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      Father Absence and Accelerated Reproductive Development in Non-Hispanic White Women in the United States

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          Abstract

          <p class="first" id="P1">Girls who experience father absence in childhood also experience accelerated reproductive development in comparison with peers with present fathers. One hypothesis advanced to explain this empirical pattern is genetic confounding, wherein gene-environment correlation (rGE) causes a spurious relationship between father absence and reproductive timing. We test this hypothesis by constructing polygenic scores for age at menarche and first birth using recently available genome-wide association study results and molecular genetic data on a sample of non-Hispanic white females from the National Longitudinal Study of Adolescent to Adult Health. We find that young women’s accelerated menarche polygenic scores are unrelated to their exposure to father absence. In contrast, polygenic scores for earlier age at first birth tend to be higher in young women raised in homes with absent fathers. Nevertheless, father absence and the polygenic scores independently and additively predict reproductive timing. We find no evidence in support of the rGE hypothesis for accelerated menarche and only limited evidence in support of the rGE hypothesis for earlier age at first birth. </p>

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          Most cited references72

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          Chapter 11: Genome-Wide Association Studies

          Genome-wide association studies (GWAS) have evolved over the last ten years into a powerful tool for investigating the genetic architecture of human disease. In this work, we review the key concepts underlying GWAS, including the architecture of common diseases, the structure of common human genetic variation, technologies for capturing genetic information, study designs, and the statistical methods used for data analysis. We also look forward to the future beyond GWAS.
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            Population stratification and spurious allelic association.

            Great efforts and expense have been expended in attempts to detect genetic polymorphisms contributing to susceptibility to complex human disease. Concomitantly, technology for detection and scoring of single nucleotide polymorphisms (SNPs) has undergone rapid development, extensive catalogues of SNPs across the genome have been constructed, and SNPs have been increasingly used as a means for investigation of the genetic causes of complex human diseases. For many diseases, population-based studies of unrelated individuals--in which case-control and cohort studies serve as standard designs for genetic association analysis--can be the most practical and powerful approach. However, extensive debate has arisen about optimum study design, and considerable concern has been expressed that these approaches are prone to population stratification, which can lead to biased or spurious results. Over the past decade, a great shift has been noted, away from case-control and cohort studies, towards family-based association designs. These designs have fewer problems with population stratification but have greater genotyping and sampling requirements, and data can be difficult or impossible to gather. We discuss past evidence for population stratification on genotype-phenotype association studies, review methods to detect and account for it, and present suggestions for future study design and analysis.
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              Timing of pubertal maturation in girls: an integrated life history approach.

              Life history theory provides a metatheoretical framework for the study of pubertal timing from an evolutionary-developmental perspective. The current article reviews 5 middle-level theories--energetics theory, stress-suppression theory, psychosocial acceleration theory, paternal investment theory, and child development theory--each of which applies the basic assumptions of life history theory to the question of environmental influences on timing of puberty in girls. These theories converge in their conceptualization of pubertal timing as responsive to ecological conditions but diverge in their conceptualization of (a) the nature, extent, and direction of environmental influences and (b) the effects of pubertal timing on other reproductive variables. Competing hypotheses derived from the 5 perspectives are evaluated. An extension of W. T. Boyce and B. J. Ellis's (in press) theory of stress reactivity is proposed to account for both inhibiting and accelerating effects of psychosocial stress on timing of pubertal development. This review highlights the multiplicity of (often unrecognized) perspectives guiding research, raises challenges to virtually all of these, and presents an alternative framework in an effort to move research forward in this arena of multidisciplinary inquiry.
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                Author and article information

                Journal
                Demography
                Demography
                Springer Nature
                0070-3370
                1533-7790
                August 2018
                July 5 2018
                August 2018
                : 55
                : 4
                : 1245-1267
                Article
                10.1007/s13524-018-0696-1
                6467216
                29978338
                b260e855-4097-4fc7-b16c-a375f29399b3
                © 2018

                http://www.springer.com/tdm

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