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Cross-sectional study finds preserved ovarian reserve alongside elevated kisspeptin in night-active women, suggesting shift work alters neuroendocrine rhythm rather than egg supply.
Shift work inverts the sleep–wake cycle and may perturb circadian-controlled reproductive hormones, yet its effect on ovarian reserve in young women is uncertain, and data on the circadian-sensitive neuropeptides kisspeptin and melatonin are scarce. We compared ovarian reserve and serum kisspeptin, melatonin, and thyroid-stimulating hormone (TSH) between night-active and day-active women. In this cross-sectional study, 90 healthy women aged 18–35 years with normal body mass index were enrolled (46 night-active, 44 day-active). On cycle day 3, ovarian reserve was assessed by ultrasonography (ovarian volume, antral follicle count [AFC]) and biochemistry (FSH, LH, estradiol, anti-Müllerian hormone [AMH]); prolactin, TSH, vitamin D, kisspeptin, and melatonin were also measured. Groups were compared with distribution-appropriate tests and covariate-adjusted ANCOVA. Ovarian reserve was similar between groups: ovarian volume ( p = 0.623), AFC (median 6.0 vs. 6.0, p = 0.791), and AMH (2.7 vs. 3.1 ng/mL, p = 0.862) did not differ, nor did FSH, LH, estradiol, prolactin, or vitamin D (all p > 0.05). Night-active women had higher median kisspeptin (889.5 vs. 336.2 ng/L, p < 0.001), melatonin (699.9 vs. 225.1 ng/L, p < 0.001), and TSH (2.0 vs. 1.5 mU/L, p = 0.020), and shorter sleep duration. The kisspeptin and melatonin differences persisted after covariate adjustment; the TSH difference did not. The primary effect of a night-active circadian rhythm was neuroendocrine rather than gonadal: ovarian reserve was not detectably altered in young, normal-BMI women, while kisspeptin, melatonin, and TSH were higher. These neuroendocrine differences are hypothesis-generating: because the groups were sampled at opposite points of the daily rhythm (~ 21:00 vs. ~ 09:00), they cannot be separated from a time-of-sampling effect and likely reflect circadian state rather than altered hormone output.
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Gungor et al. (2026) studied this question.
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