
- <Centre d'Information et de documentation du CRA Rhône-Alpes
- CRA
- Informations pratiques
-
Adresse
Centre d'information et de documentation
Horaires
du CRA Rhône-Alpes
Centre Hospitalier le Vinatier
bât 211
95, Bd Pinel
69678 Bron CedexLundi au Vendredi
Contact
9h00-12h00 13h30-16h00Tél: +33(0)4 37 91 54 65
Mail
Fax: +33(0)4 37 91 54 37
-
Adresse
Détail de l'auteur
Auteur Ronald L. SIMONS |
Documents disponibles écrits par cet auteur (9)



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)
![]()
[article]
Titre : Biological embedding of neighborhood disadvantage and collective efficacy: Influences on chronic illness via accelerated cardiometabolic age Type de document : Texte imprimé et/ou numérique 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
in Development and Psychopathology > 30-5 (December 2018) . - p.1797-1815[article] Biological embedding of neighborhood disadvantage and collective efficacy: Influences on chronic illness via accelerated cardiometabolic age [Texte imprimé et/ou numérique] / 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)
![]()
[article]
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
in Development and Psychopathology > 33-3 (August 2021) . - p.803-820[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)
![]()
[article]
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
in Development and Psychopathology > 34-2 (May 2022) . - 689-703[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 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)
![]()
[article]
Titre : Life stress, the dopamine receptor gene, and emerging adult drug use trajectories: A longitudinal, multilevel, mediated moderation analysis Type de document : Texte imprimé et/ou numérique 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
in Development and Psychopathology > 24-3 (August 2012) . - p.941-51[article] Life stress, the dopamine receptor gene, and emerging adult drug use trajectories: A longitudinal, multilevel, mediated moderation analysis [Texte imprimé et/ou numérique] / 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)
![]()
[article]
Titre : Methylation of the oxytocin receptor gene mediates the effect of adversity on negative schemas and depression Type de document : Texte imprimé et/ou numérique Auteurs : Ronald L. SIMONS, Auteur ; Man Kit LEI, Auteur ; Steven R. H. BEACH, Auteur ; Carolyn E. CUTRONA, Auteur ; Robert A. PHILIBERT, Auteur Article en page(s) : p.725-736 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Abstract Building upon various lines of research, we posited that methylation of the oxytocin receptor gene (OXTR) would mediate the effect of adult adversity on increased commitment to negative schemas and in turn the development of depression. We tested our model using structural equation modeling and longitudinal data from a sample of 100 middle-aged, African American women. The results provided strong support for the model. Analysis of the 12 CpG sites available for the promoter region of the OXTR gene identified four factors. One of these factors was related to the study variables, whereas the others were not. This factor mediated the effect of adult adversity on schemas relating to pessimism and distrust, and these schemas, in turn, mediated the impact of OXTR methylation on depression. All indirect effects were statistically significant, and they remained significant after controlling for childhood trauma, age, romantic relationship status, individual differences in cell types, and average level of genome-wide methylation. These finding suggest that epigenetic regulation of the oxytocin system may be a mechanism whereby the negative cognitions central to depression become biologically embedded. En ligne : http://dx.doi.org/10.1017/s0954579416000420 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=311
in Development and Psychopathology > 29-3 (August 2017) . - p.725-736[article] Methylation of the oxytocin receptor gene mediates the effect of adversity on negative schemas and depression [Texte imprimé et/ou numérique] / Ronald L. SIMONS, Auteur ; Man Kit LEI, Auteur ; Steven R. H. BEACH, Auteur ; Carolyn E. CUTRONA, Auteur ; Robert A. PHILIBERT, Auteur . - p.725-736.
Langues : Anglais (eng)
in Development and Psychopathology > 29-3 (August 2017) . - p.725-736
Index. décimale : PER Périodiques Résumé : Abstract Building upon various lines of research, we posited that methylation of the oxytocin receptor gene (OXTR) would mediate the effect of adult adversity on increased commitment to negative schemas and in turn the development of depression. We tested our model using structural equation modeling and longitudinal data from a sample of 100 middle-aged, African American women. The results provided strong support for the model. Analysis of the 12 CpG sites available for the promoter region of the OXTR gene identified four factors. One of these factors was related to the study variables, whereas the others were not. This factor mediated the effect of adult adversity on schemas relating to pessimism and distrust, and these schemas, in turn, mediated the impact of OXTR methylation on depression. All indirect effects were statistically significant, and they remained significant after controlling for childhood trauma, age, romantic relationship status, individual differences in cell types, and average level of genome-wide methylation. These finding suggest that epigenetic regulation of the oxytocin system may be a mechanism whereby the negative cognitions central to depression become biologically embedded. En ligne : http://dx.doi.org/10.1017/s0954579416000420 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=311 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)
![]()
PermalinkReports 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)
![]()
PermalinkThe 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)
![]()
PermalinkWhen inflammation and depression go together: The longitudinal effects of parent–child relationships / Steven R. H. BEACH in Development and Psychopathology, 29-5 (December 2017)
![]()
Permalink