Association between neighborhood poverty and ovarian reserve: the ovarian aging study.

OBJECTIVE: This study aimed to examine the association between neighborhood poverty and ovarian reserve. METHODS: Among 1,019 healthy premenopausal women in the Ovarian Aging Study, aggregate exposure to neighborhood poverty was examined in relation to biomarkers of ovarian reserve, antimüllerian hormone (AMH) and antral follicle count (AFC). Specifically, the interaction of age-x-neighborhood poverty was assessed cross-sectionally to determine whether AMH and AFC declines across women may be greater in women exposed to more neighborhood poverty. Neighborhood poverty was assessed by geocoding and linking women's residential addresses in adulthood to US Census data. RESULTS: Independent of covariates, a significant interaction term showed the association between age and AMH varied by degree of exposure to neighborhood poverty in adulthood ( b = -0.001, P < 0.05). AMH declines increased progressively across women exposed to low, medium, and high levels of neighborhood poverty. In addition, main effects showed that higher neighborhood poverty was related to higher AMH in the younger women only ( b = 0.022, P < 0.01). Results related to AFC were all nonsignificant ( P > 0.05). CONCLUSIONS: Across women, greater aggregate exposure to neighborhood poverty in adulthood was related to lower ovarian reserve, indexed by AMH. In addition, there was a positive association between neighborhood poverty and AMH in younger women that attenuated in the older women. Together, results suggest that neighborhood disadvantage may have detrimental impacts that manifest as initially higher AMH, resulting in greater ovarian follicle loss over time. However, it remains unclear whether these results examining differences across women may replicate when AMH declines by neighborhood poverty are examined longitudinally.

Is in utero exposure to maternal socioeconomic disadvantage related to offspring ovarian reserve in adulthood?

BACKGROUND: Because the ovarian follicle pool is established in utero, adverse exposures during this period may be especially impactful on the size and health of the initial follicle endowment, potentially shaping trajectories of ovarian follicle loss and the eventual onset of menopause. Building on a robust literature linking socioeconomic status (SES) and menopausal timing, the current study examined adverse prenatal exposures related to maternal SES, hypothesizing that greater maternal socioeconomic disadvantage would be associated with lower ovarian reserve in the adult offspring. METHODS: In a healthy, community-based sub-sample (n = 350) of reproductive age participants in the OVA Study (2006-2011), prenatal maternal SES was examined in relation to two biomarkers of ovarian reserve, antimullerian hormone (AMH) and antral follicle count (AFC). Prenatal maternal SES was assessed indirectly using maternal addresses abstracted from participant birth certificates, geocoded, and linked to US Census-derived variables, including neighborhood-level characteristics: education (% of individuals with a HS diploma); poverty (% of families below the poverty line); unemployment (% of individuals > 16 years who are unemployed); and income (median family income). RESULTS: In separate covariate-adjusted linear regression models (following the backward elimination of main effects with P > .10), greater maternal neighborhood education was related to higher ovarian reserve as marked by higher levels of offspring AMH (beta = .142, P < .001) and AFC (beta = .092, P < .10) with models accounting for 19.6% and 21.5% of the variance in AMH and AFC, respectively. In addition, greater maternal neighborhood poverty was related to lower ovarian reserve as marked by lower offspring AMH (beta = -.144, P < .01), with the model accounting for 19.5% of the variance in AMH. CONCLUSIONS: Maternal socioeconomic disadvantage measured indirectly at the neighborhood level was associated with lower ovarian reserve among the adult offspring, independently of offspring SES and other potential confounding factors. This suggests SES-related adversity exposures may have a detrimental impact on the size or health of the initial follicle endowment, leading to accelerated follicle loss over time.