The cholesterol theory of cardiovascular disease is a clever confidence trick. The theory states that dietary cholesterol and saturated fat cause detrimental changes to lipoproteins which result in the development of atherosclerosis, and that atherosclerotic plaques in turn are the cause of cardiovascular disease. However, the chain of evidence leading from dietary cholesterol and saturated fat to cardiovascular disease is lacking, and in fact contradictory evidence disproves the theory at every juncture. This theory is now ingrained in the minds of the general public and it this regard the propaganda has been effective. The deception that cholesterol and saturated fat in the diet can be a cause of cardiovascular disease has only been possible by the complicity of paid agents of the agenda posing as serious scientific researchers. While it is unlikely that such scientists actually receive brown envelopes stuffed with money, their deliberate participation in the process of publishing scientific propaganda for career benefits is tantamount to the same.
That such poorly designed scientific propaganda makes it through the peer review process is disappointing. However, just like criminals, scientific propaganda follows patterns, and by learning these patterns and studying the nutritional sciences we can expose such papers for what they are. One of the most common tricks used by proponents of the cholesterol theory of cardiovascular disease is the use of multiple variables within a study to deliberately create confounding variables. In this respect, inclusion or removal of fibre from the diet is a favourite confounding variable, because it is known that dietary fibre can lower plasma cholesterol levels in a highly effective manner. Diets high in cholesterol and saturated fat are by their very nature diets low in dietary fibre. The inability to separate such associations from dietary intakes calls into question any study that has not specifically highlighted this point because result that exclude exploration of confounding variables are disingenuous and misleading.
A study published in the American Journal of Clinical Nutrition in 19851, investigated the effects of two diets on the plasma lipoprotein levels of healthy women. One diet was a ‘normal’ diet high in cholesterol and saturated fat, but low in polyunsaturated fat and fibre. The other ‘prudent’ diet was low in cholesterol and saturated fat, but high in dietary fibre and polyunsaturated fat. The authors reported that the prudent diet was associated with a 30 % reduction in low density lipoprotein (LDL), a 27 % reduction in total cholesterol, and a 27 % reduction in apolipoprotein B concentrations. In the discussion the authors stated that ‘The serum cholesterol-lowering effect of the “prudent” diet as compared to the normal diet was very satisfactory’. However, the prudent diet also cause a 16 % reduction in high density lipoprotein (HDL) cholesterol and a 29 % increase in very low density lipoprotein (VLDL) concentrations (triglycerides). Both decreased HDL and increased VLDL are risk factors for cardiovascular disease.
The main problem with studies investigating the effects of dietary changes on plasma lipoprotein levels is that it is not possible to cause changes in one macronutrient, without causing changes in another. This study had so many changes in the diets of the subjects that to draw any conclusions from an objective scientific perspective is impossible. Focussing on the role of lipids within such papers, when the discussion should clearly encompass all dietary changes seriously undermines the authority of the investigators and their conclusions in such papers. Despite this, many studies with serious methodological flaws are used by proponents to show that saturated fat and cholesterol are causative agents in cardiovascular disease, despite the obvious contradictions in the data. Assumptions that creep into such literature are also concerning. For example the assumption that atherosclerosis is the cause of cardiovascular disease is problematic based on evidence that the Japanese are as artherosclerotic as Western nations but suffer lower rates of cardiovascular disease.
Another problem with this study which should have excluded it from publication is the lack of any mention of the word ‘sugar’, ‘sucrose, or ‘fructose’ in the entire paper. This is the real elephant in the room, because the fructose molecule is known to cause changes to lipoprotein metabolism in the liver. Serious researchers that are interested in the truth would surely not have written a paper on two contrasting diets and how they affect lipoproteins, without mentioning one of the primary drivers of lipoprotein metabolism and how it varies between the two diets? In addition, the ascorbic acid intake of the two diets was very dissimilar. In fact, while the prudent diet contain 325 mg per day of ascorbic acid, the normal diet had a level of ascorbic acid (42 mg per day) that would have caused scurvy in the subjects if consumed long term. As ascorbic acid is implicated in changes to lipoprotein levels, this ‘oversight’ and absence of comment shows the researchers to be incompetent or biased. Either way the paper should never have passed peer review.
RdB
