are 3.5
times that of Pfizer. However, when normalized to vaccinated people, Moderna has double to
triple the share of J&J, and the 3.5-fold greater share than Pfizer remains throughout.

The ability of each vaccine to stimulate IL-6 has not been compared head-to-head, but
Moderna’s greater antibody and T cell response might correlate with a greater cytokine
response, in which case this would align with my hypothesis that cognitive impairment is largely
driven by inflammation-induced decreases in iron and zinc status.

A Note on Novavax
Novavax was not included in the main analysis above, because it has been authorized more
recently and the data is more sparse and less robust.

At the time of writing, there are only nine Novavax reports in VAERS. However, this may easily
be explained by the fact that there have hardly been 7,000 doses distributed and it has only
been authorized for two months. More time is needed to see what reports come in. In the FDA’s
June 7 meeting when Novavax was authorized, the FDA reviewed data from several countries
where the data was considered adequately administered. If we substitute this for VAERS data,
the side effect rate per person seems to be half that of the other vaccines. Non-US data is less
transparent than US data, and is mostly available in summary form. If we look at data from the
European Union, making side-by-side comparisons of Novavax, J&J, AstraZeneca, Pfizer, and
Moderna, considering the doses administered to date, Novavax stands out as having the least
reports per dose, about four times fewer than Pfizer. However, if we look at Australia’s
AusVaxSafety surveys for Pfizer, Moderna, AstraZeneca, and Novavax, Novavax has similar
rates of total adverse effects per dose as the others, and this remains true if looking at effects
that interfere with daily activities. These data do not appear suitable for the type of analysis I
performed above.

When the Novavax trial was published last year, there was only one death in each group.134
However, in the briefing document of the FDA’s advisory board from June 7, 2022,135 when
Novavax was authorized, the followup had found twice as many deaths in the vaccine group
(11) as the placebo group (5). when Novavax was authorized, the followup had found twice as
many deaths in the vaccine group (11) as the placebo group (5). Since there were almost twice
as many people in the vaccine group as the placebo, this amounted to a 9% higher total
mortality rate in the vaccine group, but which fails to reach statistical significance.

These data do not appear suitable for the type of analysis I performed above. Therefore,
Novavax is not included in the comparison of side effect profiles across vaccines.
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49
A Note on Cardiac Deaths in mRNA Vaccine Trials

In the Pfizer trial, there were nine cardiac deaths in the vaccine group and five in the placebo
group. This represents an 80% increase, but it is not statistically significant. In the Moderna trial,
there were seven cardiac deaths in the vaccine group and five in the placebo group.113 This
represents a 40% increase, but it is not statistically significant. The J&J trial unfortunately did
not give a full accounting of the causes of death in the final 4-month followup.136 However, there
were no cardiac deaths in the vaccine group at two months even though there were three such
deaths in the placebo group.136 The AstraZeneca results are reported across different trials at
4-5 months. In the pooled results for the trials in South Africa, Brazil, and the UK, no cardiac
deaths at all were reported.130 In the pooled results for the US, Chile, and Peru, there was one
cardiac death in the placebo group and none in the vaccine group.137

While these are not statistically robust comparisons, there seems to be a trend for excess
cardiac death with the mRNA vaccines that is not emerging for the adenoviral vectored
vaccines. The trend is strongest for Pfizer and more modest for Moderna. We may invoke
Moderna’s greater immunogenicity to explain why it has a weaker trend than Pfizer, which
implicates the spike protein since that is what the immune system primarily responds to. As to
why this trend seems shared across mRNA vaccines but not the adenoviral vectored vaccines,
my speculation is that the heart is a major expressor of LPL, so takes up more spike mRNA
from Pfizer and Moderna.

Conclusions From the Adverse Effects Comparisons


These are the main conclusions I draw:

● The spike protein is the major explanation for COVID vaccine side effects. Most adverse
effects are shared across the vaccines. Where they differ from the effects of the virus
can easily be explained by different tissue distributions.

● Viral infection seems to cause a much higher rate of inflammation-induced deficiencies


of iron and zinc, although this seems robust for zinc, while for iron, VAERS and React19
surveys conflict.

● The vaccines cause a much higher rate of hypertension, heart inflammation, and
neurological disorders and have a unique impact on menstrual cycles.

● Compared across vaccines, adenoviral vectored vaccines definitely create an outsized


risk of central venous thrombosis with thrombocytopenia, although the mRNA vaccines

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50
contribute to VAERS reports for these disorders as well.

● While the toxicity of the lipid nanoparticles is very concerning for general health and may
be driving side effects for some people, no adverse effect stands out as a unique effect
of the mRNA vaccines. Greater uptake of these vaccines into the heart and brain via
LPL can explain most of the differential rates between the vaccines.

● Where Moderna has lower rates of reporting than Pfizer, it is usually best explained by a
protective effect of the greater immune response. This, in particular, argues against a
general hyperactivity of the immune response being the culprit. While autoimmune
conditions may represent overactivity of the autoantibodies, a stronger immune
response is generally a good thing when it comes to COVID vaccine side effects.

● The exception seems to be for cognitive impairment, where Moderna is worse, perhaps
due to greater inflammation-induced sequestration of iron.

What is Driving Vaccine Side Effects?


I believe spike protein toxicity is the most universal reaction to the vaccines. Whereas
autoimmunity is not a typical response to them, circulating spike protein is the universal
response.

The most likely mechanisms of spike protein toxicity are in acting as a pore-forming toxin,
increasing the production of breakdown-resistant clots, and binding to ACE2 receptors to drive
increases in hypertension.

Spike protein toxicity and autoimmunity are not mutually exclusive, but the causation starts with
the spike protein. Spike protein toxicity will cause tissue damage, and tissue damage often
causes autoimmunity.

Nevertheless, I believe that those suffering side effects can be broadly classed into those where
the immune system is doing the bulk of the damage – as in the hepatitis patient with no spike
protein in his liver but plenty of anti-spike T cells58 – and those where the immune system
running sluggish is driving the persistence of the spike protein and its enduring toxicity – as
might have been the case in the fatal myocarditis victim whose heart tissue had spike protein
found in it at the time of death.56

In support of this two-type model, a React19 survey found that corticosteroids – which have
immunosuppressive properties – were the most polarizing medication, with many people
reporting improvement but many people reporting getting worse.

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51
The immunosuppressed type is most likely driven by vaccine-induced rises in MDSCs, as
supported by the five-fold increase in arginase-expressing cells in the wake of Pfizer
vaccination.

The autoimmune type is most likely driven by anti-idiotype antibodies to the spike protein that
damage its targets, such as ACE2 and neuropilin-1, or by autoantibodies that rise in the wake of
spike protein toxicity-induced tissue damage.

Nevertheless, there are at least some people for whom inflammation-induced sequestration of
iron is the dominant theme. This is supported by the prevalence of hair loss and memory issues
in the React19 survey, the outsized reporting of cognitive issues in VAERS for the more strongly
immunogenic Moderna vaccine, and two case reports of young women in their 20s and 30s who
developed dangerous autoimmune relapses after vaccination, with dramatically increased
ferritin.138,139

How Do We Heal From Vaccine Side Effects?


The most important place to start is to consider the possibility that someone has persistent
production of spike protein as a result of a decreased immune response. Many protocols
recommend fasting to turn over spike-contaminated cells, but we have to acknowledge that 1)
all the mRNA and adenoviral vectored vaccines are designed to generate spike protein
expressed on cell surfaces and this should cause T cells to destroy those cells;50 2) poor
antibody and T cell response is correlated with antigen persistence;59 and 3) while cyclical
fasting and refeeding can help reset the immune system and will become an important part of
this protocol, the initial response to fasting is a decrease in circulating lymphocytes.140

Therefore, while these two problems are not mutually exclusive, it is critical to distinguish those
whose dominant problem is a relatively suppressed immune clearance of the spike protein from
those whose dominant problem is a hyperactive autoimmune state.

Therefore, this protocol first provides a base of nutritional support that should help both
problems simultaneously, and then bifurcates into two modifications of the Base Protocol for
each immunotype.

The Base: Vitamins A and D for Immunoregulation, Omega-3s for


Inflammation Resolution

Vitamins A and D form the base of this protocol because they synergistically eliminate T cell
suppressive MDSCs by stimulating myeloid differentiation,141–144 while simultaneously
suppressing the autoimmune-related Th17 helper T cells.145 This makes them well suited to
those of both immunotypes as well as to those of mixed type.

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52
Omega-3 fatty acids are found in small amounts in the fat of land animals, especially egg yolks,
and especially when those animals are raised on pasture, and in large amounts in fish, fish liver
oil, and cod liver oil. The most important of these are EPA and DHA.146–148 EPA can act similar
to an NSAID by obstructing the inflammatory process. This obstruction tends to prevent
inflammation from reaching as high a peak, but also prevents it from fully resolving. DHA, by
contrast, readily contributes to the active resolution of inflammation. However, aspirin is unique
among NSAIDs in that it can jumpstart the resolution of inflammation, and it can even help EPA
drive the resolution of inflammation just like DHA does on its own. Furthermore, bacteria can
enhance the ability of EPA to contribute to the resolution of inflammation, so there might be an
interaction between EPA and probiotics worth exploring. Generally speaking, it would be easiest
for moderate doses of DHA-rich fish oils (providing doses in the hundreds of milligrams) to
jumpstart inflammation resolution, while high-dose EPA (doses in the grams) would be a difficult
balancing act, since its ability to help or hurt the resolution of inflammation would depend so
much on contextual factors like aspirin and probiotics.

The Base Protocol therefore calls for 300 milligrams of DHA, obtained through one or two
servings of fatty fish per week, or using a fish or cod liver oil. Cod liver oil contains vitamins A
and D, so if used, should be counted toward the targets for those vitamins.

Differentiating Immunotypes: Immunosuppressed, Autoimmune, and Mixed

The key lab tests for determining one’s immunotype are a plasma amino acids test and
LabCorp’s ANA Profile 12.

Amino acids tests can be ordered by standard labs, by functional medicine labs, or as part of
broader functional medicine profiles, such as Genova’s NutrEval or Metabolomix+. On the
amino acids test, the key signs of MDSC-related T cell suppression are arginine and tryptophan
being near the bottom of the normal range or below it. Glycine and glutamine may also be low,
as they are in COVID,149 but this is not necessary. If there are other obvious patterns like all
amino acids across the board are low, this may cast doubt on the interpretation as it may just
reflect protein deficiency. Selectively low arginine and tryptophan, however, are an indicator of T
cell suppression, and are the basis for categorizing someone as a suppressed immunotype in
this protocol.

Anti-nuclear antibodies (ANA) are the most consistent indicator of autoimmunity in severe
COVID,75 and are likely to be elevated in post-vaccine issues caused by hyperactive
autoimmunity. In the case of the hepatitis following Pfizer vaccination that was mediated by
anti-spike T cells,58 the patient had acute hepatitis after the first dose without any evidence of
autoimmunity, but then after the second dose he had a relapse of the hepatitis and showed ANA
elevated to the 1:200 threshold. 1:200 represents the amount of dilution that can be done to the
blood while still detecting ANA. 1:200 is considerably higher than the minimal threshold of 1:40.
Caution with ANA is widely recommended, because many people have positive ANA with no
apparent autoimmune condition. However, I use a liberal approach in this protocol, because
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53
autoimmunity is an important hypothesis in otherwise poorly understood post-vaccine side
effects. Thus, someone with a positive ANA is an autoimmune type in this protocol.

If both T cell suppression markers are present and ANA is positive, someone is a mixed type.

LabCorps’s ANA Profile 12 will automatically measure 12 common autoimmune targets if ANA is
positive, to give more information about whether a specific autoimmune condition is present.

Relieving T Cell Suppression

MDSCs suppress T cells by depleting them of the arginine and tryptophan needed for growth,
by sequestering the cysteine they need to make glutathione, and by launching oxidants and
glycating agents at them.150–158

Arginine is widely reported by people with herpes to cause flareups, and reactivation of herpes
is reported as a vaccine side effect. It is possible this also applies to tryptophan.159 Therefore,
people with herpes reactivation should not use arginine and tryptophan. Apart from this
exception, this protocol calls for Immunosuppressed Types to supplement with L-arginine,
L-tryptophan, N-acetylcysteine, and glycine. The dose of arginine is taken from the dose used to
successfully treat respiratory distress in COVID patients,160 and the dose of tryptophan is
selected to match it since tryptophan is slightly more depleted in COVID patients.149

The dose of NAC has a somewhat more complex rationale. T cells are not able to access the
main form of cysteine that circulates in plasma, which is oxidized, and spelled cystine.161 They
need reduced cysteine. Usually macrophages stand in close proximity to the T cells, digest
cystine from plasma, turn it into cysteine, and feed it directly to the T cells as if they were their
babies. MDSCs displace these macrophages and siphon off the supply of cystine, never
releasing any cysteine to feed the T cells. 2.1 grams of NAC raises the free cysteine content of
plasma for three hours162 to a concentration of 50 micromoles per liter, which is sufficient to
normalize glutathione synthesis in a red blood cell that has no other supply.163 No such data are
available for T cells, but this provides proof of principle that the concentration is highly relevant
to circulating cells. Since this effect only lasts three hours, the dose is repeated every three
waking hours. This amounts to 10 grams per day, and I have only seen this used long-term in a
study where it was matched to 7.5 grams of glycine. The cysteine from NAC needs to be
combined with glycine to make glutathione, so pairing them together makes sense. The study in
question was done in healthy, older adults, and safely used these doses for 24 weeks.164

Those who show no signs of immunosuppression should not use the above protocol. In theory, it
could worsen a case of hyperactive T cells.

Autoimmune conditions usually involve elevated MDSCs. Therefore, it is actually more likely
someone is a Mixed Immunotype than an Autoimmune type.

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54
Mixed Immunotypes may carefully experiment with the protocol, and guidelines are included
for doing so.

Given that tissue damage can drive autoimmunity, the Mixed and Autoimmune types are given
followup labwork for nutritional causes of oxidative stress that could reveal deficiencies. In the
event deficiencies are revealed, they should be resolved before any fasting protocols are
initiated.

Fasting-Feeding Immunological Reset

Once deficiencies in amino acids and nutrients are corrected, those who fall into the Mixed and
Autoimmune Types may benefit from the fasting-feeding protocol, which is also used for
membrane, mitochondrial, and neurological regeneration resets below. The principle of this
approach is that, in the fasting state, dysfunctional mitochondria, immune cells, and other cells
are digested; then, in the fed state, fresh cells and mitochondria are regenerated. Animal
experiments suggest that such a protocol leads to a “reset” of the immune system.140

Pregnancy and lactation are extremely energy-intensive. In these conditions, fasting should not
be used. In fact, fasting can cause ketoacidosis in lactating women even if they are not
diabetic.165 The same animal experiments that suggest fasting-refeeding can achieve a healthy
immunological reset in adults also suggest it can cause lasting damage to the immune system
in children.166 While this is a generalization from mice to humans, there is broad concern that
fasting could hurt growth in children. Therefore, children should not use the fasting-refeeding
protocol.

Many fasting-refeeding options are available. This protocol does not select one over the others,
but it emphasizes that the refeeding part of the cycle is just as important as the fasting part, and
it adds supplements that may be able to enhance each part.

Intensifying the Fasting State


An important signal of the fasting state is adenosine monophosphate-activated protein kinase
(AMPK), which is primarily activated by energy depletion. Fasting itself will activate AMPK.
However, this can be enhanced by exercising in the fasting state. Fasting involves a shift to fatty
acid metabolism, and the exercise that burns the most fatty acids is steady-state “zone 2”
cardio. Given the prominent place of this exercise in the protocol for membrane, mitochondrial,
and neurological regeneration, which will often be used in tandem with the immunological reset
protocol, it is the form of exercise selected for enhancing the fasting state signaling.

The easiest way to know if you are in zone 2 is if you find it a modest nuisance to carry on a
sustained conversation throughout your workout, and if someone on the other end of the phone
line would know you were exercising by the way you are speaking and breathing. However, the
most accurate way to know that you are in zone 2 is to get a lactate meter, measure blood

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55
lactate levels before and immediately after exercise, and aim to have post-exercise lactate
levels less than 2 millimoles per liter, but at least 0.3 millimoles per liter above your baseline
level, aiming at first to consistently target a 0.3-0.5 millimole per liter increase over baseline.
Importantly, for someone with impaired mitochondrial health, a zone 2 workout may simply be
walking at a gentle pace. For others, it may be power walking, jogging, running, or cycling. Zone
2 workouts should last at least 30 minutes, ideally 60-90 minutes, should be used 3-5 times per
week, and should be conducted at a consistent pace of effort throughout the workout without
breaks or intervals. In the case of the fasting-refeeding cycle, zone 2 should be consistently
used in the morning of each fasting day, and then rest should be emphasized on refeeding
days.

Resveratrol further enhances AMPK signaling.167,168 2000 milligrams of resveratrol per day has
been safely used for one to four weeks.169 However, 2000 milligrams twice per day has caused
mild diarrhea in a majority of people.170 At high doses, it has a half-life of 2.5 hours, which would
lead to it being mostly gone in 12.5 hours. Food delays the absorption of resveratrol but has no
impact on the total amount absorbed.171 Therefore, this protocol calls for supplementing with
1000 milligrams of resveratrol twice a day during the fasting state, and ceasing its
supplementation during the refeeding state.

Part of the fasting process involves the activation of enzymes such as sirtuins that irreversibly
hydrolyze NAD+, a form of niacin, also known as vitamin B3. NAD+ is also broken down during
the repair of DNA during cellular injury. Therefore, spike protein toxicity is likely to deplete
NAD+. NAD+ is universally used in the fed and fasted states for energy metabolism, and does
not need to be taken specifically during the fasting state. Its retention in cells is likely to be
better in the fed state, due to the role of ATP in trapping it and most other B vitamins inside
cells. Therefore, this protocol uses nicotinamide riboside supplementation during the refeeding
phase. Dosing is poorly characterized, and so starts at 150 mg per day. It may be slowly
increased to a maximum of 2000 mg per day if this appears to improve symptoms. These doses
will also deplete methyl groups and therefore antagonize the SAMe, described below, so dosing
should be conservative.

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56
Intensifying the Feeding State

The most well established signals of the fed state come from calories, carbohydrate, and
protein. Therefore, the foundation of a strong feeding phase is to eat a calorie load that not only
meets your needs for the day but also causes a regain of all the weight lost in the fasting phase,
that includes whole-food starches and fruits at every meal, and that has at least a third of the
plate devoted to a whole-food animal protein. Protein should measure in at a minimum of 0.5
grams for every pound of bodyweight and an ideal of 1 gram per pound of bodyweight. Multiply
these by 2.2 if you are measuring your weight in kilograms.

In addition to the signals provided by calories, carbohydrate, and protein, there are specific
amino acids and derivatives that activate the mammalian target of rapamycin (MTOR) pathway
to accentuate fed state signaling. These are arginine, leucine, and S-adenosylmethionine.172
During the refeeding phase, 1600 milligrams of S-adenosylmethionine is borrowed from
unrelated trials that have successfully used this dose.173 It repeats the dose of L-arginine used in
the protocol for rejuvenating T cells, and it uses the dose 9 grams of leucine per day by
borrowing from the mid-upper range of what has typically been studied for improving lean mass
in older adults.174

Hyperpermeability vs. Hypertension

The second axis on which protocol participants are distinguished is whether the dominant
problem is hyperpermeability or hypertension.

The most likely cause of post-vaccine hypertension is direct inhibition of ACE2 by spike protein
or its inhibition by autoimmune anti-idiotype antibodies. In both cases, angiotensin II will be
elevated.

Hyperpermeability can be directly induced by whole spike proteins or their subunits infiltrating
cell membranes and causing an inflammation-mimicking response, and can also be caused by
excessive genuine inflammation. While this is not mutually exclusive with hypertension – in fact,
sustained hypertension can cause hyperpermeability of the blood vessels simply by pushing
blood against the blood vessel wall with more force – elevated angiotensin II will help reverse
spike protein-induced or inflammation-induced hyperpermeability. This is because angiotensin II
helps repair the barriers between epithelial cells. In fact, overexpression of ACE2 in mouse
heart causes arrhythmia, tachycardia, and sudden death through excessive
hyperpermeability.175

Therefore, one or the other of these problems is likely to be dominant.

If angiotensin II and blood pressure are both elevated, this makes one a Hypertension Type in
this protocol.

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If you have a persistent fever over weeks or months, especially if it is combined with low blood
pressure, cardiac dysfunction, shortness of breath, and diarrhea, or you have been diagnosed
with multisystem inflammatory syndrome,176 then you are definitely considered
Hyperpermeable Type in this protocol.177 If you have edema (swelling) of any tissues, any
symptoms of pneumonia, new-onset eczema that gets worse with exposure to soap, these are
strong indications you are a Hyperpermeable Type. The following are less obvious but possible
signs of this type: anything that could be caused by disruptions to the blood-brain barrier or to
the control of nervous system signals, such as insomnia, anxiety, palpitations, tingling and
numbness, and elevated heart rate; or any signs of a leaky gut, such as new-onset food
allergies that are very broad in their scope. Headaches are usually caused by excessive
vasodilation, which is not the same thing as hyperpermeability, but may tend to correlate with
the same underlying processes. This is because nitric oxide drives both.

If one has a mix of hypertension and hyperpermeability signs, one is a Mixed Type.

Hypertension Protocol

Hypertension Types, but not Mixed Types, would benefit most from increasing endogenous
ACE2 activity. Mixed types may try this protocol after they achieve resolution of
hyperpermeability symptoms using the hyperpermeability protocol below.

ACE2 is zinc-dependent, so zinc deficiency must be ruled out and resolved if it is present.
Vitamins A178–181 and D182–184 increase the expression of ACE2. The Base Protocol should be
used throughout and will provide a sufficient amount of these vitamins. (The Base Protocol is
used for non-hypertensive types regardless of this because they are needed for
immunoregulation.) A high calcium-to-phosphorus ratio suppresses the bone-generated
hormone FGF23, while a low calcium-to-phosphorus ratio increases it.185–187 FGF23 suppresses
ACE2,187 suggesting that a high calcium-to-phosphorus ratio might increase ACE2. Therefore,
the protocol calls for 1200 milligrams of calcium per day from food, spread across the day, and
removing all store-bought processed foods (regardless of whether they are organic or otherwise
marketed as healthy, and this includes bread and cheese), since these are often sources of
hidden, unlabeled phosphorus additives that have much stronger effects on hormones than
whole-food phosphorus has.

Nattokinase does not affect angiotensin II levels, but when it is heated to 250 degrees
Fahrenheit (121 Celsius), it is broken down into fragments that have been shown in rats to
decrease angiotensin II.188 Based on data discussed in the clotting protocol below as well as the
nattokinase content of commercial natto, 50-100 grams of cooked natto per day are included in
the hypertension protocol. Alternatively, a 2000 FU (100 mg) dose of nattokinase may be
sprinkled onto food during cooking, and thoroughly cooked with the food.

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58
Hyperpermeability Protocol

Hyperpermeable Types or Mixed Types should use the following protocol.

Hyperpermeability is driven by nitric oxide binding to the proteins that make up the junctions
between cells and causing the junctions to withdraw.189–193 Glutathione prevents nitric oxide from
binding to these proteins in the first place,194 while the selenium-dependent protein thioredoxin
removes it from them after it has bound.195 In addition, blue, green, and ultraviolet light remove
nitric oxide from these proteins.194,196 Liberal exposure of the naked skin to daytime, outdoor,
unprotected sunlight with careful attention to avoid sunburn may prove valuable for reversing
this, while internally nourishing glutathione and thioredoxin should provide the bulk of the
benefit.

However, heat exposure causes increases in heat shock protein 90, and this protein
dramatically increases the nitric oxide load caused by spike protein toxicity or inflammation.197
Therefore, avoiding sauna use is very wise for hyperpermeable types. The emphasis should
be on exposure to the sun at levels that cause neither sunburn nor flushing nor overheating, and
otherwise staying in a cool environment. Extreme cold is not recommended, as hyperpermeable
types are also likely to be leaky membrane types, discussed below, and cold exposures such as
ice water baths or even cold showers may make mitochondrial membranes temporarily more
leaky. Outside of the sun exposure, mildly cool temperatures should be sought. Air conditioning,
mattress cooling systems, or cooling head bands – such as those made by ChiliSleep – may
help.

If following the T Cell Rejuvenation Protocol, adding glutathione support is unnecessary


because it is covered by the NAC and glycine. However, if that protocol is not needed, the best
way to boost glutathione status would be 1500 milligrams of reduced glutathione taken three
times a day.

Regardless of the approach to boosting glutathione, plasma selenium must be measured,


deficiency must be ruled out, and plasma levels must be targeted to the 100-140 nanograms per
milliliter range.

For nourishing glutathione and thioredoxin, the following considerations may also be helpful:

● Adequate glutathione synthesis requires one gram of protein per kilogram of


bodyweight,198 which is roughly a half gram per pound of bodyweight and on the low end
of what appears needed for healthy body composition.

● When cysteine is no longer limiting for glutathione synthesis, glycine becomes limiting,
and they have been effectively used in combination to boost glutathione status.164

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59
● Glutathione synthesis requires magnesium, ATP, and a high ratio of insulin to
glucagon.199 Thus, magnesium deficiency and anything that can hurt energy status –
deficiencies of B vitamins, iron, copper, or sulfur; diabetes, thyroid disorders, adrenal
disorders, or rare inborn errors of metabolism; or excessive fasting –could hurt
glutathione status.

● Diabetes compromises glutathione status and this can be corrected with insulin.200 Thus,
we need to be sensitive to insulin, but also need to be exposed to insulin. This makes
correcting insulin resistance paramount, but also implies a need for carbohydrate.

● Glutathione uses selenium when it neutralizes peroxides. A similar protein, thioredoxin,


is directly selenium dependent. Both glutathione and thioredoxin are recycled with
riboflavin-dependent enzymes using NADPH, a form of niacin. NADPH is mainly
generated in the pentose phosphate pathway. This pathway requires the enzyme
glucose 6-phosphate dehydrogenase, which is the most commonly genetically defective
enzyme in the world.201 The pathway is also enhanced by calcium and magnesium,202
dependent on iron,203 and critically dependent on thiamin.204 Thus, selenium, the first
three B vitamins, calcium, and magnesium are all especially important to glutathione
status (and thioredoxin status).

● NADPH gets used up by other processes under certain circumstances. One is the
conversion of sugar to fat, which mainly increases in the follicular phase of a woman’s
menstrual cycle, and on a 60% sugar diet.205 A second is the conversion of glucose to
sorbitol when blood glucose exceeds 140 mg/dL.206–208 A third is the conversion of
galactose to galactitol during the first 15 days of a new milk-drinking habit.209,210 Thus,
avoiding high-sugar diets, keeping blood glucose under 140 mg/dL, and not starting a
new milk-drinking habit when ill might all be important glutathione-boosting strategies.

Leaky Membrane Types

Leaky Membrane Types are likely to overlap with Hyperpermeable Types, since leaky
membranes cause calcium influx that initiates the hyperpermeability cascade, and since in
many cases things leaking into cells will produce similar results as things leaking between cells.

However, the distinguishing feature of the leaky membrane type is any electrolyte (sodium,
potassium, or total CO2, which largely reflects bicarbonate) abnormality on a complete
metabolic panel, defects in acid-base handling, twitching that resolves when supplementing with
electrolytes, or elevated red blood cell calcium, which can be order from Quest Diagnostics as
“Calcium, Total, RBCs.”

Leaky mitochondrial membranes will hurt ATP production, and leaky neural membranes will lead
to neurological dysregulation. Together, these could cause fatigue, exercise intolerance, brain

Copyright © Chris Masterjohn, 2022. All rights reserved. Not for distribution. Do not store this in the files of a public web site.
This guide is for educational purposes only and does not constitute medical or nutritional advice. Do not use these strategies as a
substitute for medical advice or treatment.
60
fog, heart palpitations, muscle weakness, tingling or numbness in the extremities, and muscle
twitching.

This could also play a role in severe neurological disorders, since it would cause electrolyte
imbalances that would hurt the ability to clear glutamate from synapses, which can cause
demyelination.

Urine pH should be above 5.5 at all times and should be between 6.4-6.8 in the postprandial
state. If it is consistently (or very erratically) below 6.0 or above 7.2, this would support the leaky
membrane type, though it would be less conclusive than elevated RBC calcium.

If membrane integrity is disturbed, it can be attributed to persistence of spike protein subunits in


circulation. The Base Protocol and the T Cell Rejuvenation Protocol are designed to increase
antibody production (helper T cells are needed for this, and vitamin A is directly used for this),
which is by far and away the most effective way to stop spike protein subunits from circulating.
Since they most likely originate from the cleavage of spike proteins on the surfaces of cells,
slipping into the circulation and then into cells throughout the body is the likely route by which
the subunits arrive in cell membranes, especially those of organelles like the mitochondrion.

If this is not adequate to restore membrane integrity, it is most likely because cell membranes
are already enriched with spike protein subunits. Therefore, stimulating the breakdown of cells
and their mitochondria – autophagy and mitophagy – and the subsequent rebuilding of these
structures, is likely to be the only way to clear out spike protein subunits persisting in cell
membranes.

This approach is likely to be helpful for neurological disorders as well, because it drives the
immunological reset in case autoimmunity is involved, it regenerates the mitochondria of nerve
cells, and it degrades unuseful materials that can later be used to power myelin synthesis during
the fed state.

The Cellular, Mitochondrial, and Neurological Resets


Therefore, the accentuated fasting-feeding cycle described above is used as a general cellular,
mitochondrial, and neurological reset. The main deviation for leaky membrane types is to
warrant caution on the extremity of fasting. Fasting will lower ATP levels, which could worsen
symptoms of fatigue, brain fog, or nervous system dysregulation. Therefore, start slow,
emphasize the refeeds, and cautiously increase the fasting component according to your
tolerance.

For neurological regeneration specifically, processes involved in healing such as stem cell
differentiation and myelin synthesis are not only stimulated by the fed state signaling discussed
above, but also by acetylcholine,211, thyroid hormone,212, vitamins A and D,213,214, and the
omega-3 fatty acid DHA.215 Maintaining myelin and synthesizing it also depend on having
enough iron, but not too much, and handling it properly.216 Therefore, during the fed state, those
Copyright © Chris Masterjohn, 2022. All rights reserved. Not for distribution. Do not store this in the files of a public web site.
This guide is for educational purposes only and does not constitute medical or nutritional advice. Do not use these strategies as a
substitute for medical advice or treatment.
61
with neurological disorders should include the acetylcholine-booster alpha-GPC at 400 mg three
times a day, the dose that has been shown beneficial in Alzheimer’s.217 240 milligrams per day
ginkgo biloba has also been shown helpful in Alzheimer’s, and has natural acetylcholinesterase
inhibitors that should enhance the alpha-GPC.218 The A, D, and omega-3s in the Base Protocol
will provide sufficient dosing for neurological regeneration, although I encourage
self-experimentation to see if higher doses of omega-3s prove beneficial. Iron status and iron
handling are covered by the first-round labwork. Thyroid health is not specifically addressed in
this protocol, but it is dependent on iodine, antioxidant protection, and selenium. Selenium is
addressed in the initial lab work. For iodine and other nutrients, see Appendix 2: How to Get
Enough of Everything.

Distinguishing the Clotting/Bleeding Type

Elevated D-Dimer can be used to distinguish clotting types. If D-dimer is elevated, the protocol
uses fibrinolytic enzymes.

Clotting can increase the viscosity of the blood, which can decrease circulation. Paradoxically,
the pressure caused by increased viscosity can lead to secondary hyperpermeability, causing a
lot of overlap with symptoms discussed in that section. If we generalize from polycythemia,
where increased concentrations of red blood cells increase blood viscosity, we can imagine this
leading to fatigue, brain fog, weakness, headaches, dizziness, shortness of breath, visual
disturbances, nose bleeds, bleeding gums, heavy menstrual periods, and bruising.

The Clotting Type is addressed in this protocol using enzymes. There are many thrombolytic
enzymes available,219 and naturally occurring enzymes available as supplements include
nattokinase and serrapetase. Of them, nattokinase is the best characterized in the literature. A
single oral dose of 2,000 functional units (100 mg) of nattokinase has been shown to cause
measurable breakdown of blood clots in healthy males, and to lower the clotting activity of blood
for four hours.220 This dose has been used daily for three years in a clinical trial, where it
showed no safety concerns in men over 55 years old or in postmenopausal women.221 Since the
decreased clotting time lasts four hours, if higher doses are sought, they should be used by
repeating 2000 FU at least four hours apart, such as taking four doses every four waking hours.
However, this should not be done without close medical supervision, including monitoring the
clotting time of the blood, since the possibility of bleeding disorders has not been characterized
with such doses. This amount is found in 50-100 grams of natto, but the natto has to be raw.

If someone is a Hypertension Type and a Clotting Type, then two servings of natto or
nattokinase, one cooked, and one not cooked, should be used. The nattokinase supplement or
raw natto addresses the clotting, while the cooked natto, or cooked supplement, addresses the
hypertension.

Bleeding Types are not expected, but are distinguished by an elevated prothrombin time. This
is critical – someone with a nosebleed and elevated D-dimer but normal prothrombin time is not
Copyright © Chris Masterjohn, 2022. All rights reserved. Not for distribution. Do not store this in the files of a public web site.
This guide is for educational purposes only and does not constitute medical or nutritional advice. Do not use these strategies as a
substitute for medical advice or treatment.
62
a bleeding type. These types are determined by the underlying mechanism, and are sorted out
by the blood work, not by the symtpoms that arise to the surface.

If the prothrombin time is elevated, protein induced by vitamin K absence or antagonism


(PIVKA) should be measured. If this is elevated, including daily green leafy vegetables or
supplementing with a blend of vitamin K1 and MK-7 providing several hundred micrograms per
day should help.

If PIVKA is not elevated, the cause of elevated prothrombin time is unlikely to be nutritional.
Many causes of bleeding are outside the scope of this protocol. However, someone who is a
bleeding type with no other explanation, and who also fits the symptoms of amyloidosis listed in
Appendix 1, should discuss with their doctor whether their symptoms are extreme enough to
merit a biopsy of the tissues indicated by the symptoms. In biopsy, stains such as congo red,
thioflavin S, or thioflavin T can reveal amyloid plaques regardless of what proteins they are
made from.39 If cases of post-vaccination amyloidosis turn up, please let me know using the
protocol feedback survey.

Staying in Touch and a Final Note


Once you have had enough time to gain some experience with this protocol, please fill out the
protocol feedback survey.

To receive my free newsletter, sign up at chrismasterjohnphd.substack.com

Have a question? Ask me in the newsletter comments!

This guide focuses on nutritional support, but we also need to get good sleep, stay active
without being too hard on our bodies, manage stress well, stay connected to our families and
friends, and maintain a positive outlook. All of these things help support a healthy immune
system to clear the spike protein, and a calm immune system that will make peace with our
bodies. I know these are very difficult under these circumstances. I just want to say that I am
grateful to you for having purchased this guide, which helps support my work and my ability to
get the word out, and I hope the effort that I’ve put into this guide brings calm and clarity your
way.

Copyright © Chris Masterjohn, 2022. All rights reserved. Not for distribution. Do not store this in the files of a public web site.
This guide is for educational purposes only and does not constitute medical or nutritional advice. Do not use these strategies as a
substitute for medical advice or treatment.
63
Appendix 1: Tissue-Specific Symptoms of
Amyloidosis
If any of these symptoms are debilitating enough to warrant a biopsy, congo red, or thioflavin T
or S can be used to stain for amyloid plaques. If amyloid plaques are found post-vaccination
please let me know using the protocol feedback survey so future editions can include treatments
for this. This table is taken from reference.46

Copyright © Chris Masterjohn, 2022. All rights reserved. Not for distribution. Do not store this in the files of a public web site.
This guide is for educational purposes only and does not constitute medical or nutritional advice. Do not use these strategies as a
substitute for medical advice or treatment.
64
Appendix 2: How to Get Enough of Everything
While this protocol includes supplementation with specific nutrients that I believe are most relevant
to post-COVID vaccine side effects, any nutrient deficiency has the potential to compromise your
immune health. Therefore, it is important to make sure you’re getting enough of everything.

The simplest way to do this is to spend a few days or a week tracking what you eat in an app such
as Cronometer. There are many nutrition-tracking apps, but most others, such as MyFitnessPal, do
not track vitamins and minerals comprehensively enough for this purpose.

When using Cronometer, it is very important to make sure each food you add has 81 listed nutrients
and not much less than this. Sometimes when you enter a food you may get the exact food but it
only has 20-something nutrients listed. In that case it is best to use whatever Cronometer suggests
as the closest approximation to that food from the USDA or NCCDB databases, as these should
have 81 listed nutrients. This helps you avoid false zeros in your data.

Track your food for three days if you tend to eat the same thing all the time. If your diet is variable,
track it for one week or longer. Track however many days you need to in order to capture a
representative chunk of all the different types of foods you tend to eat.

Apart from the specific recommendations in this protocol, I recommend changing the default targets
for other nutrients within Cronometer as follows:

● Protein: anywhere from 0.5 to 1.0 grams for each pound of bodyweight; if you are overweight
you can reduce this to your ideal bodyweight. If you measure your weight in kilograms you
can use 1.0-2.0 grams per kilogram.
● Vitamin C: 150 mg; if you are highly active, or if you get sick, 400 mg. If targeting 400 mg,
spread the vitamin C-rich foods out across the day. If using supplements, divide the dose half
in the morning and half in the evening.
● Vitamin B1 (Thiamin): 3 mg
● Vitamin B2 (Riboflavin): 2 mg
● Vitamin B3 (Niacin) 20 mg
● Vitamin B5 (Pantothenic Acid): 10 mg
● Vitamin B6: 3 mg per 100 g dietary protein
● Vitamin B7: 150 mcg per 100 g dietary protein
● Vitamin B12: 3 mcg
● Selenium: 105 mcg

For the other nutrients, you can keep Cronometer’s defaults.

To learn more about getting the vitamins and minerals you need, see
https://chrismasterjohnphd.com/101

Copyright © Chris Masterjohn, 2022. All rights reserved. Not for distribution. Do not store this in the files of a public web site.
This guide is for educational purposes only and does not constitute medical or nutritional advice. Do not use these strategies as a
substitute for medical advice or treatment.
65
References
1. Turner AJ, Hiscox JA, Hooper NM. ACE2: from vasopeptidase to SARS virus receptor.
Trends Pharmacol Sci [Internet]. 2004 Jun;25(6):291–294. Available from:
http://dx.doi.org/10.1016/j.tips.2004.04.001 PMCID: PMC7119032

2. Benton DJ, Wrobel AG, Xu P, Roustan C, Martin SR, Rosenthal PB, Skehel JJ, Gamblin SJ.
Receptor binding and priming of the spike protein of SARS-CoV-2 for membrane fusion.
Nature [Internet]. 2020 Dec;588(7837):327–330. Available from:
http://dx.doi.org/10.1038/s41586-020-2772-0 PMCID: PMC7116727

3. Bos R, Rutten L, van der Lubbe JEM, Bakkers MJG, Hardenberg G, Wegmann F,
Zuijdgeest D, de Wilde AH, Koornneef A, Verwilligen A, van Manen D, Kwaks T, Vogels R,
Dalebout TJ, Myeni SK, Kikkert M, Snijder EJ, Li Z, Barouch DH, Vellinga J, Langedijk JPM,
Zahn RC, Custers J, Schuitemaker H. Ad26 vector-based COVID-19 vaccine encoding a
prefusion-stabilized SARS-CoV-2 Spike immunogen induces potent humoral and cellular
immune responses. NPJ Vaccines [Internet]. 2020 Sep 28;5:91. Available from:
http://dx.doi.org/10.1038/s41541-020-00243-x PMCID: PMC7522255

4. Feng L, Wang Q, Shan C, Yang C, Feng Y, Wu J, Liu X, Zhou Y, Jiang R, Hu P, Liu X,


Zhang F, Li P, Niu X, Liu Y, Zheng X, Luo J, Sun J, Gu Y, Liu B, Xu Y, Li C, Pan W, Zhao J,
Ke C, Chen X, Xu T, Zhong N, Guan S, Yuan Z, Chen L. An adenovirus-vectored COVID-19
vaccine confers protection from SARS-COV-2 challenge in rhesus macaques. Nat Commun
[Internet]. 2020 Aug 21;11(1):4207. Available from:
http://dx.doi.org/10.1038/s41467-020-18077-5 PMCID: PMC7442803

5. Xia X. Detailed Dissection and Critical Evaluation of the Pfizer/BioNTech and Moderna
mRNA Vaccines. Vaccines (Basel) [Internet]. 2021 Jul 3;9(7). Available from:
http://dx.doi.org/10.3390/vaccines9070734 PMCID: PMC8310186

6. Tian JH, Patel N, Haupt R, Zhou H, Weston S, Hammond H, Logue J, Portnoff AD, Norton
J, Guebre-Xabier M, Zhou B, Jacobson K, Maciejewski S, Khatoon R, Wisniewska M,
Moffitt W, Kluepfel-Stahl S, Ekechukwu B, Papin J, Boddapati S, Jason Wong C, Piedra PA,
Frieman MB, Massare MJ, Fries L, Bengtsson KL, Stertman L, Ellingsworth L, Glenn G,
Smith G. SARS-CoV-2 spike glycoprotein vaccine candidate NVX-CoV2373
immunogenicity in baboons and protection in mice. Nat Commun [Internet]. 2021 Jan
14;12(1):372. Available from: http://dx.doi.org/10.1038/s41467-020-20653-8 PMCID:
PMC7809486

7. Vogel AB, Kanevsky I, Che Y, Swanson KA, Muik A, Vormehr M, Kranz LM, Walzer KC,
Hein S, Güler A, Loschko J, Maddur MS, Tompkins K, Cole J, Lui BG, Ziegenhals T,
Plaschke A, Eisel D, Dany SC, Fesser S, Erbar S, Bates F, Schneider D, Jesionek B,
Sänger B, Wallisch AK, Feuchter Y, Junginger H, Krumm SA, Heinen AP, Adams-Quack P,
Schlereth J, Kröner C, Hall-Ursone S, Brasky K, Griffor MC, Han S, Lees JA, Mashalidis
EH, Sahasrabudhe PV, Tan CY, Pavliakova D, Singh G, Fontes-Garfias C, Pride M, Scully
IL, Ciolino T, Obregon J, Gazi M, Carrion R, Alfson KJ, Kalina WV, Kaushal D, Shi PY,
Klamp T, Rosenbaum C, Kuhn AN, Türeci Ö, Dormitzer PR, Jansen KU, Sahin U. A
prefusion SARS-CoV-2 spike RNA vaccine is highly immunogenic and prevents lung
infection in non-human primates [Internet]. bioRxiv. 2020 [cited 2022 Aug 6]. p.
2020.09.08.280818. Available from:
Copyright © Chris Masterjohn, 2022. All rights reserved. Not for distribution. Do not store this in the files of a public web site.
This guide is for educational purposes only and does not constitute medical or nutritional advice. Do not use these strategies as a
substitute for medical advice or treatment.
66
https://www.biorxiv.org/content/10.1101/2020.09.08.280818v1.full

8. Corbett KS, Edwards D, Leist SR, Abiona OM, Boyoglu-Barnum S, Gillespie RA, Himansu
S, Schäfer A, Ziwawo CT, DiPiazza AT, Dinnon KH, Elbashir SM, Shaw CA, Woods A,
Fritch EJ, Martinez DR, Bock KW, Minai M, Nagata BM, Hutchinson GB, Bahl K,
Garcia-Dominguez D, Ma L, Renzi I, Kong WP, Schmidt SD, Wang L, Zhang Y, Stevens LJ,
Phung E, Chang LA, Loomis RJ, Altaras NE, Narayanan E, Metkar M, Presnyak V, Liu C,
Louder MK, Shi W, Leung K, Yang ES, West A, Gully KL, Wang N, Wrapp D, Doria-Rose
NA, Stewart-Jones G, Bennett H, Nason MC, Ruckwardt TJ, McLellan JS, Denison MR,
Chappell JD, Moore IN, Morabito KM, Mascola JR, Baric RS, Carfi A, Graham BS.
SARS-CoV-2 mRNA Vaccine Development Enabled by Prototype Pathogen Preparedness
[Internet]. bioRxiv. 2020 [cited 2022 Aug 6]. p. 2020.06.11.145920. Available from:
https://www.biorxiv.org/content/10.1101/2020.06.11.145920v1.full

9. Sadoff J, Davis K, Douoguih M. Thrombotic Thrombocytopenia after Ad26.COV2.S


Vaccination - Response from the Manufacturer [Internet]. The New England journal of
medicine. 2021. p. 1965–1966. Available from: http://dx.doi.org/10.1056/NEJMc2106075
PMCID: PMC8117965

10. Nyström S, Hammarström P. Amyloidogenesis of SARS-CoV-2 Spike Protein. J Am Chem


Soc [Internet]. 2022 May 25;144(20):8945–8950. Available from:
http://dx.doi.org/10.1021/jacs.2c03925 PMCID: PMC9136918

11. Heinz FX, Stiasny K. Distinguishing features of current COVID-19 vaccines: knowns and
unknowns of antigen presentation and modes of action. NPJ Vaccines [Internet]. 2021 Aug
16;6(1):104. Available from: http://dx.doi.org/10.1038/s41541-021-00369-6 PMCID:
PMC8368295

12. Keech C, Albert G, Cho I, Robertson A, Reed P, Neal S, Plested JS, Zhu M, Cloney-Clark
S, Zhou H, Smith G, Patel N, Frieman MB, Haupt RE, Logue J, McGrath M, Weston S,
Piedra PA, Desai C, Callahan K, Lewis M, Price-Abbott P, Formica N, Shinde V, Fries L,
Lickliter JD, Griffin P, Wilkinson B, Glenn GM. Phase 1-2 Trial of a SARS-CoV-2
Recombinant Spike Protein Nanoparticle Vaccine. N Engl J Med [Internet]. 2020 Dec
10;383(24):2320–2332. Available from: http://dx.doi.org/10.1056/NEJMoa2026920 PMCID:
PMC7494251

13. Xia X. Domains and Functions of Spike Protein in Sars-Cov-2 in the Context of Vaccine
Design. Viruses [Internet]. 2021 Jan 14;13(1). Available from:
http://dx.doi.org/10.3390/v13010109 PMCID: PMC7829931

14. Kirchdoerfer RN, Wang N, Pallesen J, Wrapp D, Turner HL, Cottrell CA, Corbett KS,
Graham BS, McLellan JS, Ward AB. Stabilized coronavirus spikes are resistant to
conformational changes induced by receptor recognition or proteolysis. Sci Rep [Internet].
2018 Oct 24;8(1):15701. Available from: http://dx.doi.org/10.1038/s41598-018-34171-7
PMCID: PMC6200764

15. Vogel AB, Kanevsky I, Che Y, Swanson KA, Muik A, Vormehr M, Kranz LM, Walzer KC,
Hein S, Güler A, Loschko J, Maddur MS, Ota-Setlik A, Tompkins K, Cole J, Lui BG,
Ziegenhals T, Plaschke A, Eisel D, Dany SC, Fesser S, Erbar S, Bates F, Schneider D,
Jesionek B, Sänger B, Wallisch AK, Feuchter Y, Junginger H, Krumm SA, Heinen AP,
Adams-Quack P, Schlereth J, Schille S, Kröner C, de la Caridad Güimil Garcia R, Hiller T,
Copyright © Chris Masterjohn, 2022. All rights reserved. Not for distribution. Do not store this in the files of a public web site.
This guide is for educational purposes only and does not constitute medical or nutritional advice. Do not use these strategies as a
substitute for medical advice or treatment.
67
Fischer L, Sellers RS, Choudhary S, Gonzalez O, Vascotto F, Gutman MR, Fontenot JA,
Hall-Ursone S, Brasky K, Griffor MC, Han S, Su AAH, Lees JA, Nedoma NL, Mashalidis
EH, Sahasrabudhe PV, Tan CY, Pavliakova D, Singh G, Fontes-Garfias C, Pride M, Scully
IL, Ciolino T, Obregon J, Gazi M, Carrion R Jr, Alfson KJ, Kalina WV, Kaushal D, Shi PY,
Klamp T, Rosenbaum C, Kuhn AN, Türeci Ö, Dormitzer PR, Jansen KU, Sahin U. BNT162b
vaccines protect rhesus macaques from SARS-CoV-2. Nature [Internet]. 2021
Apr;592(7853):283–289. Available from: http://dx.doi.org/10.1038/s41586-021-03275-y
PMID: 33524990

16. Nguyen HL, Lan PD, Thai NQ, Nissley DA, O’Brien EP, Li MS. Does SARS-CoV-2 Bind to
Human ACE2 More Strongly Than Does SARS-CoV? J Phys Chem B [Internet]. 2020 Aug
27;124(34):7336–7347. Available from: http://dx.doi.org/10.1021/acs.jpcb.0c04511 PMCID:
PMC7433338

17. Schoenmaker L, Witzigmann D, Kulkarni JA, Verbeke R, Kersten G, Jiskoot W, Crommelin


DJA. mRNA-lipid nanoparticle COVID-19 vaccines: Structure and stability. Int J Pharm
[Internet]. 2021 May 15;601:120586. Available from:
http://dx.doi.org/10.1016/j.ijpharm.2021.120586 PMCID: PMC8032477

18. Listed NA. A Tissue Distribution Study of a [3H]-Labelled Lipid Nanoparticle-mRNA


Formulation Containing ALC-0315 and ALC-0159 Following Intramuscular Administration in
Wistar Han Rats. Available from: 125742_S1_M4_4223_185350.pdf at
https://phmpt.org/pfizers-documents/

19. Listed NA. EXPRESSION OF LUCIFERASE-ENCODING MODRNA AFTER I.M.


APPLICATION OF GMP- READY ACUITAS LIPID NANOPARTICLE FORMULATION.
Available from: http://dx.doi.org/125742_S1_M4_4223_R-20-0072.pdf at
https://phmpt.org/pfizers-documents/

20. Sebastiani F, Yanez Arteta M, Lerche M, Porcar L, Lang C, Bragg RA, Elmore CS,
Krishnamurthy VR, Russell RA, Darwish T, Pichler H, Waldie S, Moulin M, Haertlein M,
Forsyth VT, Lindfors L, Cárdenas M. Apolipoprotein E Binding Drives Structural and
Compositional Rearrangement of mRNA-Containing Lipid Nanoparticles. ACS Nano
[Internet]. 2021 Apr 27;15(4):6709–6722. Available from:
http://dx.doi.org/10.1021/acsnano.0c10064 PMCID: PMC8155318

21. Mui BL, Tam YK, Jayaraman M, Ansell SM, Du X, Tam YYC, Lin PJ, Chen S,
Narayanannair JK, Rajeev KG, Manoharan M, Akinc A, Maier MA, Cullis P, Madden TD,
Hope MJ. Influence of Polyethylene Glycol Lipid Desorption Rates on Pharmacokinetics
and Pharmacodynamics of siRNA Lipid Nanoparticles. Mol Ther Nucleic Acids [Internet].
2013 Dec 17;2:e139. Available from: http://dx.doi.org/10.1038/mtna.2013.66 PMCID:
PMC3894582

22. Sato Y, Hatakeyama H, Hyodo M, Harashima H. Relationship Between the


Physicochemical Properties of Lipid Nanoparticles and the Quality of siRNA Delivery to
Liver Cells. Mol Ther [Internet]. 2016 Apr;24(4):788–795. Available from:
http://dx.doi.org/10.1038/mt.2015.222 PMCID: PMC4886930

23. Kersten S. Physiological regulation of lipoprotein lipase. Biochim Biophys Acta [Internet].
2014 Jul;1841(7):919–933. Available from: http://dx.doi.org/10.1016/j.bbalip.2014.03.013
PMID: 24721265
Copyright © Chris Masterjohn, 2022. All rights reserved. Not for distribution. Do not store this in the files of a public web site.
This guide is for educational purposes only and does not constitute medical or nutritional advice. Do not use these strategies as a
substitute for medical advice or treatment.
68
24. Baker AT, Boyd RJ, Sarkar D, Teijeira-Crespo A, Chan CK, Bates E, Waraich K, Vant J,
Wilson E, Truong CD, Lipka-Lloyd M, Fromme P, Vermaas J, Williams D, Machiesky L,
Heurich M, Nagalo BM, Coughlan L, Umlauf S, Chiu PL, Rizkallah PJ, Cohen TS, Parker
AL, Singharoy A, Borad MJ. ChAdOx1 interacts with CAR and PF4 with implications for
thrombosis with thrombocytopenia syndrome. Sci Adv [Internet]. 2021 Dec
3;7(49):eabl8213. Available from: http://dx.doi.org/10.1126/sciadv.abl8213 PMCID:
PMC8635433

25. Nestić D, Božinović K, Pehar I, Wallace R, Parker AL, Majhen D. The Revolving Door of
Adenovirus Cell Entry: Not All Pathways Are Equal. Pharmaceutics [Internet]. 2021 Sep
29;13(10). Available from: http://dx.doi.org/10.3390/pharmaceutics13101585 PMCID:
PMC8540258

26. Almuqrin A, Davidson AD, Williamson MK, Lewis PA, Heesom KJ, Morris S, Gilbert SC,
Matthews DA. SARS-CoV-2 vaccine ChAdOx1 nCoV-19 infection of human cell lines
reveals low levels of viral backbone gene transcription alongside very high levels of
SARS-CoV-2 S glycoprotein gene transcription. Genome Med [Internet]. 2021 Mar
15;13(1):43. Available from: http://dx.doi.org/10.1186/s13073-021-00859-1 PMCID:
PMC7958140

27. FACT SHEET FOR HEALTHCARE PROVIDERS ADMINISTERING VACCINE


(VACCINATION PROVIDERS). Available from:
https://www.fda.gov/media/159897/download

28. Reimer JM, Karlsson KH, Lövgren-Bengtsson K, Magnusson SE, Fuentes A, Stertman L.
Matrix-MTM adjuvant induces local recruitment, activation and maturation of central immune
cells in absence of antigen. PLoS One [Internet]. 2012 Jul 23;7(7):e41451. Available from:
http://dx.doi.org/10.1371/journal.pone.0041451 PMCID: PMC3402407

29. (2) (PDF) DETECTION OF GRAPHENE IN COVID19 VACCINES [Internet]. ResearchGate.


[cited 2022 Aug 7]. Available from:
https://www.researchgate.net/profile/Pablo-Campra/publication/355979001_DETECTION_
OF_GRAPHENE_IN_COVID19_VACCINES/links/6187be4907be5f31b753dfcc/DETECTIO
N-OF-GRAPHENE-IN-COVID19-VACCINES.pdf

30. Applications of Graphene Oxide and Reduced Graphene Oxide [Internet]. [cited 2022 Aug
7]. Available from:
https://www.sigmaaldrich.com/US/en/technical-documents/technical-article/materials-scienc
e-and-engineering/microelectronics-and-nanoelectronics/applications-of-graphene-oxide-an
d-reduced-graphene-oxide

31. Buzhdygan TP, DeOre BJ, Baldwin-Leclair A, Bullock TA, McGary HM, Khan JA, Razmpour
R, Hale JF, Galie PA, Potula R, Andrews AM, Ramirez SH. The SARS-CoV-2 spike protein
alters barrier function in 2D static and 3D microfluidic in-vitro models of the human
blood-brain barrier. Neurobiol Dis [Internet]. 2020 Dec;146:105131. Available from:
http://dx.doi.org/10.1016/j.nbd.2020.105131 PMCID: PMC7547916

32. Asandei A, Mereuta L, Schiopu I, Park J, Seo CH, Park Y, Luchian T.


Non-Receptor-Mediated Lipid Membrane Permeabilization by the SARS-CoV-2 Spike
Protein S1 Subunit. ACS Appl Mater Interfaces [Internet]. 2020 Dec
16;12(50):55649–55658. Available from: http://dx.doi.org/10.1021/acsami.0c17044 PMID:
Copyright © Chris Masterjohn, 2022. All rights reserved. Not for distribution. Do not store this in the files of a public web site.
This guide is for educational purposes only and does not constitute medical or nutritional advice. Do not use these strategies as a
substitute for medical advice or treatment.
69
33270413

33. Colunga Biancatelli RML, Solopov PA, Sharlow ER, Lazo JS, Marik PE, Catravas JD. The
SARS-CoV-2 spike protein subunit S1 induces COVID-19-like acute lung injury in
Κ18-hACE2 transgenic mice and barrier dysfunction in human endothelial cells. Am J
Physiol Lung Cell Mol Physiol [Internet]. 2021 Aug 1;321(2):L477–L484. Available from:
http://dx.doi.org/10.1152/ajplung.00223.2021 PMCID: PMC8384477

34. Ogata AF, Cheng CA, Desjardins M, Senussi Y, Sherman AC, Powell M, Novack L, Von S,
Li X, Baden LR, Walt DR. Circulating Severe Acute Respiratory Syndrome Coronavirus 2
(SARS-CoV-2) Vaccine Antigen Detected in the Plasma of mRNA-1273 Vaccine Recipients.
Clin Infect Dis [Internet]. 2022 Mar 1;74(4):715–718. Available from:
http://dx.doi.org/10.1093/cid/ciab465 PMCID: PMC8241425

35. FDA. M7(R1) Assessment and Control of DNA Reactive (Mutagenic) Impurities in
Pharmaceuticals To Limit Potential Carcinogenic Risk Guidance for Industry. Available from:
https://www.tga.gov.au/sites/default/files/ichq3cr5.pdf

36. Röltgen K, Nielsen SCA, Silva O, Younes SF, Zaslavsky M, Costales C, Yang F, Wirz OF,
Solis D, Hoh RA, Wang A, Arunachalam PS, Colburg D, Zhao S, Haraguchi E, Lee AS,
Shah MM, Manohar M, Chang I, Gao F, Mallajosyula V, Li C, Liu J, Shoura MJ, Sindher SB,
Parsons E, Dashdorj NJ, Dashdorj ND, Monroe R, Serrano GE, Beach TG, Chinthrajah RS,
Charville GW, Wilbur JL, Wohlstadter JN, Davis MM, Pulendran B, Troxell ML, Sigal GB,
Natkunam Y, Pinsky BA, Nadeau KC, Boyd SD. Immune imprinting, breadth of variant
recognition, and germinal center response in human SARS-CoV-2 infection and
vaccination. Cell [Internet]. 2022 Mar 17;185(6):1025–1040.e14. Available from:
http://dx.doi.org/10.1016/j.cell.2022.01.018 PMCID: PMC8786601

37. Jahn K, Handtke S, Palankar R, Kohler TP, Wesche J, Wolff M, Bayer J, Wolz C,
Greinacher A, Hammerschmidt S. α-hemolysin of Staphylococcus aureus impairs thrombus
formation. J Thromb Haemost [Internet]. 2022 Jun;20(6):1464–1475. Available from:
http://dx.doi.org/10.1111/jth.15703 PMID: 35303391

38. Grobbelaar LM, Venter C, Vlok M, Ngoepe M, Laubscher GJ, Lourens PJ, Steenkamp J,
Kell DB, Pretorius E. SARS-CoV-2 spike protein S1 induces fibrin(ogen) resistant to
fibrinolysis: implications for microclot formation in COVID-19. Biosci Rep [Internet]. 2021
Aug 27;41(8). Available from: http://dx.doi.org/10.1042/BSR20210611 PMCID:
PMC8380922

39. Kell DB, Pretorius E. Proteins behaving badly. Substoichiometric molecular control and
amplification of the initiation and nature of amyloid fibril formation: lessons from and for
blood clotting. Prog Biophys Mol Biol [Internet]. 2017 Jan;123:16–41. Available from:
http://dx.doi.org/10.1016/j.pbiomolbio.2016.08.006 PMID: 27554450

40. Pretorius E, Mbotwe S, Kell DB. Lipopolysaccharide-binding protein (LBP) reverses the
amyloid state of fibrin seen in plasma of type 2 diabetics with cardiovascular co-morbidities.
Sci Rep [Internet]. 2017 Aug 29;7(1):9680. Available from:
http://dx.doi.org/10.1038/s41598-017-09860-4 PMCID: PMC5574907

41. de Villiers S, Bester J, Kell DB, Pretorius E. A Possible Role of Amyloidogenic Blood
Clotting in the Evolving Haemodynamics of Female Migraine-With-Aura: Results From a
Copyright © Chris Masterjohn, 2022. All rights reserved. Not for distribution. Do not store this in the files of a public web site.
This guide is for educational purposes only and does not constitute medical or nutritional advice. Do not use these strategies as a
substitute for medical advice or treatment.
70
Pilot Study. Front Neurol [Internet]. 2019 Nov 26;10:1262. Available from:
http://dx.doi.org/10.3389/fneur.2019.01262 PMCID: PMC6887655

42. Pretorius E, Vlok M, Venter C, Bezuidenhout JA, Laubscher GJ, Steenkamp J, Kell DB.
Persistent clotting protein pathology in Long COVID/Post-Acute Sequelae of COVID-19
(PASC) is accompanied by increased levels of antiplasmin. Cardiovasc Diabetol [Internet].
2021 Aug 23;20(1):172. Available from: http://dx.doi.org/10.1186/s12933-021-01359-7
PMCID: PMC8381139

43. Cortes-Canteli M, Paul J, Norris EH, Bronstein R, Ahn HJ, Zamolodchikov D,


Bhuvanendran S, Fenz KM, Strickland S. Fibrinogen and beta-amyloid association alters
thrombosis and fibrinolysis: a possible contributing factor to Alzheimer’s disease. Neuron
[Internet]. 2010 Jun 10;66(5):695–709. Available from:
http://dx.doi.org/10.1016/j.neuron.2010.05.014 PMCID: PMC2895773

44. Pretorius E, Mbotwe S, Bester J, Robinson CJ, Kell DB. Acute induction of anomalous and
amyloidogenic blood clotting by molecular amplification of highly substoichiometric levels of
bacterial lipopolysaccharide. J R Soc Interface [Internet]. 2016 Sep;13(122). Available from:
http://dx.doi.org/10.1098/rsif.2016.0539 PMCID: PMC5046953

45. Townsend L, Fogarty H, Dyer A, Martin-Loeches I, Bannan C, Nadarajan P, Bergin C,


O’Farrelly C, Conlon N, Bourke NM, Ward SE, Byrne M, Ryan K, O’Connell N, O’Sullivan
JM, Ni Cheallaigh C, O’Donnell JS. Prolonged elevation of D-dimer levels in convalescent
COVID-19 patients is independent of the acute phase response. J Thromb Haemost
[Internet]. 2021 Apr;19(4):1064–1070. Available from: http://dx.doi.org/10.1111/jth.15267
PMCID: PMC8013297

46. Vaxman I, Gertz M. When to Suspect a Diagnosis of Amyloidosis. Acta Haematol [Internet].
2020 Apr 27;143(4):304–311. Available from: http://dx.doi.org/10.1159/000506617 PMID:
32340017

47. Ogata AF, Maley AM, Wu C, Gilboa T, Norman M, Lazarovits R, Mao CP, Newton G, Chang
M, Nguyen K, Kamkaew M, Zhu Q, Gibson TE, Ryan ET, Charles RC, Marasco WA, Walt
DR. Ultra-Sensitive Serial Profiling of SARS-CoV-2 Antigens and Antibodies in Plasma to
Understand Disease Progression in COVID-19 Patients with Severe Disease. Clin Chem
[Internet]. 2020 Dec 1;66(12):1562–1572. Available from:
http://dx.doi.org/10.1093/clinchem/hvaa213 PMCID: PMC7499543

48. Fajnzylber J, Regan J, Coxen K, Corry H, Wong C, Rosenthal A, Worrall D, Giguel F,


Piechocka-Trocha A, Atyeo C, Fischinger S, Chan A, Flaherty KT, Hall K, Dougan M, Ryan
ET, Gillespie E, Chishti R, Li Y, Jilg N, Hanidziar D, Baron RM, Baden L, Tsibris AM,
Armstrong KA, Kuritzkes DR, Alter G, Walker BD, Yu X, Li JZ, Massachusetts Consortium
for Pathogen Readiness. SARS-CoV-2 viral load is associated with increased disease
severity and mortality. Nat Commun [Internet]. 2020 Oct 30;11(1):5493. Available from:
http://dx.doi.org/10.1038/s41467-020-19057-5 PMCID: PMC7603483

49. Bansal S, Perincheri S, Fleming T, Poulson C, Tiffany B, Bremner RM, Mohanakumar T.


Cutting Edge: Circulating Exosomes with COVID Spike Protein Are Induced by BNT162b2
(Pfizer-BioNTech) Vaccination prior to Development of Antibodies: A Novel Mechanism for
Immune Activation by mRNA Vaccines. J Immunol [Internet]. 2021 Nov
15;207(10):2405–2410. Available from: http://dx.doi.org/10.4049/jimmunol.2100637 PMID:
Copyright © Chris Masterjohn, 2022. All rights reserved. Not for distribution. Do not store this in the files of a public web site.
This guide is for educational purposes only and does not constitute medical or nutritional advice. Do not use these strategies as a
substitute for medical advice or treatment.
71
34654691

50. Merchant HA. Comment on Aldén et al. Intracellular Reverse Transcription of Pfizer
BioNTech COVID-19 mRNA Vaccine BNT162b2 In Vitro in Human Liver Cell Line. Curr.
Issues Mol. Biol. 2022, 44, 1115-1126. Curr Issues Mol Biol [Internet]. 2022 Apr
11;44(4):1661–1663. Available from: http://dx.doi.org/10.3390/cimb44040113 PMCID:
PMC9164063

51. Zhang L, Richards A, Barrasa MI, Hughes SH, Young RA, Jaenisch R. Reverse-transcribed
SARS-CoV-2 RNA can integrate into the genome of cultured human cells and can be
expressed in patient-derived tissues. Proc Natl Acad Sci U S A [Internet]. 2021 May
25;118(21). Available from: http://dx.doi.org/10.1073/pnas.2105968118 PMCID:
PMC8166107

52. Cara A, Reitz MS Jr. New insight on the role of extrachromosomal retroviral DNA. Leukemia
[Internet]. 1997 Sep;11(9):1395–1399. Available from:
http://dx.doi.org/10.1038/sj.leu.2400776 PMID: 9305590

53. Cara A, Klotman ME. Retroviral E-DNA: persistence and gene expression in nondividing
immune cells. J Leukoc Biol [Internet]. 2006 Nov;80(5):1013–1017. Available from:
http://dx.doi.org/10.1189/jlb.0306151 PMID: 16923918

54. Kilzer JM, Stracker T, Beitzel B, Meek K, Weitzman M, Bushman FD. Roles of host cell
factors in circularization of retroviral dna. Virology [Internet]. 2003 Sep 15;314(1):460–467.
Available from: http://dx.doi.org/10.1016/s0042-6822(03)00455-0 PMID: 14517098

55. Møller HD, Mohiyuddin M, Prada-Luengo I, Sailani MR, Halling JF, Plomgaard P, Maretty L,
Hansen AJ, Snyder MP, Pilegaard H, Lam HYK, Regenberg B. Circular DNA elements of
chromosomal origin are common in healthy human somatic tissue. Nat Commun [Internet].
2018 Mar 14;9(1):1069. Available from: http://dx.doi.org/10.1038/s41467-018-03369-8
PMCID: PMC5852086

56. Kawano H, Motokawa T, Kurohama H, Okano S, Akashi R, Yonekura T, Ikeda S, Izumikawa


K, Maemura K. Fulminant Myocarditis 24 Days after Coronavirus Disease Messenger
Ribonucleic Acid Vaccination. Intern Med [Internet]. 2022 Aug 1;61(15):2319–2325.
Available from: http://dx.doi.org/10.2169/internalmedicine.9800-22 PMID: 35650138

57. Yoshimura Y, Sasaki H, Miyata N, Miyazaki K, Okudela K, Tateishi Y, Hayashi H,


Kawana-Tachikawa A, Iwashita H, Maeda K, Ihama Y, Hatayama Y, Ryo A, Tachikawa N.
An autopsy case of COVID-19-like acute respiratory distress syndrome after mRNA-1273
SARS-CoV-2 vaccination. Int J Infect Dis [Internet]. 2022 Aug;121:98–101. Available from:
http://dx.doi.org/10.1016/j.ijid.2022.04.057 PMCID: PMC9054706

58. Boettler T, Csernalabics B, Salié H, Luxenburger H, Wischer L, Salimi Alizei E, Zoldan K,


Krimmel L, Bronsert P, Schwabenland M, Prinz M, Mogler C, Neumann-Haefelin C, Thimme
R, Hofmann M, Bengsch B. SARS-CoV-2 vaccination can elicit a CD8 T-cell dominant
hepatitis. J Hepatol [Internet]. 2022 Apr 21; Available from:
http://dx.doi.org/10.1016/j.jhep.2022.03.040 PMCID: PMC9021033

59. Zollner A, Koch R, Jukic A, Pfister A, Meyer M, Rössler A, Kimpel J, Adolph TE, Tilg H.
Postacute COVID-19 is Characterized by Gut Viral Antigen Persistence in Inflammatory
Copyright © Chris Masterjohn, 2022. All rights reserved. Not for distribution. Do not store this in the files of a public web site.
This guide is for educational purposes only and does not constitute medical or nutritional advice. Do not use these strategies as a
substitute for medical advice or treatment.
72
Bowel Diseases. Gastroenterology [Internet]. 2022 Aug;163(2):495–506.e8. Available from:
http://dx.doi.org/10.1053/j.gastro.2022.04.037 PMCID: PMC9057012

60. Xia J, Tang W, Wang J, Lai D, Xu Q, Huang R, Hu Y, Gong X, Fan J, Shu Q, Xu J.


SARS-CoV-2 N Protein Induces Acute Lung Injury in Mice via NF-ĸB Activation. Front
Immunol [Internet]. 2021 Dec 7;12:791753. Available from:
http://dx.doi.org/10.3389/fimmu.2021.791753 PMCID: PMC8688532

61. Ndeupen S, Qin Z, Jacobsen S, Estanbouli H, Bouteau A, Igyártó BZ. The mRNA-LNP
platform’s lipid nanoparticle component used in preclinical vaccine studies is highly
inflammatory. bioRxiv [Internet]. 2021 Jul 23; Available from:
http://dx.doi.org/10.1101/2021.03.04.430128 PMCID: PMC7941620

62. CHMP. COVID-19 mRNA Vaccine (Nucleoside-Modified). Available from:


https://www.ema.europa.eu/en/documents/assessment-report/comirnaty-epar-public-assess
ment-report_en.pdf

63. Kircheis R. Coagulopathies after Vaccination against SARS-CoV-2 May Be Derived from a
Combined Effect of SARS-CoV-2 Spike Protein and Adenovirus Vector-Triggered Signaling
Pathways. Int J Mol Sci [Internet]. 2021 Oct 6;22(19). Available from:
http://dx.doi.org/10.3390/ijms221910791 PMCID: PMC8509779

64. Palmieri V, Perini G, De Spirito M, Papi M. Graphene oxide touches blood: in vivo
interactions of bio-coronated 2D materials. Nanoscale Horiz [Internet]. 2019 Mar
1;4(2):273–290. Available from: http://dx.doi.org/10.1039/c8nh00318a PMID: 32254085

65. Polvere I, Parrella A, Zerillo L, Voccola S, Cardinale G, D’Andrea S, Madera JR, Stilo R,
Vito P, Zotti T. Humoral Immune Response Diversity to Different COVID-19 Vaccines:
Implications for the “Green Pass” Policy. Front Immunol [Internet]. 2022 May 11;13:833085.
Available from: http://dx.doi.org/10.3389/fimmu.2022.833085 PMCID: PMC9130843

66. Barbeau DJ, Martin JM, Carney E, Dougherty E, Doyle JD, Dermody TS, Hoberman A,
Williams JV, Michaels MG, Alcorn JF, Paul Duprex W, McElroy AK. Comparative analysis of
human immune responses following SARS-CoV-2 vaccination with BNT162b2,
mRNA-1273, or Ad26.COV2.S. NPJ Vaccines [Internet]. 2022 Jul 6;7(1):77. Available from:
http://dx.doi.org/10.1038/s41541-022-00504-x PMCID: PMC9258461

67. Han H, Ma Q, Li C, Liu R, Zhao L, Wang W, Zhang P, Liu X, Gao G, Liu F, Jiang Y, Cheng
X, Zhu C, Xia Y. Profiling serum cytokines in COVID-19 patients reveals IL-6 and IL-10 are
disease severity predictors. Emerg Microbes Infect [Internet]. 2020 Dec;9(1):1123–1130.
Available from: http://dx.doi.org/10.1080/22221751.2020.1770129 PMCID: PMC7473317

68. Anantharaj A, Gujjar S, Verma N, Khan NA, Shaman H, Sharanabasava P, Das A, Pandey
R, Pandey AK, Medigeshi GR. Resolution of viral load in mild COVID-19 patients is
associated with both innate and adaptive immune responses. J Clin Virol [Internet]. 2022
Jan;146:105060. Available from: http://dx.doi.org/10.1016/j.jcv.2021.105060 PMCID:
PMC8687718

69. Sonnweber T, Boehm A, Sahanic S, Pizzini A, Aichner M, Sonnweber B, Kurz K,


Koppelstätter S, Haschka D, Petzer V, Hilbe R, Theurl M, Lehner D, Nairz M, Puchner B,
Luger A, Schwabl C, Bellmann-Weiler R, Wöll E, Widmann G, Tancevski I,
Copyright © Chris Masterjohn, 2022. All rights reserved. Not for distribution. Do not store this in the files of a public web site.
This guide is for educational purposes only and does not constitute medical or nutritional advice. Do not use these strategies as a
substitute for medical advice or treatment.
73
Judith-Löffler-Ragg, Weiss G. Persisting alterations of iron homeostasis in COVID-19 are
associated with non-resolving lung pathologies and poor patients’ performance: a
prospective observational cohort study. Respir Res [Internet]. 2020 Oct 21;21(1):276.
Available from: http://dx.doi.org/10.1186/s12931-020-01546-2 PMCID: PMC7575703

70. Arunachalam PS, Scott MKD, Hagan T, Li C, Feng Y, Wimmers F, Grigoryan L, Trisal M,
Edara VV, Lai L, Chang SE, Feng A, Dhingra S, Shah M, Lee AS, Chinthrajah S, Sindher
SB, Mallajosyula V, Gao F, Sigal N, Kowli S, Gupta S, Pellegrini K, Tharp G,
Maysel-Auslender S, Hamilton S, Aoued H, Hrusovsky K, Roskey M, Bosinger SE, Maecker
HT, Boyd SD, Davis MM, Utz PJ, Suthar MS, Khatri P, Nadeau KC, Pulendran B. Systems
vaccinology of the BNT162b2 mRNA vaccine in humans. Nature [Internet]. 2021
Aug;596(7872):410–416. Available from: http://dx.doi.org/10.1038/s41586-021-03791-x
PMCID: PMC8761119

71. Bergamaschi C, Terpos E, Rosati M, Angel M, Bear J, Stellas D, Karaliota S, Apostolakou


F, Bagratuni T, Patseas D, Gumeni S, Trougakos IP, Dimopoulos MA, Felber BK, Pavlakis
GN. Systemic IL-15, IFN-γ, and IP-10/CXCL10 signature associated with effective immune
response to SARS-CoV-2 in BNT162b2 mRNA vaccine recipients. Cell Rep [Internet]. 2021
Aug 10;36(6):109504. Available from: http://dx.doi.org/10.1016/j.celrep.2021.109504
PMCID: PMC8299183

72. Willems LH, Nagy M, Ten Cate H, Spronk HMH, Jacobs LMC, Kranendonk J, van Leeuwen
M, Meijer D, Middeldorp S, Groh LA, Warlé MC. ChAdOx1 vaccination, blood coagulation,
and inflammation: No effect on coagulation but increased interleukin-6. Res Pract Thromb
Haemost [Internet]. 2021 Dec;5(8):e12630. Available from:
http://dx.doi.org/10.1002/rth2.12630 PMCID: PMC8652129

73. Greifenberg V, Ribechini E, Rössner S, Lutz MB. Myeloid-derived suppressor cell activation
by combined LPS and IFN-gamma treatment impairs DC development. Eur J Immunol
[Internet]. 2009 Oct;39(10):2865–2876. Available from:
http://dx.doi.org/10.1002/eji.200939486 PMID: 19637228

74. Hegde S, Leader AM, Merad M. MDSC: Markers, development, states, and unaddressed
complexity. Immunity [Internet]. 2021 May 11;54(5):875–884. Available from:
http://dx.doi.org/10.1016/j.immuni.2021.04.004 PMCID: PMC8709560

75. Woodruff MC, Ramonell RP, Saini AS, Haddad NS, Anam FA, Rudolph ME, Bugrovsky R,
Hom J, Cashman KS, Nguyen DC, Kyu S, Piazza M, Tipton CM, Jenks SA, Lee FEH, Sanz
I. Relaxed peripheral tolerance drives broad de novo autoreactivity in severe COVID-19.
medRxiv [Internet]. 2021 Jul 27; Available from:
http://dx.doi.org/10.1101/2020.10.21.20216192 PMCID: PMC7587839

76. Murphy WJ, Longo DL. A Possible Role for Anti-idiotype Antibodies in SARS-CoV-2
Infection and Vaccination. N Engl J Med [Internet]. 2022 Jan 27;386(4):394–396. Available
from: http://dx.doi.org/10.1056/NEJMcibr2113694 PMID: 34818473

77. Murphy WJ, Longo DL. Anti-idiotype Antibodies in SARS-CoV-2 Infection and Vaccination.
Reply [Internet]. The New England journal of medicine. 2022. p. 898–899. Available from:
http://dx.doi.org/10.1056/NEJMc2119443 PMID: 35108468

78. Hajjo R, Sabbah DA, Tropsha A. Analyzing the Systems Biology Effects of COVID-19
Copyright © Chris Masterjohn, 2022. All rights reserved. Not for distribution. Do not store this in the files of a public web site.
This guide is for educational purposes only and does not constitute medical or nutritional advice. Do not use these strategies as a
substitute for medical advice or treatment.
74
mRNA Vaccines to Assess Their Safety and Putative Side Effects. Pathogens [Internet].
2022 Jun 29;11(7). Available from: http://dx.doi.org/10.3390/pathogens11070743 PMCID:
PMC9320269

79. Healey Q, Sheikh A, Daines L, Vasileiou E. Symptoms and signs of long COVID: A rapid
review and meta-analysis. J Glob Health [Internet]. 2022 May 21;12:05014. Available from:
http://dx.doi.org/10.7189/jogh.12.05014 PMCID: PMC9125197

80. Lopez-Leon S, Wegman-Ostrosky T, Perelman C, Sepulveda R, Rebolledo PA, Cuapio A,


Villapol S. More than 50 long-term effects of COVID-19: a systematic review and
meta-analysis. Sci Rep [Internet]. 2021 Aug 9;11(1):16144. Available from:
http://dx.doi.org/10.1038/s41598-021-95565-8 PMCID: PMC8352980

81. Ceban F, Ling S, Lui LMW, Lee Y, Gill H, Teopiz KM, Rodrigues NB, Subramaniapillai M, Di
Vincenzo JD, Cao B, Lin K, Mansur RB, Ho RC, Rosenblat JD, Miskowiak KW, Vinberg M,
Maletic V, McIntyre RS. Fatigue and cognitive impairment in Post-COVID-19 Syndrome: A
systematic review and meta-analysis. Brain Behav Immun [Internet]. 2022 Mar;101:93–135.
Available from: http://dx.doi.org/10.1016/j.bbi.2021.12.020 PMCID: PMC8715665

82. Wang S, Mortazavi J, Hart JE, Hankins JA, Katuska LM, Farland LV, Gaskins AJ, Wang YX,
Tamimi RM, Terry KL, Rich-Edwards JW, Missmer SA, Chavarro JE. A prospective study of
the association between SARS-CoV-2 infection and COVID-19 vaccination with changes in
usual menstrual cycle characteristics. Am J Obstet Gynecol [Internet]. 2022 Jul 13;
Available from: http://dx.doi.org/10.1016/j.ajog.2022.07.003 PMCID: PMC9277995

83. Ahmed A Ibrahim E, Isam Farah Hassan R, Abbasher Hussien Mohamed Ahmed K, Taha
Salah E, Eltahier Abdalla Omer M, S Haroun M. Neurological manifestations of COVID-19:
A potential gate to the determinants of a poor prognosis. Brain Behav [Internet]. 2022
Jun;12(6):e2587. Available from: http://dx.doi.org/10.1002/brb3.2587 PMCID: PMC9110897

84. Khayat-Khoei M, Bhattacharyya S, Katz J, Harrison D, Tauhid S, Bruso P, Houtchens MK,


Edwards KR, Bakshi R. COVID-19 mRNA vaccination leading to CNS inflammation: a case
series. J Neurol [Internet]. 2022 Mar;269(3):1093–1106. Available from:
http://dx.doi.org/10.1007/s00415-021-10780-7 PMCID: PMC8417681

85. Matteo E, Romoli M, Calabrò C, Piccolo L, Lazzarotto T, Suserea M, Contardi S, Stagni S,


Gabrielli L, Forlivesi S, Bassi M, Borsari M, Sacripanti C, Merli E, Naldi F, Kaveh KM, Borghi
A, Magni E, Simonetti L, Descovich C, Vegezzi E, Gastaldi M, Zini A. Combined Central
and Peripheral Demyelination with Anti-Neurofascin155 IgG Following COVID-19
Vaccination. Can J Neurol Sci [Internet]. 2021 Dec 13;1–3. Available from:
http://dx.doi.org/10.1017/cjn.2021.256 PMCID: PMC8814467

86. Oshida S, Akamatsu Y, Matsumoto Y, Suzuki T, Sasaki T, Kondo Y, Fujiwara S, Kashimura


H, Kubo Y, Ogasawara K. Intracranial aneurysm rupture within three days after receiving
mRNA anti-COVID-19 vaccination: Three case reports. Surg Neurol Int [Internet]. 2022 Mar
31;13:117. Available from: http://dx.doi.org/10.25259/SNI_1144_2021 PMCID:
PMC9062907

87. Waheed W, Carey ME, Tandan SR, Tandan R. Post COVID-19 vaccine small fiber
neuropathy. Muscle Nerve [Internet]. 2021 Jul;64(1):E1–E2. Available from:
http://dx.doi.org/10.1002/mus.27251 PMCID: PMC8250971
Copyright © Chris Masterjohn, 2022. All rights reserved. Not for distribution. Do not store this in the files of a public web site.
This guide is for educational purposes only and does not constitute medical or nutritional advice. Do not use these strategies as a
substitute for medical advice or treatment.
75
88. Iseki M, Nakayama H, Watanabe M, Uchibori A, Chiba A, Mizutani S. [A case of
polyneuropathy after COVID-19 vaccine]. Rinsho Shinkeigaku [Internet]. 2022 Jul
29;62(7):558–562. Available from: http://dx.doi.org/10.5692/clinicalneurol.cn-001750 PMID:
35753790

89. Karimi Galougahi K. Autonomic dysfunction post-inoculation with ChAdOx1 nCoV-19


vaccine. Eur Heart J Case Rep [Internet]. 2021 Dec;5(12):ytab472. Available from:
http://dx.doi.org/10.1093/ehjcr/ytab472 PMCID: PMC8672656

90. Reddy S, Reddy S, Arora M. A Case of Postural Orthostatic Tachycardia Syndrome


Secondary to the Messenger RNA COVID-19 Vaccine. Cureus [Internet]. 2021 May
4;13(5):e14837. Available from: http://dx.doi.org/10.7759/cureus.14837 PMCID:
PMC8101507

91. Vitturi BK, Grandis M, Beltramini S, Orsi A, Schenone A, Icardi G, Durando P.


Parsonage-Turner syndrome following coronavirus disease 2019 immunization with
ChAdOx1-S vaccine: a case report and review of the literature. J Med Case Rep [Internet].
2021 Dec 13;15(1):589. Available from: http://dx.doi.org/10.1186/s13256-021-03176-8
PMCID: PMC8667016

92. Queler SC, Towbin AJ, Milani C, Whang J, Sneag DB. Parsonage-Turner Syndrome
Following COVID-19 Vaccination: MR Neurography. Radiology [Internet]. 2022
Jan;302(1):84–87. Available from: http://dx.doi.org/10.1148/radiol.2021211374 PMCID:
PMC8488809

93. Flikkema K, Brossy K. Parsonage-Turner Syndrome After COVID-19 Vaccination: A Case


Report. JBJS Case Connect [Internet]. 2021 Dec 22;11(4). Available from:
http://dx.doi.org/10.2106/JBJS.CC.21.00577 PMID: 34936579

94. Coffman JR, Randolph AC, Somerson JS. Parsonage-Turner Syndrome After SARS-CoV-2
BNT162b2 Vaccine: A Case Report. JBJS Case Connect [Internet]. 2021 Sep 24;11(3).
Available from: http://dx.doi.org/10.2106/JBJS.CC.21.00370 PMID: 34559695

95. Kim SI, Seok HY, Yi J, Cho JH. Leg paralysis after AstraZeneca COVID-19 vaccination
diagnosed as neuralgic amyotrophy of the lumbosacral plexus: a case report. J Int Med Res
[Internet]. 2021 Nov;49(11):3000605211056783. Available from:
http://dx.doi.org/10.1177/03000605211056783 PMCID: PMC8649466

96. Crespo Burillo JA, Loriente Martínez C, García Arguedas C, Mora Pueyo FJ. Amyotrophic
neuralgia secondary to Vaxzevri (AstraZeneca) COVID-19 vaccine. Neurologia [Internet].
2021 Sep;36(7):571–572. Available from: http://dx.doi.org/10.1016/j.nrleng.2021.05.002
PMCID: PMC8316086

97. Koh JS, Goh Y, Tan BYQ, Hui ACF, Hoe RHM, Makmur A, Kei PL, Vijayan J, Ng KWP,
Quek AML, Thirugnanm U. Neuralgic amyotrophy following COVID-19 mRNA vaccination.
QJM [Internet]. 2021 Nov 5;114(7):503–505. Available from:
http://dx.doi.org/10.1093/qjmed/hcab216 PMID: 34347105

98. Narasimhalu K, Lee WC, Salkade PR, De Silva DA. Trigeminal and cervical radiculitis after
tozinameran vaccination against COVID-19. BMJ Case Rep [Internet]. 2021 Jun 21;14(6).
Available from: http://dx.doi.org/10.1136/bcr-2021-242344 PMCID: PMC8217939
Copyright © Chris Masterjohn, 2022. All rights reserved. Not for distribution. Do not store this in the files of a public web site.
This guide is for educational purposes only and does not constitute medical or nutritional advice. Do not use these strategies as a
substitute for medical advice or treatment.
76
99. Kaya A, Kaya SY. A case of trigeminal neuralgia developing after a COVID-19 vaccination.
J Neurovirol [Internet]. 2022 Feb;28(1):181–182. Available from:
http://dx.doi.org/10.1007/s13365-021-01030-7 PMCID: PMC8647511

100. Morena J, Gyang TV. Myelin Oligodendrocyte Glycoprotein Antibody-Associated


Disease and Transverse Myelitis Probably Associated With SARS-CoV-2 mRNA Vaccines:
Two Case Reports. Neurohospitalist [Internet]. 2022 Jul;12(3):536–540. Available from:
http://dx.doi.org/10.1177/19418744221090426 PMCID: PMC9214935

101. Tahir N, Koorapati G, Prasad S, Jeelani HM, Sherchan R, Shrestha J, Shayuk M.


SARS-CoV-2 Vaccination-Induced Transverse Myelitis. Cureus [Internet]. 2021
Jul;13(7):e16624. Available from: http://dx.doi.org/10.7759/cureus.16624 PMCID:
PMC8384391

102. Hsiao YT, Tsai MJ, Chen YH, Hsu CF. Acute Transverse Myelitis after COVID-19
Vaccination. Medicina [Internet]. 2021 Sep 25;57(10). Available from:
http://dx.doi.org/10.3390/medicina57101010 PMCID: PMC8540274

103. Pagenkopf C, Südmeyer M. A case of longitudinally extensive transverse myelitis


following vaccination against Covid-19. J Neuroimmunol [Internet]. 2021 Sep
15;358:577606. Available from: http://dx.doi.org/10.1016/j.jneuroim.2021.577606 PMCID:
PMC8223023

104. Tan WY, Yusof Khan AHK, Mohd Yaakob MN, Abdul Rashid AM, Loh WC, Baharin J,
Ibrahim A, Ismail MR, Inche Mat LN, Wan Sulaiman WA, Basri H, Hoo FK. Longitudinal
extensive transverse myelitis following ChAdOx1 nCOV-19 vaccine: a case report. BMC
Neurol [Internet]. 2021 Oct 12;21(1):395. Available from:
http://dx.doi.org/10.1186/s12883-021-02427-x PMCID: PMC8506086

105. Notghi AA, Atley J, Silva M. Lessons of the month 1: Longitudinal extensive transverse
myelitis following AstraZeneca COVID-19 vaccination. Clin Med [Internet]. 2021
Sep;21(5):e535–e538. Available from: http://dx.doi.org/10.7861/clinmed.2021-0470 PMCID:
PMC8439525

106. Hirose S, Hara M, Koda K, Natori N, Yokota Y, Ninomiya S, Nakajima H. Acute


autoimmune transverse myelitis following COVID-19 vaccination: A case report. Medicine
[Internet]. 2021 Dec 23;100(51):e28423. Available from:
http://dx.doi.org/10.1097/MD.0000000000028423 PMCID: PMC8701778

107. Khan E, Shrestha AK, Colantonio MA, Liberio RN, Sriwastava S. Acute transverse
myelitis following SARS-CoV-2 vaccination: a case report and review of literature. J Neurol
[Internet]. 2022 Mar;269(3):1121–1132. Available from:
http://dx.doi.org/10.1007/s00415-021-10785-2 PMCID: PMC8418691

108. Vegezzi E, Ravaglia S, Buongarzone G, Bini P, Diamanti L, Gastaldi M, Prunetti P,


Rognone E, Marchioni E. Acute myelitis and ChAdOx1 nCoV-19 vaccine: Casual or causal
association? J Neuroimmunol [Internet]. 2021 Oct 15;359:577686. Available from:
http://dx.doi.org/10.1016/j.jneuroim.2021.577686 PMCID: PMC8325554

109. Malhotra HS, Gupta P, Prabhu V, Kumar Garg R, Dandu H, Agarwal V. COVID-19
vaccination-associated myelitis. QJM [Internet]. 2021 Nov 5;114(8):591–593. Available
Copyright © Chris Masterjohn, 2022. All rights reserved. Not for distribution. Do not store this in the files of a public web site.
This guide is for educational purposes only and does not constitute medical or nutritional advice. Do not use these strategies as a
substitute for medical advice or treatment.
77
from: http://dx.doi.org/10.1093/qjmed/hcab069 PMCID: PMC8083508

110. Sadoff J, Gray G, Vandebosch A, Cárdenas V, Shukarev G, Grinsztejn B, Goepfert PA,


Truyers C, Fennema H, Spiessens B, Offergeld K, Scheper G, Taylor KL, Robb ML, Treanor
J, Barouch DH, Stoddard J, Ryser MF, Marovich MA, Neuzil KM, Corey L, Cauwenberghs
N, Tanner T, Hardt K, Ruiz-Guiñazú J, Le Gars M, Schuitemaker H, Van Hoof J, Struyf F,
Douoguih M, ENSEMBLE Study Group. Safety and Efficacy of Single-Dose Ad26.COV2.S
Vaccine against Covid-19. N Engl J Med [Internet]. 2021 Jun 10;384(23):2187–2201.
Available from: http://dx.doi.org/10.1056/NEJMoa2101544 PMCID: PMC8220996

111. Voysey M, Costa Clemens SA, Madhi SA, Weckx LY, Folegatti PM, Aley PK, Angus B,
Baillie VL, Barnabas SL, Bhorat QE, Bibi S, Briner C, Cicconi P, Clutterbuck EA, Collins
AM, Cutland CL, Darton TC, Dheda K, Dold C, Duncan CJA, Emary KRW, Ewer KJ,
Flaxman A, Fairlie L, Faust SN, Feng S, Ferreira DM, Finn A, Galiza E, Goodman AL,
Green CM, Green CA, Greenland M, Hill C, Hill HC, Hirsch I, Izu A, Jenkin D, Joe CCD,
Kerridge S, Koen A, Kwatra G, Lazarus R, Libri V, Lillie PJ, Marchevsky NG, Marshall RP,
Mendes AVA, Milan EP, Minassian AM, McGregor A, Mujadidi YF, Nana A, Padayachee SD,
Phillips DJ, Pittella A, Plested E, Pollock KM, Ramasamy MN, Ritchie AJ, Robinson H,
Schwarzbold AV, Smith A, Song R, Snape MD, Sprinz E, Sutherland RK, Thomson EC,
Török ME, Toshner M, Turner DPJ, Vekemans J, Villafana TL, White T, Williams CJ,
Douglas AD, Hill AVS, Lambe T, Gilbert SC, Pollard AJ, Oxford COVID Vaccine Trial Group.
Single-dose administration and the influence of the timing of the booster dose on
immunogenicity and efficacy of ChAdOx1 nCoV-19 (AZD1222) vaccine: a pooled analysis
of four randomised trials. Lancet [Internet]. 2021 Mar 6;397(10277):881–891. Available
from: http://dx.doi.org/10.1016/S0140-6736(21)00432-3 PMCID: PMC7894131

112. Thomas SJ, Moreira ED Jr, Kitchin N, Absalon J, Gurtman A, Lockhart S, Perez JL,
Pérez Marc G, Polack FP, Zerbini C, Bailey R, Swanson KA, Xu X, Roychoudhury S, Koury
K, Bouguermouh S, Kalina WV, Cooper D, Frenck RW Jr, Hammitt LL, Türeci Ö, Nell H,
Schaefer A, Ünal S, Yang Q, Liberator P, Tresnan DB, Mather S, Dormitzer PR, Şahin U,
Gruber WC, Jansen KU, C4591001 Clinical Trial Group. Safety and Efficacy of the
BNT162b2 mRNA Covid-19 Vaccine through 6 Months. N Engl J Med [Internet]. 2021 Sep
15; Available from: http://dx.doi.org/10.1056/NEJMoa2110345 PMCID: PMC8461570

113. El Sahly HM, Baden LR, Essink B, Doblecki-Lewis S, Martin JM, Anderson EJ, Campbell
TB, Clark J, Jackson LA, Fichtenbaum CJ, Zervos M, Rankin B, Eder F, Feldman G,
Kennelly C, Han-Conrad L, Levin M, Neuzil KM, Corey L, Gilbert P, Janes H, Follmann D,
Marovich M, Polakowski L, Mascola JR, Ledgerwood JE, Graham BS, August A, Clouting
H, Deng W, Han S, Leav B, Manzo D, Pajon R, Schödel F, Tomassini JE, Zhou H, Miller J,
COVE Study Group. Efficacy of the mRNA-1273 SARS-CoV-2 Vaccine at Completion of
Blinded Phase. N Engl J Med [Internet]. 2021 Nov 4;385(19):1774–1785. Available from:
http://dx.doi.org/10.1056/NEJMoa2113017 PMCID: PMC8482810

114. Peter Doshi: Pfizer and Moderna’s “95% effective” vaccines—we need more details and
the raw data [Internet]. The BMJ. 2021 [cited 2022 Aug 7]. Available from:
https://blogs.bmj.com/bmj/2021/01/04/peter-doshi-pfizer-and-modernas-95-effective-vaccin
es-we-need-more-details-and-the-raw-data/

115. Polack FP, Thomas SJ, Kitchin N, Absalon J, Gurtman A, Lockhart S, Perez JL, Pérez
Marc G, Moreira ED, Zerbini C, Bailey R, Swanson KA, Roychoudhury S, Koury K, Li P,
Kalina WV, Cooper D, Frenck RW Jr, Hammitt LL, Türeci Ö, Nell H, Schaefer A, Ünal S,
Copyright © Chris Masterjohn, 2022. All rights reserved. Not for distribution. Do not store this in the files of a public web site.
This guide is for educational purposes only and does not constitute medical or nutritional advice. Do not use these strategies as a
substitute for medical advice or treatment.
78
Tresnan DB, Mather S, Dormitzer PR, Şahin U, Jansen KU, Gruber WC, C4591001 Clinical
Trial Group. Safety and Efficacy of the BNT162b2 mRNA Covid-19 Vaccine. N Engl J Med
[Internet]. 2020 Dec 31;383(27):2603–2615. Available from:
http://dx.doi.org/10.1056/NEJMoa2034577 PMCID: PMC7745181

116. Liuzzi JP, Lichten LA, Rivera S, Blanchard RK, Aydemir TB, Knutson MD, Ganz T,
Cousins RJ. Interleukin-6 regulates the zinc transporter Zip14 in liver and contributes to the
hypozincemia of the acute-phase response. Proc Natl Acad Sci U S A [Internet]. 2005 May
10;102(19):6843–6848. Available from: http://dx.doi.org/10.1073/pnas.0502257102 PMCID:
PMC1100791

117. Han Y, Huang W, Meng H, Zhan Y, Hou J. Pro-inflammatory cytokine


interleukin-6-induced hepcidin, a key mediator of periodontitis-related anemia of
inflammation. J Periodontal Res [Internet]. 2021 Aug;56(4):690–701. Available from:
http://dx.doi.org/10.1111/jre.12865 PMID: 33656216

118. Granero R, Pardo-Garrido A, Carpio-Toro IL, Ramírez-Coronel AA, Martínez-Suárez PC,


Reivan-Ortiz GG. The Role of Iron and Zinc in the Treatment of ADHD among Children and
Adolescents: A Systematic Review of Randomized Clinical Trials. Nutrients [Internet]. 2021
Nov 13;13(11). Available from: http://dx.doi.org/10.3390/nu13114059 PMCID: PMC8618748

119. Kim HB, Park B, Shim JY. Anemia in Association with Cognitive Impairment: A
Systematic Review and Meta-Analysis. J Alzheimers Dis [Internet]. 2019;72(3):803–814.
Available from: http://dx.doi.org/10.3233/JAD-190521 PMID: 31640093

120. Rutjes AW, Denton DA, Di Nisio M, Chong LY, Abraham RP, Al-Assaf AS, Anderson JL,
Malik MA, Vernooij RW, Martínez G, Tabet N, McCleery J. Vitamin and mineral
supplementation for maintaining cognitive function in cognitively healthy people in mid and
late life. Cochrane Database Syst Rev [Internet]. 2018 Dec 17;12:CD011906. Available
from: http://dx.doi.org/10.1002/14651858.CD011906.pub2 PMCID: PMC6353240

121. Warthon-Medina M, Moran VH, Stammers AL, Dillon S, Qualter P, Nissensohn M,


Serra-Majem L, Lowe NM. Zinc intake, status and indices of cognitive function in adults and
children: a systematic review and meta-analysis. Eur J Clin Nutr [Internet]. 2015
Jun;69(6):649–661. Available from: http://dx.doi.org/10.1038/ejcn.2015.60 PMID: 25920424

122. Warner MJ, Kamran MT. Iron Deficiency Anemia. StatPearls [Internet]. Treasure Island
(FL): StatPearls Publishing; 2021. Available from:
https://www.ncbi.nlm.nih.gov/pubmed/28846348 PMID: 28846348

123. Trost LB, Bergfeld WF, Calogeras E. The diagnosis and treatment of iron deficiency and
its potential relationship to hair loss. J Am Acad Dermatol [Internet]. 2006
May;54(5):824–844. Available from: http://dx.doi.org/10.1016/j.jaad.2005.11.1104 PMID:
16635664

124. Park SY, Na SY, Kim JH, Cho S, Lee JH. Iron plays a certain role in patterned hair loss. J
Korean Med Sci [Internet]. 2013 Jun;28(6):934–938. Available from:
http://dx.doi.org/10.3346/jkms.2013.28.6.934 PMCID: PMC3678013

125. Zappa M, Verdecchia P, Spanevello A, Visca D, Angeli F. Blood pressure increase after
Pfizer/BioNTech SARS-CoV-2 vaccine. Eur J Intern Med [Internet]. 2021 Aug;90:111–113.
Copyright © Chris Masterjohn, 2022. All rights reserved. Not for distribution. Do not store this in the files of a public web site.
This guide is for educational purposes only and does not constitute medical or nutritional advice. Do not use these strategies as a
substitute for medical advice or treatment.
79
Available from: http://dx.doi.org/10.1016/j.ejim.2021.06.013 PMCID: PMC8206586

126. Frangež R, Šuput D, Molgó J, Benoit E. Ostreolysin A/Pleurotolysin B and Equinatoxins:


Structure, Function and Pathophysiological Effects of These Pore-Forming Proteins. Toxins
[Internet]. 2017 Apr 5;9(4). Available from: http://dx.doi.org/10.3390/toxins9040128 PMCID:
PMC5408202

127. Martini J, Cabrales P, Tsai AG, Intaglietta M. Mechanotransduction and the homeostatic
significance of maintaining blood viscosity in hypotension, hypertension and haemorrhage.
J Intern Med [Internet]. 2006 Apr;259(4):364–372. Available from:
http://dx.doi.org/10.1111/j.1365-2796.2006.01622.x PMID: 16594904

128. Li C, Chen Y, Zhao Y, Lung DC, Ye Z, Song W, Liu FF, Cai JP, Wong WM, Yip CCY,
Chan JFW, To KKW, Sridhar S, Hung IFN, Chu H, Kok KH, Jin DY, Zhang AJ, Yuen KY.
Intravenous Injection of Coronavirus Disease 2019 (COVID-19) mRNA Vaccine Can Induce
Acute Myopericarditis in Mouse Model. Clin Infect Dis [Internet]. 2022 Jun
10;74(11):1933–1950. Available from: http://dx.doi.org/10.1093/cid/ciab707 PMCID:
PMC8436386

129. Gilley RP, González-Juarbe N, Shenoy AT, Reyes LF, Dube PH, Restrepo MI, Orihuela
CJ. Infiltrated Macrophages Die of Pneumolysin-Mediated Necroptosis following
Pneumococcal Myocardial Invasion. Infect Immun [Internet]. 2016 May;84(5):1457–1469.
Available from: http://dx.doi.org/10.1128/IAI.00007-16 PMCID: PMC4862731

130. Voysey M, Clemens SAC, Madhi SA, Weckx LY, Folegatti PM, Aley PK, Angus B, Baillie
VL, Barnabas SL, Bhorat QE, Bibi S, Briner C, Cicconi P, Collins AM, Colin-Jones R,
Cutland CL, Darton TC, Dheda K, Duncan CJA, Emary KRW, Ewer KJ, Fairlie L, Faust SN,
Feng S, Ferreira DM, Finn A, Goodman AL, Green CM, Green CA, Heath PT, Hill C, Hill H,
Hirsch I, Hodgson SHC, Izu A, Jackson S, Jenkin D, Joe CCD, Kerridge S, Koen A, Kwatra
G, Lazarus R, Lawrie AM, Lelliott A, Libri V, Lillie PJ, Mallory R, Mendes AVA, Milan EP,
Minassian AM, McGregor A, Morrison H, Mujadidi YF, Nana A, O’Reilly PJ, Padayachee
SD, Pittella A, Plested E, Pollock KM, Ramasamy MN, Rhead S, Schwarzbold AV, Singh N,
Smith A, Song R, Snape MD, Sprinz E, Sutherland RK, Tarrant R, Thomson EC, Török ME,
Toshner M, Turner DPJ, Vekemans J, Villafana TL, Watson MEE, Williams CJ, Douglas AD,
Hill AVS, Lambe T, Gilbert SC, Pollard AJ, Oxford COVID Vaccine Trial Group. Safety and
efficacy of the ChAdOx1 nCoV-19 vaccine (AZD1222) against SARS-CoV-2: an interim
analysis of four randomised controlled trials in Brazil, South Africa, and the UK. Lancet
[Internet]. 2021 Jan 9;397(10269):99–111. Available from:
http://dx.doi.org/10.1016/S0140-6736(20)32661-1 PMCID: PMC7723445

131. Ozonoff A, Nanishi E, Levy O. Bell’s palsy and SARS-CoV-2 vaccines. Lancet Infect Dis
[Internet]. 2021 Apr;21(4):450–452. Available from:
http://dx.doi.org/10.1016/S1473-3099(21)00076-1 PMCID: PMC7906673

132. Safavi F, Gustafson L, Walitt B, Lehky T, Dehbashi S, Wiebold A, Mina Y, Shin S, Pan B,
Polydefkis M, Oaklander AL, Nath A. Neuropathic symptoms with SARS-CoV-2 vaccination.
medRxiv [Internet]. 2022 May 17; Available from:
http://dx.doi.org/10.1101/2022.05.16.22274439 PMCID: PMC9128783

133. Cirillo N, Doan R. Bell’s palsy and SARS-CoV-2 vaccines-an unfolding story [Internet].
The Lancet infectious diseases. 2021. p. 1210–1211. Available from:
Copyright © Chris Masterjohn, 2022. All rights reserved. Not for distribution. Do not store this in the files of a public web site.
This guide is for educational purposes only and does not constitute medical or nutritional advice. Do not use these strategies as a
substitute for medical advice or treatment.
80
http://dx.doi.org/10.1016/S1473-3099(21)00273-5 PMCID: PMC8184125

134. Heath PT, Galiza EP, Baxter DN, Boffito M, Browne D, Burns F, Chadwick DR, Clark R,
Cosgrove C, Galloway J, Goodman AL, Heer A, Higham A, Iyengar S, Jamal A, Jeanes C,
Kalra PA, Kyriakidou C, McAuley DF, Meyrick A, Minassian AM, Minton J, Moore P,
Munsoor I, Nicholls H, Osanlou O, Packham J, Pretswell CH, San Francisco Ramos A,
Saralaya D, Sheridan RP, Smith R, Soiza RL, Swift PA, Thomson EC, Turner J, Viljoen ME,
Albert G, Cho I, Dubovsky F, Glenn G, Rivers J, Robertson A, Smith K, Toback S,
2019nCoV-302 Study Group. Safety and Efficacy of NVX-CoV2373 Covid-19 Vaccine. N
Engl J Med [Internet]. 2021 Sep 23;385(13):1172–1183. Available from:
http://dx.doi.org/10.1056/NEJMoa2107659 PMCID: PMC8262625

135. FDA. Vaccines and Related Biological Products Advisory Committee Meeting June 7,
2022. Available from: https://www.fda.gov/media/158912/download

136. Sadoff J, Gray G, Vandebosch A, Cárdenas V, Shukarev G, Grinsztejn B, Goepfert PA,


Truyers C, Van Dromme I, Spiessens B, Vingerhoets J, Custers J, Scheper G, Robb ML,
Treanor J, Ryser MF, Barouch DH, Swann E, Marovich MA, Neuzil KM, Corey L, Stoddard
J, Hardt K, Ruiz-Guiñazú J, Le Gars M, Schuitemaker H, Van Hoof J, Struyf F, Douoguih M,
ENSEMBLE Study Group. Final Analysis of Efficacy and Safety of Single-Dose
Ad26.COV2.S. N Engl J Med [Internet]. 2022 Mar 3;386(9):847–860. Available from:
http://dx.doi.org/10.1056/NEJMoa2117608 PMCID: PMC8849184

137. Falsey AR, Sobieszczyk ME, Hirsch I, Sproule S, Robb ML, Corey L, Neuzil KM, Hahn
W, Hunt J, Mulligan MJ, McEvoy C, DeJesus E, Hassman M, Little SJ, Pahud BA, Durbin A,
Pickrell P, Daar ES, Bush L, Solis J, Carr QO, Oyedele T, Buchbinder S, Cowden J, Vargas
SL, Guerreros Benavides A, Call R, Keefer MC, Kirkpatrick BD, Pullman J, Tong T,
Brewinski Isaacs M, Benkeser D, Janes HE, Nason MC, Green JA, Kelly EJ, Maaske J,
Mueller N, Shoemaker K, Takas T, Marshall RP, Pangalos MN, Villafana T, Gonzalez-Lopez
A, AstraZeneca AZD1222 Clinical Study Group. Phase 3 Safety and Efficacy of AZD1222
(ChAdOx1 nCoV-19) Covid-19 Vaccine. N Engl J Med [Internet]. 2021 Dec
16;385(25):2348–2360. Available from: http://dx.doi.org/10.1056/NEJMoa2105290 PMCID:
PMC8522798

138. Jeon YH, Lim DH, Choi SW, Choi SJ. A flare of Still’s disease following COVID-19
vaccination in a 34-year-old patient. Rheumatol Int [Internet]. 2022 Apr;42(4):743–748.
Available from: http://dx.doi.org/10.1007/s00296-021-05052-6 PMCID: PMC8602986

139. Muench F, Krusche M, Sander LE, Rose T, Burmester GR, Schneider U. Macrophage
activation syndrome in a patient with adult-onset Still’s disease following first COVID-19
vaccination with BNT162b2. BMC Rheumatol [Internet]. 2021 Dec 28;5(1):60. Available
from: http://dx.doi.org/10.1186/s41927-021-00237-9 PMCID: PMC8712099

140. Longo VD, Cortellino S. Fasting, dietary restriction, and immunosenescence. J Allergy
Clin Immunol [Internet]. 2020 Nov;146(5):1002–1004. Available from:
http://dx.doi.org/10.1016/j.jaci.2020.07.035 PMID: 32853639

141. Miyaura C, Abe E, Suda T, Kuroki T. Alternative differentiation of human promyelocytic


leukemia cells (HL-60) induced selectively by retinoic acid and 1 alpha,25-dihydroxyvitamin
D3. Cancer Res [Internet]. 1985 Sep;45(9):4244–4248. Available from:
https://www.ncbi.nlm.nih.gov/pubmed/2992776 PMID: 2992776
Copyright © Chris Masterjohn, 2022. All rights reserved. Not for distribution. Do not store this in the files of a public web site.
This guide is for educational purposes only and does not constitute medical or nutritional advice. Do not use these strategies as a
substitute for medical advice or treatment.
81
142. Ozawa K, Sato N, Urabe A, Takaku F. Modulation of normal myelopoiesis in vitro by
retinoic acid. Biochem Biophys Res Commun [Internet]. 1984 Aug 30;123(1):128–132.
Available from: http://dx.doi.org/10.1016/0006-291x(84)90389-9 PMID: 6477579

143. Prus E, Fibach E. Retinoic acid induction of CD38 antigen expression on normal and
leukemic human myeloid cells: relationship with cell differentiation. Leuk Lymphoma
[Internet]. 2003 Apr;44(4):691–698. Available from:
http://dx.doi.org/10.1080/1042819031000060564 PMID: 12769347

144. Koeffler HP, Amatruda T, Ikekawa N, Kobayashi Y, DeLuca HF. Induction of macrophage
differentiation of human normal and leukemic myeloid stem cells by 1,25-dihydroxyvitamin
D3 and its fluorinated analogues. Cancer Res [Internet]. 1984 Dec;44(12 Pt 1):5624–5628.
Available from: https://www.ncbi.nlm.nih.gov/pubmed/6594194 PMID: 6594194

145. Ikeda U, Wakita D, Ohkuri T, Chamoto K, Kitamura H, Iwakura Y, Nishimura T.


1α,25-Dihydroxyvitamin D3 and all-trans retinoic acid synergistically inhibit the
differentiation and expansion of Th17 cells. Immunol Lett [Internet]. 2010 Nov
30;134(1):7–16. Available from: http://dx.doi.org/10.1016/j.imlet.2010.07.002 PMID:
20655952

146. Duvall MG, Levy BD. DHA- and EPA-derived resolvins, protectins, and maresins in
airway inflammation. Eur J Pharmacol [Internet]. Elsevier; 2016 Aug 15;785:144–155.
Available from: https://www.sciencedirect.com/science/article/pii/S001429991530340X
PMCID: pmc4854800

147. Arita M, Clish CB, Serhan CN. The contributions of aspirin and microbial oxygenase to
the biosynthesis of anti-inflammatory resolvins: novel oxygenase products from omega-3
polyunsaturated fatty acids. Biochem Biophys Res Commun [Internet]. 2005 Dec
9;338(1):149–157. Available from: http://dx.doi.org/10.1016/j.bbrc.2005.07.181 PMID:
16112645

148. Obata T, Nagakura T, Masaki T, Maekawa K, Yamashita K. Eicosapentaenoic acid


inhibits prostaglandin D2 generation by inhibiting cyclo-oxygenase-2 in cultured human
mast cells. Clin Exp Allergy [Internet]. 1999 Aug;29(8):1129–1135. Available from:
http://dx.doi.org/10.1046/j.1365-2222.1999.00604.x PMID: 10457118

149. Rees CA, Rostad CA, Mantus G, Anderson EJ, Chahroudi A, Jaggi P, Wrammert J,
Ochoa JB, Ochoa A, Basu RK, Heilman S, Harris F, Lapp SA, Hussaini L, Vos MB, Brown
LA, Morris CR. Altered amino acid profile in patients with SARS-CoV-2 infection. Proc Natl
Acad Sci U S A [Internet]. 2021 Jun 22;118(25). Available from:
http://dx.doi.org/10.1073/pnas.2101708118 PMCID: PMC8237604

150. De Kleer I, Willems F, Lambrecht B, Goriely S. Ontogeny of myeloid cells. Front Immunol
[Internet]. 2014 Sep 3;5:423. Available from: http://dx.doi.org/10.3389/fimmu.2014.00423
PMCID: PMC4153297

151. Veglia F, Sanseviero E, Gabrilovich DI. Myeloid-derived suppressor cells in the era of
increasing myeloid cell diversity. Nat Rev Immunol [Internet]. 2021 Aug;21(8):485–498.
Available from: http://dx.doi.org/10.1038/s41577-020-00490-y PMCID: PMC7849958

152. Grover A, Sanseviero E, Timosenko E, Gabrilovich DI. Myeloid-Derived Suppressor


Copyright © Chris Masterjohn, 2022. All rights reserved. Not for distribution. Do not store this in the files of a public web site.
This guide is for educational purposes only and does not constitute medical or nutritional advice. Do not use these strategies as a
substitute for medical advice or treatment.
82
Cells: A Propitious Road to Clinic. Cancer Discov [Internet]. 2021 Nov;11(11):2693–2706.
Available from: http://dx.doi.org/10.1158/2159-8290.CD-21-0764 PMID: 34635571

153. Gabrilovich DI. Myeloid-Derived Suppressor Cells. Cancer Immunol Res [Internet]. 2017
Jan;5(1):3–8. Available from: http://dx.doi.org/10.1158/2326-6066.CIR-16-0297 PMCID:
PMC5426480

154. Gabrilovich DI, Nagaraj S. Myeloid-derived suppressor cells as regulators of the immune
system. Nat Rev Immunol [Internet]. 2009 Mar;9(3):162–174. Available from:
http://dx.doi.org/10.1038/nri2506 PMCID: PMC2828349

155. Cassetta L, Baekkevold ES, Brandau S, Bujko A, Cassatella MA, Dorhoi A, Krieg C, Lin
A, Loré K, Marini O, Pollard JW, Roussel M, Scapini P, Umansky V, Adema GJ. Deciphering
myeloid-derived suppressor cells: isolation and markers in humans, mice and non-human
primates. Cancer Immunol Immunother [Internet]. 2019 Apr;68(4):687–697. Available from:
http://dx.doi.org/10.1007/s00262-019-02302-2 PMCID: PMC6447515

156. Dorhoi A, Glaría E, Garcia-Tellez T, Nieuwenhuizen NE, Zelinskyy G, Favier B, Singh A,


Ehrchen J, Gujer C, Münz C, Saraiva M, Sohrabi Y, Sousa AE, Delputte P, Müller-Trutwin
M, Valledor AF. MDSCs in infectious diseases: regulation, roles, and readjustment. Cancer
Immunol Immunother [Internet]. 2019 Apr;68(4):673–685. Available from:
http://dx.doi.org/10.1007/s00262-018-2277-y PMID: 30569204

157. Fresno M, Gironès N. Myeloid-Derived Suppressor Cells in Trypanosoma cruzi Infection.


Front Cell Infect Microbiol [Internet]. 2021 Aug 27;11:737364. Available from:
http://dx.doi.org/10.3389/fcimb.2021.737364 PMCID: PMC8430253

158. Cuenca AG, Delano MJ, Kelly-Scumpia KM, Moreno C, Scumpia PO, Laface DM,
Heyworth PG, Efron PA, Moldawer LL. A paradoxical role for myeloid-derived suppressor
cells in sepsis and trauma. Mol Med [Internet]. 2011 Mar;17(3-4):281–292. Available from:
http://dx.doi.org/10.2119/molmed.2010.00178 PMCID: PMC3060988

159. Mehraj V, Routy JP. Tryptophan Catabolism in Chronic Viral Infections: Handling
Uninvited Guests. Int J Tryptophan Res [Internet]. 2015 Aug 4;8:41–48. Available from:
http://dx.doi.org/10.4137/IJTR.S26862 PMCID: PMC4527356

160. Fiorentino G, Coppola A, Izzo R, Annunziata A, Bernardo M, Lombardi A, Trimarco V,


Santulli G, Trimarco B. Effects of adding L-arginine orally to standard therapy in patients
with COVID-19: A randomized, double-blind, placebo-controlled, parallel-group trial. Results
of the first interim analysis. EClinicalMedicine [Internet]. 2021 Sep 9;101125. Available
from: http://dx.doi.org/10.1016/j.eclinm.2021.101125 PMCID: PMC8428476

161. Sandstrom PA, Mannie MD, Buttke TM. Inhibition of activation-induced death in T cell
hybridomas by thiol antioxidants: oxidative stress as a mediator of apoptosis. J Leukoc Biol
[Internet]. 1994 Feb;55(2):221–226. Available from: http://dx.doi.org/10.1002/jlb.55.2.221
PMID: 7507967

162. Burgunder JM, Varriale A, Lauterburg BH. Effect of N-acetylcysteine on plasma cysteine
and glutathione following paracetamol administration. Eur J Clin Pharmacol [Internet].
1989;36(2):127–131. Available from: http://dx.doi.org/10.1007/BF00609183 PMID: 2721538

Copyright © Chris Masterjohn, 2022. All rights reserved. Not for distribution. Do not store this in the files of a public web site.
This guide is for educational purposes only and does not constitute medical or nutritional advice. Do not use these strategies as a
substitute for medical advice or treatment.
83
163. Whillier S, Raftos JE, Chapman B, Kuchel PW. Role of N-acetylcysteine and cystine in
glutathione synthesis in human erythrocytes. Redox Rep [Internet]. 2009;14(3):115–124.
Available from: http://dx.doi.org/10.1179/135100009X392539 PMID: 19490753

164. Kumar P, Liu C, Hsu JW, Chacko S, Minard C, Jahoor F, Sekhar RV. Glycine and
N-acetylcysteine (GlyNAC) supplementation in older adults improves glutathione deficiency,
oxidative stress, mitochondrial dysfunction, inflammation, insulin resistance, endothelial
dysfunction, genotoxicity, muscle strength, and cognition: Results of a pilot clinical trial. Clin
Transl Med [Internet]. 2021 Mar;11(3):e372. Available from:
http://dx.doi.org/10.1002/ctm2.372 PMCID: PMC8002905

165. Hudak SK, Overkamp D, Wagner R, Häring HU, Heni M. Ketoacidosis in a non-diabetic
woman who was fasting during lactation. Nutr J [Internet]. 2015 Nov 4;14:117. Available
from: http://dx.doi.org/10.1186/s12937-015-0076-2 PMCID: PMC4634581

166. Cheng CW, Adams GB, Perin L, Wei M, Zhou X, Lam BS, Da Sacco S, Mirisola M,
Quinn DI, Dorff TB, Kopchick JJ, Longo VD. Prolonged fasting reduces IGF-1/PKA to
promote hematopoietic-stem-cell-based regeneration and reverse immunosuppression. Cell
Stem Cell [Internet]. 2014 Jun 5;14(6):810–823. Available from:
http://dx.doi.org/10.1016/j.stem.2014.04.014 PMCID: PMC4102383

167. Zhang J, Chiu J, Zhang H, Qi T, Tang Q, Ma K, Lu H, Li G. Autophagic cell death


induced by resveratrol depends on the Ca(2+)/AMPK/mTOR pathway in A549 cells.
Biochem Pharmacol [Internet]. 2013 Jul 15;86(2):317–328. Available from:
http://dx.doi.org/10.1016/j.bcp.2013.05.003 PMID: 23680031

168. Price NL, Gomes AP, Ling AJY, Duarte FV, Martin-Montalvo A, North BJ, Agarwal B, Ye
L, Ramadori G, Teodoro JS, Hubbard BP, Varela AT, Davis JG, Varamini B, Hafner A,
Moaddel R, Rolo AP, Coppari R, Palmeira CM, de Cabo R, Baur JA, Sinclair DA. SIRT1 is
required for AMPK activation and the beneficial effects of resveratrol on mitochondrial
function. Cell Metab [Internet]. 2012 May 2;15(5):675–690. Available from:
http://dx.doi.org/10.1016/j.cmet.2012.04.003 PMCID: PMC3545644

169. Dash S, Xiao C, Morgantini C, Szeto L, Lewis GF. High-dose resveratrol treatment for 2
weeks inhibits intestinal and hepatic lipoprotein production in overweight/obese men.
Arterioscler Thromb Vasc Biol [Internet]. 2013 Dec;33(12):2895–2901. Available from:
http://dx.doi.org/10.1161/ATVBAHA.113.302342 PMID: 24072699

170. la Porte C, Voduc N, Zhang G, Seguin I, Tardiff D, Singhal N, Cameron DW.


Steady-State pharmacokinetics and tolerability of trans-resveratrol 2000 mg twice daily with
food, quercetin and alcohol (ethanol) in healthy human subjects. Clin Pharmacokinet
[Internet]. 2010 Jul;49(7):449–454. Available from:
http://dx.doi.org/10.2165/11531820-000000000-00000 PMID: 20528005

171. Vaz-da-Silva M, Loureiro AI, Falcao A, Nunes T, Rocha JF, Fernandes-Lopes C, Soares
E, Wright L, Almeida L, Soares-da-Silva P. Effect of food on the pharmacokinetic profile of
trans-resveratrol. Int J Clin Pharmacol Ther [Internet]. 2008 Nov;46(11):564–570. Available
from: http://dx.doi.org/10.5414/cpp46564 PMID: 19000554

172. Gu X, Orozco JM, Saxton RA, Condon KJ, Liu GY, Krawczyk PA, Scaria SM, Harper JW,
Gygi SP, Sabatini DM. SAMTOR is an S-adenosylmethionine sensor for the mTORC1
Copyright © Chris Masterjohn, 2022. All rights reserved. Not for distribution. Do not store this in the files of a public web site.
This guide is for educational purposes only and does not constitute medical or nutritional advice. Do not use these strategies as a
substitute for medical advice or treatment.
84
pathway. Science [Internet]. 2017 Nov 10;358(6364):813–818. Available from:
http://dx.doi.org/10.1126/science.aao3265 PMCID: PMC5747364

173. Mischoulon D, Alpert JE, Arning E, Bottiglieri T, Fava M, Papakostas GI. Bioavailability of
S-adenosyl methionine and impact on response in a randomized, double-blind,
placebo-controlled trial in major depressive disorder. J Clin Psychiatry [Internet]. 2012
Jun;73(6):843–848. Available from: http://dx.doi.org/10.4088/JCP.11m07139 PMCID:
PMC4156851

174. Xu ZR, Tan ZJ, Zhang Q, Gui QF, Yang YM. The effectiveness of leucine on muscle
protein synthesis, lean body mass and leg lean mass accretion in older people: a
systematic review and meta-analysis. Br J Nutr [Internet]. 2015 Jan 14;113(1):25–34.
Available from: http://dx.doi.org/10.1017/S0007114514002475 PMID: 25234223

175. Donoghue M, Wakimoto H, Maguire CT, Acton S, Hales P, Stagliano N,


Fairchild-Huntress V, Xu J, Lorenz JN, Kadambi V, Berul CI, Breitbart RE. Heart block,
ventricular tachycardia, and sudden death in ACE2 transgenic mice with downregulated
connexins. J Mol Cell Cardiol [Internet]. 2003 Sep;35(9):1043–1053. Available from:
http://dx.doi.org/10.1016/s0022-2828(03)00177-9 PMID: 12967627

176. Parums DV. Editorial: Multisystem Inflammatory Syndrome in Adults (MIS-A) and the
Spectrum of COVID-19. Med Sci Monit [Internet]. 2021 Oct 11;27:e935005. Available from:
http://dx.doi.org/10.12659/MSM.935005 PMCID: PMC8518511

177. Fink MP, Delude RL. Epithelial barrier dysfunction: a unifying theme to explain the
pathogenesis of multiple organ dysfunction at the cellular level. Crit Care Clin [Internet].
2005 Apr;21(2):177–196. Available from: http://dx.doi.org/10.1016/j.ccc.2005.01.005 PMID:
15781156

178. Choudhary R, Palm-Leis A, Scott RC 3rd, Guleria RS, Rachut E, Baker KM, Pan J.
All-trans retinoic acid prevents development of cardiac remodeling in aortic banded rats by
inhibiting the renin-angiotensin system. Am J Physiol Heart Circ Physiol [Internet]. 2008
Feb;294(2):H633–44. Available from: http://dx.doi.org/10.1152/ajpheart.01301.2007 PMID:
18156191

179. Zhong JC, Huang DY, Yang YM, Li YF, Liu GF, Song XH, Du K. Upregulation of
angiotensin-converting enzyme 2 by all-trans retinoic acid in spontaneously hypertensive
rats. Hypertension [Internet]. 2004 Dec;44(6):907–912. Available from:
http://dx.doi.org/10.1161/01.HYP.0000146400.57221.74 PMID: 15477383

180. Zhou TB, Wu WF, Qin YH, Yin SS. Association of all-trans retinoic acid treatment with
the renin-angiotensin aldosterone system expression in glomerulosclerosis rats. J Renin
Angiotensin Aldosterone Syst [Internet]. 2013 Dec;14(4):299–307. Available from:
http://dx.doi.org/10.1177/1470320312465220 PMID: 23144044

181. Zhou TB, Ou C, Rong L, Drummen GPC. Effect of all-trans retinoic acid treatment on
prohibitin and renin-angiotensin-aldosterone system expression in hypoxia-induced renal
tubular epithelial cell injury. J Renin Angiotensin Aldosterone Syst [Internet]. 2014
Sep;15(3):243–249. Available from: http://dx.doi.org/10.1177/1470320314542727 PMID:
25031298

Copyright © Chris Masterjohn, 2022. All rights reserved. Not for distribution. Do not store this in the files of a public web site.
This guide is for educational purposes only and does not constitute medical or nutritional advice. Do not use these strategies as a
substitute for medical advice or treatment.
85
182. Xu J, Yang J, Chen J, Luo Q, Zhang Q, Zhang H. Vitamin D alleviates
lipopolysaccharide induced acute lung injury via regulation of the renin angiotensin
system. Mol Med Rep [Internet]. 2017 Nov;16(5):7432–7438. Available from:
http://dx.doi.org/10.3892/mmr.2017.7546 PMCID: PMC5865875

183. Lin M, Gao P, Zhao T, He L, Li M, Li Y, Shui H, Wu X. Calcitriol regulates


angiotensin-converting enzyme and angiotensin converting-enzyme 2 in diabetic kidney
disease. Mol Biol Rep [Internet]. 2016 May;43(5):397–406. Available from:
http://dx.doi.org/10.1007/s11033-016-3971-5 PMID: 26968558

184. Cui C, Xu P, Li G, Qiao Y, Han W, Geng C, Liao D, Yang M, Chen D, Jiang P. Vitamin D
receptor activation regulates microglia polarization and oxidative stress in spontaneously
hypertensive rats and angiotensin II-exposed microglial cells: Role of renin-angiotensin
system. Redox Biol [Internet]. 2019 Sep;26:101295. Available from:
http://dx.doi.org/10.1016/j.redox.2019.101295 PMCID: PMC6831892

185. Goltzman D, Mannstadt M, Marcocci C. Physiology of the Calcium-Parathyroid


Hormone-Vitamin D Axis. Front Horm Res [Internet]. 2018 Mar 29;50:1–13. Available from:
http://dx.doi.org/10.1159/000486060 PMID: 29597231

186. Tsai WC, Wu HY, Peng YS, Hsu SP, Chiu YL, Yang JY, Chen HY, Pai MF, Lin WY, Hung
KY, Chu FY, Tsai SM, Chien KL. Short-Term Effects of Very-Low-Phosphate and
Low-Phosphate Diets on Fibroblast Growth Factor 23 in Hemodialysis Patients: A
Randomized Crossover Trial. Clin J Am Soc Nephrol [Internet]. 2019 Oct
7;14(10):1475–1483. Available from: http://dx.doi.org/10.2215/CJN.04250419 PMCID:
PMC6777602

187. Dai B, David V, Martin A, Huang J, Li H, Jiao Y, Gu W, Quarles LD. A comparative


transcriptome analysis identifying FGF23 regulated genes in the kidney of a mouse CKD
model. PLoS One [Internet]. 2012 Sep 6;7(9):e44161. Available from:
http://dx.doi.org/10.1371/journal.pone.0044161 PMCID: PMC3435395

188. Fujita M, Ohnishi K, Takaoka S, Ogasawara K, Fukuyama R, Nakamuta H.


Antihypertensive effects of continuous oral administration of nattokinase and its fragments
in spontaneously hypertensive rats. Biol Pharm Bull [Internet]. 2011;34(11):1696–1701.
Available from: http://dx.doi.org/10.1248/bpb.34.1696 PMID: 22040882

189. Han X, Fink MP, Uchiyama T, Yang R, Delude RL. Increased iNOS activity is essential
for pulmonary epithelial tight junction dysfunction in endotoxemic mice. Am J Physiol Lung
Cell Mol Physiol [Internet]. 2004 Feb;286(2):L259–67. Available from:
http://dx.doi.org/10.1152/ajplung.00187.2003 PMID: 12896879

190. Olson N, Greul AK, Hristova M, Bove PF, Kasahara DI, van der Vliet A. Nitric oxide and
airway epithelial barrier function: regulation of tight junction proteins and epithelial
permeability. Arch Biochem Biophys [Internet]. 2009 Apr 15;484(2):205–213. Available
from: http://dx.doi.org/10.1016/j.abb.2008.11.027 PMCID: PMC2753865

191. Marín N, Zamorano P, Carrasco R, Mujica P, González FG, Quezada C, Meininger CJ,
Boric MP, Durán WN, Sánchez FA. S-Nitrosation of β-catenin and p120 catenin: a novel
regulatory mechanism in endothelial hyperpermeability. Circ Res [Internet]. 2012 Aug
17;111(5):553–563. Available from: http://dx.doi.org/10.1161/CIRCRESAHA.112.274548
Copyright © Chris Masterjohn, 2022. All rights reserved. Not for distribution. Do not store this in the files of a public web site.
This guide is for educational purposes only and does not constitute medical or nutritional advice. Do not use these strategies as a
substitute for medical advice or treatment.
86
PMCID: PMC3966064

192. Durán WN, Beuve AV, Sánchez FA. Nitric oxide, S-nitrosation, and endothelial
permeability. IUBMB Life [Internet]. 2013 Oct;65(10):819–826. Available from:
http://dx.doi.org/10.1002/iub.1204 PMCID: PMC4004350

193. Guequén A, Carrasco R, Zamorano P, Rebolledo L, Burboa P, Sarmiento J, Boric MP,


Korayem A, Durán WN, Sánchez FA. S-nitrosylation regulates VE-cadherin phosphorylation
and internalization in microvascular permeability. Am J Physiol Heart Circ Physiol [Internet].
2016 Apr 15;310(8):H1039–44. Available from:
http://dx.doi.org/10.1152/ajpheart.00063.2016 PMCID: PMC4867340

194. Forrester MT, Foster MW, Stamler JS. Assessment and application of the biotin switch
technique for examining protein S-nitrosylation under conditions of pharmacologically
induced oxidative stress. J Biol Chem [Internet]. 2007 May 11;282(19):13977–13983.
Available from: http://dx.doi.org/10.1074/jbc.M609684200 PMID: 17376775

195. Benhar M, Forrester MT, Hess DT, Stamler JS. Regulated protein denitrosylation by
cytosolic and mitochondrial thioredoxins. Science [Internet]. 2008 May
23;320(5879):1050–1054. Available from: http://dx.doi.org/10.1126/science.1158265
PMCID: PMC2754768

196. Suschek CV, Opländer C, van Faassen EE. Non-enzymatic NO production in human
skin: effect of UVA on cutaneous NO stores. Nitric Oxide [Internet]. 2010 Feb
15;22(2):120–135. Available from: http://dx.doi.org/10.1016/j.niox.2009.10.006 PMID:
19879370

197. Colunga Biancatelli RML, Solopov PA, Gregory B, Khodour Y, Catravas JD. HSP90
Inhibitors Modulate SARS-CoV-2 Spike Protein Subunit 1-Induced Human Pulmonary
Microvascular Endothelial Activation and Barrier Dysfunction. Front Physiol [Internet]. 2022
Mar 21;13:812199. Available from: http://dx.doi.org/10.3389/fphys.2022.812199 PMCID:
PMC8979060

198. Courtney-Martin G, Rafii M, Wykes LJ, Ball RO, Pencharz PB. Methionine-adequate
cysteine-free diet does not limit erythrocyte glutathione synthesis in young healthy adult
men. J Nutr [Internet]. 2008 Nov;138(11):2172–2178. Available from:
http://dx.doi.org/10.3945/jn.108.093302 PMID: 18936215

199. Lu SC. Glutathione synthesis. Biochim Biophys Acta [Internet]. 2013


May;1830(5):3143–3153. Available from: http://dx.doi.org/10.1016/j.bbagen.2012.09.008
PMCID: PMC3549305

200. Bravi MC, Armiento A, Laurenti O, Cassone-Faldetta M, De Luca O, Moretti A, De Mattia


G. Insulin decreases intracellular oxidative stress in patients with type 2 diabetes mellitus.
Metabolism [Internet]. 2006 May;55(5):691–695. Available from:
http://dx.doi.org/10.1016/j.metabol.2006.01.003 PMID: 16631447

201. Nkhoma ET, Poole C, Vannappagari V, Hall SA, Beutler E. The global prevalence of
glucose-6-phosphate dehydrogenase deficiency: a systematic review and meta-analysis.
Blood Cells Mol Dis [Internet]. 2009 May;42(3):267–278. Available from:
http://dx.doi.org/10.1016/j.bcmd.2008.12.005 PMID: 19233695
Copyright © Chris Masterjohn, 2022. All rights reserved. Not for distribution. Do not store this in the files of a public web site.
This guide is for educational purposes only and does not constitute medical or nutritional advice. Do not use these strategies as a
substitute for medical advice or treatment.
87
202. Cho SW, Joshi JG. Characterization of glucose-6-phosphate dehydrogenase isozymes
from human and pig brain. Neuroscience [Internet]. 1990;38(3):819–828. Available from:
http://dx.doi.org/10.1016/0306-4522(90)90074-e PMID: 2270145

203. Liang W, Ouyang S, Shaw N, Joachimiak A, Zhang R, Liu ZJ. Conversion of D-ribulose
5-phosphate to D-xylulose 5-phosphate: new insights from structural and biochemical
studies on human RPE. FASEB J [Internet]. 2011 Feb;25(2):497–504. Available from:
http://dx.doi.org/10.1096/fj.10-171207 PMCID: PMC6188353

204. Mocali A, Paoletti F. Transketolase from human leukocytes. Isolation, properties and
induction of polyclonal antibodies. Eur J Biochem [Internet]. 1989 Mar 1;180(1):213–219.
Available from: http://dx.doi.org/10.1111/j.1432-1033.1989.tb14636.x PMID: 2495942

205. Hellerstein MK. De novo lipogenesis in humans: metabolic and regulatory aspects. Eur J
Clin Nutr [Internet]. 1999 Apr;53 Suppl 1:S53–65. Available from:
http://dx.doi.org/10.1038/sj.ejcn.1600744 PMID: 10365981

206. Tigchelaar C, van Zuylen ML, Hulst AH, Preckel B, van Beek AP, Kema IP, Hermanides
J, Absalom AR. Elevated cerebrospinal fluid glucose levels and diabetes mellitus are
associated with activation of the neurotoxic polyol pathway. Diabetologia [Internet]. 2022
Jul;65(7):1098–1107. Available from: http://dx.doi.org/10.1007/s00125-022-05693-7
PMCID: PMC9174140

207. Lapolla A, Tessari P, Franchin A, Gerhardinger C, Valerio A, Proto N, Fedele D. Red cell
sorbitol concentration in relation to short- and medium-term variation of plasma glucose.
Acta Diabetol Lat [Internet]. 1989 Jul;26(3):211–216. Available from:
http://dx.doi.org/10.1007/BF02581387 PMID: 2618527

208. Ciuchi E, Odetti P, Prando R. Relationship between glutathione and sorbitol


concentrations in erythrocytes from diabetic patients. Metabolism [Internet]. 1996
May;45(5):611–613. Available from: http://dx.doi.org/10.1016/s0026-0495(96)90032-3
PMID: 8622605

209. Coelho AI, Berry GT, Rubio-Gozalbo ME. Galactose metabolism and health. Curr Opin
Clin Nutr Metab Care [Internet]. 2015 Jul;18(4):422–427. Available from:
http://dx.doi.org/10.1097/MCO.0000000000000189 PMID: 26001656

210. Birlouez-Aragon I, Alloussi S. Effect of prolonged galactose consumption on galactose


tolerance in young healthy humans. Ann Nutr Metab [Internet]. 1990;34(1):1–7. Available
from: http://dx.doi.org/10.1159/000177563 PMID: 2331135

211. Onishchenko LS, Gaikova ON, Yanishevskii SN. Changes at the focus of experimental
ischemic stroke treated with neuroprotective agents. Neurosci Behav Physiol [Internet].
2008 Jan;38(1):49–54. Available from: http://dx.doi.org/10.1007/s11055-008-0007-1 PMID:
18097760

212. Baldassarro VA, Krężel W, Fernández M, Schuhbaur B, Giardino L, Calzà L. The role of
nuclear receptors in the differentiation of oligodendrocyte precursor cells derived from fetal
and adult neural stem cells. Stem Cell Res [Internet]. 2019 May;37:101443. Available from:
http://dx.doi.org/10.1016/j.scr.2019.101443 PMID: 31022610

Copyright © Chris Masterjohn, 2022. All rights reserved. Not for distribution. Do not store this in the files of a public web site.
This guide is for educational purposes only and does not constitute medical or nutritional advice. Do not use these strategies as a
substitute for medical advice or treatment.
88
213. López-Barahona M, Miñano M, Mira E, Iglesias T, Stunnenberg HG, Rodríguez-Peña A,
Bernal J, Muñoz A. Retinoic acid posttranscriptionally up-regulates proteolipid protein gene
expression in C6 glioma cells. J Biol Chem [Internet]. 1993 Dec 5;268(34):25617–25623.
Available from: https://www.ncbi.nlm.nih.gov/pubmed/7503983 PMID: 7503983

214. Baas D, Prüfer K, Ittel ME, Kuchler-Bopp S, Labourdette G, Sarliève LL, Brachet P. Rat
oligodendrocytes express the vitamin D(3) receptor and respond to 1,25-dihydroxyvitamin
D(3). Glia [Internet]. 2000 Jul;31(1):59–68. Available from:
http://dx.doi.org/10.1002/(sici)1098-1136(200007)31:1<59::aid-glia60>3.0.co;2-y PMID:
10816607

215. Weiser MJ, Butt CM, Mohajeri MH. Docosahexaenoic Acid and Cognition throughout the
Lifespan. Nutrients [Internet]. 2016 Feb 17;8(2):99. Available from:
http://dx.doi.org/10.3390/nu8020099 PMCID: PMC4772061

216. Khattar N, Triebswetter C, Kiely M, Ferrucci L, Resnick SM, Spencer RG, Bouhrara M.
Investigation of the association between cerebral iron content and myelin content in
normative aging using quantitative magnetic resonance neuroimaging. Neuroimage
[Internet]. 2021 Oct 1;239:118267. Available from:
http://dx.doi.org/10.1016/j.neuroimage.2021.118267 PMCID: PMC8370037

217. De Jesus Moreno Moreno M. Cognitive improvement in mild to moderate Alzheimer’s


dementia after treatment with the acetylcholine precursor choline alfoscerate: a multicenter,
double-blind, randomized, placebo-controlled trial. Clin Ther [Internet]. 2003
Jan;25(1):178–193. Available from: http://dx.doi.org/10.1016/s0149-2918(03)90023-3
PMID: 12637119

218. Tan MS, Yu JT, Tan CC, Wang HF, Meng XF, Wang C, Jiang T, Zhu XC, Tan L. Efficacy
and adverse effects of ginkgo biloba for cognitive impairment and dementia: a systematic
review and meta-analysis. J Alzheimers Dis [Internet]. 2015;43(2):589–603. Available from:
http://dx.doi.org/10.3233/JAD-140837 PMID: 25114079

219. Kumar SS, Sabu A. Fibrinolytic Enzymes for Thrombolytic Therapy. Adv Exp Med Biol
[Internet]. 2019;1148:345–381. Available from:
http://dx.doi.org/10.1007/978-981-13-7709-9_15 PMID: 31482506

220. Kurosawa Y, Nirengi S, Homma T, Esaki K, Ohta M, Clark JF, Hamaoka T. A single-dose
of oral nattokinase potentiates thrombolysis and anti-coagulation profiles. Sci Rep [Internet].
2015 Jun 25;5:11601. Available from: http://dx.doi.org/10.1038/srep11601 PMCID:
PMC4479826

221. Hodis HN, Mack WJ, Meiselman HJ, Kalra V, Liebman H, Hwang-Levine J, Dustin L,
Kono N, Mert M, Wenby RB, Huesca E, Rochanda L, Li Y, Yan M, St John JA, Whitfield L.
Nattokinase atherothrombotic prevention study: A randomized controlled trial. Clin
Hemorheol Microcirc [Internet]. 2021;78(4):339–353. Available from:
http://dx.doi.org/10.3233/CH-211147 PMID: 33843667

Copyright © Chris Masterjohn, 2022. All rights reserved. Not for distribution. Do not store this in the files of a public web site.
This guide is for educational purposes only and does not constitute medical or nutritional advice. Do not use these strategies as a
substitute for medical advice or treatment.
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