What if your ovaries aren't out of eggs at all and what you're feeling is a reversible slowdown

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Hello and welcome to Dr. Mercola's cellular wisdom. I'm Ethan Foster. Today we're asking whether menopause is an irreversible endpoint or a metabolic state you can influence.

We'll look at new findings on egg cell mitochondria, clinical attempts to restart ovarian function, and the

specific metabolic supports under investigation.

I'm Alara Sky.

We'll keep this focused on what the research describes, how uocytes appear to resist typical

mitochondrial aging, why that matters for your hormones, and which experimental and

nutritional strategies are being studied without adding anything beyond the article's content.

A recent science advances study looked directly at mitochondrial DNA in human egg cells.

The researchers analyzed 80 single usites from 22 women, age 20 to 42, undergoing IVF,

comparing them to each woman's blood and saliva.

Using duplex sequencing, they expected to see age-related MTDNA mutations in eggs just as in other tissues,

but they didn't.

Blood and saliva showed the usual rise in MTDNA mutations with age, yet

U-Sites maintained mitochondrial genetic stability across the two decades studied. The authors interpreted

the pattern as evidence of protective mechanisms in egg cells that limit function disrupting

mutations, at least into the early 40s.

That stability challenges the idea that menopause must be driven by egg decay alone.

Clinical observations point in the same direction.

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