Twelve weeks of supplementation led to increased plasma levels of CoQ10, with unchanged levels in muscle tissue and isolated mitochondria. No differences in mitochondrial function, glucose homeostasis, and physical performance were found in a cohort of robust older adults.
A useless supplement.
Thank you for that, one less supplement to worry about. Did the population include statin users? This is on the main context that I hear Coq10 can be helpful.
That was my personal experience. No benefit I could tell. I quit coq10 a few years ago.
Right. I never took it, because I could never find any convincing evidence it worked. I remember some 20 years ago there was a lot of talk about it on the CR list, but very quickly two camps formed, and I agreed with the skeptics. The “statin users benefit” seemed plausible mechanistically, but no study ever showed a clear benefit. Some claim the form you take it in is important, but here it shows that regardless - it’s present in the serum, but does nothing much, at least in these outcomes.
For my part, I took 200-400mg every day for 6 weeks, compared levels before and after, and didn’t see much change. I’m a statin user.
According to my Claude Opus 4.5 AI health agent:
Based on my search, I believe you’re referring to the NHANES observational study (Liang et al., 2025) showing CoQ10 supplementation was not associated with all-cause or CVD mortality in general US adults (HR 1.00 for all-cause, HR 1.30 for CVD, neither significant).
How damning is this?
Not very. Here’s why:
Limitations of the NHANES study:
Functional outcome RCTs that refute the “CoQ10 is useless” interpretation:
| Trial | Population | Design | Result |
|---|---|---|---|
| Q-SYMBIO (2014) | 420 patients, moderate-severe heart failure | RCT, 300 mg/day, 2 years | 42% reduction all-cause mortality (p=0.018), 43% reduction CV mortality (p=0.026), 50% reduction in MACE (p=0.003) |
| KiSel-10 (2013, 12-yr follow-up 2018) | 443 elderly Swedes (70-88 years) | RCT, CoQ10 200 mg + selenium 200 mcg, 4 years | 53% reduction CV mortality at 4 years, effect persisted at 12-year follow-up (28.1% vs 38.7% CV mortality) |
| European Q-SYMBIO subgroup (2019) | 231 European HF patients | Post-hoc | Confirmed mortality reduction, significant LVEF improvement |
The key distinction:
The NHANES study asks: “Do random Americans who happen to take CoQ10 live longer than those who don’t?” Answer: No signal.
The RCTs ask: “Does CoQ10 at therapeutic doses improve outcomes in people with documented mitochondrial compromise (heart failure, elderly)?” Answer: Yes, significantly.
I put more stock in functional outcomes than mechanistic measurements.
The only use case is in people on statins and even there the evidence is mixed and the human body only needs like 0.5mg per day.
I have seen at least 5 primary providers since I was first prescribed a statin. Not one doctor suggested that I take a CoQ10 supplement.
I was recently surprised when my nephrologist told me that he had never heard of Berberine.
What is the expected time to see structural mitochondrial changes. I know this is at the early edge of expectations for Urolithin-A, as a somewhat related case. Four to six months is the stabilization target. I can’t recall when a single study involving humans was determinative of much.
Well if it has no benefit, then why would people on statins show improvement with Q10 added? I believe there are even some newer statin formulations already included…
Agreed, which is why I was REFUTING that it had no benefit.
CoQ10 often gets brought up in the context of statin use and Mitochondria but I think it’s a waste of time still exploring those things when the best evidence is for systolic heart failure. While it isn’t a slam dunk for that, there is enough of a signal to me to use it for anyone who is worried about their hearts and especially for people who already have some degree of heart failure. It might not be THAT great but I would rather be safe than sorry in that case.
From ConsumerLab
“Long-term supplementation with CoQ10 may be beneficial in people with congestive heart failure, while evidence that it’s helpful for diastolic heart failure is mixed. Preliminary studies suggest CoQ10 may modestly lower cholesterol levels in people not on statin medication, lower homocysteine levels, and protect the heart during aortic heart valve replacement. CoQ10 does not appear to further lower cholesterol in people taking statins.
Taken orally, coenzyme Q10 may help treat congestive heart failure, a disease in which the heart doesn’t adequately maintain circulation. CoQ10’s role in cell energy production may be the mechanism by which it assists the heart. An analysis of 13 clinical studies found that taking coenzyme Q10 (usually 100 mg daily) significantly improves how well the heart pumps blood (i.e., ejection fraction) by about 3.7% compared to placebo in people with mild-to-moderate heart failure (Fotino, Am J Clin Nutr 2013). The largest and longest clinical study to date found that taking 100 mg three times daily of coenzyme Q10 for 2 years significantly reduced the chance of an adverse cardiovascular event (e.g., hospitalization, worsening heart failure, or death) by almost 50% compared to placebo in people with moderate-to-severe heart failure and significantly improved measures of quality of life such as activity levels, fatigue, and shortness of breath. It’s important to note that these benefits from CoQ10 may require long-term supplementation (2 years); when researchers checked after just 3 months of supplementation, no significant improvements were found (Mortensen, JACC Heart Failure 2014). In all of these studies, coenzyme Q10 was used in addition to prescription heart failure treatment, not in place of it.“
From Grok
Major Trial: Q-SYMBIO (2014)
This is the most influential modern RCT — a multicenter, double-blind, placebo-controlled trial of 420 patients with moderate to severe chronic heart failure (NYHA class III-IV). Patients received 300 mg/day CoQ10 (100 mg three times daily) or placebo for up to 2 years, added to standard therapy.
• It showed a significant reduction in the primary endpoint (major adverse cardiovascular events: CV death, HF hospitalization, urgent transplant, or mechanical support): 15% vs. 26% (HR 0.50, 95% CI 0.32-0.80, p=0.003).
• Secondary benefits: lower CV mortality (9% vs. 16%), all-cause mortality (10% vs. 18%), HF hospitalizations, and improved NYHA class.
• It was safe, with no major adverse effects beyond mild issues.
This trial renewed interest in CoQ10, though it had limitations like smaller event numbers and challenges in recruitment.
Meta-Analyses and Systematic Reviews
Multiple meta-analyses (pooling RCTs) support modest benefits:
• A recent large meta-analysis (33 RCTs) found CoQ10 reduced all-cause mortality (RR 0.64, moderate-quality evidence), HF hospitalizations (RR 0.50, moderate quality), improved NYHA class, lowered BNP levels, boosted left ventricular ejection fraction (LVEF) slightly, and enhanced 6-minute walk test distance — all without major safety concerns.
• The Cochrane review (updated 2021, including multiple RCTs) concluded moderate-quality evidence that CoQ10 probably reduces all-cause mortality and HF hospitalizations.
• Other overviews and meta-analyses (e.g., 10-26 studies) report reductions in mortality (e.g., 31-40%), HF hospitalizations (up to 61% risk reduction in some), improved exercise capacity, and small LVEF gains (often ~2-3.7%), though effects on LVEF or exercise are inconsistent or low-quality evidence in some analyses.
• Benefits appear more consistent for mortality/hospitalizations than for LVEF or symptoms in some reviews.
Earlier meta-analyses (pre-2014) focused more on LVEF improvements (e.g., +3.67%), often in older or less severe cases.
The only drug really effective for heart failure = SGLT2. Using CoQ10 for that is a joke compared to the real massive effect of SGLT2i.
Yes of course there is no comparison between the two but it could be beneficial as an add on to an SGLT2. They act very differently.
I’m convinced this is a pretty solid good heart failure supplement but people seem distracted by the fact it isn’t any more effective for people on statins or have benefits on mitochondria, which are commonly cited (faulty) reasons for taking it. It should certainly not replace heart failure medication, but I do believe it is additive since it acts different mechanistically. This is a recent study that showed it was effective, even on a low-dose of 120mg.
But guys, do you suffer from heart failure, or are on the way to heart failure? No? Then of what relevance is any study, especially small or janky ones maybe showing beneficial effects of CoQ10 on heart failure patients? Honestly, this is just straight up bizarre.
Again, lets look at specific benefits of supplementing with CoQ10 if you have no heart disease. If there are, I can’t find any, but maybe I’m not searching hard enough.
There are literally thousands of drugs and supplements out there. You can’t take them all. You have to have some criteria for which ones you are going to privilege enough to make the cut into your stack. That’s a very, very, very, elite group, where each compound has to justify its place under rigorous scrutiny - like if there are 30,000 supps and drugs out there, and your stack ends up being 30 in total number (still pretty high!), that’s 1 in a 1000! That’s a very high bar to pass, seems to me?
Now ask yourself, why would you take a supp like CoQ10, which has no documented benefits (unless you have heart failure), and for the sake of that you picked it over 999 others? Has it really made the cut? Why?
All the years that I’ve been aware of CoQ10, I’ve never seen a single reason to bother with it. Not one.
Null findings, like the OP study linked to by Antoine, do nothing to change my mind - I still see no reason to take it. I guess I’m extremely resistant to hype and “fashionable moments”. I never took resveratrol for the same reason: where’s the solid evidence of benefits? For resveratrol all they had was some benefits for mice on terrible high fat diets; zero evidence of impact on lifespan in normal mice. And that was literally all - the rest was just a stream of empty hype about red wine and suspicious blabber by Sinclair (that was the moment - all those years ago - when I declared on the CR list that David Sinclair was a huckster in my view, based on his MO - he acted like a huckster, so duck, walk, quack, Quack). What’s the hurry? If a compound has benefits, time will tell - I’m not jumping on it, I am happy to wait. And if decades pass and still no clear evidence of benefits, I’m not wasting any time on it. So to me CoQ10 is a nothingburger. But of coursse to each their own, if you feel it helps you, more power to you. YMMV.
Well cardiovascular disease is the #1 risk of death. Many of us take drugs/supplements/exercise/etc in order to prevent something like heart failure. When we have a supplement where its direct purpose is to improve heart failure, it would serve as a good choice for people who are concerned with getting it to begin with. Prevention is the name of the game.
Now if someone gets full heart work-ups and their heart is in great shape with an ejection fraction of 65%, then yes they are probably better off saving their money. For others, it is a decent insurance policy.
If a supplement showed promise for something else like improving hearing loss or something, then yes that might not be worth it since that’s not exactly fatal like heart failure is.