Childhood adversity is linked to adult health among African Americans via adolescent weight gain and effects are genetically moderated / Steven R. H. BEACH in Development and Psychopathology, 33-3 (August 2021)  

Public ISBD [article]  inDevelopment and Psychopathology > 33-3 (August 2021) . - p.803-820 Titre : Childhood adversity is linked to adult health among African Americans via adolescent weight gain and effects are genetically moderated Type de document : Texte imprimé et/ou numérique Auteurs : Steven R. H. BEACH, Auteur ; Mei Ling ONG, Auteur ; Man-Kit LEI, Auteur ; Eric KLOPACK, Auteur ; Sierra E. CARTER, Auteur ; Ronald L. SIMONS, Auteur ; Frederick X. GIBBONS, Auteur ; Justin A. LAVNER, Auteur ; Robert A. PHILIBERT, Auteur ; Kaixiong YE, Auteur Article en page(s) : p.803-820 Langues : Anglais (eng) Mots-clés : African American  childhood adversity  genetic risk  health disparities  obesity Index. décimale : PER Périodiques Résumé : Identifying the mechanisms linking early experiences, genetic risk factors, and their interaction with later health consequences is central to the development of preventive interventions and identifying potential boundary conditions for their efficacy. In the current investigation of 412 African American adolescents followed across a 20-year period, we examined change in body mass index (BMI) across adolescence as one possible mechanism linking childhood adversity and adult health. We found associations of childhood adversity with objective indicators of young adult health, including a cardiometabolic risk index, a methylomic aging index, and a count of chronic health conditions. Childhood adversities were associated with objective indicators indirectly through their association with gains in BMI across adolescence and early adulthood. We also found evidence of an association of genetic risk with weight gain across adolescence and young adult health, as well as genetic moderation of childhood adversity's effect on gains in BMI, resulting in moderated mediation. These patterns indicated that genetic risk moderated the indirect pathways from childhood adversity to young adult health outcomes and childhood adversity moderated the indirect pathways from genetic risk to young adult health outcomes through effects on weight gain during adolescence and early adulthood. En ligne : http://dx.doi.org/10.1017/S0954579420000061 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=457 [article] Childhood adversity is linked to adult health among African Americans via adolescent weight gain and effects are genetically moderated [Texte imprimé et/ou numérique] / Steven R. H. BEACH, Auteur ; Mei Ling ONG, Auteur ; Man-Kit LEI, Auteur ; Eric KLOPACK, Auteur ; Sierra E. CARTER, Auteur ; Ronald L. SIMONS, Auteur ; Frederick X. GIBBONS, Auteur ; Justin A. LAVNER, Auteur ; Robert A. PHILIBERT, Auteur ; Kaixiong YE, Auteur . - p.803-820. Langues : Anglais (eng) in Development and Psychopathology > 33-3 (August 2021) . - p.803-820 Mots-clés : African American  childhood adversity  genetic risk  health disparities  obesity Index. décimale : PER Périodiques Résumé : Identifying the mechanisms linking early experiences, genetic risk factors, and their interaction with later health consequences is central to the development of preventive interventions and identifying potential boundary conditions for their efficacy. In the current investigation of 412 African American adolescents followed across a 20-year period, we examined change in body mass index (BMI) across adolescence as one possible mechanism linking childhood adversity and adult health. We found associations of childhood adversity with objective indicators of young adult health, including a cardiometabolic risk index, a methylomic aging index, and a count of chronic health conditions. Childhood adversities were associated with objective indicators indirectly through their association with gains in BMI across adolescence and early adulthood. We also found evidence of an association of genetic risk with weight gain across adolescence and young adult health, as well as genetic moderation of childhood adversity's effect on gains in BMI, resulting in moderated mediation. These patterns indicated that genetic risk moderated the indirect pathways from childhood adversity to young adult health outcomes and childhood adversity moderated the indirect pathways from genetic risk to young adult health outcomes through effects on weight gain during adolescence and early adulthood. En ligne : http://dx.doi.org/10.1017/S0954579420000061 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=457

Childhood adversity predicts black young adults? DNA methylation-based accelerated aging: A dual pathway model / Steven R. H. BEACH in Development and Psychopathology, 34-2 (May 2022)  

Public ISBD [article]  inDevelopment and Psychopathology > 34-2 (May 2022) . - 689-703 Titre : Childhood adversity predicts black young adults? DNA methylation-based accelerated aging: A dual pathway model Type de document : Texte imprimé et/ou numérique Auteurs : Steven R. H. BEACH, Auteur ; Frederick X. GIBBONS, Auteur ; Sierra E. CARTER, Auteur ; Mei Ling ONG, Auteur ; Justin A. LAVNER, Auteur ; Man-Kit LEI, Auteur ; Ronald L. SIMONS, Auteur ; Meg GERRARD, Auteur ; Robert A. PHILIBERT, Auteur Article en page(s) : 689-703 Langues : Anglais (eng) Mots-clés : discrimination  DNAm-aging  FKBP5  Life History Index. décimale : PER Périodiques Résumé : We expand upon prior work (Gibbons et al., ) relating childhood stressor effects, particularly harsh childhood environments, to risky behavior and ultimately physical health by adding longer-term outcomes ? deoxyribonucleic acid (DNA) methylation-based measures of accelerated aging (DNAm-aging). Further, following work on the effects of early exposure to danger (McLaughlin et al., ), we also identify an additional pathway from harsh childhood environments to DNAm-aging that we label the danger/FKBP5 pathway, which includes early exposure to dangerous community conditions that are thought to impact glucocorticoid regulation and pro-inflammatory mechanisms. Because different DNAm-aging indices provide different windows on accelerated aging, we contrast effects on early indices of DNAm-aging based on chronological age with later indices that focused on predicting biological outcomes. We utilize data from Family and Community Health Study participants (N = 449) from age 10 to 29. We find that harshness influences parenting, which, in turn, influences accelerated DNAm-aging through the risky cognitions and substance use (i.e., behavioral) pathway outlined by Gibbons et al. (). Harshness is also associated with increased exposure to threat/danger, which, in turn, leads to accelerated DNAm-aging through effects on FKBP5 activity and enhanced pro-inflammatory tendencies (i.e., the danger/FKBP5 pathway). En ligne : http://dx.doi.org/10.1017/s0954579421001541 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=474 [article] Childhood adversity predicts black young adults? DNA methylation-based accelerated aging: A dual pathway model [Texte imprimé et/ou numérique] / Steven R. H. BEACH, Auteur ; Frederick X. GIBBONS, Auteur ; Sierra E. CARTER, Auteur ; Mei Ling ONG, Auteur ; Justin A. LAVNER, Auteur ; Man-Kit LEI, Auteur ; Ronald L. SIMONS, Auteur ; Meg GERRARD, Auteur ; Robert A. PHILIBERT, Auteur . - 689-703. Langues : Anglais (eng) in Development and Psychopathology > 34-2 (May 2022) . - 689-703 Mots-clés : discrimination  DNAm-aging  FKBP5  Life History Index. décimale : PER Périodiques Résumé : We expand upon prior work (Gibbons et al., ) relating childhood stressor effects, particularly harsh childhood environments, to risky behavior and ultimately physical health by adding longer-term outcomes ? deoxyribonucleic acid (DNA) methylation-based measures of accelerated aging (DNAm-aging). Further, following work on the effects of early exposure to danger (McLaughlin et al., ), we also identify an additional pathway from harsh childhood environments to DNAm-aging that we label the danger/FKBP5 pathway, which includes early exposure to dangerous community conditions that are thought to impact glucocorticoid regulation and pro-inflammatory mechanisms. Because different DNAm-aging indices provide different windows on accelerated aging, we contrast effects on early indices of DNAm-aging based on chronological age with later indices that focused on predicting biological outcomes. We utilize data from Family and Community Health Study participants (N = 449) from age 10 to 29. We find that harshness influences parenting, which, in turn, influences accelerated DNAm-aging through the risky cognitions and substance use (i.e., behavioral) pathway outlined by Gibbons et al. (). Harshness is also associated with increased exposure to threat/danger, which, in turn, leads to accelerated DNAm-aging through effects on FKBP5 activity and enhanced pro-inflammatory tendencies (i.e., the danger/FKBP5 pathway). En ligne : http://dx.doi.org/10.1017/s0954579421001541 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=474

Children's genotypes interact with maternal responsive care in predicting children's competence: Diathesis–stress or differential susceptibility? / Grazyna KOCHANSKA in Development and Psychopathology, 23-2 (May 2011)  

Public ISBD [article]  inDevelopment and Psychopathology > 23-2 (May 2011) . - p.605-616 Titre : Children's genotypes interact with maternal responsive care in predicting children's competence: Diathesis–stress or differential susceptibility? Type de document : Texte imprimé et/ou numérique Auteurs : Grazyna KOCHANSKA, Auteur ; Sanghag KIM, Auteur ; Robin A. BARRY, Auteur ; Robert A. PHILIBERT, Auteur Année de publication : 2011 Article en page(s) : p.605-616 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : We examined Genotype × Environment (G × E) interactions between children's genotypes (the serotonin transporter linked promoter region [5-HTTLPR] gene) and maternal responsive care observed at 15, 25, 38, and 52 months on three aspects of children's competence at 67 months: academic skills and school engagement, social functioning with peers, and moral internalization that encompassed prosocial moral cognition and the moral self. Academic and social competence outcomes were reported by both parents, and moral internalization was observed in children's narratives elicited by hypothetical stories and in a puppet interview. Analyses revealed robust G × E interactions, such that children's genotype moderated the effects of maternal responsive care on all aspects of children's competence. Among children with a short 5-HTTLPR allele (ss/sl), those whose mothers were more responsive were significantly more competent than those whose mothers were less responsive. Responsiveness had no effect for children with two long alleles (ll). For academic and social competence, the G × E interactions resembled the diathesis–stress model: ss/sl children of unresponsive mothers had particularly unfavorable outcomes, but ss/sl children of responsive mothers had no worse outcomes than ll children. For moral internalization, the G × E interaction reflected the differential susceptibility model: whereas ss/sl children of unresponsive mothers again had particularly unfavorable outcomes, ss/sl children of responsive mothers had significantly better outcomes than ll children. En ligne : http://dx.doi.org/10.1017/S0954579411000071 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=121 [article] Children's genotypes interact with maternal responsive care in predicting children's competence: Diathesis–stress or differential susceptibility? [Texte imprimé et/ou numérique] / Grazyna KOCHANSKA, Auteur ; Sanghag KIM, Auteur ; Robin A. BARRY, Auteur ; Robert A. PHILIBERT, Auteur . - 2011 . - p.605-616. Langues : Anglais (eng) in Development and Psychopathology > 23-2 (May 2011) . - p.605-616 Index. décimale : PER Périodiques Résumé : We examined Genotype × Environment (G × E) interactions between children's genotypes (the serotonin transporter linked promoter region [5-HTTLPR] gene) and maternal responsive care observed at 15, 25, 38, and 52 months on three aspects of children's competence at 67 months: academic skills and school engagement, social functioning with peers, and moral internalization that encompassed prosocial moral cognition and the moral self. Academic and social competence outcomes were reported by both parents, and moral internalization was observed in children's narratives elicited by hypothetical stories and in a puppet interview. Analyses revealed robust G × E interactions, such that children's genotype moderated the effects of maternal responsive care on all aspects of children's competence. Among children with a short 5-HTTLPR allele (ss/sl), those whose mothers were more responsive were significantly more competent than those whose mothers were less responsive. Responsiveness had no effect for children with two long alleles (ll). For academic and social competence, the G × E interactions resembled the diathesis–stress model: ss/sl children of unresponsive mothers had particularly unfavorable outcomes, but ss/sl children of responsive mothers had no worse outcomes than ll children. For moral internalization, the G × E interaction reflected the differential susceptibility model: whereas ss/sl children of unresponsive mothers again had particularly unfavorable outcomes, ss/sl children of responsive mothers had significantly better outcomes than ll children. En ligne : http://dx.doi.org/10.1017/S0954579411000071 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=121

Developmental interplay between children's biobehavioral risk and the parenting environment from toddler to early school age: Prediction of socialization outcomes in preadolescence / Grazyna KOCHANSKA in Development and Psychopathology, 27-3 (August 2015)  

Public ISBD [article]  inDevelopment and Psychopathology > 27-3 (August 2015) . - p.775-790 Titre : Developmental interplay between children's biobehavioral risk and the parenting environment from toddler to early school age: Prediction of socialization outcomes in preadolescence Type de document : Texte imprimé et/ou numérique Auteurs : Grazyna KOCHANSKA, Auteur ; Lea J. BOLDT, Auteur ; Sanghag KIM, Auteur ; Jeung Eun YOON, Auteur ; Robert A. PHILIBERT, Auteur Article en page(s) : p.775-790 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : We followed 100 community families from toddler age to preadolescence. Each mother– and father–child dyad was observed at 25, 38, 52, 67, and 80 months (10 hr/child) to assess positive and power-assertive parenting. At age 10 (N = 82), we obtained parent- and child-reported outcome measures of children's acceptance of parental socialization: cooperation with parental monitoring, negative attitude toward substance use, internalization of adult values, and callous–unemotional tendencies. Children who carried a short serotonin transporter linked polymorphic region gene (5-HTTLPR) allele and were highly anger prone, based on anger observed in laboratory from 25 to 80 months, were classified as high in biobehavioral risk. The remaining children were classified as low in biobehavioral risk. Biobehavioral risk moderated links between parenting history and outcomes. For low-risk children, parenting measures were unrelated to outcomes. For children high in biobehavioral risk, variations in positive parenting predicted cooperation with monitoring and negative attitude toward substance use, and variations in power-assertive parenting predicted internalization of adult values and callous–unemotional tendencies. Suboptimal parenting combined with high biobehavioral risk resulted in the poorest outcomes. The effect for attitude toward substance use supported differential susceptibility: children high in biobehavioral risk who received optimal parenting had a more adaptive outcome than their low-risk peers. The remaining effects were consistent with diathesis–stress. En ligne : http://dx.doi.org/10.1017/S0954579414000777 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=263 [article] Developmental interplay between children's biobehavioral risk and the parenting environment from toddler to early school age: Prediction of socialization outcomes in preadolescence [Texte imprimé et/ou numérique] / Grazyna KOCHANSKA, Auteur ; Lea J. BOLDT, Auteur ; Sanghag KIM, Auteur ; Jeung Eun YOON, Auteur ; Robert A. PHILIBERT, Auteur . - p.775-790. Langues : Anglais (eng) in Development and Psychopathology > 27-3 (August 2015) . - p.775-790 Index. décimale : PER Périodiques Résumé : We followed 100 community families from toddler age to preadolescence. Each mother– and father–child dyad was observed at 25, 38, 52, 67, and 80 months (10 hr/child) to assess positive and power-assertive parenting. At age 10 (N = 82), we obtained parent- and child-reported outcome measures of children's acceptance of parental socialization: cooperation with parental monitoring, negative attitude toward substance use, internalization of adult values, and callous–unemotional tendencies. Children who carried a short serotonin transporter linked polymorphic region gene (5-HTTLPR) allele and were highly anger prone, based on anger observed in laboratory from 25 to 80 months, were classified as high in biobehavioral risk. The remaining children were classified as low in biobehavioral risk. Biobehavioral risk moderated links between parenting history and outcomes. For low-risk children, parenting measures were unrelated to outcomes. For children high in biobehavioral risk, variations in positive parenting predicted cooperation with monitoring and negative attitude toward substance use, and variations in power-assertive parenting predicted internalization of adult values and callous–unemotional tendencies. Suboptimal parenting combined with high biobehavioral risk resulted in the poorest outcomes. The effect for attitude toward substance use supported differential susceptibility: children high in biobehavioral risk who received optimal parenting had a more adaptive outcome than their low-risk peers. The remaining effects were consistent with diathesis–stress. En ligne : http://dx.doi.org/10.1017/S0954579414000777 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=263

Exploring genetic moderators and epigenetic mediators of contextual and family effects: From Gene × Environment to epigenetics / Steven R. H. BEACH in Development and Psychopathology, 28-4 pt2 (November 2016)  

Public ISBD [article]  inDevelopment and Psychopathology > 28-4 pt2 (November 2016) . - p.1333-1346 Titre : Exploring genetic moderators and epigenetic mediators of contextual and family effects: From Gene × Environment to epigenetics Type de document : Texte imprimé et/ou numérique Auteurs : Steven R. H. BEACH, Auteur ; Gene H. BRODY, Auteur ; Allen W. BARTON, Auteur ; Robert A. PHILIBERT, Auteur Article en page(s) : p.1333-1346 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : In the current manuscript, we provide an overview of a research program at the University of Georgia's Center for Family Research designed to expand upon rapid and ongoing developments in the fields of genetics and epigenetics. By placing those developments in the context of translational research on family and community determinants of health and well-being among rural African Americans, we hope to identify novel, modifiable environments and biological processes. In the first section of the article, we review our earlier work on genotypic variation effects on the association between family context and mental and physical health outcomes as well as differential responses to family-based intervention. We then transition to discuss our more recent research on the association of family and community environments with epigenetic processes. In this second section of the article, we begin by briefly reviewing terminology and basic considerations before describing evidence that early environments may influence epigenetic motifs that potentially serve as mediators of long-term effects of early family and community environments on longer term health outcomes. We also provide evidence that genotype may sometimes influence epigenetic outcomes. Finally, we describe our recent efforts to use genome-wide characterization of epigenetic patterns to better understand the biological impact of protective parenting on long-term shifts in inflammatory processes and its potential implications for young adult health. As will be clear, research on epigenetics as a mediator of the connections between family/community processes and a range of health outcomes is still in its infancy, but the potential to develop important insights regarding mechanisms linking modifiable environments to biological processes and long-term health outcomes already is coming into view. En ligne : http://dx.doi.org/10.1017/s0954579416000882 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=294 [article] Exploring genetic moderators and epigenetic mediators of contextual and family effects: From Gene × Environment to epigenetics [Texte imprimé et/ou numérique] / Steven R. H. BEACH, Auteur ; Gene H. BRODY, Auteur ; Allen W. BARTON, Auteur ; Robert A. PHILIBERT, Auteur . - p.1333-1346. Langues : Anglais (eng) in Development and Psychopathology > 28-4 pt2 (November 2016) . - p.1333-1346 Index. décimale : PER Périodiques Résumé : In the current manuscript, we provide an overview of a research program at the University of Georgia's Center for Family Research designed to expand upon rapid and ongoing developments in the fields of genetics and epigenetics. By placing those developments in the context of translational research on family and community determinants of health and well-being among rural African Americans, we hope to identify novel, modifiable environments and biological processes. In the first section of the article, we review our earlier work on genotypic variation effects on the association between family context and mental and physical health outcomes as well as differential responses to family-based intervention. We then transition to discuss our more recent research on the association of family and community environments with epigenetic processes. In this second section of the article, we begin by briefly reviewing terminology and basic considerations before describing evidence that early environments may influence epigenetic motifs that potentially serve as mediators of long-term effects of early family and community environments on longer term health outcomes. We also provide evidence that genotype may sometimes influence epigenetic outcomes. Finally, we describe our recent efforts to use genome-wide characterization of epigenetic patterns to better understand the biological impact of protective parenting on long-term shifts in inflammatory processes and its potential implications for young adult health. As will be clear, research on epigenetics as a mediator of the connections between family/community processes and a range of health outcomes is still in its infancy, but the potential to develop important insights regarding mechanisms linking modifiable environments to biological processes and long-term health outcomes already is coming into view. En ligne : http://dx.doi.org/10.1017/s0954579416000882 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=294

G × E interaction in the organization of attachment: mothers'responsiveness as a moderator of children's genotypes / Robin A. BARRY in Journal of Child Psychology and Psychiatry, 49-12 (December 2008)  

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Interplay of genes and early mother–child relationship in the development of self-regulation from toddler to preschool age / Grazyna KOCHANSKA in Journal of Child Psychology and Psychiatry, 50-11 (November 2009)  

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Is serotonin transporter genotype associated with epigenetic susceptibility or vulnerability? Examination of the impact of socioeconomic status risk on African American youth / Steven R. H. BEACH in Development and Psychopathology, 26-2 (May 2014)  

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Life stress, the dopamine receptor gene, and emerging adult drug use trajectories: A longitudinal, multilevel, mediated moderation analysis / Gene H. BRODY in Development and Psychopathology, 24-3 (August 2012)  

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Methylation of the oxytocin receptor gene mediates the effect of adversity on negative schemas and depression / Ronald L. SIMONS in Development and Psychopathology, 29-3 (August 2017)  

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Perceived discrimination, serotonin transporter linked polymorphic region status, and the development of conduct problems / Gene H. BRODY in Development and Psychopathology, 23-2 (May 2011)  

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Smoking in young adulthood among African Americans: Interconnected effects of supportive parenting in early adolescence, proinflammatory epitype, and young adult stress / Steven R. H. BEACH in Development and Psychopathology, 29-3 (August 2017)  

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When inflammation and depression go together: The longitudinal effects of parent–child relationships / Steven R. H. BEACH in Development and Psychopathology, 29-5 (December 2017)  

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