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 . Atherosclerosis, in turn, increases your chance of getting and dying from cardiovascular (heart) disease . 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:
- A (dietary saturated fat) leads to B (high circulating total and LDL cholesterol concentrations)
- B (high cholesterol) leads to C (atherosclerosis)
- C (atherosclerosis) leads to D (heart disease and death from heart disease)
- 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 . 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 . The implication of these recommendations remains relevant, as they were adopted globally (including within South Africa ) and have remained relatively unchanged .
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 . 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 . 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 .
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 . 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  is based on the assumption that dietary cholesterol raises circulating cholesterol concentrations, which in turn is thought to raise CVD risk (as mentioned above) . 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 . Similarly, lowering blood levels of total and LDL cholesterol using statin medications [5-6] or dietary intervention  does not reduce your chances of having a heart attack or stroke or dying of heart disease . In other words, blood concentrations of total and LDL cholesterol are not related to heart disease risk .
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) . 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 . LCHF and keto diets also consistently lower inflammatory markers  and prevent further deteriorations in CAC scores . 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.
- Help! Keto raised my cholesterol! (it’s OK. Here’s why), Dr Ken Berry https://www.youtube.com/watch?v=-QwD4xoSmRg
- Why we need ‘bad’ cholesterol, with Dave Feldman https://www.youtube.com/watch?v=rui6NC4jnDk
- Cholesterol Code FAQ, Dave Feldman
- TEDx (East): The big fat surprise, Nina Teicholz https://www.youtube.com/watch?v=1CHGiid6N9Q
- High Cholesterol on a ketogenic diet, Paul Mason https://www.youtube.com/watch?v=TRB0jOfymLk
- Vorster HH, B.J., Venter CS, An introduction to the revised food-based dietary guidelines for South Africa. S Afr J Clin Nutr, 2013. 26(3): p. S1-S164.
- Dehghan, M., et al., Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study. The Lancet, 2017. 390(10107): p. 2050-2062.
- 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.
- Demasi, M., R.H. Lustig, and A. Malhotra, The cholesterol and calorie hypotheses are both dead—it is time to focus on the real culprit: insulin resistance. Pharmaceutical Journal doi, 2017. 10.
- DuBroff, R., Cholesterol paradox: a correlate does not a surrogate make. BMJ Evidence-Based Medicine, 2017. 22(1): p. 15-19.
- Vancheri, F., et al., Time trends in statin utilisation and coronary mortality in Western European countries. BMJ open, 2016. 6(3): p. e010500.
- Harcombe, Z., et al., Evidence from randomised controlled trials did not support the introduction of dietary fat guidelines in 1977 and 1983: a systematic review and meta-analysis. Open heart, 2015. 2(1): p. e000196.
- U.S. Department of Health and Human Services, Dietary guidelines for Americans 2015-2020. 2017: Skyhorse Publishing Inc.
- Ramsden, C.E., et al., Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73). bmj, 2016. 353: p. i1246.
- Hamley, S., The effect of replacing saturated fat with mostly n-6 polyunsaturated fat on coronary heart disease: a meta-analysis of randomised controlled trials. Nutrition journal, 2017. 16(1): p. 30.
- De Souza, R.J., et al., Intake of saturated and trans unsaturated fatty acids and risk of all cause mortality, cardiovascular disease, and type 2 diabetes: systematic review and meta-analysis of observational studies. Bmj, 2015. 351: p. h3978.
- Siri-Tarino, P.W., et al., Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. The American journal of clinical nutrition, 2010. 91(3): p. 535-546.
- Liu, S., et al., A prospective study of dietary glycemic load, carbohydrate intake, and risk of coronary heart disease in US women–. The American journal of clinical nutrition, 2000. 71(6): p. 1455-1461.
- Anderson, T.J., et al., 2016 Canadian Cardiovascular Society guidelines for the management of dyslipidemia for the prevention of cardiovascular disease in the adult. Canadian Journal of Cardiology, 2016. 32(11): p. 1263-1282.
- Micha, R. and D. Mozaffarian, Saturated fat and cardiometabolic risk factors, coronary heart disease, stroke, and diabetes: a fresh look at the evidence. Lipids, 2010. 45(10): p. 893-905.
- Mozaffarian, D., R. Micha, and S. Wallace, Effects on coronary heart disease of increasing polyunsaturated fat in place of saturated fat: a systematic review and meta-analysis of randomized controlled trials. PLoS medicine, 2010. 7(3): p. e1000252.
- Hooper, L., et al., Reduction in saturated fat intake for cardiovascular disease. Cochrane database of systematic reviews, 2015(6).
- Wang, C.C., et al., Acute effects of different diet compositions on skeletal muscle insulin signalling in obese individuals during caloric restriction. Metabolism, 2013. 62(4): p. 595-603.
- Adochio, R.L., et al., Early responses of insulin signaling to high-carbohydrate and high-fat overfeeding. Nutr Metab (Lond), 2009. 6: p. 37.
- Berger, S., et al., Dietary cholesterol and cardiovascular disease: a systematic review and meta-analysis–3. The American journal of clinical nutrition, 2015. 102(2): p. 276-294.
- De Lorgeril, M., et al., Mediterranean alpha-linolenic acid-rich diet in secondary prevention of coronary heart disease. The Lancet, 1994. 343(8911): p. 1454-1459.
- Niewdorp M., et al. Loss of Endothelial Glycocalyx During Acute Hyperglycemia Coincides With Endothelial Dysfunction and Coagulation Activation In Vivo. Diabetes, 2006. 55:480-486
- IItabe H, Obama T, Kato R. The dynamics of oxidized LDL during atherogenesis. Journal of lipids, 2011. 2011:9 pages
- Tsimikas, S., et al. High-Dose Atorvastatin Reduces Total Plasma Levels of Oxidized Phospholipids and Immune Complexes Present on Apolipoprotein B-100 in Patients With Acute Coronary Syndromes in the MIRACL Trial. Circulation, 2004. 110:1406–1412
- Goldstein, JL., and Brown, MS. Regulation of the Mevalonate pathway. Nature, 1990. 343:425-430
- Mohammad, J., et al. High Prevalence of Vitamin D Deficiency and Correlation of Serum Vitamin D with Cardiovascular Risk in Patients with Metabolic Syndrome. Metabolic Syndrome and Related Disorders.Jun 2017.15(5): p213-219.
- 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.
- Meng, Y., et al., Efficacy of low carbohydrate diet for type 2 diabetes mellitus management: A systematic review and meta-analysis of randomized controlled trials. diabetes research and clinical practice, 2017. 131: p. 124-131.
- 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.
- Siri-Tarino, P.W., et al., Saturated fat, carbohydrate, and cardiovascular disease–. The American journal of clinical nutrition, 2010. 91(3): p. 502-509.
- 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
- Hu, T., et al. Low-carbohydrate diets and prevalence, incidence and progression of coronary artery calcium in the Multi-Ethnic Study of Atherosclerosis (MESA). British Journal of Nutrition. 2019 . 121(4):461-468