The cholesterol theory of cardiovascular disease states that dietary cholesterol raises plasma levels of certain lipoproteins, and that this in turn is the cause of the atherosclerosis that subsequently increases the risk of cardiovascular disease. However, the basis of the theory is of questionable logic because evidence is lacking for adequate mechanisms at each juncture of the hypothesis. In fact, if a theory ever warranted the title of being unscientific, the cholesterol theory of cardiovascular disease would be a strong contender. The unfounded nature of the theory is demonstrated consistently by the lack of adequate controls in many of the studies feeding low lipid diets to subjects while reporting beneficial blood lipids effects. Often in such studies, the results do not match the conclusions, which demonstrates the desperation of the authors to show a valid connection between dietary cholesterol and cardiovascular disease. The fact that low lipid diets are also high fibre diets, and that fibre is a known cholesterol lowering agent, is often conveniently forgotten.
For example, in one study1, researchers treated a group of coronary artery disease patients a diet with less than 100 mg of cholesterol a day. Fat in the diet was limited to 10 % of energy intake, while protein and carbohydrate made up 15 and 75 % of energy, respectively. In 3 months the diet caused a 41 % reduction in serum low density lipoprotein (LDL) and a 33 % reduction in serum total cholesterol. At this point the researchers asked the subjects to maintain their fat intakes as low as possible, and after a further 9 months a diet recall questionnaire showed that mean total total fat intake in the subjects was 21.4 % of energy. At the conclusion to the study after 12 months, serum total, LDL and VLDL (very low density lipoprotein) cholesterol had fallen 14, 18, 27 %, respectively (from baseline). In addition, high density lipoprotein (HDL) cholesterol had increased 18 %. The authors claimed that the changes in serum lipids were correlated with changes in fat, but this claim is not possible from their data based on their methodology (which is severely lacking).
The authors concluded that serum lipids can be improved through use of low fat diets, and even suggested that the reason for this was the low intake of saturated fat and cholesterol. However, the subjects were advised to lower sugar intake and increase consumption of whole grains products which included legumes. High intakes of fibre and legumes and low intakes of sugar have been shown to beneficially alter plasma lipoprotein levels and cause weight loss. That the mean body weight of the subjects also fell is interesting because body weight reductions are also known to cause reductions in plasma lipoprotein levels. Therefore this data can just as easily be used to claim that high fibre, low sugar diets are able to cause weight loss, which subsequently improved lipoprotein levels. Many studies investigating the role of cholesterol in cardiovascular disease have drawn similar conclusions. Disparities between data and conclusions highlight the bias inherent in such investigations and question the motive of the authors propagating such cholesterol myths.
RdB
