The idea that cholesterol is the primary cause of heart disease has come under increasing scrutiny in recent years. While high cholesterol levels, particularly LDL, have long been labeled a major risk factor, a growing body of research suggests that this relationship is far more nuanced. Many individuals who suffer heart attacks have normal cholesterol levels, and markers like inflammation, insulin resistance, and particle size may be more predictive of cardiovascular risk. This has led some experts to argue that the “cholesterol hypothesis” is an oversimplification and in many cases, a myth that has distracted from more meaningful root causes of heart disease.
Here is a collection of published research that seriously challenges the cholesterol hypothesis:
“National dietary guidelines were introduced in 1977 and 1983, by the US and UK governments, respectively, with the ambition of reducing coronary heart disease (CHD) by reducing fat intake. There were no differences in all-cause mortality and non-significant differences in CHD mortality, resulting from the dietary interventions.”
18 Oct 2010 [77] Do statins have a role in primary prevention? An update.
- “The claimed mortality benefit of statins for primary prevention is more likely a measure of bias than a real effect.
- The reduction in major coronary heart disease serious adverse events with statins as compared to placebo is not reflected in a reduction in total serious adverse events.
- Statins do not have a proven net health benefit in primary prevention populations and thus when used in that setting do not represent good use of scarce health care resources.”
LDL-C does not cause cardiovascular disease: a comprehensive review of the current literature
“Despite the fact that LDL-C is routinely referred to as the ‘bad cholesterol’, we have shown that high LDL-C levels appear to be unrelated to the risk of CVD, both in FH individuals and in the general population and that the benefit from the use of cholesterol-lowering drugs is questionable.”
“High LDL-C is inversely associated with mortality in most people over 60 years. This finding is inconsistent with the cholesterol hypothesis (ie, that cholesterol, particularly LDL-C, is inherently atherogenic). Since elderly people with high LDL-C live as long or longer than those with low LDL-C, our analysis provides reason to question the validity of the cholesterol hypothesis. Moreover, our study provides the rationale for a re-evaluation of guidelines recommending pharmacological reduction of LDL-C in the elderly as a component of cardiovascular disease prevention strategies.”
“substituting dietary linoleic acid in place of saturated fats increased the rates of death from all causes, coronary heart disease, and cardiovascular disease. An updated meta-analysis of linoleic acid intervention trials showed no evidence of cardiovascular benefit.
“replacement of saturated fat in the diet with linoleic acid effectively lowers serum cholesterol but does not support the hypothesis that this translates to a lower risk of death from coronary heart disease or all causes.”
Our study provides an updated epidemiological indication of possible errors in the CVD risk algorithms of many clinical guidelines. If our findings are generalizable, clinical and public health recommendations regarding the ‘dangers’ of cholesterol should be revised. This is especially true for women, for whom moderately elevated cholesterol (by current standards) may prove to be not only harmless but even beneficial.
