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That the mortality of patients with cardiogenic shock is inversely associated with low-density-lipoprotein cholesterol (LDL-C), as documented by Jin et al.1 is in accordance with our reviews of 38 studies, where the authors had followed more than six million people of all ages for several years after having measured their LDL-C.2,3 In almost all of the studies those with high LDL-C lived just as long or longer than those with normal or low LDL-C. These findings are of course most surprising because according to the official guidelines, high LDL-C is an important risk factor for cardiovascular disease (CVD), the commonest cause of death in most countries.
However, many other contradictory observations have been ignored by the guideline authors as well.4,5 For example, people with low cholesterol become just as atherosclerotic as people with high cholesterol;5 LDL-C of patients with acute myocardial infarction is lower than normal and if it is lowered even more, their risk of dying prematurely increases.5 Furthermore, there is no exposure-response in the statin trials.5
Familial hypercholesterolemia (FH) is seen as a strong argument for the view that high cholesterol is the main cause of CVD, although multiple studies are contradictive.6 For instance, three large follow-up studies of people with FH have found that on average, they lived just as long or longer than other people.6 The few who suffer prematurely from CVD have inherited increased levels of vario...
Familial hypercholesterolemia (FH) is seen as a strong argument for the view that high cholesterol is the main cause of CVD, although multiple studies are contradictive.6 For instance, three large follow-up studies of people with FH have found that on average, they lived just as long or longer than other people.6 The few who suffer prematurely from CVD have inherited increased levels of various types of coagulation factors as well, but their cholesterol does not differ from that of healthy FH individuals´.6 In accordance, rabbits with FH have significantly higher levels of factor VIII and fibrinogen compared with normal rabbits and in an experiment with these rabbits, atherosclerosis was prevented with probucol, which lowered factor VIII and fibrinogen whereas their serum cholesterol was unchanged.6
A relevant question is why high LDL-C is beneficial. The cause is most likely that LDL partakes in the immune system by adhering to and inactivating all kinds of microorganisms and their toxic products; a little-known fact although it has been documented in many ways by more than a dozen research groups.7 The reason why the association between high LDL-C and mortality in the study by Jin et al. was noted only in patients with acute coronary syndrome may be that there is much evidence that infections is a major cause of CVD.8
1. Jin J, Shi Z, Pang X. Association between low- density lipoprotein cholesterol level and mortality in patients with cardiogenic shock: a retrospective cohort study. BMJ Open 2021;11:e044668. doi:10.1136/ bmjopen-2020-044668
2. Ravnskov U, Diamond DM, Hama R, et al. Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly: a systematic review. BMJ Open 2016;6: e010401. doi:10.1136/ bmjopen-2015-010401
3. Ravnskov U, de Lorgeril M, Diamond DM, et al. The LDL paradox: Higher LDL-cholesterol is associated with greater longevity. A Epidemiol Public Health 2020;3:1040-7.
4. Ravnskov, Alabdulgader A, de Lorgeril M, et al. The new European guidelines for prevention of cardiovascular disease are misleading. Exp Rev Clin Pharm 2020;13:1289-94. doi.org/10.1080/17512433.2020.1841635
5. Ravnskov U, de Lorgeril M, Diamond DM, et al. LDL-C does not cause cardiovascular disease: a comprehensive review of the current literature. Expert Rev Clin Pharm 2018;11:959-70. doi: 10.1080/17512433.2018.1519391.
6. Ravnskov U, de Lorgeril M, Kendrick M, et al. Inborn coagulation factors are more important cardiovascular risk factors than high LDL-cholesterol in familial hypercholesterolemia. Med Hypotheses 2018;121:60–3. doi.org/10.1016/j.mehy.2018.09.019
7. Ravnskov U, McCully KS. Review and Hypothesis: Vulnerable plaque formation from obstruction of vasa vasorum by homocysteinylated and oxidized lipoprotein aggregates complexed with microbial remnants and LDL autoantibodies. Ann Clin Lab Sci 2009;39:3-16. PMID: 19201735.
8. Ravnskov U, McCully KS. Infections may be causal in the pathogenesis of atherosclerosis. Am J Med Sci 2012;344:391-4. doi: 10.1097/MAJ.0b013e31824ba6e0.