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Title:Variation in age at menarche and adult reproductive function: the role of energetic and psychosocial stressors
Author(s):Rogers, Mary Patricia
Director of Research:Clancy, Kathryn B.H.; Malhi, Ripan S.
Doctoral Committee Chair(s):Clancy, Kathryn B.H.; Malhi, Ripan S.
Doctoral Committee Member(s):Roseman, Charles; Uddin, Monica
Department / Program:Anthropology
Degree Granting Institution:University of Illinois at Urbana-Champaign
Subject(s):age at menarche
reproductive ecology
gene methylation
reproductive function
energetic stressors
psychosocial stressors
Abstract:Reproductive ecology has long examined the flexibility of women’s reproductive function in the face of variable environments. The timing of a woman’s first menses, or age at menarche, is both used as a proxy of childhood stressors and correlated with adolescent and adult reproductive function. This research seeks to understand the connections between childhood environments, pubertal timing, and adult reproductive function, and I specifically 1) identify a need for including social support measures in studies of pubertal timing through empirical evidence that positive parental-child interactions affect age at menarche, 2) demonstrate that psychosocial and energetic stressors experienced during childhood correlate with pubertal timing and adult reproductive function, 3) compare timing of menarche and variation in reproductive hormones between two populations with similar geographic origins but different subsistence environments, and 4) investigate gene methylation as a potential mechanism mediating the relationship between key stressors and reproductive function. I first investigated relationships between parent-adolescent communication and age at menarche in a diverse sample of 128 post-menarcheal, American girls aged 12-17. I found that measures of close family relationships, specifically open communication with parents, were correlated with age at menarche in this sample. I further found that mother-adolescent and father-adolescent open communication scores had opposing directional effects on menarcheal timing. These findings suggest that maternal and paternal communication may signal different things about the developmental and reproductive environment. This research underscores the importance of including measures of family support in future studies of adolescent reproductive trait timing, as well as the consideration that positive psychosocial factors, rather than only negative psychosocial factors, may be associated with accelerated menarcheal development. I further investigated the secular trend of declining ages at menarche in in the rural Beskid Wyspowy region of southern Poland and investigated relationships between childhood stressors, age at menarche, and adult reproductive function. I found that age at menarche has declined over time in rural Poland. Helping on farms and with farm animals as a child were associated with later ages at menarche. Women with a higher number of adverse childhood experiences tended to have earlier age at menarche, although this difference was not statistically significant. Despite different effects on age at menarche, all types of childhood stressors were associated with lower adult E1G concentrations. The results of this study support a model under which developmental conditions affect adult reproductive function, but challenge the use of age at menarche alone as a proxy for childhood stressors. I compared differences in reproductive traits between women in rural Poland and Polish American women in urban areas of the United States. We found that ages at menarche are earlier in Polish American women. Further, there is a generational effect where Polish American women whose parents were born in Poland did not have significant difference in average ages at menarche compared to women in Poland, but Polish American women whose grandparents were born in Poland had earlier ages at menarche compared to women in Poland. Additionally, we found that the Polish American sample had a significantly longer average luteal phase length compared to the Polish sample. These differences may indicate that, while rural Poland is undergoing many transitions, there are still environmental stressors affecting reproductive function. Finally, I investigated gene methylation as a potential mechanism mediating the relationship between stress and reproductive function. Epigenetic traits, like gene methylation, are modified by early environmental variables, and, thus, gene methylation is a likely mediator connecting early life environments with timing of menarche and adult reproductive hormones. I found that methylation at a promoter of the gene coding for aromatase (CYP19A1) along with farming during childhood significantly predicted age at menarche in a rural Polish population. We further identified a potential pathway by which increased cortisol concentrations increases CYP19A1 promoter I.4 methylation, which likely decreases aromatase activity and downstream estrogen and estrone concentrations. This pathway adds another potential pathway helping to explain inter-individual differences in estrogen concentrations. Overall, the results of this research underscore that epigenetic factors like gene methylation play a role in reproductive ecology and may provide a piece of the lacking intermediate structure between early environmental experiences and reproductive traits.
Issue Date:2018-07-12
Rights Information:Copyright 2018 Mary Rogers
Date Available in IDEALS:2018-09-27
Date Deposited:2018-08

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