Cholesterol testing is currently popular in the allopathic medicine, despite its questionable validity as a diagnostic tool. The current paradigm states that dietary cholesterol raises level of plasma cholesterol, and this in turn leads to the formation of atherosclerosis which we are told is pivotal in the aetiology of cardiovascular disease. However, this theory is provably false because evidence from the nutritional literature contradict the foundations of the theory. Firstly, studies show that dietary cholesterol does not raise plasma levels of cholesterol and so the initial assumption is false. Secondly, plasma cholesterol does not cause atherosclerosis, but is mearly associated with it. While elevated levels of some cholesterol carrying lipoproteins are a risk factor for cardiovascular disease, the cause and effect is not proven. Thirdly, the presence of atherosclerotic plaques does not determine cardiovascular risk as some populations such as the Japanese develop high rates of atherosclerosis, but have low rates of cardiovascular disease.
That the cholesterol theory of cardiovascular disease is provably false, based on sound evidence in the nutritional literature, should not necessarily eliminate the usefulness of cholesterol testing. An association between some plasma cholesterol carrying lipoproteins and cardiovascular disease does exist, albeit for different reasons than believed by proponents of the cholesterol theory of cardiovascular disease. For example, elevated plasma levels of the small dense low density lipoprotein (LDL), elevated levels of lipoprotein(a), elevated levels of very low density lipoprotein (VLDL; triglycerides) and depressed levels of high density lipoprotein (HDL) are all associated with an increase risk of cardiovascular disease. Understanding these associations has only become possible as more detailed analytical techniques have elucidated the various subgroups within the lipoprotein fractions. Indeed, detailed testing of these specific markers is now often required in a research setting in order to give the study any kind of validity.
However, clinical cholesterol testing does not measure the various subtypes of lipoproteins in detail but instead relies only on measures of LDL, HDL and total cholesterol. This lack of detailed lipoprotein subgroup analysis detracts from the usefulness of the test and raises questions about the validity of cholesterol testing in a clinical setting. For example, while the ratio of LDL to HDL is often touted as an important diagnostic indicator of cardiovascular disease, the truth is that without measuring the subgroups of LDL, that is to say lipoprotein(a), small dense LDL and large buoyant LDL, the results of the test are of little benefit. For example, elevated levels of small dense LDL are associated with an increase risk of cardiovascular disease, while increased levels of large buoyant LDL are not associated with an increase risk. Total cholesterol is also of questionable value as it shows only a very weak association with cardiovascular disease and as a result has been almost completely ignored in recent years as a valid diagnostic tool in research.
In addition, it has been known for some time that total cholesterol is also under the influence of seasonal variation, and so the time a cholesterol test is taken can have a huge influence on the results. For example, in one study1, researchers noticed that plasma cholesterol concentrations rose in the autumn months and declined in the summer months. Similar results have been reported in other earlier studies (here). A number of explanations have been proposed to explain the influence of seasonal factors on cholesterol metabolism. Some researchers have suggested that the increased temperature of the summer combined with greater physical activity levels decreases the volume of plasma2. However, another explanation for the variation may relate to higher conversion of subcutaneous cholesterol to vitamin D in the summer month. In countries such as Finland the variation in seasonal cholesterol levels may be as much as 100 mg/mL (2.59 mmol/L). Based on these findings, the validity of cholesterol screening in a clinical setting is questionable.
