High fat, low carb diets

and the evidence

Dr Trudi Deakin
Confused? Has the X-PERT
Programme become low carb?

X-PERT Health is a charity with a mission to provide accurate and

up-to-date information for the prevention and treatment of
diabetes.

Version 12 & 13 of the manual acknowledges the latest evidence

for a very low carb/high fat lifestyle, it doesn’t prescribe it.

The X-PERT Programme is based on the empowerment approach

with informed decisions. If patients wish to adopt a low carb/high
fat lifestyle, it is another option for them to lose weight and
improve glycaemic control.

Thus, the X-PERT Diabetes Programme continues the same but

with less emphasis on low fat and supporting participants with
trying different dietary approaches.
 Common concerns

1. Saturated fat clogs the arteries

2. Carbohydrate is an essential nutrient
3. A LCHF diet is a nutrient deficient
diet
4. It’s a fad diet – people wont stick to it
5. If they do stick to it – it’ll cause health
problems
Macronutrient changes in diabetes
dietary guidelines

Nutrient 1930s 1970s 1980s 1990s 2000s

CHO 15% 40% >50% 50-55% 60-70% with

MUFA
(% energy)
FAT 68% 45% <35% 30-35% <35%
(% energy)
Protein 17% 15% 15% 10-15% 10-15%
(% energy)
Added None None A little as <25g/day <10%
part of mixed
sucrose
meal

↑Carbs and ↓fat over the decades

Diabetes UK Evidence Based
Nutrition Guidelines (2011)

– Weight management is the key nutritional

strategy that can improve glycaemic control
for overweight pts with T2DM (A)

– Total carbohydrate strong predictor of

glycaemic response. Monitoring intake key
strategy for glycaemic control. No evidence
to recommend specific amount (A)
Diabetes UK Evidence Based
Nutrition Guidelines (2011)

• A range of approaches should be considered. Focus on

calorie restriction
• Risks/benefits of each approach should be discussed
– Low fat/healthy eating
– Very low calorie liquid diet
– Meal replacements
– Commercial Slimming Clubs
– Low Carbohydrate
• American Diabetes Association [ADA] (2013)
recommend the mix of carbohydrate, protein, and fat be
adjusted to meet metabolic goals and individual preferences
Reference Intakes became
legislation in December 2014

for an HEALTHY
ADULT
Does this include
T2DM?
 Research to Practice Gap

Guidelines often out of date when published

17-year time lag translating research into practice1

1Morris ZS, Wooding S & Grant J (2011) J R Soc Med 2011 104: 510-520
 Professional Code for Conduct Standards
state the requirement to deliver
evidence-based practice For example:

 best interests of service users

 keep skills and knowledge up to date
 provide information necessary to make informed decisions
 engage in evidence-based practice & evaluate practice
 use research to determine appropriate actions
 critically evaluate research in order to inform practice
Challenges to traditional
dietetic advice

 Treatment focus – cause or effect

 Diabetes remission
 Intermittent fasting
 To snack or not?
 Dietary fats
 Low carb diet
Does Type 2 diabetes need to be a
progressive condition?
Normal IGR IGT Type 2 Diabetes
Insulin resistance

Post-meal glucose

Fasting glucose

Insulin
concentration

No – the progression can be halted and even reversed!

Adapted from Ramlo-Halsted & Edelman (2000) Clinical Diabet;18:80-5
Does Type 2 diabetes have to be a
progressive condition?
Poor self-
management /
Unhealthy
lifestyle
Insulin
 CVD resistance
risk
Β-cell function

 Hypoglycaemia
Weight gain HbA1c, FPG & PPG
deteriorates
Prescribed
medication

A different series of events lead to halting & even reversing progression

Does Type 2 diabetes have to be a
progressive condition?
Poor self-
Good self-
management /
management/
Unhealthy
Healthy lifestyle
lifestyle
Insulin

 CVD
CVD Insulin resistance
resistance
risk
risk Β-cell function
Β-cell function

Hypoglycaemia
Hypoglycaemia
Weight gain HbA1c, FPG
HbA1c, FPG&&PPG
PPG
Weight gain improves
deteriorates
Prescribed
Prescribed
medication
medication

A different series of events lead to halting & even reversing progression

 Normoglyaemia = 3.5 to 7.8 mmol/l
How much glucose is this?

to

to

Only 6g to 14g of glucose should be in the blood at any one time!

What is the cause and effect of Type 2 diabetes?
Insulin resistance is the cause……

………………raised blood glucose is the

effect

Are we treating the right thing?

What causes resistance?

Antibiotics! Viruses!
 Repeated drug exposure causes
resistance

Increasing insulin doses reduce glucose disposal rate

Insulin causes insulin resistance

Insulin Action

• Inhibits glycogenolysis
• Inhibits gluconeogenesis
• Stimulates de novo lipogenesis (DNL)
Insulin drives fat storage

Lack of insulin drives weight loss

 Weight loss

Low Insulin

• Type 1 diabetes • Type 2 diabetes

• Omission • Insulin
• Low carb diet • High carb diet
• Fasting • Snacking
• Exercise • Sedentary
• ↓Snacking Weight gain lifestyle
Hyperinsulinaemia causes fatty liver

Ryysy L et al. Diabetes 2000; 49(5): 749-58.

Insulin causes Insulin Resistance
Intensive Conventional Insulin
Therapy for Type II Diabetes
Diabetes Care 1993 16:23-31 Henry RR

Increasing insulin
resistance!
8.7 kg weight gain!
 Insulin secretion is primary
Increasing resistance with duration of obesity

Diabetes 43:696-702; 1994 Le Stunff C

Time Sequence of Juvenile Obesity

Genetics Increased Insulin

Obesity
insulin Resistance
Insulin resistance comes first
Obesity is secondary
Mothers with insulin resistance have big babies
High maternal
Insulin levels

High infant
Insulin levels

Infant obesity
 Insulin resistance and diet success

• Women divided
into tertiles based
on insulin
resistance

• Weight loss at 12
months – only
insulin sensitive
achieve target on
low fat diet

Low fat diet only effective in insulin sensitive individuals

Diabetes Obes Metab. 2013 January ; 15(1): 87–90. doi:10.1111/j.1463-1326.2012.01668.x.

Can Type 2 diabetes be reversed?
 Method and results
• Liquid diet formula (46.4% carb, 32.5% protein, 20.1% fat)
510 kcal + 3 portions non-starchy veg. Total 600 kcal
• Regular telephone contact
• At 8 weeks returned to normal eating but information
provided re healthy eating and portion control
• FPG 9.2±0.4 to 5.7±0.5 mmol/l (p=0.003)
• HbA1c 57±3 to 42±2 mmol/mol (7.4±0.3 to 6±0.2%)
• ↓ pancreatic fat from 8.0±1.6% to 6.2±1.1% and hepatic fat
from 12.8±2.4% to 2.9±0.2%
Critical appraisal

• An early stage clinical trial of involving 11 people

• All participants reversed their diabetes by drastically cutting their
food intake to just 600 calories a day for two months.
• However, only seven remained free of diabetes at three months.
• We wait with interest to see the long-term effect of the study.
• Insufficient evidence to recommend such an approach to people
outside a research setting.
• Diabetes UK now funding (£2.4m) randomised clinical trial of 140
people following a VLCDs for 8 to 20wks with a 2year follow-up
and comparison to 140 people receiving standard care.
87% with T2DM
<4 years and 50% > 8
years can achieve
normoglycaemia after
8 weeks

Can it be maintained?
Intermittent fasting

• Calorie restriction or short periods of fasting could achieve

a number of health benefits
- reduce cancer & aging1,2,3
- reduce diabetes & CVD4
- improve memory and balance5
• Alternate Day fasting (ADF) or 5:2 diet (Horizon: Eat, Fast
and Live Longer - BBC Two 6/8/12)
• Calorie restriction < GDA. Fasting days
~ 500kcal 600kcal 

1 Fontana L et al (2008). Aging Cell; 7(5): 681-687

2 Pallavi R et al (2012). Front Physiol; 3: 318
3 Lee C et al (2012). Sci Transl Med; 7(4): 124
4 Wallander M et al (2007). Diabetes Care; 30: 2343-2348
5 Colman RJ et al (2009). Science; 325: 201-204.
 The IGF-1 hormone
(insulin-like growth factor)
• IGF-1 is a growth hormone
• High levels lead to accelerated ageing and age-
related diseases
• Low levels are protective
• Laron syndrome, a rare condition that affects
fewer than 350 people worldwide. The very low
levels of IGF-1 their bodies produce means they
are short, but this also seems to protect them
against cancer and diabetes.
Proposed mechanism
• IGF-1 drives the body into “go-go” mode, with cells
driven to reproduce (fine when the body is growing,
but not so good later in life).
• There is now evidence suggesting that IGF-1 levels
can be lowered through diet (calorie restriction and
fasting).
• Reducing protein intake to RIs is also deemed to be
necessary.
• When the body no longer has access to food it
switches from "growth mode" to "repair mode".
• As levels of the IGF-1 hormone drop, a number of
repair genes appear to get switched on according to
ongoing research by Professor Valter Longo of the
University of Southern California.

http://fasten.tv/en/vortraege/longo
Increased frequency of eating
= increased insulin
= ↑ insulin resistance

Source: Dr Jason Fung http://intensivedietarymanagement.com/

Why were we led to believe that
saturated fat is bad for us?
 Flawed Science

Ancel Keys concluded that dietary fat increased CHD

Keys A. Coronary heart disease in seven countries.
Summary. Circulation 1970;41(4 Suppl):I186–95
Self-selected studies

e.g. choosing
Finland, Italy,
Ireland,
Switzerland,
West Germany
and Holland
would show that
the opposite is
true

http://www.perfecthealthinstitute.com/aANCELKEYS.html
 Diet-Heart Hypothesis
Assumptions
1. Saturated fat → Raised LCL-C [A → B]
2. Raised LDL-C causes CVD [B → C]
3. Saturated fat causes CVD [A → C]

Evidence
1. Limited – individual variation
2. No cause & effect evidence & some inverse correlations
3. No evidence
1. Saturated fat → Raised LCL-C
[A → B]

Shekelle et al. N Engl J Med. 1981; 304:65–70

Observational study – not cause and effect

Conclusions due not always reflect findings!
Increased
risk:
↓ HDL-C
↑ TG
↑ ApoB
↓ ApoA-1
↑ Lp(a)
↑ TC/HDL
↑ TG/HDL
Discussion
“Consumption of the Step 1 and Low-Sat diets was also associated with
significant reductions in HDL cholesterol and significant increases in Lp(a)
concentrations.
Plasma triglycerides rose minimally in our normolipidemic subjects. The
impact of these potentially atherogenic changes in response to reducing
dietary total and saturated fats must be weighed against the clearly
demonstrated benefit of reducing LDL cholesterol levels”
Randomised controlled Trial: 18% saturated fat did not increase LDL-C
No correlation between diet and
cholesterol level
 “No association is evident
between what these men
ate and their individual
cholesterol levels: diet
thus does not seem to
account for the wide
range in cholesterol
values
that was found. This
range may be crucial to
the chances of developing
ischaemic heart disease,
and other causes of it
should be sought.”

Morris JN, et al. Diet and Plasma Cholesterol in 99 Bank Men. British Medical Journal
1963; 1(5330): 571-6.
Reiser R. Am J Clin Nutr 1973; 26(5): 524-55.
 Dietary Saturated Fat and
Cholesterol Levels
Author Journal Type Number Impact on lipids

Morris BMJ Observational: 99 black men No correlation

1963 weighed diet between SFA & TC
Stulb AJCN Observational: 52 men No correlation
1965 dietary interview between SFA & TC
Nichols AJCN Observational: 2039 (men & No correlation
1976 24-hr diet record women) between SFA & TC/TG
Morris BMJ Observational: 7- 337 men 30- CHD not associated
1977 day weighed diet 67 years with TF or SFA
Shekelle NEJM Observational: 1900 middle- SFA correlated with
1981 diet score (Keys) to aged men ↑TC
serum cholesterol
Frantz Arterio- RCT – diets 9057 ♀ & ♂ ↓TC in 9% group
1989 sclerosis 18% SF/38% TF Mental → TC in 18%
9% SF/38% TF Institutions No diff in CVD
events
 Dietary Saturated Fat and
Cholesterol Levels
Author Journal Type Number Impact on lipids

Mensink Arterioscler Meta-analysis of 27 controlled Replacement carbs by fat

1992 osis and total fat (TF), trials = ↓TG.
Thrombosis unsaturated (UFA), UFA = ↑HDL to LDL
(SFA & carbs ratio
Ginsberg Arterioscler RCT – Diets: 103 Step 1 & low SFA
1998 Thromb AAD 34% fat & 15% Aged 22 to 67 ↓TC, LDL-C, HDL-C,
Vasc Biol. SFA; Step 1, 29% fat years ApoA-1
& 9% SFA; Low- ↑TG, ApoB, Lp(a),
Sat, 25% fat & 6% TC/HDL, TG/HDL
SFA.
Katan AJCN Review --- ↓HDL by LF, high-carb
1998 diet constitutes a
distinct disadvantage
that can no longer be
ignored
 Dietary Saturated Fat and
Cholesterol Levels
Author Journal Type Number Impact on lipids
Müller Journal of RCT - crossover 25 women TC & LDL did not
2003 Nutrition high fat - 38.4% (20-40 change between high
high SFA diet years) and low SFA diet but
Low fat 19.7% ↑HDL with high SFA
Low SFA diet & TG/VLDL higher
HUFA diet with low SFA diet
Mensink AJCN Meta-analysis of 60 Replacement of carbs
2003 dietary fats on controlled with tropical
TC:HDL ratio trials oils ↑TC, ↑HDL & ↓apo
B. Carbs ↑TG. UFA ↓
TC:HDL
Mozaffar AJCN Observational: 235 PM ♀ ↑SFA associated with ↓
ian diet & progression with progression of coronary
2004 of coronary established atherosclerosis, whereas
atherosclerosis CHD carb intake associated
with ↑ progression.
 Observation: Countries that consume more
saturated fat have lower heart disease
mortality and vice versa

http://news.bitofnews.com/war-on-fat-was-a-huge-mistake/
 Observation

Increased
saturated fat =
lower death rate

Allender S, Scarborough P, Peto V, Rayner M. European

Cardiovascular Disease Statistics: British Heart Foundation
Health Promotion Research Group, 2008.
No evidence SFA are harmful

Ann Intern Med. 2014;160:398-406.

643,226 participants
Which fats are harmful? Trans
Which fats are health promoting?
Omega-3
 Long-chain
w-3 protective
but ratio
currently
unbalanced in
favour of
omega-6

Simopoulos, A.P., Exp Biol

Med 2008. 233(6):
p. 674-88.
Largely ignored in 2010
Secondary prevention?

Schwingshackl L,
Hoffmann G. BMJ
Open 2014; 4:
e004487.
doi:10.1136/bmjopen-
2013-004487
Saturated fat clogs the arteries
doesn’t it?

No cause & effect

evidence
Offer Ravnskov, MD, PhD

Nutr Health 2010, part 2, p 109-119

http://www.ravnskov.nu/is_saturated_fat_bad.htm
 2. Raised LDL-C causes CVD [B → C]

World Health Organisation. WHO Global Infobase: Data for Saving

Lives https://apps.who.int/infobase/Comparisons.aspx
 2. Raised LDL-C causes CVD [B → C]

World Health Organisation. WHO Global Infobase: Data for Saving

Lives https://apps.who.int/infobase/Comparisons.aspx
 Dietary Saturated Fat and
Cholesterol Levels
Author Journal Type Number Impact on mortality
Salmond BMJ Observational 17 630 aged 25- Sig inverse relations with
1985 years 74 ♀ & ♂ TC for total, cancer &
other causes of mortality
Anderson JAMA Observational: 30yr 4374 ♀ & ♂ > 50 yrs no increased
1987 f/up of the overall mortality with
Framingham Study either high or low serum
cholesterol levels.
Neaton Arch Intern Observational: 350 977 Inverse relationship
1992 Med 12yr f/up of Multiple men aged 35 between TC<4.14 and
Risk Factor to 57 years stoke, cancer, hepatic
Intervention Trial cirrhosis, suicide and
alcohol dependence
Kaplan Ann N Y Review ----- (1) Low TC marker for
1997 Acad Sci risk of suicide/traumatic
death (2) TC lowering
may have adverse effects
 Dietary Saturated Fat and
Cholesterol Levels
Author Journal Type Number Impact on mortality
He BMJ Observational: 43 732 men No association between
2003 Health aged 40-75 intake of total fat,
professional years cholesterol, or specific types
follow up study of fat and risk of stroke in
with 14 year men.
follow up.
Ulmer Journal of Observational: 67,413 men ↑↓ TC related to mortality.
2004 Women's VHM&PP and 82,237 Low TC mortality occurs in
Health 15 year f/up women aged younger pts contradicting
20–95 years marker for frailty occurring
with age.
Wang Clinical Observational: 84 429 Hypercholesterolemia
2009 Cardiology newly diagnosed patients associated with lower in-
hypercholesterole hospital mortality.
mia and mortality
3. Saturated fat causes CVD [A → C]

Citation: Hooper L, et al

Reduced or modified
dietary fat for preventing
cardiovascular disease

Cochrane Database of
Systematic Reviews 2012,
Issue 5. Art. No.: CD002137.
DOI:
10.1002/14651858.CD002137.
pub3.
Total mortality
There was no effect of:
• any dietary fat intervention compared to usual or
control diet on mortality (RR 0.98, 95% CI 0.93 to
1.04, I2 0%, 71,790 participants)
• any modified fat vs usual diet (RR 1.02, 95%CI 0.88 to
1.18, I2 34%, 11,441 participants)
• any reduced fat vs usual diet (RR 0.97, 95% CI 0.90 to
1.04, I2 0%, 58,130 participants)
• any reduced and modified fat vs usual diet (RR 0.97,
95% CI 0.76 to 1.23, I2 0%, 2219 participants)
Cardiovascular mortality
There was no effect of:
• any dietary fat intervention compared to
usual diet (RR 0.94, 95% CI 0.85 to 1.04, I2
0%, 65,978 participants)
• modified fat diet vs usual diet RR 0.92 (95%
CI 0.73 to 1.15, I2 45%, 10,788 participants)
• reduced fat vs usual diet RR 0.96 (95% CI
0.82 to 1.13, I2 0%, 52,971 participants)
• reduced and modified fat vs usual diet RR
0.98 (95%CI 0.76 to 1.27, I2 0%, 2219
participants)
Cardiovascular events
Heterogeneity was examined using the
I2 test, and considered important where
> 50%
There was a reduction in cardiovascular events for any
dietary fat intervention compared with usual diet (RR 0.86,
95% CI 0.77 to 0.96, I2 50%, 65,508 participants)
None of the subgroups of types of dietary fat change showed a
clear effect of dietary fat change compared with usual diet
• modified fat vs usual fat RR 0.82 (95% CI 0.66 to 1.02, I2
61%, 11,660 participants)
• reduced and modified fat vs usual diet RR 0.77 (95% CI
0.57 to 1.03, I2 40%, 3193 participants).
• There was no suggestion of an effect on cardiovascular
events in studies that compared reduced fat vs usual intake
(RR 0.97, 95%CI 0.87 to 1.08, I2 17%, 50,655 participants)
Secondary outcomes

No effects for:
• Total myocardial infarction
• Stroke
• Cancer deaths
• Cancer diagnosis
• Non-fatal myocardial infarction
• Quality of life
Cochrane SR - summary
• Low fat or modified fat diets not shown to reduce total
mortality
• Low fat or modified fat diets not shown to reduce CVD
mortality
• Low fat or modified fat diets may reduce CVD events when all
studies types merged together but heterogeneity becomes
significant and reduces the quality of the evidence i.e. classed
at moderate quality evidence “further research is likely to have
an important impact on our confidence in the estimate of
effect”. No low fat or modified fat diet subgroups were
shown to reduce CVD events.
• Low fat or modified fat diets not shown to reduce heart
attacks, strokes or cancer
The largest clinical trial on low fat diets

50,000 participants!

Howard BV. JAMA 2006; 295(6): 655-66.

 The longest observational study

4,374 patients

“After age 50 years there is no increased overall mortality with

either high or low serum cholesterol levels. For individuals
older than 50 years, lipoprotein fractions and apolipoprotein
values are likely to be more appropriate screening devices than
measurements of total cholesterol.”

JAMA 1987;257:2176-2180
Does the
latest
evidence base
support this?

No!

Why?
 Dietary Fat
 No foods have 100% one type of fat – they tend
to have a combination of the SFA, MUFA &
PUFA

 Processed food is often confused with

saturated fat

 Processed food is usually a combination of

refined carbohydrate and processed vegetable
oils e.g. crisps, French fried & biscuits

 Rich sources of saturated fat come from more

natural foods such as milk, cheese, cream,
meat, butter & lard
All about the bonds

1. No double bonds = hard at room temperature

2. One double bond = liquid at room temp and solid when chilled
3. Several double bonds = liquid at room temp & when chilled
4. ↑ number of double bonds = increased oxidation and free
radicals production = harmful
5. Partial hydrogenation of double bonds = trans fats = harmful
Cholesterol synthesis
We can make cholesterol
out of dietary fat but only
when fatty acids undergo β
oxidation to release HMG-
CoA

Unlikely as this will only

happen in the absence of
insulin and then ketone
pathway dominates

More likely to synthesise

cholesterol from carbs via
acetyl-CoA

Kendrick M 2006: The Great Cholesterol Con; p35

But dietary recommendations
from 1983 still advised low fat

Some nutrition researchers

were sceptical

“credibility of nutritionists and

dietitians will diminish if the
advice we offer is not effective”

M. J. Gibney Dietary guidelines: a critical appraisal. JHND 1990; 3, 245-254

 Fat & sugar have a inverse relationship

“The Seven Countries study classified

processed foods, primarily carbohydrates, as
saturated fats -biscuits, cakes, pastries and
savoury snacks as saturated fats.

Processed foods should be the target of

public health advice but not natural fats, in
which the UK diet is deficient. The macro
and micro nutrients found in meat, fish, eggs
and dairy products, are vital for human
health and consumption of these nutritious
foods should be encouraged.”

M. J. Gibney Dietary guidelines: a critical appraisal. JHND 1990; 3, 245-254

Dietary recommendations were
introduced in the absence of
supporting evidence from RCTs

Open Heart 2015;2:e000196. doi:10.1136/openhrt-2014-000196

National Diet and Nutrition Survey
2008/09 to 2010/11
Adults 19 to 64 years
• Energy intake: 2151 kcal for men aged and 1614 kcal for
women
• Protein: 17-18% √
• Fat: < 35% √
In the main dietary guidelines
• SFA: 12.7%
are being followed
• MUFA: 12-13% √
• Trans fats: 0.7-0.8% √
• Carbs: 50% √
• Fibre: 13.3-13.8g per day

http://webarchive.nationalarchives.gov.uk/20130402145952/http:/
/transparency.dh.gov.uk/2012/07/25/ndns-3-years-report/
Change in food consumption

Source: Department for Environment Food and Rural Affairs –

National Food Surveys
Major sources of carbohydrate -
world production 1961-1994

UK citizens eat 40g of butter per

week (1) compared with 1,423g
of flour (2) and 731g of sugar (3)

1. DEFRA, Family Food Survey,

(Table 1.1), (2008).
2.http://www.fabflour.co.uk/co
ntent/1/31/facts-aboutbread-
in-the-uk.html
3.http://www.whocollab.od.ma
h.se/expl/globalsugar.html

Source: http://www.fao.org/docrep/w8079e/w8079e0g.htm
Change in food consumption

Source: Department for Environment Food and Rural Affairs –

National Food Surveys
Change in food consumption

Source: Department for Environment Food and Rural Affairs –

National Food Surveys
Change in food consumption

Source: Department for Environment Food and Rural Affairs –

National Food Surveys
Change in food consumption

Source: Department for Environment Food and Rural Affairs –

National Food Surveys
Change in food consumption

Source: Department for Environment Food and Rural Affairs –

National Food Surveys
 Obesity prevalence
– tripled and growing
60

50

40
Percentage (%)

30
Men
Women
20

10

0
1980 1993 2013 2035 2050
Year

Health & Social Care Information Centre 2014

 Diabetes prevalence (%)
– quadrupled and growing
7

0
1993 2003 2013

Diabetes UK “State of the Nation: Challenges for 2015 and beyond” 2014
What should we do?

What does cause atherosclerosis?

Cholesterol is essential for life

A fat-soluble lipid (not a fat) - no calories. Cholesterol is a sterol

Cholesterol is essential to life. Functions:
• Brain synapses – the vital connections between the nerve cells
in the brain.
• Hormone production. Cholesterol plays a part in producing
hormones such as oestrogen, testosterone, progesterone,
aldosterone and cortisone.
• Vitamin D production. Vitamin D is produced when the sun’s
ultraviolet rays reach the human skin surface.
• Bile production. Cholesterol produces bile acids which aid in
digestion and vitamin absorption.
• Cell membrane support. Cholesterol plays a very important
part in both the creation and maintenance of human cell
membrane (waterproof / flexibility).
~ 25%
~ 75%
Cholesterol cannot travel in the
blood on it’s own. It needs to be
carried by lipoproteins
There isn’t good or bad cholesterol
– it all about the lipoprotein
Different types of lipoproteins:
- LDLs contain the most cholesterol
- VLDL & Chylomicrons contain the most triglyceride
When VLDL & Chylomicron release TG
for fuel they convert to IDL & LDL
Only oxidised LDL form fatty plaques
Small dense LDL more likely to
oxidise
Why LDL particles (LDL-P) are
important

The truck is a large fluffy The car is the small dense

LDL-P LDL-P

LDL-P is the number of cholesterol carriers (vehicles)

LDL-C is the amount of cholesterol
 Two people can have the same LDL-C
but different LDL-P

LDL-P = 3 LDL-P = 6
LDL-C = 3 LDL-C = 3

Dr Peter Attia http://authoritynutrition.com/diet-cholesterol-and-lipoproteins-explained/

Don’t blame the backseat passenger
for the car crash!

Small dense LDL-P more

easily slither into
endothelium wall and
oxidise [an abundance of
cars on the road are more
likely to crash – it doesn’t
matter how many
passengers they are
carrying]

http://biohackme.net/cholesterol-nut-shell/
LDL-P is more of a risk factor
than LDL-C
How do we know how many LDL-P we
have? Monitor ApoB (a protein on
each LDL-P)

2/3 people admitted to hospital with a diagnosis of acute MI

have the metabolic syndrome—but 75% have completely
normal total cholesterol concentrations
Is monitoring total and LDL
cholesterol useful?
Cholesterol is measured by breaking open the Lipoproteins
and measuring the underlying Cholesterol. The Lipid Profile
test = degree of estimation and approximation as not all
Cholesterol is measured.

TC = HDL + LDL + IDL + VLDL + Chylomicron + a couple of other

Cholesterol types

Assumption 1: IDL and Chylomicron are negligible. So they are set

to 0. TC = HDL + LDL + VLDL

Assumption 2: LDL is calculated, not measured

Cholesterol in VLDL is approximately 46% of total Triglycerides
(TG)
In the test TC, HDL and TG are measured and based on the results
LDL is calculated.
TC (mmol/l) = HDL + LDL + (TG/2.17)
An example,
TC = 5 HDL = 1 and TG = 1.5 LDL = 5 – 1 – 0.69 (1.5/2.17)
LDL = 3.31 mmol/l But not accurate with high or low TGs
 Limitations with monitoring Total
Cholesterol and LDL-Cholesterol

NICE (2014 lipid guidelines) advise that we

monitor non-HDL-C instead of LDL-C

Ratio’s are more informative e.g.

T.Chol to HDL-C < 4.5 Triglycerides to HDL-C < 0.87
What is the healthiest LDL profile?
Low LDL-P and not low LDL-C

100mg/dl = 2.59mmo/l

Source: Journal of Clinical Lipidology 2011: 5; 338

 Metabolic syndrome is associated
with small dense LDL-P

Dr Peter Attia http://authoritynutrition.com/diet-cholesterol-and-lipoproteins-explained/

 What is the cause of ↑ LDL-P?

Carbohydrate pathway to LDL

VLDLs are
produced in the
liver from carbs –
when they off
load the TG for
energy or fat
storage they
become small
dense LDL

Taskinen MR, Boren J. New insights into the pathophysiology of dyslipidemia in type 2
diabetes. Atherosclerosis 2015; 239(2): 483-95.
“Replacement of saturated fat by
carbohydrates,
particularly refined carbohydrates and added
sugars, increases levels of triglyceride and
small LDL particles and reduces high-density
lipoprotein cholesterol, effects that are of
particular concern in the context of the
increased prevalence of obesity and insulin
resistance.”

Curr Atheroscler Rep (2010) 12:384–390

Lipid Technology 2012; 24 (5) 106-107
 Summary - lipids

• Cholesterol is vital for life

• The cholesterol we eat has little to do with the cholesterol in the body
• Problems occur when cholesterol ends up in the artery wall macrophages
• The only way this can happen if the cholesterol is carried there by an apoB
lipoprotein (LDL)
• The higher the LDL-P i.e. the more LDL particles, the higher the risk. Fewer
LDL-P (trucks) carrying more cholesterol (sand) reduces risk
• PUFA is more prone to oxidation. Oxidation causes free radicals that can lead
cell damage increasing the risk of heart disease and cancer.
• The ratio between omega-6 and omega-3 fatty acids is important to reduce
systemic inflammation.
• Consumption of carbohydrate at a level where people are not using it for
energy but instead storing it as fat is more likely to increase LDL-P.
Have we become a nation of carb junkies?
 What is an essential nutrient?
“A nutrient in which an organism must obtain
from the environment or from a dietary source
since the organism is unable to synthesize it”
Fatty acids α-Linolenic acid (ALA, 18:3), an omega-3 fatty acid
Linoleic acid (LA, 18:2), an omega-6 fatty acid
Amino Isoleucine, Lysine, Leucine, Methionine, Cystine, Phenylalanine, Threonine,
acids Tryptophan, Valine, Histidine, Arginine
Vitamins Vitamin A (beta-carotene, retinol), Vitamin B1 (thiamin), Vitamin B2 (riboflavin,
vitamin G), Vitamin B3 (niacin, vitamin P, vitamin PP), Vitamin B5 (pantothenic
acid), Vitamin B6 (pyridoxine, pyridoxamine, or pyridoxal), Vitamin B7 (biotin,
vitamin H), Vitamin B9 (folic acid, folate, vitamin M), Vitamin B12 (cobalamin),
Vitamin C (ascorbic acid), Vitamin D (ergocalciferol D2, or cholecalciferol D3),
Vitamin E (tocopherol), Vitamin K (naphthoquinoids)
Minerals Calcium (Ca), Chloride (Cl−), Chromium (Cr), Cobalt (Co) (as part of Vitamin B12),
Copper (Cu),
Iodine (I), Iron (Fe), Magnesium (Mg), Manganese (Mn), Molybdenum (Mo),
Phosphorus (P), Potassium (K), Selenium (Se), Sodium (Na), Zinc (Zn)
Others Choline

Carbohydrate is not an essential nutrient

 130g Carbohydrate
requirement

Carbohydrate
100g 400g storage
RDIs for carbohydrate

EAR for adults 100 g/d of carbohydrate

• The RDI for carbohydrate is set by using a coefficient
variant of 15 percent based on the variation in brain
glucose utilisation EAR plus twice the CV to cover the
needs of 97 to 98 percent of the individuals
RDI for adults 130 g/d of carbohydrate
• Nevertheless, the brain can adapt to a carbohydrate-free,
energy-sufficient diet, by utilising ketoacids for part of
its fuel requirements. When glucose production or
availability decreases there is a rise in ketoacid
production in the liver in order to provide the brain with
an alternative fuel. This has been referred to as “ketosis.”
RDIs for carbohydrate

• Approximately 0.56 g of glucose can be derived from every

1g of protein ingested (100g protein can make 56g glucose)
• Approximately 0.1g of glucose can be derived from every 1g
of fat (triglyceride) ingested (100g fat can make 10g glucose)
• Thus, a combination of protein and fat utilisation is
required to supply the small amount of glucose still
required by the brain in a person fully adapted a
carbohydrate-free diet.
• “The lower limit of dietary carbohydrate compatible with life
apparently is zero, provided that adequate amounts of
protein and fat are consumed” (p.275)
Gluconeogensesis
Are Ketones harmful?

• In individuals fully adapted,

ketoacid oxidation can
account for approximately 80
percent of the brain’s energy
requirements. Thus, only 22 to
28 g/d of glucose are required
to fuel the brain.
• Confusion about the
difference between ketosis
and ketoacidosis is a major
issue. The latter results in 10-
fold higher blood ketones and
only occurs with insufficiency
of insulin and high blood
glucose levels
A LCHF diet is not high protein

• Ingestion of 25 to 50 g of protein at a single

time stimulates insulin secretion despite a
lack of carbohydrate intake. This rise in insulin
would result in a diminution in the release of fatty
acids from adipose cells and as a consequence,
reduce ketoacid formation and fatty acid oxidation
• Environmental friendly – grass fed animals, free
range eggs, less processed food, locally sourced &
grown, sustainable
• Ketoacids are an important source of fuel for the
developing brain. The infant brain is fully capable
of using ketoacids as fuel.
Is a LCHF diet a nutrient deficient diet?
A typical
LCHF diet

Frequency
of eating: 2
or 3 meals
per day
A typical low fat diet (LFHC)
Frequency of eating: 5-6 times per day
 Omega-6 to omega-3 ratio

Calorie Carbs Protein Fat (g) Alcohol Fibre

s (kacl) (g) (g) (g) (g)
LCHF 1,998 23 109 152 16 (6%) 19g
(4%) (22%) (68%)
LFHC 1,972 253 103 56 16 (6%) 22g
(48%) (21%) (25%)
SFA (g) MUFA PUFA Omega Omega O6:O3
(g) (g) -6 (g) -3 (g) ratio
LCHF 58 60 20 12.5 5.1 2.5 to 1
LFHC 20 21 11 6.1 0.9 6.7 to 1

Analysed with Nutritics software

 Vitamin A Vitamin E Vitamin D Thiamin Riboflavin
(B1) (B2)
LCHF 2999 16.9 18 1.2 2.5
LFHC 2187 12.4 4.0 1.8 1.6
RDA 800µg 12mg 5µg 1.1mg 1.4mg
Niacin EQ Vitamin Folic Acid Vitamin Vitamin C
(B3) B6 B12

LCHF 43 2.1 366 13.1 162

LFHC 68 3.6 295 4.1 128
RDA 16mg 1.4mg 200µg 2.5µg 80mg
Potassium Calcium Magnesiu Iron Zinc
(mg) (mg) m (mg) (mg) (mg)
LCHF 3303 857 331 14.8 14.8
LFHC 4533 755 318 11.8 6.5
RDA 2000 800 375 14 10
A low fat high carb diet is more
likely to be nutrient deficient than a
low carb high fat diet – especially in
Vit D, Calcium, Iron & Zinc
Is It a fad diet? Can people stick to it?
Twelve case studies from diabetes.co.uk
Take home message from 12 case studies
from diabetes.co.uk

• Mean duration from 11 case studies

= 23 months (not including case
study 1 of 51 years)
• Mean daily carb intake 50g
• Mean reduction in HbA1c 22.3
mmol/mol
• Mean reduction in weight 15.6kg
• General – less hunger, more energy,
better sleep, less brain fog

Can we ignore this?

An n=1 case study tells the
experience of one
individual. While most
people downplay the
importance of a study like
this, a lot of information
can be obtained from one
person’s experience—
especially if that
experience is new or
unusual
Active listening

Listening to
people’s
experiences
helps to
understand
their journey
and facilitate
better self-
management
Science conclusion

“HbA1c, fasting glucose, weight and

some lipid fractions
(triglycerides/HDL) improved with
lower carbohydrate−content diets.”

Sustainability
Limitation
Individual needs – sustainable
approach in ~ 50% of patients
Low Carb Ketogenic Diet

PLOS ONE | www.plosone.org | April 2014 |

Volume 9 | Issue 4 | e91027
The 2 diets
• MCCR group 45% to 50% calories from
carbohydrates. Taught to count
carbohydrates using 15 grams of
carbohydrates as a unit. 3 carbohydrate
units per meal and 1 per snack (~165
grams of carbohydrates a day)

• LCKD group low carbohydrate, high fat,

non calorie-restricted diet. Reduce carb
intake over 7–10 days to 20–50g carbs with
the goal of achieving nutritional ketosis,
defined as a blood beta-hydroxybutyrate
level between 0.5 and 3 mM.
Results
MCCR LCKD
Carbs at baseline (% of kcal) 207.8g (39.5%) 208.9g (38.1%)

Carbs at 3 months (% of 138.5g (40.7%) 57.8g (14.4%)

kcal)
Calories at baseline 2,172.9 kcal 2,390.6 kcal
Calories at 3 months 1,380.8 kcal 1,693.7 kcal
HbA1c at baseline 6.9% 6.6%
HbA1c at 3 months 6.9 % 6.0%
Weight at baseline 99.7 kg 100.1 kg
Weight at 3 months 97.1 kg 94.6 kg
Fasting insulin at baseline 10.1 mIU/mL 12.2 mIU/mL
Fasing insulin at 3 months 11.1 mIU/mL 9.3 mIU/mL
Triglyceride at baseline 172.2 mg/dL 123.6 mg/dL
Triglyceride at 3 months 168..3 mg/dL 101.3 mg/dL
Reduced diabetes medication 11% 44%
Take home message

• very low carbohydrate diet may improve

glycaemic control and weight loss in pre-
diabetes and type 2 diabetes while allowing
decreases in diabetes medications

• long-term effects of low carbohydrate diets

highlights the importance of larger
randomized clinical trial testing the
effectiveness and safety of low
carbohydrate diets for individuals with type
2 diabetes over sustained periods of time
In practice

Practical Diabetes 2014;

31(2): 76–79
Diabesity: perhaps we can make a difference
after all? Diabesity in Practice 2014: 3 (4)
A call to revise the diabetes
dietary guidelines
 Will a LCHF diet cause harm?
• The low fat high carb diet was introduced without evidence
- a human experiment?
• 2-year dietary-intervention study, the low-carbohydrate diets is an
effective alternative for weight loss and appears to be just as safe as the
low-fat diet (1).
• There are several populations around the world that have eaten almost
no carbohydrates for very long periods of times (their whole lives).
• These include the Inuit, which ate almost no plant foods, and the
Masai in Africa which ate mostly meat and drank raw milk and blood.
• Both of these populations ate lots of meat and fat, were in excellent
health, with no evidence of many of the chronic diseases that are
killing Western populations.
• Long-term studies on low-fat diets (Women’s Health Intervention)
almost 50,000 women 50 to 79 (studied 8 years). Gold standard RCT. A
low fat diet did not reduce heart disease, stroke or cancer (or mortality
rates from these) (2, 3)

1) N Engl J Med 2008; 359:229-24 2) JAMA. 2006;295(6):643-654 3) JAMA. 2006;295(6):643-654.

 Working with the University of
Hertfordshire & East Anglia University

• Low carb audit

• Literature review
• Feasibility study
• Multi-centre RCT
• Small audit
• Excellent completion
• ↑ Empowerment
• Possible to reduce carbs
in multi-ethnic patients
• Significantly more
weight loss in LC
• Reduction of PAID
greater in XD
X-PERT Diabetes Handbook v11 p.21
X-PERT Diabetes Handbook v11 p.21
Options for weight loss.....
X-PERT Diabetes Handbook v11 p.27
Dietary
approaches
p.28-32
Take home message
Encourage:
long-term strategies and not quick fix
diets
experimentation with different strategies
as it is clear that one approach does not
suit all
a varied diet i.e. “no food is bad unless
eaten to excess” as the evidence base is not
strong enough to support any one dietary
approach except the promotion of F&V
Promotion of real unprocessed foods
People wishing to try an alternative
dietary approach should first of all
discuss it with their GP
Summary
• No rules
• Choices and consequences
• Informed decisions
• Support participants in self-
assessing their diets
 “”””In the past 30 years, as obesity has rocketed, there has
been little change in physical activity levels in the
Western population.2 This places the blame for our
expanding waist lines directly on the type
and amount of calories consumed”

Malhotra A, et al. Br J Sports Med 2015 http://bjsm.bmj.com/content/early

/2015/04/21/bjsports-2015-094911.full.pdf+html
 Thank you for your attention!

@ X-PERT Health

X-PERT Health

trudi.deakin@xperthealth.org.uk www.xperthealth.org.uk
Interested to know more?
 X-PERT Position Statements
• Evidence supporting a low carb dietary approach
• Saturated fat does not increase CVD

Available from the download section of the X-PERT Health Website:

http://www.xperthealth.org.uk/home/downloads-library