Every claim, every source.

This 2025 systematic review specifically addresses how intermittent fasting affects fertility and reproductive hormones in women with polycystic ovary syndrome (PCOS) — the most common endocrine disorder of reproductive-aged women, characterized by hyperandrogenism, insulin resistance, and menstrual irregularity. The authors synthesized three included studies of time-restricted feeding (TRF) and related IF protocols in PCOS patients. The findings were notably favorable. Menstrual regularity improved in 33–40 percent of participants — meaning a third or more of women with previously irregular cycles reported normalized cycling after TRF intervention. Hormonal changes pointed in the right direction for the PCOS phenotype: total testosterone fell about 9 percent, free androgen index dropped 26 percent, sex hormone-binding globulin rose, and anti-Müllerian hormone and luteinizing hormone both decreased. The review concludes that intermittent fasting, particularly time-restricted feeding, shows potential as a non-pharmacological adjunct intervention for improving reproductive health and fertility in women with PCOS by addressing the core pathophysiological mechanisms (insulin resistance, hyperandrogenism) that drive the syndrome.

This Nutrients review is the first to synthesize specifically what human trials of intermittent fasting (not animal work, not religious fasting) show about sex-hormone shifts in women and men. The authors identified seven human trials total: five testing time-restricted eating, one testing a 5:2 protocol, and one studying meal timing. Their headline findings for premenopausal women with obesity: intermittent fasting reduces testosterone and the free androgen index, and increases sex hormone-binding globulin — particularly when the eating window is restricted to earlier in the day. Estrogen, luteinizing hormone, and follicle-stimulating hormone showed no statistically meaningful change in the trials reviewed. In men, intermittent fasting reduced total and free testosterone in some studies, with implications for libido and lean-mass maintenance that the authors flag as concerning at longer protocol durations. The honest summary: female reproductive hormone effects are real but modest, mostly favorable for PCOS-spectrum profiles, and depend heavily on eating-window timing.

Anne Loucks's 2003 review consolidates a foundational principle for women's exercise and nutrition science: it is energy availability — calories left over after subtracting exercise expenditure from intake — that regulates reproductive function, not body fatness. Through a series of careful in-laboratory studies measuring LH (luteinizing hormone) pulsatility as a surrogate for menstrual cycle integrity, Loucks and colleagues found that reproductive disruption begins when energy availability falls below a threshold between 20 and 30 kcal per kilogram of lean body mass per day. Above the threshold, women maintain normal reproductive endocrine function; below it, even with adequate body fat, LH pulsatility breaks down and menstrual disruption follows. The implication is that "thinness" itself does not cause amenorrhea; sustained energy deficit does. The framework gave rise to the modern Female Athlete Triad and RED-S (Relative Energy Deficiency in Sport) clinical concepts, which are now standard in sports medicine. The 30 kcal/kg LBM/day threshold remains the most-cited clinical cutoff for evaluating energy-availability risk in active women.