Download `Saturated fat doesn`t increase coronary heart

Debate
‘Saturated fat doesn’t increase coronary heart
disease in people with diabetes’
For
Dr Trudi Deakin, X-PERT Health (registered charity), Hebden
Bridge, West Yorkshire, UK
Have we been fighting the wrong demons? Despite significant advances in management strategies, coronary heart
disease (CHD) remains the leading cause of morbidity
and mortality. Diabetes increases risk of myocardial infarction by 55% and, between 2010–2012, 37 000 people with
diabetes in England/Wales were hospitalised with CHD.1
Given the role played by fatty plaque (containing cholesterol) earlier thinking demonised dietary saturated fat.
Why was saturated fat implicated in the aetiology
of CHD? Was it justified?
Researchers since the 1950s focused on the diet-heart
hypothesis but with severe methodological limitations.2
There was also a failure to establish a cause and effect
relationship between dietary saturated fat and CHD.3
The diet-heart hypothesis did appear simple, logical and
well-founded suggesting that death from CHD can be prevented. However, despite it having been the cornerstone of
dietary recommendations for almost 40 years, it has never
been proven.2 Although a low saturated fat diet has been
shown to reduce LDL-C levels in some studies,4 these findings have not been consistent5 and often have a detrimental
impact on HDL-C6 without preventing CHD in people with
and without diabetes.7,8 Some studies have even shown an
inverse correlation between cholesterol levels and mortality.9 Thus, neither the level of serum lipids nor CHD can be
related to saturated fat.10,11 A Cochrane systematic review of
randomised controlled trials (RCTs) concluded that there
was no evidence that reduced saturated fat diets reduce total
or CHD mortality and, although there was a moderate effect
for CHD events, there was high heterogeneity and the effect
disappeared when only studies that significantly reduced
saturated fat were included.12 Recent systematic reviews and
meta-analyses conclude that current evidence does not
support cardiovascular guidelines that encourage high
consumption of polyunsaturated fatty acids and low consumption of total saturated fats in the primary and
secondary prevention of CHD, and there is no significant
evidence for concluding that dietary saturated fat is associated with an increased risk of CHD.13,14
Low fat/saturated fat dietary recommendations were
launched in the US2/UK15 in the absence of supporting
evidence from RCTs.16 Since then, the prevalence of obesity has tripled from 6% of women/8% of men to 25%.
Diabetes prevalence has quadrupled from 1.4% to 6%.17,18
What is saturated fat?
Fat is a component of every cell, serves as the primary
energy reserve and is transported as triglyceride (TG).
Saturated fats contain no double bonds, allowing the
hydrocarbon chains to pack closely together making them
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PRACTICAL DIABETES VOL. 32 NO. 7
solid at room temperature. Fatty acids can vary from
within and between TG molecules depending on their
availability. No food contains 100% of one type of fatty
acid or TG. Dietary TGs are broken down by lipases
before being packaged into chylomicrons and entering
the plasma. Triglycerides generated by the liver are transported in very low density lipoproteins (VLDLs).
Fat storage and plasma saturated fat
Adipose tissue lipogenesis and lipolysis are regulated by
many hormones including insulin and glucagon.
Triglycerides are synthesised from non-esterified fatty
acids. In the liver, saturated fat, palmitate (C16:0), is synthesised from dietary carbohydrates by de novo lipogenesis
(DNL); (Figure 1). Thus, glucose promotes plasma levels
of saturated fat.19,20
What is CHD?
CHD is multifactorial. The diet-heart hypothesis focuses on
atherosclerosis. The cascade of events involves systemic
inflammation resulting from oxidised lipoproteins,
enhanced monocyte-derived macrophages uptake and foam
cell formation. Resulting plaques protruding into the arterial lumen can rupture, leading to myocardial infarction.21
Why is cholesterol implicated in CHD?
Around 25% of cholesterol comes from the diet (exogenous) with 75% made by cells (endogenous) reducing the
demand for plasma cholesterol.22 Cholesterol is available as
unesterified (UC) or as cholesterol esters (CE). Dietary
cholesterol needs to be de-esterified before absorption and
the absorption rate is poor. Bile cholesterol can be reabsorbed by gut enterocytes.23
Blood cholesterol has been used to assess risk of CHD.
LDL cholesterol (LDL-C) is commonly termed bad cholesterol and HDL-cholesterol (HDL-C), good cholesterol.
However, all cholesterol is essential. The only negative is
when cholesterol is deposited inside the artery wall.
Cholesterol is hydrophobic and requires a protein
carrier to be transported in the blood. The combination
of cholesterol, TG and phospholipids and apolipoprotein
forms lipoproteins. Small dense lipoproteins may enter
the arterial wall, be oxidised and scavenged by monocytes
and converted to macrophages and foam cells causing
CHD. Cholesterol is merely the innocent passenger.
Not all lipoproteins are the same. Chylomicrons
(ApoB-48) are produced after a meal. VLDLs (ApoB-100)
are produced by the liver and are the predominant carriers of TGs. LDLs are by-products of VLDL metabolism and
are usually the primary carriers of plasma cholesterol.
HDL particles (HDL-P), produced by the liver and intestine, mature and become enriched with ApoA-1. HDLs
protect against atherosclerosis by anti-inflammatory properties and reverse cholesterol transport.24,25 The size and
density differ between and within types of lipoprotein due
to lipidation and delipidation and this makes the standard
COPYRIGHT © 2015 JOHN WILEY & SONS
Debate
‘Saturated fat doesn’t increase coronary heart disease in people with diabetes’
Sugar
(sucrose)
Starches
(polysaccharides)
Fat
(triglycerides)
Glucose
Transported in
chylomicrons
Stimulated
by glucagon
Stimulated
by insulin
Fructose
Glycogen
Lipogenesis
↑ Body fat
Glycolysis
Lipolysis
↓ Body fat
Stimulated by
glucagon
De novo
lipogenesis
↑ Blood
triglycerides
Pyruvate
Stimulated
by insulin
Acetyl CoA
Stimulated by glucagon
Stimulated by insulin
HMG CoA
Krebs cycle
HMG CoA
↑ Blood
cholesterol
Energy
↑ Blood
ketones
Figure 1. Metabolic pathways of dietary carbohydrate and fat
lipid profile (LDL-C, HDL-C, and TG) less reliable measures for assessing CHD risk.26
LDL-C is not the problem
Lowering LDL-C became a primary goal in CHD prevention but has limitations:
• LDL-C can be measured but is usually calculated using the
Friedewald equation, which can underestimate or overestimate the cholesterol content in LDL particles (LDL-P).27
• LDL-C is only an indirect marker of CHD risk as it is
solely the lipoprotein which initiates atherosclerosis.
LDL-P is a strong predictor of CHD as an abundance of
small dense LDL-P has been shown to be atherogenic as
they are much more likely to become oxidised and lodged
PRACTICAL DIABETES VOL. 32 NO. 7
in the arteries.28,29 ApoB-100 and LDL-P indicate the number of atherogenic particles (<1000nmol/L is considered
ideal).30 Size of LDL-P can also be measured (<25nm is
associated with an increased risk of CHD).31 People with
diabetes and CHD often have normal levels of LDL-C but
increased numbers of small dense LDL-P32,33 resulting in a
three- to six-fold greater risk of CHD.28,34
Liver DNL drives the production of TG-rich VLDLs,
which cause LDL and HDL to become cholesterol-poor
and TG-rich. Remnant VLDLs are smaller, carrying predominantly CE which is associated with increased CHD
risk.35 Small HDL-P are excreted in the kidney further contributing to dyslipidaemia. Hepatic LDL receptors do not
recognise small LDL-P so they remain in the plasma for
fuelling high levels of atherogenic LDL-P (Figure 2).36–38
COPYRIGHT © 2015 JOHN WILEY & SONS
255
Debate
‘Saturated fat doesn’t increase coronary heart disease in people with diabetes’
LDL and HDL particle abnormalities in hypertrigliceridaemia
TG
CETP
Excess dietary
carbohydrate
De novo
lipogenesis
TG-rich
VLDL
HL
Large LDL-P
(ApoB-100)
Small dense
LDL-P
Not
recognised
by liver LDL
receptors
Abundance
of small
dense
LDL-P
Oxidised
LDL-P
CE
CETP
Large HDL-P
(ApoA-1)
TG
Small
HDL-P
Excreted
via the
kidney
Low levels
of HDL-C
Macrophages
HL
Fatty plaques
TG: triglyceride; VLDL: very low density lipoprotein; CETP: cholesterol ester transfer protein; CE: cholesterol ester; LDL-P: low density lipoprotein particles;
HDL-P: high density lipoprotein particles; HL: hepatic lipase; HDL-C: high density lipoprotein cholesterol.
Figure 2. Creation of atherogenic small dense LDL particles
Controversy exists as to whether LDL-P size, LDL-P number or discordant LDL-C and LDL-P leads to the greatest
risk.39 In patients with diabetes who presented with ideal
LDL-C, HDL-C and TG levels, LDL-P was only concordant
with LDL-C in 22% of cases.23 Thus, when TGs are elevated
and HDL-C is low, small LDL-P predominate despite
normal/low LDL-C.40
Although ApoB-100 and LDL-P are believed to be better
risk predictors of CHD than LDL-C, they are not routinely
monitored in the UK. Non-HDL cholesterol is a better predictor of CHD risk than LDL-C and can be calculated from
a non-fasting lipid profile.32 NICE has now recommended it
instead of LDL-C.41 The TG/HDL-C ratio has been shown
to be a good predictor of LDL-P size42 and correlates
strongly with the incidence and extent of CHD43 in men44
and women.45 A ratio of <0.87 is ideal (mmol/L [2 for
mg/dl]) whereas a ratio >1.74 (mmol/L [4mg/dl]) is a
powerful independent predictor of developing CHD.
In epidemiological studies seeking a relationship
between LDL-C and the risk of CHD, up to half of patients
with CHD have cholesterol levels in the normal range.46
The Framingham Heart Study demonstrated that
increased total-C can be protective against mortality risk
with increasing age, and lipoprotein/apolipoprotein values are likely to be more appropriate screening devices
because two individuals may have an identical LDL-C but
differ with respect to particle size and concentration.47
What are the real risk factors for CHD in people
with diabetes?
Increased risk of CHD in people with diabetes is unlikely to
be associated with total-C as, in England and Wales, 40% of
patients achieve a cholesterol level <4mmol/L and 77%
<5mmol/L.1 In comparison, the general population UK
average for men is 5.5mmol/L and 5.6mmol/L for women,
with 22% of the adult population having a cholesterol level
>6.5mmol/L.48 Correlation does not prove causation but of
interest is the weak negative correlation between mean total
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PRACTICAL DIABETES VOL. 32 NO. 7
cholesterol and mortality, indicating that higher cholesterol levels may protect from CVD and diabetes mortality.
The orange marker in Figures 3 to 6 denotes the UK.49
Modifiable risk factors include dyslipidaemia (above),
hyperinsulinaemia, hyperglycaemia, hepatic insulin resistance and non-alcoholic fatty liver disease (NAFLD).26,50–52
If saturated fat is not implicated in the aetiology of
CHD, what dietary factors are?
What can we learn from our human ancestors? Evidence
from archaeological records suggests that hunter-gatherers consumed a high animal fat diet53 and the modal age
of death for those who survived past 15 was 72.54 Teeth
were free from dental caries and there is no evidence that
the diet caused any of the long-term conditions that are
experienced today.55 If saturated fat caused heart disease,
it would have been evident in this population.
Modern-day diets since have seen an increase in calorie intake mainly from sugars, breakfast cereals and
processed vegetable oils with a dramatic reduction in
eggs, meat, full fat milk/dairy products and vegetables
(Figures 7 and 8).56,57
The likely dietary culprits that influence CHD
• Trans fats due to insulin resistance, inflammation and
endothelial dysfunction.58
• PUFA from processed vegetable oils due to an unbalanced intake of omega-6:omega-3 fatty ratio59 and
omega-6 fats pro-inflammatory impacts on health.60,61
• Processed food and snacks that have become the norm
increasing refined vegetable fat and carbohydrate
intakes.20,56
• Excessive consumption of sugars and refined starches
due to the low-fat dietary recommendations and food
manufacturer influences which have been shown to be
detrimental to health,62 increase insulin resistance,63
atherogenic dyslipidemia,64–67 NAFLD inflammation68
and energy expenditure.69
COPYRIGHT © 2015 JOHN WILEY & SONS
Debate
‘Saturated fat doesn’t increase coronary heart disease in people with diabetes’
Diabetes deaths per 100 000
CVD deaths per 1000 000
1200
1000
800
600
400
200
0
4.5
4.7
4.9
5.1 5.3 5.5 5.7 5.9
Mean cholesterol (mmol/L)
6.1
6.3
800
700
600
500
400
300
200
100
0
4.7
4.9
5.1 5.3 5.5 5.7 5.9
Mean cholesterol (mmol/L)
6.1
1980
Cakes and pastries
Breakfast cereal
Sugar sweetened
beverages
2000
Figure 7. UK starch and sugar intake per adult 1980–2013
In contrast, diets lower in carbohydrate70,71 which include
animal foods that are naturally high in fat tend to be
healthy and nutritious (non-factory farmed meat,72 eggs,73
milk and dairy products74,75 and coconut products76).
Why should we stop demonising saturated fat?
It is now accepted by the Academy of Nutrition and
Dietetics that carbohydrate contributes a greater amount
to CVD risk than saturated fat.77 The diet-heart hypothesis
has been meticulously measured and found incorrect. The
PRACTICAL DIABETES VOL. 32 NO. 7
5.1 5.3 5.5 5.7 5.9
Mean cholesterol (mmol/L)
6.1
6.3
30
25
20
15
10
5
0
4.7
4.9
5.1
5.3 5.5
5.7
Mean cholesterol (mmol/L)
5.9
6.1
Figure 6. Females in European countries: diabetes death rates per mean
country cholesterol level. (Orange marker denotes the UK)
350
300
250
200
150
100
50
0
2013
Biscuits
Sugar, preserves and
confectionary
4.9
35
4.5
Amount per adult per week (ml)
900
800
700
600
500
400
300
200
100
0
4.7
Figure 4. Males in European countries: diabetes death rates per mean
country cholesterol level. (Orange marker denotes the UK)
6.3
Figure 5. Females in European countries: CVD death rates per mean
country cholesterol level. (Orange marker denotes the UK)
Amount per adult per week (g)
4.5
Diabetes deaths per 100 000
CVD deaths per 100 000
Figure 3. Males in European countries: CVD death rates per mean country
cholesterol level. (Orange marker denotes the UK)
4.5
40
35
30
25
20
15
10
5
0
1980
Butter
2000
Margarine
Vegetable oils
2013
Total fats
Figure 8. UK fats and oils intake per adult 1980–2013
simple fact is dietary saturated fat does not increase blood levels
of cholesterol and cause CHD. It is now time to retire that theory and concentrate on researching and recommending a
diet to people with diabetes that will benefit their health
and reduce risk of morbidity and mortality.
Declaration of interests
The author is Chief Executive of the charitable not-forprofit organisation, X-PERT Health.
References
References are available in Practical Diabetes online at
www.practicaldiabetes.com.
COPYRIGHT © 2015 JOHN WILEY & SONS
257
Debate
‘Saturated fat doesn’t increase coronary heart disease in people with diabetes’
Against
Leonie Garden, Senior Diabetes Specialist Dietitian, The James
Cook University Hospital, NHS South Tees, Middlesbrough, UK
National dietary guidelines were introduced in the UK in
1983 by the National Advisory Committee on Nutritional
Education recommending that overall fat consumption
be reduced to 30% of total energy intake with saturated
fat intakes comprising no more than 10% of total
energy.1 This equates to no more than 20g per day for
women and 30g per day for men. These guidelines followed the publication of the Seven Countries Study by
Keys in 1970 which highlighted a link between high
serum cholesterol levels and coronary heart disease
(CHD) incidence, with higher levels of saturated fat consumption tending to be related to CHD disease.2,3 Recent
publications have questioned this guidance and whether
we should continue to follow its dietary principles.4–6
The risk of CHD is multifactorial and cannot be
blamed on one single nutrient or lifestyle factor. It is
therefore essential to consider the diet as a whole and
move away from recommendations built on one particular nutrient.7
The science
The carbon atoms in saturated fats are linked only by
single bonds. Principally derived from animal fats, they
have a relatively high melting temperature and are solid
at room temperature.8
Evidence has shown that low-density lipoprotein
(LDL) receptors are down-regulated by the consumption
of saturated fat thus reducing the rate of LDL removal
from the circulation.9 The consequence of this is a raised
level of LDL, and therefore total cholesterol in the blood.
The process of atherogenesis is enhanced by an increased
intake of saturated fat leading to an increase in the risk of
CHD.3 An increase in total fat intake results in postprandial activation of factor VII and suppresses clot breakdown. Saturated fat increases platelet activity, whereas
polyunsaturated fats have the opposite effect.8
Death from CHD is significantly elevated in those
with diabetes mellitus. They are three to four times more
likely to die from CHD and two to three times more
likely to suffer a stroke.10 This risk is not related to hyperglycaemia per se but to disturbances in other metabolic
parameters such as blood lipids, which occur in the presence of poor glycaemic control. Diabetes is a non-modifiable risk factor for CHD. However, dietary approaches
resulting in a reduction in total cholesterol and LDL
cholesterol have been shown to improve CHD outcomes
in people with diabetes.11
No-one can ignore the overwhelming body of evidence which shows that a diet rich in saturated fat leads
to an increase in total serum cholesterol levels.7,12
Palmitic, myristic and lauric acid are three fatty acids
which have been shown in both clinical studies and
meta-analysis to raise levels of LDL cholesterol.13 An elevated LDL level is a significant modifiable risk factor for
CHD. It has been shown that saturated fat looks as if it
interferes with the way in which the body regulates cholesterol.8 Cutting down on saturated fat and substituting
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PRACTICAL DIABETES VOL. 32 NO. 7
it with unsaturated fat leads to reductions in LDL cholesterol, total cholesterol to high-density lipoprotein
(HDL) ratio and therefore CHD risk.14
Recent publications
Recent controversy over saturated fat consumption
began in 2013 when Malhotra published a paper in the
British Medical Journal suggesting that saturated fat has
been falsely demonised.4 However, he concluded by suggesting that we should all consume a Mediterranean
style diet which is high in monounsaturated fats – surely
contradicting his original claims?
In March 2014, the Annals of Internal Medicine
followed suit publishing a meta-analysis of 72 studies
examining the effect of different fats on CHD risk.5 They
concluded that ‘current evidence does not clearly
support guidelines that encourage high consumption of
polyunsaturated fatty acids and low consumption of total
saturated fat’. The study contained flaws which included
erroneously identifying a study examining omega-3 fatty
acids to show a negative effect when in fact it had shown
a strong positive effect. They also omitted two key
studies on omega-6 fatty acids from their analysis.
However, the main issue was that the studies reviewed
failed to take into account what people consumed when
they reduced their saturated fat intake.5
A further study published in 2014 in the Open Heart
journal also calls into question the value of low saturated
fat diets but incorrectly declares that current UK dietary
guidelines encourage the replacement of saturated fats
with carbohydrates.6 This is untrue and the guidelines
make no such statement.1 It is important to note that no
new evidence has actually been produced in any of the
aforementioned recent publications.
Nutritional science is complicated and multifaceted.
This can therefore result in compelling arguments
regarding the effect of dietary components on health
and CHD risk. However, recent studies contradict 50
years of evidence-based practice despite there being an
undisputed link between high levels of saturated fat consumption and LDL cholesterol levels.14 Researchers will
often try to pull apart nutrients in order to assess their
individual health benefits. This often results in misleading guidelines as nutrients are rarely eaten in isolation.
It is very difficult to measure the effect of diet on
health and therefore draw solid conclusions from the
data. Studies assessing diet are more challenging to conduct than drug trials, as ensuring that people stick to a
prescribed diet is near impossible and carefully controlling the diet of thousands of people over many years
would be unfeasible. Dietary assessment techniques
often result in flawed data. A 24-hour dietary recall may
not represent a ‘typical day’, but also people tend to
underestimate their intake which also happens when an
average dietary intake is asked for. Food frequency questionnaires only list a certain number of foods so therefore are unlikely to represent all foods consumed for all
participants. Dietary assessments are performed at the
beginning of studies but people change their dietary
habits over time.9
Many of the studies included in the meta-analysis did
not take into account what people consumed in place of
COPYRIGHT © 2015 JOHN WILEY & SONS
Debate
‘Saturated fat doesn’t increase coronary heart disease in people with diabetes’
Foodstuff
Calories (kcal)
Saturated fat (g)
Total calories (kcal)
Total saturated fat (g)
Full fat versions
20g butter
300ml full-cream milk
30g cheddar cheese
148
198
125
11
8
6
471kcal
25g
Low fat versions
20g low-fat spread
300ml skimmed-milk
30g half-fat cheddar
56
96
82
1
0
4
234kcal
5g
237kcal
20g
Difference
Table 1. The calorie and saturated fat savings that could be made by switching from high fat dairy products to low fat alternatives19
Food
Low fat alternative
Calorie saving (kcal)
Saturated fat saving (g)
35g sugar coated cereal with
100ml whole milk
25g porridge oats with 200ml skimmed milk
35
3
Apple Danish
Slice of toast with jam and margarine
186
5
Chocolate muffin
Slice of malt loaf
315
11
Bakewell tart
160g cherries
128
5
Beef burger – grilled
Roast beef – 75g
159
7
Chicken Kiev
Chicken breast – 95g
207
8
130g battered fish
Baked cod/haddock – 125g
154
5
168g deep fried chips
195g boiled new potatoes
330
4
120g potato salad (with mayo)
160g sweet potato mash
210
5
50g milk chocolate
Banana
179
9
4 chocolate digestives
125g natural yoghurt, 140g strawberries
59
8
Croissant
Slice of granary bread with 5g light margarine
98
5
Chocolate cornflake cake
30g cornflakes with 100ml skimmed milk
104
6
80g apple pie
30g dried apple rings
143
3
50g tortilla chips
30g dried fruit and nuts
97
1
Table 2. Examples of the calorie and saturated fat savings that could be made by switching from high fat processed foods to low fat alternatives19
saturated fat. It is possible that numerous people may
have increased their intake of refined carbohydrates
which in turn may increase their risk of CHD.
Current advice
Current advice remains to state that we should consume
no more than 10% of energy from saturated fat.
Saturated fat should be replaced with unsaturated fats,
particularly monounsaturated fats not carbohydrates.15
This comes from evidence collected from various randomised controlled trials. For example the RISCK trial
analysed results from 548 participants over a six-month
period. They concluded that total cholesterol and LDL
PRACTICAL DIABETES VOL. 32 NO. 7
cholesterol levels were significantly lower after consumption of a low saturated fat diet in comparison to a control
group.16 In 2009, a meta-analysis was carried out looking
at 16 studies which modified the amount of saturated fat
consumed. Results showed that in the studies where
serum cholesterol was reduced by replacing saturated fat
with polyunsaturated fat myocardial infarction rates and
deaths from CHD were significantly reduced.17
The year 2015 has seen the publication of a Cochrane
Collaboration systematic review which concluded that
cardiovascular events could be reduced by 17% by reducing saturated fat consumption by lowering and/or
modifying fat intake.18
COPYRIGHT © 2015 JOHN WILEY & SONS
259
Debate
‘Saturated fat doesn’t increase coronary heart disease in people with diabetes’
What also needs to be considered is that foods containing high levels of saturated fat also contain numerous calories. Table 1 shows the calorie and saturated fat
savings that could be made by switching from high fat
dairy products to low fat alternatives.19 Considering the
current obesity epidemic, a reduction in calories consumed can only be a positive result and therefore this
alone has to be one of the leading influences for continuing with current dietary guidelines.
What to eat in place of saturated fat?
Recent studies reporting that saturated fat has been
falsely vilified have been embraced by the media and
have led to newspaper headlines such as ‘Butter is NOT
bad for you’ and ‘Saturated fat is ok after all’. This is
likely to lead to confusion and will possibly result in an
increase in consumption of high fat processed foods.
One of the most important things to consider when
reducing any nutrient in the diet is what is eaten in its
place. Replacing saturated fat with refined carbohydrates
has potentially negative side effects and can result in
insulin resistance and dyslipideamia.5
In 2009, Jakobsen et al. showed that substitution of saturated fat with polyunsaturated fat resulted in a significant
reduction in coronary heart disease risk whereas exchanging it for carbohydrates resulted in a modest increase in
risk.20 A meta-analysis carried out by Mozaffarian et al. in
2010 found a significant reduction in risk of CHD events
where a reduction in saturated fat was accomplished by
substitution primarily with polyunsaturated fat.21
We should be aiming to decrease overall energy
intake by reducing the amount of high fat processed
foods we consume. See Table 2 for examples.19
Conclusion
Dietary recommendations will not fit all individuals
when taking into account disease status, age and activity
levels. In those with diabetes, the reduction in amounts
of carbohydrate foods consumed may be beneficial;
however, these should not be replaced with saturated
fats, but rather monounsaturated fats, lean protein
foods and vegetables.
Advice continues to suggest limiting foods which
contain high levels of saturated fat, particularly meat
products, and swapping these for foods rich in unsaturated fats, such as fish and nuts. Diets which are known
to be cardio-protective – including the Mediterranean
diet, a vegetarian diet and the DASH diet (Dietary
Approaches to Stop Hypertension) – all advocate a low
intake of saturated fat. A diet focused on fruit, vegetables, legumes, nuts and whole grains will have limited
space for saturated fats. However, when considering
weight control, it is important to remember that even
monounsaturated fats are high in calories. Just because
a diet is low in fat does not mean it needs to be high in
carbohydrate. Moderation is key and focusing on overall intake is essential.
Dietary intake is an individual choice but I for one
will not be increasing the saturated fat content of my diet
in light of this ‘new’ research!
Declaration of interests
There are no conflicts of interest declared.
References
References are available in Practical Diabetes online at
www.practicaldiabetes.com.
POEMs
In T2DM, intensive glucose control modestly reduces CV events, but not mortality, after 10 years
Clinical question
Are there long-term benefits to more intensive
glycaemic control in patients with type 2 diabetes?
Reference
Hayward RA, et al., for the VADT Investigators. Followup of glycemic control and cardiovascular outcomes in
type 2 diabetes. N Engl J Med 2015;372(23):2197–206.
Synopsis
The Veterans Affairs Diabetes Trial (VADT)
originally randomised 1791 veterans with type 2
diabetes mellitus to receive intensive or usual
glycaemic control, and achieved mean HbA1c levels of
6.9% and 8.4%, respectively, after a median of 5.6
years. The original trial found a non-significant trend
toward fewer cardiovascular events in the intensive
therapy group, but no change in mortality. Two other
large, similar trials reported similar findings,
although one found increased mortality in the
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PRACTICAL DIABETES VOL. 32 NO. 7
intensive glycaemic control group. Follow-up studies
for these two other trials have had mixed results, one
finding increased mortality and no change in events,
with the other finding fewer events but no change in
mortality. The current study linked patients in the
original VADT to national disease registries (92% of
participants) and also to regular record reviews and
surveys (77% agreed to participate). The median
follow up was 9.8 years for cardiovascular events and
11.8 years for assessment of total mortality. They
found a small but statistically significant reduction in
the primary combined outcome of myocardial
infarction, stroke, new or worsening heart failure,
cardiovascular death, or amputation (44.1 versus
52.7 per 1000 person-years; p=0.04). There was no
significant difference between groups in the
likelihood of cardiovascular death or all-cause
mortality. The greatest contribution to the reduction
in cardiovascular events was fewer non-fatal
myocardial infarctions.
COPYRIGHT © 2015 JOHN WILEY & SONS
Debate
‘Saturated fat doesn’t increase coronary heart disease in people with diabetes’
For
Dr Trudi Deakin, X-PERT Health (registered charity), Hebden
Bridge, West Yorkshire, UK
References
1. Diabetes UK. Are diabetes services in England and Wales measuring up? A
summary of findings from the National Diabetes Audit 2011–12 for people with
diabetes and anyone interested in the quality of diabetes care. https://www.
diabetes.org.uk/Upload/Professionals/Service%20improvement/NDA%20201112%20Summary_Report_printer-ready.pdf [accessed 9 June 2015].
2. Hite AH, et al. In the face of contradictory evidence: report of the Dietary
Guidelines for Americans Committee. Nutrition 2010;26(10):915–24.
3. Ravnskov U. Is atherosclerosis caused by high cholesterol? QJM 2002;
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Leonie Garden, Senior Diabetes Specialist Dietitian, The James
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