Abstract
BackgroundBecause 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.MethodsIn 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).ResultsIn 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.ConclusionsMaternal 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.
Highlights
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
The racial/ethnic composition of the sample was 24.9% white, 43.4% African-American, 14% Latina, 13.7% Chinese, and 4.0% Filipina. This distribution differs from the total Ovarian Aging (OVA) Ovarian Aging Study (Study) sample (N = 1019; 27.4% white, 24.1% AfricanAmerican, 22.6% Latina, 21.9% Chinese, and 4.0% Filipina) due to the greater number of African-American women who were born in the state of California and, had a birth certificate available for analysis
Greater maternal neighborhood education was related to higher ovarian reserve as marked by higher levels of offspring Antimullerian hormone (AMH) and Antral follicle count (AFC) with models accounting for 19.6% and 21.5% of the variance in AMH and AFC, respectively
Summary
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. Recent methodological advances are enabling the examination of the real-time loss of ovarian follicles underlying variability in the timing of menopause, termed “ovarian aging” [14,15,16] Using such methods by which the number of ovarian follicles remaining in the primordial pool (or ovarian reserve) is estimated, it is possible—for the first time—to characterize trajectories of ovarian aging over the life course. In parallel to findings in the menopausal timing literature, that even among younger, pre-menopausal women, more accelerated ovarian aging may be associated with an increase in cardiovascular risk [17,18,19,20,21] In this context, elucidating factors that explain variability in ovarian aging is of critical importance as it raises the possibility that such factors may be modified through intervention efforts targeting the slowing of ovarian aging and/or the amelioration of its sequelae in at-risk women
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