Statins
Statins block cholesterol synthesis and are mass-prescribed for heart risk scores. They lower a lab number while cholesterol is a raw material for steroids and membrane repair. Muscle and energy side effects (pain, fatigue) and glucose changes are commonly reported by patients, though incidence and causality are debated in literature versus clinics.
Primary prevention and coronary calcium
[edit]A 13,644-patient cohort followed a median of 9.4 years found statin use cut major adverse cardiovascular events only in people who already had detectable coronary artery calcium (CAC) on scan (adjusted subhazard ratio 0.76, p=0.015); in patients with a CAC score of zero, statins showed no measurable benefit (adjusted subhazard ratio 1.00, p=0.99). The benefit scaled with CAC severity, from a number-needed-to-treat of 100 over 10 years at low CAC (1-100) down to 12 at CAC over 100.[1] This is a specific claim about a CAC score of zero, not a blanket claim about anyone without coronary artery disease broadly, and doesn't extend to secondary prevention (people who've already had a cardiac event).
CoQ10 depletion and mitochondrial stress
[edit]Statins block HMG-CoA reductase, the same mevalonate-pathway step that produces the farnesyl pyrophosphate needed for Coenzyme Q10 synthesis, so blocking cholesterol production also blocks a shared precursor for the electron-transport-chain molecule CoQ10 depends on; circulating CoQ10 commonly falls 20-40% within weeks of starting a statin.[2] The elderly, hypothyroid, magnesium-deficient, and high-dose statin users are more often flagged as susceptible to statin-associated muscle symptoms, consistent with lower baseline mitochondrial reserve. The evidence for muscle-tissue (not just blood) CoQ10 depletion specifically is mixed: one controlled trial found statins reduced measured muscle mitochondrial respiration without a corresponding drop in muscle CoQ10 levels, pointing to other mechanisms (reduced small GTP-binding proteins, altered calcium handling, or fatty-acid-oxidation changes) contributing alongside or instead of CoQ10 loss.[2]
Practice
[edit]Medical decision with full context. Prefer thyroid and metabolic repair for hypothyroid high cholesterol. Coenzyme Q10 is sometimes discussed as an adjunct for side effects. A CAC score of zero is one input worth discussing with a physician before starting a statin purely for primary prevention. See Cholesterol, Heart, Thyroid, Pregnenolone, Harm reduction.
See also
[edit]References
[edit]- ↑ Mitchell JD, Fergestrom N, Gage BF, et al. "Impact of Statins on Cardiovascular Outcomes Following Coronary Artery Calcium Scoring," J Am Coll Cardiol. 2018;72(25):3233-3242. PMID 30409567.
- ↑ 2.0 2.1 Mollazadeh H, et al. "Effects of statins on mitochondrial pathways," J Cachexia Sarcopenia Muscle. 2021;12(2):237-251. PMID 33511728.