Purpose of review The aim of this review is to evaluate biological, life history, environmental, and lifestyle factors and exposures that cause variability in menstrual cycle length (MCL). Recent findings Recent literature has detailed a number of factors that influence MCL, with particular emphasis placed on novel environmental exposures, such as air pollution and endocrine disrupting chemicals. Summary MCL varies widely in response to intrinsic and extrinsic inputs and is a useful predictor of reproductive health and fecundability. Video abstract

Objective: To determine the dose-dependent effect of contemporary marijuana exposure on female menstrual cyclicity and reproductive endocrine physiology in a nonhuman primate model. Design: Research animal study. Setting: Research institute environment. Animals: Adult female rhesus macaques (6-12 years of age; n ¼ 8). Intervention(s): Daily delta-9-tetrahydrocannabinol (THC) edible at medically and recreationally relevant contemporary doses. Main Outcome Measure(s): Menstrual cycle length (MCL), anti-M€ ullerian hormone, prolactin, basal follicle-stimulating hormone (FSH), estradiol (E2) and progesterone, luteinizing hormone (LH), and thyroid-stimulating hormone. Result(s): The average before THC weight was 6.9 kg (standard deviation, 0.8), and at the highest THC dosing, the average weight was 7.2 kg (standard deviation, 0.8). With increasing THC dosing, MCL and FSH concentrations increased, while basal E2 concentration was stable. The average MCL concentration increased 4.0 days for each mg/7 kg/day of THC (95% CI, 1.4-6.6 days). Follicle-stimulating hormone concentration increased significantly with increasing THC dose, 0.34 ng/mL for each mg/7 kg/day of THC (95% CI, 0.14-0.57 ng/mL). No significant trends were observed between THC dosing and average basal progesterone, anti-M€ ullerian hormone, prolactin, LH, or thyroid-stimulating hormone concentrations. Conclusion(s):In rhesus macaques, a dose response toward increased MCL and basal FSH concentrations but plateau of basal E2 and LH concentrations was observed with increasing THC dosing, suggesting ovulatory dysfunction. Further studies are needed to determine the effects of a longer duration of exposure and whether the significant increase in MCL and FSH concentrations results in reduced fecundity.

Within this review, the literature and outcomes from animal models of maternal marijuana use and cigarette smoking are summarized. The existing data demonstrate that prenatal marijuana and nicotine exposure both have multifaceted adverse effects on maternal, gestational, placental, and fetal outcomes. These include placental function and development, fetal growth and birth weight, and offspring neurodevelopment.