Cholesterol-lowering treatment may worsen the outcome of a Covid-19 infection.
According to Hu et al. serum cholesterol is significantly lower among Chinese patients with Covid-19 (1). The reason may be that low cholesterol predisposes to infectious diseases, because LDL partake in the immune system by adhering to and inactivating almost all types of microorganisms and their toxic products. This is a little-known fact but it has been documented in many ways by more than a dozen research groups (2,3) For instance, human LDL inactivates up to 90% of staphylococcus aureus -toxin and rats injected with mortal bacterial toxins survive if they are injected with human LDL as well (3).
The anti-infectious property of LDL has been documented in human studies as well. In a meta-analysis of 19 cohort studies including almost 70,000 deaths, Jacobs et al. found an inverse association between serum cholesterol and mortality from respiratory and gastrointestinal diseases, most of which are of an infectious origin (4). It is unlikely that the low cholesterol was caused by these diseases because the associations remained after exclusion of deaths occurring during the first 5 years. Furthermore, in a 15-year follow-up of more than 120,000 adult, multiethnic people, Iribarren et al. found a strong, inverse association between initially determined cholesterol and the risk of being admitted to hospital later in life due to an infectious disease (5).
As LDL-cholesterol is able to inactivate virus as well (6,7) patients on cholesterol-lowering treatment and with a life-threatening Covid-19-infection should cease this treatment; at least until they have recovered from the infection.
1. Hu, X, Chen D, Wu L, He G, Ye W. Low Serum Cholesterol level among patients with COVID-19 infection in Wenzhou, China (February 21, 2020). Available at SSRN: https://ssrn.com/abstract=3544826.
2. Ravnskov U, McCully KS. 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.
3. Ravnskov U, McCully KS. Infections may be causal in the pathogenesis of atherosclerosis. Am J Med Sci. 2012;344:391–394. https://doi.org/10.1097/MAJ.0b013e31824ba6e0
4. Jacobs D, Blackburn H, Higgins M, Reed D, Iso H, McMillan G, Neaton J, Nelson J, Potter J, Rifkind B. Report of the conference on low blood cholesterol: Mortality associations. Circulation 1992; 86:1046–60. https://doi.org/10.1161/01.cir.86.3.1046
5. Iribarren C, Jacobs DR Jr, Sidney S, Claxton AJ, Feingold KR. Cohort study of serum total cholesterol and in-hospital incidence of infectious diseases. Epidemiol Infect 1998; 121:335–47. https://doi.org/10.1017/s0950268898001435
6. Huemer HP, Menzel HJ, Potratz D et al. Herpes simplex virus binds to human serum lipoprotein. Intervirology 1988;29:68-76. https://doi.org/10.1159/000150031
7. Superti F, Seganti L, Marchetti M, Marziano ML, Orsi N. SA-11 rotavirus binding to human serum lipoproteins. Med Microbiol Immunol 1992;181:77-86. https://doi.org/10.1007/bf00189426
Competing interests: No competing interests