Government nutrition guidelines recommend a high carbohydrate diet regardless of the ample evidence of the health risks it promotes. Yet, chronic diseases and obesity rates have risen in correlation with a reduced intake of dietary fat. The Food Standards Agency states all individuals’ diets should contain “plenty of starchy foods such as rice, bread, pasta and potatoes”. In addition to this, “just a little saturated fat”.
While science has moved on, nutritional advice lags behind. And in a new study published in Open Heart, a group of researchers concludes that national dietary advice on fat consumption issued to millions in the 1970s to reduce the risk of heart disease which suggested that fat should form no more than 30% of daily food intake lacked any solid trial evidence and shouldn’t have been introduced.
While more circumspect, cardiologist Rahul Bahl wrote in a linked editorial:
There is certainly a strong argument that an over-reliance in public health on saturated fat as the main dietary villain for cardiovascular disease has distracted from the risks posed by other nutrients, such as carbohydrates.
Fat and High-Carb Meals
Fat intake decreased from 36.6% to 33.7% from 1971 to 2006, while the intake of carbohydrates rose from 44.0% to 48.7%. Yet obesity levels have escalated.
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Fat contains more than twice the calories (9kcal) per gramme than carbohydrates (4kcal). So if you eat a high-fat meal it is more calorific than a high-carb one, but there is evidence to also show that carbohydrates can lead to feelings of increased hunger. A recent study in The American Journal of Clinical Nutrition found that eating carbohydrate foods with a high glycemic index (bread, rice, pasta) caused effects on the brain that led to feelings of increased hunger, which could in turn lead to eating more.
Another study in 2013 found high-carb meals could leave you feeling hungrier hours later compared to a low-carb meal with more fibre, protein and fat. The team behind the research attributed this to the plummeting levels of blood sugar that regularly follows high-carb meals.
The Diet-Heart Hypothesis
At the University of Hull we’ve been also looking at the effects of saturated fats on triglyceride levels – a type of fat (lipid) found in the blood. Using coconut oil because of its high (90%) saturated fat content, we found that when coupled with exercise, it significantly reduced triglyceride levels. A recent Brazilian rat study also found that coconut oil and exercise could lower blood pressure.
So where does our unshakable idea that fat leads to heart disease come from? The diet-heart hypothesis, that low density lipoproteins (LDL) cholesterol is raised in the blood by eating saturated fat, which then leads to clogged arteries and eventual heart disease, is not a credible claim.
This theory linking saturated fat and heart disease has been around since 1955 when Ansel Keys introduced his lipid hypothesis. Despite it being the foundation of dietary recommendations, it has never been proven and we have been advised to avoid certain foods including meat, dairy products and coconuts. And these myths are so deeply embedded in our minds, that recent science advocates have seen how hard it is to challenge established thinking.
Saturated Fat and Cholesterol
When we talk about high-density lipoprotein (HDL) or LDL – often referred to as good and bad cholesterol – we aren’t actually referring to cholesterol itself. These lipoproteins actually carry cholesterol, fat and fat soluble vitamins in the bloodstream. It appears that elevated levels of cholesterol (or more accurately, cholesterol which is transported around the blood by lipioproteins) is correlated with an increase in the risk of heart disease.
However, correlation does not mean causation. Very low cholesterol is linked with an increased risk of death (though not from heart disease). And in the very old, research suggests cholesterol can be protective. So it’s fair to say the relationship between cardiovascular disease and total cholesterol is complex.
Type of cholesterol is important. The “good” (HDL) cholesterol is strongly linked with a reduced risk of heart disease. However, LDL, the “bad” cholesterol, is associated with an increased risk of heart disease. But it turns out that there are in fact subtypes of LDL which make this black and white picture more complicated. The actual size of the LDL particle is significant. Individuals are at a heightened risk of heart disease if they have most small, dense LDL particles, that may more easily lodge in the arteries, as opposed to those who have large LDL particles.
Your blood lipid profile is frequently used as a medical screening tool for abnormalities in lipids (including triglycerides and cholesterol). These blood lipid profile tests can identify approximate risks for cardiovascular disease and specific genetic diseases. Studies have also shown that saturated fats do not harm your blood lipid profile – and can actually improve it. Saturated fats could lower the risk of heart disease by shifting LDL cholesterol from dense small LDL to large LDL.
Numerous short-term feeding trials have shown that an increase in saturated fat consumption leads to a rise in overall LDL. Nevertheless, the result is inconsistent and weak. The methods used in a number of these research studies have been criticised – and plenty of studies support the contrary, that no association exists between total LDL and saturated fat consumption.
Cause and Correlation
If it was true that saturated fat did cause heart disease, then it follows that people who consume more would be at higher risk. But observational studies – again only illustrative of correlation not cause – haven’t shown this. One study looked at a population of 347,747 subjects from a total of 21 studies and concluded that there was “no significant evidence for concluding that dietary saturated fat is associated with an increased risk of coronary heart or cardiovascular disease”. This has also been the conclusion of other reviews.
So what about randomised controlled trials? One such study divided 12,866 male subjects at a high risk of heart disease into a low-fat or Western diet group. After six years, no difference was found between them. The Women’s Health Imitative, the biggest randomised controlled trial in diet history, comprised of 48,835 postmenopausal women who were also divided into two similar groups and came up with similar findings.
The Coconut Oil Example
If you don’t care for the science, then take an everyday example. Look at the large populations of the Masai in Africa who consume large amounts of saturated fat but have low levels of coronary heart disease. Or the Tokelauans of New Zealand who consume a massive amount of saturated fat through coconuts: more than 60% of their daily calories come from coconuts. These populations have no history of heart disease. And the health benefits of coconut oil are now becoming known more widely.
We’re learning so much more about fats and that there is no evidence that saturated fat causes heart disease. Leading nutrition experts have been calling for an amendment to dietary recommendations for more than ten years. But despite these calls and the high-quality evidence assembled throughout the past decade, doctors, governments – and by extension the public – still take extraordinarily little notice. But a decade of research to the contrary would suggest it’s time we moved away from entrenched thinking, towards a more enlightened attitude to saturated fat.
About the Author
Craig Scott graduated with a BSc (Hons) degree from Leeds Metropolitan in Sport in 2013. Following this, he decided to pursue postgraduate study. Craig joined the University of Hull in November 2013 to undertake an MSc in Sport and Exercise Science. Craig's undergraduate thesis looked at the glycemic response following acute supplementation of Virgin Coconut oil. He has now progressed his undergraduate thesis into postgraduate research. His research is now looking at the acute effects of Virgin Coconut Oil and aerobic exercise following postprandial hypertriglyceridemia. The study will be looking at blood lipid profiles and endothelial function.