In girls with polycystic ovary syndrome and obesity, a 4-month ketogenic diet is linked to the return of regular menstrual cycles and a decrease in testosterone levels.
Mechanism
Synthesis from 1 study
Cutting carbs lowers insulin, which stops the ovaries from making too much testosterone. At the same time, the body makes ketones that calm inflammation in the ovaries, allowing eggs to mature and periods to return. This dual effect restores normal reproductive function.
Most probable mechanism
Eating very few carbohydrates lowers blood sugar and insulin levels. Lower insulin tells the ovaries to stop making too much testosterone and tells the liver to make more protein that traps testosterone, making less of it active. At the same time, the body produces ketones that calm inflammation in the ovaries, allowing follicles to develop normally and ovulation to restart. This brings back regular periods.
Carbohydrate intake is restricted to below 40 grams per day, eliminating postprandial glucose spikes and reducing pancreatic insulin secretion
Fasting insulin levels decrease significantly, removing chronic stimulation of ovarian theca cells that drive androgen synthesis
Reduced insulin increases hepatic production of sex hormone-binding globulin, which binds testosterone and lowers its bioavailable fraction
Ketone bodies, particularly beta-hydroxybutyrate, accumulate in circulation and inhibit the NLRP3 inflammasome in ovarian tissue
Inhibition of ovarian NLRP3 inflammasome reduces NF-kB signaling and local inflammation, restoring follicular development and reducing atresia
Normalized ovarian function reestablishes gonadotropin rhythm and triggers resumption of spontaneous ovulation and menstrual cycles
Less supported by current evidence, but not ruled out
Ketones activate a receptor on fat cells that triggers the release of adiponectin, a hormone that improves how muscle and liver respond to insulin. This further lowers insulin levels, indirectly reducing testosterone production.
Beta-hydroxybutyrate activates the GPR109A receptor on adipocytes
GPR109A activation stimulates adiponectin synthesis and secretion
Adiponectin enhances insulin sensitivity in skeletal muscle and liver via AMPK and PPARα pathways
Improved insulin sensitivity further suppresses ovarian androgen production
Fat loss, especially around the abdomen, reduces the enzyme that reactivates cortisol in fat tissue. Lower inflammation and improved insulin sensitivity also reduce stress signaling to the adrenal glands, lowering cortisol levels.
Visceral adipose tissue mass decreases, reducing local cortisol regeneration by 11β-HSD1
Beta-hydroxybutyrate inhibits NLRP3 inflammasome, reducing systemic inflammation that drives HPA axis overactivity
Reduced HPA axis activation lowers adrenal cortisol secretion
Evidence from Studies
Supporting (1)
Community contributions welcome
Low-Carbohydrate (Ketogenic) Diet in Children with Obesity: Part 2—Hormonal Effects of the Ketogenic Diet
Contradicting (0)
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