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)  

Public ISBD [article]  inDevelopment and Psychopathology > 26-2 (May 2014) . - p.289-304 Titre : Is serotonin transporter genotype associated with epigenetic susceptibility or vulnerability? Examination of the impact of socioeconomic status risk on African American youth Type de document : Texte imprimé et/ou numérique Auteurs : Steven R. H. BEACH, Auteur ; Gene H. BRODY, Auteur ; Man Kit LEI, Auteur ; Sangjin KIM, Auteur ; Juan CUI, Auteur ; Robert A. PHILIBERT, Auteur Article en page(s) : p.289-304 Index. décimale : PER Périodiques Résumé : We hypothesized that presence of the short allele in the promoter region of the serotonin transporter would moderate the effect of early cumulative socioeconomic status (SES) risk on epigenetic change among African American youth. Contrasting hypotheses regarding the shape of the interaction effect were generated using vulnerability and susceptibility frameworks and applied to data from a sample of 388 African American youth. Early cumulative SES risk assessed at 11–13 years based on parent report interacted with presence of the short allele to predict differential methylation assessed at age 19. Across multiple tests, a differential susceptibility perspective rather than a diathesis–stress framework best fit the data for genes associated with depression, consistently demonstrating greater epigenetic response to early cumulative SES risk among short allele carriers. A pattern consistent with greater impact among short allele carriers also was observed using all cytosine nucleotide–phosphate–guanine nucleotide sites across the genome that were differentially affected by early cumulative SES risk. We conclude that the short allele is associated with increased responsiveness to early cumulative SES risk among African American youth, leading to epigenetic divergence for depression-related genes in response to exposure to heightened SES risk among short allele carriers in a “for better” or “for worse” pattern. En ligne : http://dx.doi.org/10.1017/S0954579413000990 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=230 [article] Is serotonin transporter genotype associated with epigenetic susceptibility or vulnerability? Examination of the impact of socioeconomic status risk on African American youth [Texte imprimé et/ou numérique] / Steven R. H. BEACH, Auteur ; Gene H. BRODY, Auteur ; Man Kit LEI, Auteur ; Sangjin KIM, Auteur ; Juan CUI, Auteur ; Robert A. PHILIBERT, Auteur . - p.289-304. in Development and Psychopathology > 26-2 (May 2014) . - p.289-304 Index. décimale : PER Périodiques Résumé : We hypothesized that presence of the short allele in the promoter region of the serotonin transporter would moderate the effect of early cumulative socioeconomic status (SES) risk on epigenetic change among African American youth. Contrasting hypotheses regarding the shape of the interaction effect were generated using vulnerability and susceptibility frameworks and applied to data from a sample of 388 African American youth. Early cumulative SES risk assessed at 11–13 years based on parent report interacted with presence of the short allele to predict differential methylation assessed at age 19. Across multiple tests, a differential susceptibility perspective rather than a diathesis–stress framework best fit the data for genes associated with depression, consistently demonstrating greater epigenetic response to early cumulative SES risk among short allele carriers. A pattern consistent with greater impact among short allele carriers also was observed using all cytosine nucleotide–phosphate–guanine nucleotide sites across the genome that were differentially affected by early cumulative SES risk. We conclude that the short allele is associated with increased responsiveness to early cumulative SES risk among African American youth, leading to epigenetic divergence for depression-related genes in response to exposure to heightened SES risk among short allele carriers in a “for better” or “for worse” pattern. En ligne : http://dx.doi.org/10.1017/S0954579413000990 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=230

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)  

Public ISBD [article]  inDevelopment and Psychopathology > 29-3 (August 2017) . - p.725-736 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 [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

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)  

Public ISBD [article]  inDevelopment and Psychopathology > 29-3 (August 2017) . - p.957-969 Titre : Smoking in young adulthood among African Americans: Interconnected effects of supportive parenting in early adolescence, proinflammatory epitype, and young adult stress Type de document : Texte imprimé et/ou numérique Auteurs : Steven R. H. BEACH, Auteur ; Man Kit LEI, Auteur ; Gene H. BRODY, Auteur ; Gregory E. MILLER, Auteur ; Edith CHEN, Auteur ; Jelani MANDARA, Auteur ; Robert A. PHILIBERT, Auteur Article en page(s) : p.957-969 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Abstract We examined two potentially interacting, connected pathways by which parental supportiveness during early adolescence (ages 1–13) may come to be associated with later African American young adult smoking. The first pathway is between parental supportiveness and young adult stress (age 19), with stress, in turn, predicting increased smoking at age 20. The second pathway is between supportive parenting and tumor necrosis factor (TNF) gene methylation (i.e., TNFm), a proinflammatory epitype, with low levels indicating greater inflammatory potential and forecasting increased risk for smoking in response to young adult stress. In a sample of 382 African American youth residing in rural Georgia, followed from early adolescence (age 10–11) to young adulthood (age 20), supportive parenting indirectly predicted smoking via associations with young adult stress, IE = –0.071, 95% confidence interval [–0.132, –0.010]. In addition, supportive parenting was associated with TNFm measured at age 20 (r = .177, p = .001). Further, lower TNFm was associated with a significantly steeper slope (b = 0.583, p = .003) of increased smoking in response to young adult stress compared to those with higher TNFm (b = 0.155, p = .291), indicating an indirect, amplifying role for supportive parenting via TNFm. The results suggest that supportive parenting in early adolescence may play a role in understanding the emergence of smoking in young adulthood. En ligne : http://dx.doi.org/10.1017/s0954579416000961 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=312 [article] Smoking in young adulthood among African Americans: Interconnected effects of supportive parenting in early adolescence, proinflammatory epitype, and young adult stress [Texte imprimé et/ou numérique] / Steven R. H. BEACH, Auteur ; Man Kit LEI, Auteur ; Gene H. BRODY, Auteur ; Gregory E. MILLER, Auteur ; Edith CHEN, Auteur ; Jelani MANDARA, Auteur ; Robert A. PHILIBERT, Auteur . - p.957-969. Langues : Anglais (eng) in Development and Psychopathology > 29-3 (August 2017) . - p.957-969 Index. décimale : PER Périodiques Résumé : Abstract We examined two potentially interacting, connected pathways by which parental supportiveness during early adolescence (ages 1–13) may come to be associated with later African American young adult smoking. The first pathway is between parental supportiveness and young adult stress (age 19), with stress, in turn, predicting increased smoking at age 20. The second pathway is between supportive parenting and tumor necrosis factor (TNF) gene methylation (i.e., TNFm), a proinflammatory epitype, with low levels indicating greater inflammatory potential and forecasting increased risk for smoking in response to young adult stress. In a sample of 382 African American youth residing in rural Georgia, followed from early adolescence (age 10–11) to young adulthood (age 20), supportive parenting indirectly predicted smoking via associations with young adult stress, IE = –0.071, 95% confidence interval [–0.132, –0.010]. In addition, supportive parenting was associated with TNFm measured at age 20 (r = .177, p = .001). Further, lower TNFm was associated with a significantly steeper slope (b = 0.583, p = .003) of increased smoking in response to young adult stress compared to those with higher TNFm (b = 0.155, p = .291), indicating an indirect, amplifying role for supportive parenting via TNFm. The results suggest that supportive parenting in early adolescence may play a role in understanding the emergence of smoking in young adulthood. En ligne : http://dx.doi.org/10.1017/s0954579416000961 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=312

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)  

Public ISBD [article]  inDevelopment and Psychopathology > 29-5 (December 2017) . - p.1969-1986 Titre : When inflammation and depression go together: The longitudinal effects of parent–child relationships Type de document : Texte imprimé et/ou numérique Auteurs : Steven R. H. BEACH, Auteur ; Man Kit LEI, Auteur ; Ronald L. SIMONS, Auteur ; Ashley B. BARR, Auteur ; Leslie G. SIMONS, Auteur ; Katherine EHRLICH, Auteur ; Gene H. BRODY, Auteur ; Robert A. PHILIBERT, Auteur Article en page(s) : p.1969-1986 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Parent–child relationships have long-term effects on health, particularly later inflammation and depression. We hypothesized that these effects would be mediated by later romantic partner relationships and elevated stressors in young adulthood, helping promote chronic, low grade, inflammation as well as depressive symptoms, and driving their covariation. It has been proposed recently that youth experiencing harsher parenting may also develop a stronger association between inflammation and depressive symptoms in adulthood and altered effects of stressors on outcomes. In the current investigation, we test these ideas using an 18-year longitudinal study of N = 413 African American youth that provides assessment of the parent–child relationship (at age 10), pro-inflammatory cytokine profile and depressive symptoms (at age 28), and potential mediators in early young adulthood (assessed at ages 21 and 24). As predicted, the effect of harsher parent–child relationships (age 10) on pro-inflammatory state and increased depressive symptoms at age 28 were fully mediated through young adult stress and romantic partner relationships. In addition, beyond these mediated effects, parent–child relationships at age 10 moderated the concurrent association between inflammation and depressive symptoms, as well as the prospective association between romantic partner relationships and inflammation, and resulted in substantially different patterns of indirect effects from young adult mediators to outcomes. The results support theorizing that the association of depression and inflammation in young adulthood is conditional on earlier parenting, and suggest incorporating this perspective into models predicting long-term health outcomes. En ligne : http://dx.doi.org/10.1017/S0954579417001523 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=324 [article] When inflammation and depression go together: The longitudinal effects of parent–child relationships [Texte imprimé et/ou numérique] / Steven R. H. BEACH, Auteur ; Man Kit LEI, Auteur ; Ronald L. SIMONS, Auteur ; Ashley B. BARR, Auteur ; Leslie G. SIMONS, Auteur ; Katherine EHRLICH, Auteur ; Gene H. BRODY, Auteur ; Robert A. PHILIBERT, Auteur . - p.1969-1986. Langues : Anglais (eng) in Development and Psychopathology > 29-5 (December 2017) . - p.1969-1986 Index. décimale : PER Périodiques Résumé : Parent–child relationships have long-term effects on health, particularly later inflammation and depression. We hypothesized that these effects would be mediated by later romantic partner relationships and elevated stressors in young adulthood, helping promote chronic, low grade, inflammation as well as depressive symptoms, and driving their covariation. It has been proposed recently that youth experiencing harsher parenting may also develop a stronger association between inflammation and depressive symptoms in adulthood and altered effects of stressors on outcomes. In the current investigation, we test these ideas using an 18-year longitudinal study of N = 413 African American youth that provides assessment of the parent–child relationship (at age 10), pro-inflammatory cytokine profile and depressive symptoms (at age 28), and potential mediators in early young adulthood (assessed at ages 21 and 24). As predicted, the effect of harsher parent–child relationships (age 10) on pro-inflammatory state and increased depressive symptoms at age 28 were fully mediated through young adult stress and romantic partner relationships. In addition, beyond these mediated effects, parent–child relationships at age 10 moderated the concurrent association between inflammation and depressive symptoms, as well as the prospective association between romantic partner relationships and inflammation, and resulted in substantially different patterns of indirect effects from young adult mediators to outcomes. The results support theorizing that the association of depression and inflammation in young adulthood is conditional on earlier parenting, and suggest incorporating this perspective into models predicting long-term health outcomes. En ligne : http://dx.doi.org/10.1017/S0954579417001523 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=324

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