I often joke, “With nutrition, if you do the exact opposite of what you have been taught in the last 40 years, you stand the highest chance of getting it right”. With Ischaemia Heart Disease (IHD,) I think we have got the nutrition message very wrong, with respect to dietary Fat.
The Diet/Heart Hypothesis, the Lipid Hypothesis and the Cholesterol Hypothesis (1) are the theories that the current nutrition guidelines are based on. These theories are credited to Dr Ancel Keys. He presented the 7 countries study (2), which showed a clear correlation between dietary fat and ischaemic heart disease. (This study has been heavily criticised both at the time and more recently) The hypothesis was then refined to focus on the cholesterol component of saturated dietary fats, resulting in the food pyramid introduced by the US Dept of agriculture in 1977, advocating for low dietary fats and 6 to 11 servings of grains and cereals per day. (3).
The reduction of dietary fat resulted in the food industry adding sugar, particularly high fructose corn syrup to foods.
Cholesterol lowering has become the focus of both the cardiovascular risk assessment tools, dietary advice for the prevention and treatment of IHD and the statin industry. Despite recent reductions in death rates from CVD, I would like to challenge the current diet advise for IHD. As seems to be true in most aspects of medicine, the truth is in the deeper layers of detail. This is indeed the case when it comes to Saturated Fat and Cholesterol.
Unfortunately, we need to review some of the biochemistry before we can proceed. I will make this as painless as I can.
Cholesterol. This is an essential waxy substance. Cholesterol is an important component of every cell wall. It is the precursor of Vitamin D and the sex hormones. Low levels of cholesterol are linked with depression and cognitive decline.
Saturated Fat. A saturated fat contains only double bonds, making it stable and able to be heated to high temperatures without changing structure. Saturated fats are mostly found in animals with the main exception being coconut oil, a plant derived saturated fat. Saturated fats can come from the diet or can be made in the liver from excess carbohydrate. This process is called Denovo lipogenesis (the making of new fat). These fats made by the liver are saturated fats.
Atherosclerosis. This is the process of laying down cholesterol plaque in the artery wall, resulting in narrowing of that artery. This process can result in the artery blocking and causing heart attacks, strokes and peripheral vascular disease. The process is much more complicated with oxidative stress, inflammation, thrombosis and calcification all being involved.
Lipoproteins. These are complex structures made by the liver that transport triglycerides and cholesterol to the tissues. As lipoproteins deposit their cargo, they become denser and contain a greater percentage of cholesterol. The largest are called VLDL. After delivering some of their content they become smaller IDL, then LDL and finally HDL. HDL is taken back up by the liver. Each of these lipoproteins have binding sites that allow then to be taken back up by the liver and recycled. As well as transporting fuel and cholesterol lipoproteins have a role in removing pathogens and cancer cells from the body.
The new science.
More than 40 years on we have learned more about these topics. The study the opened my eyes the most is the Epic-InterAct case-cohort study, published in 2014. (4). This paper shows that dietary saturated fats have fatty acid tails adding up to odd numbers 15 and 17. The saturated fats, made in the liver from denovo lipogenesis are even numbers, 14, 16 and 18. The even numbered saturated fats where strongly associated with type 2 diabetes and the odd numbered chains were protective against diabetes. So, let’s just repeat that, saturated fat in the diet, e.g. those coming from full fat dairy products and grass fed meat are protective against diabetes!! Dietary saturated fats are transported by chylomicrons (Ultra-low density lipoproteins) to tissues where they are used as fuel. Now that is directly contradicting the usual diet advice, but does suggest that saturated fat is a problem, however it is the fat we make not the fat we eat.
But this is diabetes. How does that link to IHD? What is the connection?
More biochemistry, sorry, but this connection is really at the centre of the new science.
Excess carbohydrate, not used immediately for fuel or stored as glycogen, is converted, by the liver, via denono lipogenesis into saturated fat, more specifically triglyceride. This is packaged, with cholesterol into lipoproteins (VLDL to IDL to LDL to HDL) and transported to every cell of the body to be used as fuel. These lipoproteins are then taken back up by the liver and recycled. Now this is the interesting part. We have called LDL ‘bad’ and HDH ‘good’. Remember how I said the truth is in the next layer of detail. That is indeed the truth here. LDL is not bad, unless you damage it. Let me repeat that because it is important. You must damage LDL to make it atherogenic. You damage it either by glycation, adding glucose to it or by oxidation, meaning oxidative damage from free radicals. Damaged LDL becomes smaller and denser, called ‘small dense LDL’. The binding site is damaged, and it cannot be taken up by the liver. It remains in circulation for longer. So how is it removed from circulation you ask. And this is perhaps the missing part of the puzzle. This piece of info is so important that we need a drum roll. It is removed by specialised cells, phagocytic macrophages in the artery wall. So, we now have glycated, oxidised, highly inflammatory cholesterol deposits in the artery wall, causing the atherogenic plaque. (5)
But we still need to connect diabetes and IHD. We know that T2 Diabetes is the strongest risk factor for IHD, specifically, you are up to 1000% higher risk of IHD if you have T2 Diabetes.(6) The connection between these 2 conditions is’ insulin resistance’. The best explanation for insulin resistance is that Fructose from sugar is a direct liver toxin. (7). Fructose impairs the liver insulin receptor so that higher and higher levels of insulin is required to allow glucose into the cell. This creates hyperinsulinemia. Insulin is a fat storage hormone. Hyperinsulinemia causes obesity. Insulin resistance causes glucose levels in the blood to raise. Sugar in the diet probably initiates the process. Also involved is inflammation. This is a multifactored process but seed oil such as canola oil are highly inflammatory and contribute significantly to the oxidative damage to LDL. So, we can see how the features of a modern processed diet, highly processed foods, directly cause both diabetes and IHD.
So, the solution is simple. Avoid sugar, in fact view sugar as a direct toxin, certainly don’t poison our children by feeding them sugar. Avoid processed foods containing cheep inflammatory seed oils. Eat unprocessed foods, particularly above ground veges. There is no need to fear animal sources of fat and protein. Saturated fat from fatty meats and chicken skin, from butter and Greek yogurt is in fact protective. These fats are not incorporated into lipoproteins. Lower carbohydrates, especially those that are processed. The science supports Low Carb, Healthy Fat as the cure for Ischaemic heart disease and the low saturated fat diet is likely to be contributing to the problem.
Dr Glen Davies 23/8/2021
- https://en.wikipedia.org/wiki/Food_pyramid_(nutrition) (4)
- Making sense of LDL https://www.youtube.com/watch?v=2p-mkbNutvQ