This 2018 review presented evidence that:
“For half a century, a high level of total cholesterol (TC) or low-density lipoprotein cholesterol (LDL-C) has been considered to be the major cause of atherosclerosis and cardiovascular disease (CVD), and statin treatment has been widely promoted for cardiovascular prevention. However, there is an increasing understanding that the mechanisms are more complicated and that statin treatment, in particular when used as primary prevention, is of doubtful benefit.
The authors of three large reviews recently published by statin advocates have attempted to validate the current dogma. This article delineates the serious errors in these three reviews as well as other obvious falsifications of the cholesterol hypothesis.
Our search for falsifications of the cholesterol hypothesis confirms that it is unable to satisfy any of the Bradford Hill criteria for causality and that the conclusions of the authors of the three reviews are based on:
- Misleading statistics,
- Exclusion of unsuccessful trials and by
- Ignoring numerous contradictory observations.
The association between the absolute risk reduction of total mortality in 26 statin trials [squares] included in the study by Silverman et al. and in 11 ignored trials [triangles] and the year where the trial protocols were published. The vertical line indicates the year where the new trial regulations were introduced.
In 2004–2005, health authorities in Europe and the United States introduced New Clinical Trial Regulations, which specified that all trial data had to be made public. Since 2005, claims of benefit from statin trials have virtually disappeared.“
This paradigm was proven wrong eighty years ago! How much longer will its harmful consequences continue?
https://www.tandfonline.com/doi/full/10.1080/17512433.2018.1519391 “LDL-C does not cause cardiovascular disease: a comprehensive review of the current literature”
Surface Your Real Self 
OK, You’ll have to explain to me why having very high levels of LDL and low levels of HDL for most of my adult life eventually led to a heart attack at age 44. Genetics matter, is in my case. And how do you explain so many children with homozygous familial hypercholesteraemia getting heart attacks in their teenage years?
Bruce, we agree that group statistics often don’t represent an individual. It’s a problem discussed in https://surfaceyourrealself.com/2018/07/22/group-statistics-dont-necessarily-describe-an-individual/
This review suggested in Section 6 “Does cholesterol-lowering treatment lower the risk of CVD?”:
“If high LDL-C were the major cause of CVD, the benefit from statin treatment should be better the more LDL-C is lowered; for example, there should be a systematic exposure-response relationship.
The authors of the three reviews assert that statin trials have demonstrated such dose-responses. As proof, they have compared the outcomes in various trials with the degree of LDL-C lowering, and it is impossible to know whether the greater effect of a trial using a higher statin dose may be caused by its cholesterol-lowering effect or pleiotropic effects.
True exposure-response is based on a comparison between the degree of cholesterol lowering in each patient in a single trial and the absolute reduction of their risk. True exposure-response has only been calculated in three clinical statin trials, and it was absent in all three.
Even a correctly calculated exposure-response does not prove causality, because an innocent risk factor, for instance, LDL-C, may change in the same direction as the real cause, but the absence of exposure-response is a strong argument against causality.”
What did you think about Section 7 “Does FH prove that high LDL-C causes CVD?”
By the way, this review was published by the Cholesterol Skeptics, also known as THINCS. It’s been widely criticized in the literature because this group is known to cherry pick their studies to fit their agenda. Cholesterol matters. Don’t believe these guys.
Hi Bruce! A careful reading of this review is warranted.
What are the contrary arguments that are based on scientific merits?
It is true that placing all the emphasis on LDL c is simplistic. Population studies have suggested that HDL ( and its subclasses) the sweeper of the arteries is as important or more important than LDLc. Unfortunately we have no pharmaceutical agents to boost the level ( and the efficiency) of HDL. Unable to increase “the sanitation department “ we can only work on the “ garbage “ the LDLc. Medications that lowered the LDL c have been around for decades but did nothing to improve outcome and in the eighties our units were still full of patients with ACS or full ST elevation MI and optimal cholesterol. Current evidence points to inflammation as the triggering factor that causes an ACS. Statin have a anti inflammatory effect that makes them superior agents…