Why I think everyone should take a statin, part 1

In this episode, I talk about why I take a statin even though I am in my 30s and have no major risk factors or short-term risk of cardiovascular disease, and why I believe everyone should do the same. The main reason is this: cardiovascular disease is the number one cause of death in the United States. It remains a major cause of death and disability even in my demographic. In one paper published in the Journal of the American Medical Association, one of the most important medical journals in the world, in 2012, men at age 45 who had risk factors that were all optimal (systolic and diastolic blood pressure <120 and <80 respectively, total cholesterol <180 mg/dL, no diabetes, and no tobacco smoking), still had a risk of having a cardiovascular event of 15% by age 80. Men with just one risk factor that was not optimal had a risk of a full 35% by age 85 (PMID 23117780). Subclinical atherosclerosis, which affects quality of life, sexual, and physical functioning, is even more prevalent than these figures indicate. Why should anyone take any chances? Take a statin.

We know that statins reduce cardiovascular risk regardless of whether or not lipids are elevated. This is because LDL cholesterol is necessary for atherosclerosis. The lower LDL cholesterol goes, the more risk is reduced in a log-linear relationship, regardless of baseline risk, with larger risk reductions the longer one’s lipids are lower (PMID 28444290). The benefits of LDL reduction are cumulative. This is because impact of LDL cholesterol on cardiovascular disease risk is itself cumulative, similar to pack-years in tobacco smoking. Although there is scant evidence for the prevention of cardiovascular disease in people younger than 40, such an approach is supported by a convergence of evidence. Indeed, as an article called “Time to Relax the 40-Year Age Threshold for Pharmacologic Cholesterol Lowering” published in the Journal of the American College of Cardiology points out: “LDL-C exposure in early adulthood may pose greater risk than the same level of exposure later in life” (PMID 34763773). Current guidelines on statin treatment are excessively conservative and at odds with the currently available body of evidence.

What’s more, the side effects of statins are minimal and dramatically overstated in the popular media. As a classic meta-analysis by Feingold and colleagues of 29 randomized controlled trials involving more than 83,000 patients showed, “only a small minority of symptoms reported on statins are genuinely due to statins” (PMID 24623264). And a paper published this month showed very clearly that even intensive lipid lowering of LDL cholesterol levels below 40 mg/dL due to statins produced benefits that far exceeded risks. The risks are even smaller in those treated with the newer classes of lipid-lowering agents such as ezetimibe and the PCSK9 inhibitors (https://doi.org/10.1093/ehjopen/oeac038). Indeed, the injectable PCSK9 inhibitor inclisiran, which requires treatment only twice per year, halves LDL cholesterol and is a candidate for universal lipid reduction such as I am proposing.

In my case, I take 2.5 mg of rosuvastatin and 5 mg of ezetimibe, a combination therapy that produces most of the LDL-lowering effects of higher doses while minimizing side effects. I experience no side effects whatsoever, despite a highly active lifestyle as a combat sports athlete. To me it only seems obvious. For people who experience a similarly non-existent side effect profile of lipid lowering, I think the decision to use these drugs to minimize long-term cardiovascular disease risk is cut-and-dry. Everyone should try it and do it if they can tolerate it.

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