Excess dietary fat, particularly saturated fat, has unfairly been demonised for too long. It has not been proven that saturated fat causes heart disease. It has not even been proven that there is a consistent association between saturated fat consumption and heart disease.
So why then have we been told to avoid saturated fat for so many years? How could all the policy-makers have gotten this all wrong?
The original diet-heart hypothesis, that cholesterol was related to coronary heart disease, originated from the work of Russian pathologists in the early 20th century, after observing fatty deposits in arteries during post-mortems of rabbits.
In the 1950s, Dr Ancel Keys tested this hypothesis in human subjects. When Keys failed to find a connection between dietary cholesterol and cholesterol or the development of atherosclerosis (the buildup of fats, cholesterol and other substances in and on your artery walls (plaque), he turned his attention to dietary fat.
From 1956-58, Keys conducted his famous Seven Countries Study and published his findings in 1970. Keys concluded that there was no relationship between total fat and heart disease, but that there was a strong correlation between saturated fat intake and coronary heart disease in cross country comparison. Four years after Keys’ original paper, Yerushalmy and Hillebroe published a paper rebutting Keys’ conclusion, presenting data from a further 15 countries. By this time however, Keys’ work had already rapidly gained support and by 1977, the US Senate Select Committee on Nutrition and Human Needs formally recommended that Americans should reduce their consumption of total and saturated fat. These guidelines were followed by UK public health dietary advice issued by the National Advisory Committee on Nutritional Education in 1983.
More recent analysis of the evidence available to the dietary committees at the time the guidelines were introduced did not support the recommendations made. A 2015 systematic review and meta-analysis of RCTs available in 1977/1983, where a dietary fat intervention had been made, revealed identical all-cause mortality (30% in intervention and control groups) and no statistically significant difference in deaths from coronary heart disease. The review also found that fewer than 2500 sick men had been studied (note no women or healthy men), with no evidence in support of introducing dietary fat guidelines. If we fast forward to today, the evidence still does not offer any additional support.
These dietary guidelines gave rise to the modern low-fat, high-carbohydrate diet. We have been told for many years that the fat we eat is the fat we wear, and so we should switch to low-fat foods at all costs.
Processed low fat foods that are often high in refined carbohydrates, and paradoxically, have been linked to the epidemic of diabetes and coronary heart disease. Low fat diets that reduce serum cholesterol, and replace saturated fat with polyunsaturated fat do not reduce cardiovascular events or mortality. The PURE (Prospective Urban Rural Epidemiology) study (2017), which examined the dietary intake of over 135,000 individuals from 18 countries using validated food frequency questionnaires, found that over a median follow-up period of 7.4 years, high carbohydrate diets were associated with a higher risk of total mortality. In contrast, higher total fat intake, including saturated fat, was related to lower total mortality. Comparison of the highest and lowest quintiles of carbohydrate intake found a total mortality hazard ratio of 1.28 [1.12-1.46], reflecting a 28% increased chance of dying in those on the highest carbohydrate diets.
As the diet-heart hypothesis evolved, the focus shifted from the effect of dietary fat on total cholesterol to low-density lipoprotein-cholesterol (LDL-c). In 1986, Nobel laureates Brown and Goldstein declared that there was a ‘causal relation between an elevated level of circulating LDL and atherosclerosis’, thereby establishing the dogma that LDL-C is inherently atherogenic. But where was their evidence? Commentaries and reviews in recent years have challenged the view that LDL-C causes cardiovascular disease.
The limited utility of LDL-C as a marker of CVD risk is perhaps best illustrated in studies assessing lipids and the coronary artery calcium score, which a reliable risk marker of future coronary events. A substantial percentage of individuals with very high LDL-C (>190 mg/dl) have a coronary artery calcium score of zero. We are beginning to understand that LDL-c can further be broken down into large buoyant (lbLDL) and small dense LDL (sdLDL), which have different effects on cardiovascular risk. This distinction between LDL particle subclasses is important because sdLDL, unlike lbLDL, is a component of an atherogenic dyslipidemia risk triad composed of elevated levels of triglycerides and sdLDL, in conjunction with low levels of HDL. LDL is not “bad cholesterol”. It is just not that simple.
Cholesterol is essential for life as a key constituent of cell membranes and bile acids, and as a precursor of vitamin D and steroid hormones. As humans, we must consume fat. Hence the term “essential fats”. There are two essential fats (omega-3 and omega-6) and four fat soluble vitamins (A, D, E and K). All food that contains fat contains all three natural fats: saturated; monounsaturated and polyunsaturated. It is impossible to consume unsaturated fat without saturated fat, or vice versa, in whole unprocessed food.
Years of critique of a low-carbohydrate high-fat diets have largely focused on the cardiovascular consequences of unrestricted consumption of fat. If we listen to Keys’ diet-heart hypothesis, consumption of saturated fat raises serum cholesterol levels, which increases one’s risk of developing coronary heart disease. The problem, however, is that the evidence shows that dietary intake of saturated fat and serum levels of cholesterol is not linear, and is not causal for coronary heart disease.
The highest level of available evidence today on saturated fat and cardiovascular disease is the 2020 Cochrane Review “Reduction in saturated fat intake for cardiovascular disease”. Hooper et al 2020 reviewed 15 randomised controlled trials with a minimum of 24 months duration, involving approximately 59,000 people, which focused on the impact of reducing saturated fat on mortality, coronary heart disease and stroke. There was no significant effect from reducing saturated fat on total mortality, coronary heart disease mortality, fatal heart attacks or strokes.
So what happens to our cardiovascular risk profile if we follow a low carbohydrate diet instead of a low-fat diet? Researchers examined this question in a 2015 meta-analysis of nearly 2000 patients. Compared to low fat diets, low carbohydrate diets were associated with significantly greater reduction in weight and significantly lower risk of atherosclerotic cardiovascular disease events. Although weight loss often improves to a greater extent in response to a low carbohydrate diet, the improvements in atherogenic dyslipidemia are a primary result of carbohydrate restriction, as opposed to weight or fat loss. The consistent and significant reduction in these biomarkers in response to low-carbohydrate diets supports the view that carbohydrate restriction lowers the risk for heart disease.
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