You ask a rhetorical question, and then follow it with a concluding statement that bears no relationship to the preceding paragraph unless one rejects on principle large numbers of people being on statins (or other lipid-lowering therapies). The causality and resulting long-term risk should drive the decision. One should not wait until a person already has advanced disease discernible on CAC.
One uses MRs to indirectly gather indirect evidence on questions that can’t be answered directly by clinical trials. We don’t need an MR to assess the effects of statins on dementia risk: they are the most studied drugs in the history of the world, and we have multiple clinical trials and extensive observational data. I posted two meta-analyses of such data earlier: they have no effect or may even be protective.
Note also that the MRs are not actually of statins, of course, but are of genetic variants affecting HMG-CoA-reductatse. These variant genes are active in neurons, which will lower the cholesterol available to the brain. Hydrophilic statins do not do this to any meaningful degree — though both of the meta-analyses I posted earlier find no increased risk even from lipophilic statins.
Much of this is nocebo effects,including people who get random muscle pains or even tendinitis and attribute it to a statin they recently started. In clinical trials — where a placebo can distinguish causality — muscle pain from statins occurs in less than 7% of patients.
Moreover, in people on statins in the community,
Setting Primary care across 50 sites in the United Kingdom, December 2016 to April 2018.
Participants 200 participants who had recently stopped or were considering stopping treatment with statins because of muscle symptoms.
Interventions Participants were randomised to a sequence of six double blinded treatment periods (two months each) of atorvastatin 20 mg daily or placebo.
Results … Overall, no difference in muscle symptom scores was found between the statin and placebo periods (mean difference statin minus placebo −0.11, 95% confidence interval −0.36 to 0.14; P=0.40)). Withdrawals because of intolerable muscle symptoms were 18 participants (9%) during a statin period and 13 (7%) during a placebo period. Two thirds of those completing the trial reported restarting long term treatment with statins.
Conclusions No overall effect of atorvastatin 20 mg on muscle symptoms compared with placebo was found in participants who had previously reported severe muscle symptoms when taking statins.
https://www.bmj.com/content/372/bmj.n135
If someone really is one of the rare souls who get statin-induced muscle pain — or one of the more common people whose glucoregulation declines with statin use — there are several other lipid-lowering medications available, all of them also better-studied than the supplements you list:
You may correct me, but to my knowledge we do not have hard outcomes efficacy data on any of these interventions, and with the exception of Metamucil only small short-term studies to guess at safety.
All medications have side-effects, including medications that happen to be originally derived from plants. Statins are the best-studied drugs in the history of the world. We understand their safety and efficacy very well. We have very little idea about the safety or hard-outcomes efficacy for any of these various supplements, with the exception of safety for Metamucil.
Yes — exactly.
