Background: This systematic review summarises association between short interpregnancy intervals and adverse perinatal health outcomes in high‐resource settings to inform recommendations for healthy birth spacing for the United States.Methods: Five databases and a previous systematic review were searched for relevant articles published between 1966 and 1 May 2017. We included studies meeting the following criteria: (a) reporting of perinatal health outcomes after a short interpregnancy interval since last livebirth; (b) conducted within a high‐resource setting; and (c) estimates were adjusted for maternal age and at least one socio‐economic factor.Results: Nine good‐quality and 18 fair‐quality studies were identified. Interpregnancy intervals <6 months were associated with a clinically and statistically significant increased risk of adverse outcomes in studies of preterm birth (eg, aOR ≥ 1.20 in 10 of 14 studies); spontaneous preterm birth (eg, aOR ≥ 1.20 in one of two studies); small‐for‐gestational age (eg, aOR ≥ 1.20 in 5 of 11 studies); and infant mortality (eg, aOR ≥ 1.20 in four of four studies), while four studies of perinatal death showed no association. Interpregnancy intervals of 6‐11 and 12‐17 months generally had smaller point estimates and confidence intervals that included the null. Most studies were population‐based and few included adjustment for detailed measures of key confounders.Conclusions: In high‐resource settings, there is some evidence showing interpregnancy intervals <6 months since last livebirth are associated with increased risks for preterm birth, small‐for‐gestational age and infant death; however, results were inconsistent. Additional research controlling for confounding would further inform recommendations for healthy birth spacing for the United States.

Background: Stress has been shown to suppress ovulation in experimental models, but its effect on human reproduction at the population level is unclear. Methods: Healthy women (n = 259), aged 18–44 years from Western New York, were followed for 2 menstrual cycles (2005–2007). Women completed daily perceived stress assessments, a 4-item Perceived Stress Scale (PSS-4) up to 4 times each cycle, and a 14-item PSS at baseline. Mixed model analyses were used to assess effects of stress on log reproductive hormone concentrations and sporadic anovulation. Results: High versus low daily stress was associated with lower estradiol (−9.5% [95% confidence interval (CI) = −15.6% to −3.0%]), free estradiol (−10.4% [−16.5% to −3.9%]), and luteinizing hormone (−14.8% [−21.3% to −7.7%]) and higher follicle-stimulating hormone (6.2% [95% CI = 2.0% to 10.5%]) after adjusting for age, race, percent body fat, depression score, and time-varying hormones and vigorous exercise. High versus low daily stress was also associated with lower luteal progesterone (−10.4% [95% CI = −19.7% to −0.10%]) and higher odds of anovulation (adjusted odds ratio = 2.2 [95% CI = 1.0 to 4.7]). For each unit increase in daily stress level, women had a 70% higher odds of an anovulatory episode (odds ratio = 1.7 [1.1 to 2.4]). Similar but attenuated results were found for the association between the PSS-4 and reproductive hormones, while null findings were found for the baseline PSS. Conclusion: Daily perceived stress does appear to interfere with menstrual cycle function among women with no known reproductive disorders, warranting further research to explore potential population-level impacts and causal biologic mechanisms.

Context: Although adequate luteal hormone production is essential for establishing pregnancy, luteal phase deficiency (LPD) is poorly characterized among eumenorrheic women. Objective: We assessed the prevalence and overlap of two established LPD diagnostic criteria: short luteal phase duration less than10 days (clinical LPD) and suboptimal luteal progesterone of 5 ng/mL or less (biochemical LPD) and their relationship with reproductive hormone concentrations. Design, Setting, and Participants: We conducted a prospective study in western New York (2005–2007) following 259 women, aged 18–44 years, for up to two menstrual cycles. Results: Among ovulatory cycles with recorded cycle lengths (n = 463), there were 41 cycles (8.9%) with clinical LPD, 39 cycles (8.4%) with biochemical LPD, and 20 cycles (4.3%) meeting both criteria. Recurrent clinical and biochemical LPD was observed in eight (3.4%) and five (2.1%) women, respectively. Clinical and biochemical LPD were each associated with lower follicular estradiol (both P ≤ .001) and luteal estradiol (P = .03 and P = .02, respectively) after adjusting for age, race, and percentage body fat. Clinical, but not biochemical, LPD was associated with lower LH and FSH across all phases of the cycle (P ≤ .001). Conclusions: Clinical and biochemical LPD were evident among regularly menstruating women. Estradiol was lower in LPD cycles under either criterion, but LH and FSH were lower only in association with shortened luteal phase (ie, clinical LPD), indicating that clinical and biochemical LPD may reflect different underlying mechanisms. Identifying ovulation in combination with a well-timed luteal progesterone measurement may serve as a cost-effective and specific tool for LPD assessment by clinicians and researchers.