They looked at “elderly Swedish population low in selenium” and gave them selenium + CoQ10 and concluded it was good. Are you old? Low in selenium? Do we know if the positive outcome was due to selenium, CoQ10, or the combination? Would you get the same outcome with selenium + Nutella?
No, no, no. NOT AT ALL. They conclude:
In 2013, the American College of Cardiology Foundation and the American Heart Association recommended against the use of nutritional supplements (including coenzyme Q10) for the treatment of heart failure.5 The 2017 update to this practice guideline did not address coenzyme Q10. The approximate cost of a one-month supply of the 200-mg dose of coenzyme Q10 is $10.6 At this time, there is insufficient evidence to support, or refute, the use of coenzyme Q10 in patients with heart failure.
Their conclusion is based on the latest Cochrane review, Coenzyme Q10 for heart failure that concluded:
The included studies provide moderate‐quality evidence that coenzyme Q10 probably reduces all‐cause mortality and hospitalisation for heart failure. There is low‐quality evidence of inconclusive results as to whether coenzyme Q10 has an effect on the risk of myocardial infarction, or stroke. Because of very low‐quality evidence, it is very uncertain whether coenzyme Q10 has an effect on either left ventricular ejection fraction or exercise capacity. There is low‐quality evidence that coenzyme Q10 may increase the risk of adverse effects, or have little to no difference.
There is currently no convincing evidence to support or refute the use of coenzyme Q10 for heart failure. Future trials are needed to confirm our findings.
Q10 is not recommended by any medical society for heart failure. See for instance the latest Complementary and Alternative Medicines in the Management of Heart Failure: A Scientific Statement From the American Heart Association 2022
Coenzyme Q10 (CoQ10) naturally occurs in small amounts in organ meats and oily fish and is a cofactor in many biological pathways including oxidative phosphorylation. Because HF results in an ATP-depleted state, exogenous administration of CoQ10 has been hypothesized to result in metabolic benefit. Researchers found modest benefit with CoQ10 supplementation by improving LV ejection fraction and quality of life in small-scale studies. In the largest randomized trial of CoQ10 in 420 patients with HF, Q-SYMBIO (Coenzyme Q10 as Adjunctive Treatment of Chronic Heart Failure With Focus on Symptoms, Biomarker Status [Brain-Natriuretic Peptide], and Long-Term Outcome [Hospitalizations/Mortality]), CoQ10 treatment was not associated with any significant changes in 6-minute walk distance, or N-terminal pro-B type natriuretic peptide levels compared with placebo, but was associated with a significant improvement of New York Heart Association functional class and reduction in major adverse cardiovascular events at 2 years (hazard ratio [HR], 0.50 [95% CI, 0.32–0.80]; P=0.003). Furthermore, in a more recent literature analysis, CoQ10 treatment was associated with a reduction in all-cause mortality. However, larger-scale randomized-controlled trials are needed before any definitive conclusion can be reached. Therefore, CoQ10 supplementation remains of uncertain value in HF at this time.
That’s one trial in a specific sub-type of heart failure. Another trial from the same year found no benefits: Coenzyme Q10 in the Treatment of Heart Failure with Preserved Ejection Fraction: A Prospective, Randomized, Double-Blind, Placebo-Controlled Trial 2022.
This 2022 meta-review (Coenzyme Q10 to manage chronic heart failure with a reduced ejection fraction: a systematic review and economic evaluation) concluded:
Many trials were reported poorly and were rated as having a high or unclear risk of bias in at least one domain. Meta-analysis suggested a possible benefit of coenzyme Q10 on all-cause mortality (seven trials, 1371 participants; relative risk 0.68, 95% confidence interval 0.45 to 1.03).
Available evidence suggested that, if prescribed, coenzyme Q10 has the potential to be clinically effective and cost-effective for heart failure with a reduced ejection fraction. However, given important concerns about risk of bias, plausibility of effect sizes and applicability of the evidence base, establishing whether or not coenzyme Q10 is genuinely effective in a typical UK population is important, particularly as coenzyme Q10 has not been subject to the scrutiny of drug-licensing processes. Stronger evidence is needed before considering its prescription in the NHS.
Conclusions:
- CoQ10 lowers lifespan in mice and rats at human equivalent doses >60 mg/day. (This does NOT mean that at these doses in humans CoQ10 would also lower lifespan: we don’t know.)
- CoQ10 is not proven to improve outcomes in humans with heart failure.
There might still be a case for CoQ10, but the above two points are undeniable facts (that could still change, for instance, if a future RCT finds benefits from CoQ10 in heart failure or another condition).
