Biological embedding of neighborhood disadvantage and collective efficacy: Influences on chronic illness via accelerated cardiometabolic age / Man-Kit LEI in Development and Psychopathology, 30-5 (December 2018)  

Public ISBD [article]  inDevelopment and Psychopathology > 30-5 (December 2018) . - p.1797-1815 Titre : Biological embedding of neighborhood disadvantage and collective efficacy: Influences on chronic illness via accelerated cardiometabolic age Type de document : texte imprimé Auteurs : Man-Kit LEI, Auteur ; Steven R.H. BEACH, Auteur ; Ronald L. SIMONS, Auteur Article en page(s) : p.1797-1815 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : The present study extends prior research on the link between neighborhood disadvantage and chronic illness by testing an integrated model in which neighborhood characteristics exert effects on health conditions through accelerated cardiometabolic aging. Hypotheses were tested using a sample of 408 African Americans from the Family and Community Health Study. Using four waves of data spanning young adulthood (ages 18–29), we first found durable effects of neighborhood disadvantage on accelerated cardiometabolic aging and chronic illness. Then, we used marginal structural modeling to adjust for potential neighborhood selection effects. As expected, accelerated cardiometabolic aging was the biopsychosocial mechanism that mediated much of the association between neighborhood disadvantage and chronic illness. This finding provides additional support for the view that neighborhood disadvantage can influence morbidity and mortality by creating social contexts that becomes biologically embedded. Perceived neighborhood collective efficacy served to buffer the relationship between neighborhood disadvantage and biological aging, identifying neighborhood-level resilience factor. Overall, our results indicate that neighborhood context serves as a fundamental cause of weathering and accelerated biological aging. Residing in a disadvantaged neighborhood increases biological wear and tear that ultimately leads to onset of chronic illness, but access to perceived collective efficacy buffers the impact of these neighborhood effects. From an intervention standpoint, identifying such an integrated model may help inform future health-promoting interventions. En ligne : http://dx.doi.org/10.1017/S0954579418000937 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=370 [article] Biological embedding of neighborhood disadvantage and collective efficacy: Influences on chronic illness via accelerated cardiometabolic age [texte imprimé] / Man-Kit LEI, Auteur ; Steven R.H. BEACH, Auteur ; Ronald L. SIMONS, Auteur . - p.1797-1815. Langues : Anglais (eng) in Development and Psychopathology > 30-5 (December 2018) . - p.1797-1815 Index. décimale : PER Périodiques Résumé : The present study extends prior research on the link between neighborhood disadvantage and chronic illness by testing an integrated model in which neighborhood characteristics exert effects on health conditions through accelerated cardiometabolic aging. Hypotheses were tested using a sample of 408 African Americans from the Family and Community Health Study. Using four waves of data spanning young adulthood (ages 18–29), we first found durable effects of neighborhood disadvantage on accelerated cardiometabolic aging and chronic illness. Then, we used marginal structural modeling to adjust for potential neighborhood selection effects. As expected, accelerated cardiometabolic aging was the biopsychosocial mechanism that mediated much of the association between neighborhood disadvantage and chronic illness. This finding provides additional support for the view that neighborhood disadvantage can influence morbidity and mortality by creating social contexts that becomes biologically embedded. Perceived neighborhood collective efficacy served to buffer the relationship between neighborhood disadvantage and biological aging, identifying neighborhood-level resilience factor. Overall, our results indicate that neighborhood context serves as a fundamental cause of weathering and accelerated biological aging. Residing in a disadvantaged neighborhood increases biological wear and tear that ultimately leads to onset of chronic illness, but access to perceived collective efficacy buffers the impact of these neighborhood effects. From an intervention standpoint, identifying such an integrated model may help inform future health-promoting interventions. En ligne : http://dx.doi.org/10.1017/S0954579418000937 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=370

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 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] / 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 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] / 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

Childhood exposure to danger increases Black youths’ alcohol consumption, accelerated aging, and cardiac risk as young adults: A test of the incubation hypothesis / Steven R. H. BEACH in Development and Psychopathology, 38-1 (February 2026)  

Public ISBD [article]  inDevelopment and Psychopathology > 38-1 (February 2026) . - p.156-171 Titre : Childhood exposure to danger increases Black youths’ alcohol consumption, accelerated aging, and cardiac risk as young adults: A test of the incubation hypothesis Type de document : texte imprimé Auteurs : Steven R. H. BEACH, Auteur ; Sierra E. CARTER, Auteur ; Mei Ling ONG, Auteur ; Justin A. LAVNER, Auteur ; Steven M. KOGAN, Auteur ; Katherine B. EHRLICH, Auteur ; Man-Kit LEI, Auteur ; Ronald L. SIMONS, Auteur ; Olutosin ADESOGAN, Auteur ; Frederick X. GIBBONS, Auteur ; Meg GERRARD, Auteur ; Robert A. PHILIBERT, Auteur Article en page(s) : p.156-171 Langues : Anglais (eng) Mots-clés : DNAm-based aging Danger Inflammation alcohol cardiac risk Index. décimale : PER Périodiques Résumé : Using the dual-pathway framework (Beach et al., a), we tested a Neuro-immune Network (NIN) hypothesis: i.e., that chronically elevated inflammatory processes may have delayed (i.e., incubation) effects on young adult substance use, leading to negative health outcomes. In a sample of 449 participants in the Family and Community Health Study who were followed from age 10 to age 29, we examined a non-self-report index of young adult elevated alcohol consumption (EAC). By controlling self-reported substance use at the transition to adulthood, we were able to isolate a significant delayed (incubation) effect from childhood exposure to danger to EAC (β = −.157, p = .006), which contributed to significantly worse aging outomes. Indirect effects from danger to aging outcomes via EAC were: GrimAge (IE = .010, [.002, .024]), Cardiac Risk (IE = −.004, [−.011, −.001]), DunedinPACE (IE = .002, [.000, .008]). In exploratory analyses we examined potential sex differences in effects, showing slightly stronger incubation effects for men and slightly stronger effects of EAC on aging outcomes for women. Results support the NIN hypothesis that incubation of immune pathway effects contributes to elevated alcohol consumption in young adulthood, resulting in accelerated aging and elevated cardiac risk outcomes via health behavior. En ligne : https://dx.doi.org/10.1017/S0954579425000264 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=579 [article] Childhood exposure to danger increases Black youths’ alcohol consumption, accelerated aging, and cardiac risk as young adults: A test of the incubation hypothesis [texte imprimé] / Steven R. H. BEACH, Auteur ; Sierra E. CARTER, Auteur ; Mei Ling ONG, Auteur ; Justin A. LAVNER, Auteur ; Steven M. KOGAN, Auteur ; Katherine B. EHRLICH, Auteur ; Man-Kit LEI, Auteur ; Ronald L. SIMONS, Auteur ; Olutosin ADESOGAN, Auteur ; Frederick X. GIBBONS, Auteur ; Meg GERRARD, Auteur ; Robert A. PHILIBERT, Auteur . - p.156-171. Langues : Anglais (eng) in Development and Psychopathology > 38-1 (February 2026) . - p.156-171 Mots-clés : DNAm-based aging Danger Inflammation alcohol cardiac risk Index. décimale : PER Périodiques Résumé : Using the dual-pathway framework (Beach et al., a), we tested a Neuro-immune Network (NIN) hypothesis: i.e., that chronically elevated inflammatory processes may have delayed (i.e., incubation) effects on young adult substance use, leading to negative health outcomes. In a sample of 449 participants in the Family and Community Health Study who were followed from age 10 to age 29, we examined a non-self-report index of young adult elevated alcohol consumption (EAC). By controlling self-reported substance use at the transition to adulthood, we were able to isolate a significant delayed (incubation) effect from childhood exposure to danger to EAC (β = −.157, p = .006), which contributed to significantly worse aging outomes. Indirect effects from danger to aging outcomes via EAC were: GrimAge (IE = .010, [.002, .024]), Cardiac Risk (IE = −.004, [−.011, −.001]), DunedinPACE (IE = .002, [.000, .008]). In exploratory analyses we examined potential sex differences in effects, showing slightly stronger incubation effects for men and slightly stronger effects of EAC on aging outcomes for women. Results support the NIN hypothesis that incubation of immune pathway effects contributes to elevated alcohol consumption in young adulthood, resulting in accelerated aging and elevated cardiac risk outcomes via health behavior. En ligne : https://dx.doi.org/10.1017/S0954579425000264 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=579

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)  

Public ISBD [article]  inDevelopment and Psychopathology > 24-3 (August 2012) . - p.941-51 Titre : Life stress, the dopamine receptor gene, and emerging adult drug use trajectories: A longitudinal, multilevel, mediated moderation analysis Type de document : texte imprimé Auteurs : Gene H. BRODY, Auteur ; Yi-Fu CHEN, Auteur ; Tianyi YU, Auteur ; Steven R.H. BEACH, Auteur ; Steven M. KOGAN, Auteur ; Ronald L. SIMONS, Auteur ; Michael WINDLE, Auteur ; Robert A. PHILIBERT, Auteur Année de publication : 2012 Article en page(s) : p.941-51 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : This study was designed to examine the prospective relations of life stress and genetic status with increases in drug use. African Americans (N = 399) in rural Georgia (Wave 1 mean age = 17 years) provided three waves of data across 27.5 months and a saliva sample from which the dopamine receptor D4 (DRD4) gene was genotyped. Multilevel growth curve modeling analysis indicated that emerging adults manifested the highest escalations in drug use when they reported high life stress and carried an allele of DRD4 with 7 or more repeats (7 + R allele). In addition, emerging adults who reported high life stress and carried the 7 + R allele evinced the largest increases in two proximal risk factors for drug use: affiliations with drug-using companions and drug use vulnerability cognitions. Furthermore, when the Gene × Environment interaction effects on the increases in affiliations with drug-using companions and vulnerability cognitions were entered into the model forecasting drug use, the Life Stress × DRD4 Status interaction on drug use became nonsignificant in the presence of the risk mechanisms. This finding provides an example of “second generation” Gene × Environment interaction research in which the interaction's effects on proximal risk mechanisms account for its effects on outcomes. En ligne : http://dx.doi.org/10.1017/S0954579412000466 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=178 [article] Life stress, the dopamine receptor gene, and emerging adult drug use trajectories: A longitudinal, multilevel, mediated moderation analysis [texte imprimé] / Gene H. BRODY, Auteur ; Yi-Fu CHEN, Auteur ; Tianyi YU, Auteur ; Steven R.H. BEACH, Auteur ; Steven M. KOGAN, Auteur ; Ronald L. SIMONS, Auteur ; Michael WINDLE, Auteur ; Robert A. PHILIBERT, Auteur . - 2012 . - p.941-51. Langues : Anglais (eng) in Development and Psychopathology > 24-3 (August 2012) . - p.941-51 Index. décimale : PER Périodiques Résumé : This study was designed to examine the prospective relations of life stress and genetic status with increases in drug use. African Americans (N = 399) in rural Georgia (Wave 1 mean age = 17 years) provided three waves of data across 27.5 months and a saliva sample from which the dopamine receptor D4 (DRD4) gene was genotyped. Multilevel growth curve modeling analysis indicated that emerging adults manifested the highest escalations in drug use when they reported high life stress and carried an allele of DRD4 with 7 or more repeats (7 + R allele). In addition, emerging adults who reported high life stress and carried the 7 + R allele evinced the largest increases in two proximal risk factors for drug use: affiliations with drug-using companions and drug use vulnerability cognitions. Furthermore, when the Gene × Environment interaction effects on the increases in affiliations with drug-using companions and vulnerability cognitions were entered into the model forecasting drug use, the Life Stress × DRD4 Status interaction on drug use became nonsignificant in the presence of the risk mechanisms. This finding provides an example of “second generation” Gene × Environment interaction research in which the interaction's effects on proximal risk mechanisms account for its effects on outcomes. En ligne : http://dx.doi.org/10.1017/S0954579412000466 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=178

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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Reports of perceived racial discrimination among African American children predict negative affect and smoking behavior in adulthood: A sensitive period hypothesis / Frederick X. GIBBONS in Development and Psychopathology, 30-5 (December 2018)  

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The effect of neighborhood disadvantage, social ties, and genetic variation on the antisocial behavior of African American women: A multilevel analysis / Man-Kit LEI in Development and Psychopathology, 26-4 (Part 1) (November 2014)  

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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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