roponents of the dietary cholesterol theory of cardiovascular disease claim that high intakes of dietary cholesterol and saturated fat are the cause of elevated plasma lipid levels, and this in turn is the cause of atherosclerosis. Despite this theory being provably erroneous, low fat high carbohydrate diets have been widely presented as the solution to fighting cardiovascular disease by the mainstream medical establishment. However, high carbohydrate diets have been a disaster for health, with recent evidence suggesting high intakes of carbohydrates, particularly sugars and refined carbohydrates, are implicated in the development of metabolic syndrome, diabetes and even cardiovascular disease itself. Only carbohydrates diets containing high fibre whole grain sources, which eliminate all sugar, appear to be beneficial to long term health. This raises the question as to where the evidence for the benefit of high carbohydrate diets originated.
Much of the early research investigating the effects of diet on plasma lipoprotein levels used models based on populations with genetic defects in lipoprotein metabolism. The Framingham study, one of the first epidemiological studies to show a link between dietary cholesterol and cardiovascular disease, has been criticised for including subjects with familial hypercholesterolaemia. Sufferers of familial hypercholesterolaemia have raised levels of plasma cholesterol and die early due to cardiovascular disease. In such individuals, reducing dietary cholesterol levels does improve plasma lipid levels, but this does not mean that the same is true of healthy subjects. Examples of studies including subjects with genetic defects in lipoprotein metabolism to investigate the cholesterol theory of cardiovascular disease are common in the literature. For example, one study published in the American Journal of Nutrition used subjects with familial hypertriglyceridaemia to test the effects of low carbohydrate diets1.
Familial hypertriglyceridaemia is characterised by a deficiency of lipoprotein lipase and an overproduction of VLDL, which decreases the ability to correctly metabolism dietary triglycerides. In the study, 10 sufferers were fed a low fat, high carbohydrate diet consisting of 60 % carbohydrate, 25 % fat and 15 % protein for 12 weeks. Compared to the baseline diet that contained 45 % of energy from fat and 40 % from carbohydrate, subjects showed a significant reduction in total plasma triglycerides mainly in the form of very low density lipoprotein (VLDL), as might be expected. From these data the authors concluded that high carbohydrate diets ‘may be a useful tool in the management of hypertriglyceridaemia’, suggesting that the effects of reducing fat from the diet of genetic sufferers of hypertriglyceridaemia would be expected to be similar to that in healthy individuals. However, this conclusion is in no way justified from the results.
This is another example of a poorly constructed study, with weak methodology that should not have passed the peer review process. The effects of reducing the triglycerides content of the diet for such individuals was not novel, suggesting that the study had been set up with the sole purpose of adding a conclusion to support the cholesterol theory of cardiovascular disease. Not surprisingly, a look at the list of authors reveals that they were all medical doctors, which is common in such papers. Interestingly, the high carbohydrate diet in the study increased the low density lipoprotein (LDL) plasma levels of the subjects, something that would have increased their risk for cardiovascular disease. Other studies have shown that high carbohydrate diets, when not rigorously controlled to contain whole grains also raise levels of LDL in healthy individuals, possibly because of the refined nature of such diets.
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