Informational only - Not a substitute for medical advice
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Egg quality is inferred from the proportion of embryos that are chromosomally abnormal, and it tracks strongly with age: aneuploidy rises from about 26.9% in women under 30 to 62% in women over 40. No supplement has been shown convincingly to improve human egg quality.
Egg quality means the chance an egg produces a chromosomally normal embryo. It is not measured directly — it is inferred from how many embryos turn out abnormal when they are tested.
That inference is why so much writing on the subject is vague. There is no test that scores an egg before retrieval, so every statement about quality is really a statement about a population.
What determines chromosomal normality is whether the egg divides its chromosomes correctly as it matures. That process becomes less reliable with age, and no blood test taken beforehand can inspect it.
Conflating quantity with quality is the commonest error here, and it runs both ways. A woman of 42 with a reassuring reserve result is told her eggs are fine; a woman of 31 with a low one is told they are poor. Neither follows.
Quantity and competence are separate properties, and only one is routinely measured. Our explanation of what diminished ovarian reserve means covers the distinction.
Substantially, and steeply. In one PGT-A cohort the aneuploidy rate was 26.9% in patients under 30, rising to 62% in women over 40.
Read the other way, 62% aneuploidy at over 40 means nearly four in ten embryos were normal. The problem is usually not that no normal embryo exists — it is that more eggs are needed to find one.
Two things follow. A woman over 40 often needs more eggs to reach one normal embryo, which changes how a cycle is planned rather than whether it is worth attempting. And age is doing most of the work in these numbers.
Any intervention claiming to improve egg quality is competing against a variable moving ten percent a year on its own.
These are population proportions, not individual predictions — which is why two women of the same age can have very different outcomes without either being surprising. We cover the wider picture in how age impacts female fertility.
No supplement has been shown convincingly to improve human egg quality. CoQ10 is the most studied, and the results are suggestive rather than conclusive.
In a randomised trial of women aged 35 to 43, aneuploidy was 46.5% on CoQ10 against 62.8% on placebo — a difference that looks meaningful but did not reach statistical significance.
A later review concluded the available data do not clearly prove CoQ10 improves human oocyte quality. That is genuinely uncertain — not the same as negative, and not the same as positive.
The gap between laboratory and human findings is the part worth understanding. Work in animal models has shown improvements in maturation and chromosomal abnormality. Those results are real, and they are routinely quoted as though they were human clinical results, which they are not.
A trial showing a sizeable difference without statistical significance is the most misreported result in this field. It means chance could not be ruled out — usually because the trial was too small to settle the question.
DHEA has better trial support than CoQ10, but in a narrower group. A Cochrane review of eight randomised trials in poor ovarian responders found higher rates of live birth or ongoing pregnancy, with an odds ratio of 1.81.
Two caveats. The evidence concerns poor ovarian responders specifically, not women with normal reserve. And most poor responders do not respond to DHEA clinically.
An odds ratio of 1.81 is also easier to misread than it looks. It describes how the odds shifted across a trial population, not the chance it works for one person. Where most participants do not respond, that average is produced by a minority who do.
DHEA is a hormone, not a vitamin, and it is available over the counter in several countries — which is precisely the problem. Easy availability is not evidence of safety in a given individual.
It is a prescribing decision. If it is worth trying in your case, that is a conversation with the clinician managing your cycle.
A useful test for any claim about egg quality is to ask what it was measured against. Improvements in animal models are not changes in live birth.
The one variable with an unambiguous effect is time, and it moves in one direction. Six months on a supplement protocol is itself part of the decision, and on the figures above it is the larger part.
A woman choosing between starting treatment now and spending six months on a supplement protocol first is not choosing between two neutral options. That is uncomfortable to read and it is the most useful sentence on this page.
None of this means supplements are pointless. Wanting to contribute something to an outcome otherwise out of your hands is an ordinary human response, and a low-risk supplement is a harmless way to do it. The distinction worth holding is between something that might help a little and something that changes the picture.
IVY can read your results alongside your age and reserve, and set out what the evidence supports for your situation — and what it does not.
What people ask once they understand that age is doing most of the work.
No supplement has been shown convincingly to improve human egg quality. CoQ10 is the most studied and its randomised trial data did not reach statistical significance. Age is the dominant factor, with aneuploidy rising roughly 10% for each additional year. That is not a counsel of despair, but it does mean interventions are competing against a fast-moving variable.
No. Ovarian reserve markers estimate how many eggs remain, not whether those eggs will produce chromosomally normal embryos. The two questions are separate, and a reassuring reserve result at 41 does not change the aneuploidy figures for that age.
The evidence is genuinely uncertain rather than negative. A randomised trial in women aged 35 to 43 found lower aneuploidy on CoQ10 than placebo, but the difference did not reach statistical significance, and a later review concluded the data do not clearly prove a benefit in humans. It is a reasonable thing to discuss with a clinician; it is not a reason to delay treatment.
Only on advice. DHEA is a hormone, not a vitamin. The Cochrane evidence supporting it concerns poor ovarian responders specifically, with an odds ratio of 1.81 for live birth or ongoing pregnancy, and most poor responders do not respond clinically. That evidence does not transfer to women with normal ovarian reserve.