Proponents of the lipid hypothesis of cardiovascular disease claim that dietary saturated fat and cholesterol are the cause of cardiovascular disease. The theory states that high intakes of dietary cholesterol and saturated fat cause increases in the low density lipoprotein (LDL) particles in the plasma and these in turn then accumulate in arteries causing atherosclerosis which in turn develops into various forms of cardiovascular disease. While the theory sounds plausible, it is based mainly on conjecture and assumption and is not supported by empirical scientific evidence. The main problem with the theory is that dietary cholesterol does not cause changes to plasma cholesterol levels and the effects of saturated fatty acids on plasma cholesterol are varied depending on the chain length of the fat. In this regard some saturated fatty acids may have beneficial effects. Further as LDL is present in the plasma naturally, it has never been explained why atherosclerosis does not develop in everyone, as it should if LDL was a pathogenic particle.
In order to support their theory proponents of the lipid hypothesis often uses evidence from feeding trials. Such trials involved feeding subjects high cholesterol and saturated fatty acid diets and assessing their plasma lipoprotein levels. Many such studies have been performed and superficially they appear to show that dietary cholesterol and saturated fatty acids do negatively affect plasma levels of lipoproteins as the theory suggests. However, a deeper look at many of these studies shows them to be poorly designed and the lack of controls results in the presence of possible confounding variables that make drawing any scientific conclusions from the studies difficult, and in many cases invalidates the studies. One of the most common confounding variable in such studies are polyunsaturated fatty acids. Polyunsaturated fatty acids are known to be able to lower plasma cholesterol levels and so studies that have replaced saturated fat and cholesterol with polyunsaturated fatty acids should be read with caution.
As polyunsaturated fatty acids have been shown to possess certain plasma cholesterol lowering effects, the polyunsaturated fatty acid content of any test diets investigating the effects of dietary cholesterol and saturated fatty acids on plasma cholesterol levels should always be controlled to prevent changes to polyunsaturated fatty acids. However, this is quite often not the case. For example, in one study1, researchers tested the effects of a high cholesterol high saturated fatty acid diet and a low cholesterol high polyunsaturated fatty acid diet on the on the plasma lipoprotein levels of healthy subjects. The results showed that consumption of the high cholesterol high saturated fatty acid diet caused significant increases in cholesterol contained in LDL (+59 %), significant increases plasma levels of LDL (+15 %) and significant increases plasma levels of high density lipoprotein (+30 %). These changes caused the LDL to HDL ratio to fall from 1.78 to 1.58, suggesting that cardiovascular risk had been increased.
Just how studies such as this can be used as proof that dietary cholesterol and saturated fatty acids are a cause of cardiovascular disease is a mystery. Clearly the polyunsaturated fatty acids could have influenced these results and therefore it is not possible to claim detrimental effects for the dietary cholesterol or saturated fatty acids. Further the study design did not involve a randomised cross over design, and as such all the subjects consumed the low cholesterol diet, followed by the high cholesterol diet. This further weakens the validity of the study results. In addition, the subjects consumed a mean energy intake of 1945 kcal per day on their regular diet and this fell to 1897 kcal per day on the low cholesterol diet. As energy intake is related to lipoprotein production, this may have influenced the levels of plasma cholesterol. Then when the subjects consumed their high cholesterol diet the energy intake of the diet increased to 2063 kcal per day, which could then explain the subsequent increase in plasma cholesterol levels.
Further, the authors made no attempt to control the diets of the individuals for fibre content and so it is unknown how this may have affected the results, fibre being a particularly efficient plasma cholesterol lowering agent. It should also be noted that the study contain just 6 subjects, which is far too few to give a meaningful extrapolation to the population as a whole. On top of all of these problems we have to consider the fact that LDL in itself is now recognised to be a particle with considerable heterogeneity, existing as a small dense particle and a large buoyant particle. Only the small dense particle increases the risk of cardiovascular disease, and as this paper was published before this information was available, it is not possible to state whether the increase in LDL plasma levels were even detrimental. Credit to the authors however as they did not try to hide the known effects of polyunsaturated fatty acids on plasma cholesterol from their results. However, the title of the paper is misleading in this respect.
RdB
