Does dietary fat cause heart disease?

 In Blog

By Tamzyn Murphy, Rd, Msc (Dist.) 

 

Does eating fat really clog your arteries and cause heart attacks and strokes? Let’s take a closer look…

 

A faulty hypothesis based on flawed logic

Perhaps the greatest concern around low carbohydrate high fat (LCHF) and keto diets are that their high fat (particularly saturated fat) content raises LDL cholesterol, also thought of as “bad cholesterol”; as well as total cholesterol concentrations in the blood, thereby increasing heart disease risk. The “lipid” (i.e. fat) or “diet-heart” hypothesis postulates that this dietary saturated fat-associated rise in circulating total and LDL cholesterol concentrations leads to increased cholesterol build-up (plaques) in artery walls (endothelium) – a process called atherosclerosis [1]. Atherosclerosis, in turn, increases your chance of getting and dying from cardiovascular (heart) disease [1]. So if the diet-heart hypothesis is to be believed then dietary saturated fat increases your chances of getting and dying of heart disease.  

 

The diet-heart hypothesis’s logic goes like this:

  1. A (dietary saturated fat) leads to B (high circulating total and LDL cholesterol concentrations)
  2. B (high cholesterol) leads to C (atherosclerosis)
  3. C (atherosclerosis) leads to D (heart disease and death from heart disease)
  4. THEREFORE, A (dietary saturated fat) leads to C (heart disease)

 

The trouble with this simplistic model is that B does NOT lead to C. Without this erroneous leap in logic intact, A CANNOT be expected to result in D. Indeed LCHF and keto diets (A) are associated with an increase in total and LDL cholesterol concentrations (B) in SOME people. However, this increase in circulating cholesterol concentrations (B) does NOT translate to an increased risk of atherosclerosis (C), nor chances of getting or dying from cardiovascular disease (D) [2-3]. In fact, people with higher LDL cholesterol are at no higher risk of dying from heart disease than those with lower LDL cholesterol concentrations (4). And lowering LDL cholesterol with statin medication does NOT reduce your risk of dying from heart disease [4-6]. Clearly LDL cholesterol has had a bad rap and isn’t the black sheep of the cholesterol family after all. 

 

Origins of the faulty hypothesis

So where did this faulty diet-heart hypothesis emanate from in the first place? And how did it come to gain so much traction that it was deemed an undeniable truth? The diet-heart hypothesis was first punted by a scientist named Ancel Keys. It was based on his landmark epidemiological Seven Countries Study, which found associations between saturated fat intake and circulating cholesterol concentrations, as well as associations between circulating cholesterol concentrations and heart disease prevalence [7]. Studies based on observations about populations (called epidemiological studies), such as this one, cannot prove causation, as there’s too much chance that the outcome that you’re looking for (e.g. heart disease) could have been affected by factors that you didn’t even think of or control for. For example, you find that heart disease risk increases alongside higher saturated fat intake, but forget to look at sugar, which also rises alongside heart disease risk. Then you conclude that it was the saturated fat that CAUSED the increase in heart disease risk, you may have missed the true culprit, which could have been sugar. Or you may discount population groups that didn’t support your hypothesis, or record dietary intake at a time when the population you’re looking at is eating differently to their usual fare (all of which apply to Keys’ Seven Country Study). Despite the inability of this epidemiological evidence to prove causation, and the lack of supporting evidence from gold-standard studies at the time  (called randomised controlled trials or RCTs, which can actually prove causation), the USA and UK introduced dietary guidelines (in 1977 and 1983 respectively) recommending reducing total fat intake to less than 30 % and saturated fat intake to less than 10 % of total daily energy intake [8]. The implication of these recommendations remains relevant, as they were adopted globally (including within South Africa [9]) and have remained relatively unchanged [10]. 

 

Debunking the faulty hypothesis

More recent epidemiological studies contradict Keys’ conclusions associating total and saturated fat intake with heart disease [11-12]. The PURE study, in 135,335 individuals from 18 countries, found that total fat and the various types of fat (including saturated fat) were not associated with heart disease, heart disease-associated deaths, or deaths from any cause [11]. Plus this study found that the more saturated fat people ate, the less chance they had of having a stroke. Studies that summarised and analysed the results from all observational studies to date (called systematic reviews and meta-analyses) also found no link between saturated fat intake and heart disease, stroke or death from any cause [13-14]. 

 

Eating less fat may actually increase heart disease risk – say what?!

Energy in the diet comes from three macronutrients: carbohydrates, protein and fat. You need a certain amount of energy to meet your body’s needs. So, if you eat less of one macronutrient (e.g. fat or saturated fat) you’ll need to make up that energy deficit by eating more of one of the other macronutrients (i.e. protein or carbohydrates). There’s a hard cap on how much protein a person can and should eat. As such, eating less saturated fat invariably means making up the deficit by eating more of other types of fats (e.g. polyunsaturated fats) or carbohydrates. The health effects of these substitutions must be considered when issuing dietary recommendations to reduce saturated fat. The PURE study showed that unlike saturated fat intake, carbohydrate intake was linked to increased deaths from all-causes [11]. Results from the Nurse’s Health Study found that replacing saturated fat with refined, high glycaemic load carbohydrate was associated with increased heart disease risk [15]. 

So, saturated fat appears to be better for the heart and blood vessels than carbohydrates. But what about the effects of substituting saturated fat with unsaturated fats instead? Most observational population studies (epidemiological studies, which can’t prove causation) indicate that when people eat less saturated fat and instead fill that deficit with unsaturated fats, they may experience a lower risk of heart disease [16]. However, the gold-standard RCT studies show either no [83, 84], or only slightly reduced [17-19] heart disease or death risk associated with reducing saturated fat intake in favour of omega-6 polyunsaturated fats. 

 

Forget saturated fat then, what about dietary cholesterol?

The recommendation to limit dietary cholesterol to less than 300mg per day [1] is based on the assumption that dietary cholesterol raises circulating cholesterol concentrations, which in turn is thought to raise CVD risk (as mentioned above) [14]. While epidemiological (observational population) evidence does indicate that diets high in cholesterol (which usually co-occur in the same foods that are high in saturated fat) are associated with increased blood total, LDL and HDL cholesterol concentrations, this does not translate to increased heart disease risk [20]. Similarly, lowering blood levels of total and LDL cholesterol using statin medications [5-6] or dietary intervention [21] does not reduce your chances of having a heart attack or stroke or dying of heart disease [4]. In other words, blood concentrations of total and LDL cholesterol are not related to heart disease risk [4]. 

 

Total and LDL cholesterol: white sheep after all?

Clearly, blood levels of total and LDL cholesterol don’t predict your chances of getting heart disease, a heart attack or stroke, or of dying. Yet, it’s an undeniable truth that LDL cholesterol is a key component of atherosclerotic plaques. How does that work? Well, LDL cholesterol only ends up in arterial plaques when it or the blood vessel walls are damaged (by things like high free radicals (oxidants) and blood glucose (sugar)) [22,23]. That could explain why statins used to lower cholesterol don’t lower heart disease risk – as statins are only able to get the liver to take up undamaged cholesterol, thereby lowering circulating cholesterol concentrations, while damaged cholesterol remains in circulation [24, 25], lodging in the arterial walls promoting atherosclerosis.  It appears to be those damagers of LDL cholesterol and blood vessel walls that increase heart disease risk, rather than the absolute amount of circulating LDL cholesterol. It is possible that LDL cholesterol is raised to perform very important functions – e.g. transporting more fat to cells when eating a high fat diet, fighting inflammation or fixing things (See the Dave Feldman’s resources in the list below) – or it may be a marker (rather than a cause) of something wrong (e.g. low vitamin D production) [26]. If that’s the case, there’s another reason it’s probably better not to artificially lower cholesterol levels using statin medications in case there are unintended undesirable consequences.

 

Better markers of heart disease risk than total and LDL cholesterol concentrations

Recent reviews indicate that biomarkers other than total and LDL-cholesterol concentration are better predictors of atherosclerotic heart disease risk. Amongst these are inflammatory markers, other lipid components (triglycerides, LDL particle number, HDL cholesterol) and coronary artery calcium scores. LCHF and keto diets consistently result in superior improvements in the lipid components mentioned above – specifically resulting in reductions in triglycerides and elevations in HDL concentrations compared to conventional dietary interventions [27-29], indicating a protective cardiovascular effect. Contrastingly, replacing dietary saturated with carbohydrate, as seen in conventional low-fat diets, raises triglycerides and atherogenic small dense LDL cholesterol, while lowering HDL cholesterol concentrations – a profile associated with increased heart disease risk [30]. LCHF and keto diets also consistently lower inflammatory markers [31] and prevent further deteriorations in CAC scores [32]. These improvements clearly indicate that rather than LCHF and keto diets’ high saturated fat and cholesterol contents increasing heart disease risk, they’re far more likely to lower it. 

 

Resources:

 

References:

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  3. Halton, T.L., et al., Low-carbohydrate-diet score and the risk of coronary heart disease in women. New England Journal of Medicine, 2006. 355(19): p. 1991-2002.
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  25. Goldstein, JL., and Brown, MS.  Regulation of the Mevalonate pathway. Nature, 1990. 343:425-430
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  27. Huntriss, R., M. Campbell, and C. Bedwell, The interpretation and effect of a low-carbohydrate diet in the management of type 2 diabetes: a systematic review and meta-analysis of randomised controlled trials. European journal of clinical nutrition, 2017: p. 1.
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  29. Bhanpuri, N.H., et al., Cardiovascular disease risk factor responses to a type 2 diabetes care model including nutritional ketosis induced by sustained carbohydrate restriction at 1 year: an open label, non-randomized, controlled study. Cardiovascular diabetology, 2018. 17(1): p. 56.
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  31. 31.Pinto, A., et al. Anti-Oxidant and Anti-Inflammatory Activity of Ketogenic Diet: New Perspectives for Neuroprotection in Alzheimer’s Disease. Antioxidants, 2018. 7(5), 63
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