09/26/2026
A hormone specialist said she fixed her low progesterone by regulating her cortisol.
She’s right, and I’ll say that clearly before I disagree with anything cortisol doesn’t just compete with progesterone, it blocks progesterone receptors.
Then she said how: phosphatidylserine, pregnenolone, ashwagandha.
And for blood sugar, chromium, inositol, alpha lipoic acid and a continuous glucose monitor.
That’s where we part ways, not on the mechanism, on the layer.
Every one of those first three works at cortisol. But cortisol wasn’t the origin.
It spiked to stabilise blood sugar; that was the job it had been given.
Blunt it and you’ve quieted the messenger while the message is still true.
Which is why adaptogens work for a while and then stop the signal was accurate, and suppressing it never changed what generated it.
Here’s the tell in her own story: she also regulated her blood sugar.
That’s the piece that actually worked. Once glucose was stable, cortisol had no reason to keep spiking, and progesterone got its receptors back.
She did the right thing and credited the wrong bottle.
But the blood sugar tools work at insulin and leptin controls insulin, not the other way around. Insulin resistance isn’t the starting point — it’s downstream of a broken leptin-light relationship.
Leptin goes quiet when you never see morning sun, when you eat after dark, when you scroll in bed. Your hypothalamus reads famine.
Your mitochondria drop out of hormone production. Steroid synthesis gets deprioritised, your adrenals compensate with cortisol, and cortisol blocks progesterone.
That’s the chain. She climbed it from the bottom and stopped two floors short.
And melatonin and insulin compete for the same pancreatic receptor melatonin cuts insulin secretion by roughly a quarter at night.
Every hour of light after sunset puts insulin where melatonin belongs. No chromium outruns that.
You don’t need a monitor to tell you your blood sugar is unstable.
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