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1.
Psychol Med ; 47(15): 2628-2639, 2017 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-28803556

RESUMO

BACKGROUND: Adults who were victims of childhood maltreatment tend to have poorer health compared with adults who did not experience abuse. However, many are in good health. We tested whether safe, supportive, and nurturing relationships buffer women with a history of childhood maltreatment from poor health outcomes in later life. METHODS: Participants included women from the Environmental Risk (E-Risk) Longitudinal Twin Study who were involved in an intimate relationship at some point by the time their twin children were 10 years old. Women were initially interviewed in 1999-2000 (mean age = 33 years) and 2, 5, and 7 years later. They reported on their physical and mental health, and their health-risk behaviours. RESULTS: Compared with women who did not experience abuse in childhood, women with histories of maltreatment were at elevated risk for mental, physical, and health-risk behaviours, including major depressive disorder, sleep, and substance use problems. Cumulatively, safe, supportive, and nurturing relationships characterized by a lack of violence, emotional intimacy, and social support buffered women with a history of maltreatment from poor health outcomes. CONCLUSIONS: Our findings emphasize that negative social determinants of health - such as a childhood history of maltreatment - confer risk for psychopathology and other physical health problems. If, however, a woman's current social circumstances are sufficiently positive, they can promote good health, particularly in the face of past adversity.


Assuntos
Sobreviventes Adultos de Maus-Tratos Infantis/estatística & dados numéricos , Transtorno Depressivo Maior/epidemiologia , Nível de Saúde , Relações Interpessoais , Pobreza/estatística & dados numéricos , Transtornos do Sono-Vigília/epidemiologia , Apoio Social , Transtornos Relacionados ao Uso de Substâncias/epidemiologia , Adulto , Transtornos de Ansiedade/epidemiologia , Inglaterra/epidemiologia , Feminino , Humanos , Estudos Longitudinais , Fatores de Proteção , Fatores de Risco , Parceiros Sexuais , País de Gales/epidemiologia
2.
Mol Psychiatry ; 19(10): 1071-7, 2014 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-25199917

RESUMO

Youth with high callous-unemotional traits (CU) are at risk for early-onset and persistent conduct problems. Research suggests that there may be different developmental pathways to CU (genetic/constitutional vs environmental), and that the absence or presence of co-occurring internalizing problems is a key marker. However, it is unclear whether such a distinction is valid. Intermediate phenotypes such as DNA methylation, an epigenetic modification regulating gene expression, may help to clarify etiological pathways. This is the first study to examine prospective inter-relationships between environmental risk (prenatal/postnatal) and DNA methylation (birth, age 7 and 9) in the prediction of CU (age 13), for youth low vs high in internalizing problems. We focused on DNA methylation in the vicinity of the oxytocin receptor (OXTR) gene as it has been previously implicated in CU. Participants were 84 youth with early-onset and persistent conduct problems drawn from the Avon Longitudinal Study of Parents and Children. For youth with low internalizing problems (46%), we found that (i) OXTR methylation at birth associated with higher CU (age 13) as well as decreased experience of victimization during childhood (evocative epigenetic-environment correlation; birth-age 7), (ii) higher prenatal parental risks (maternal psychopathology, criminal behaviors, substance use) associated with higher OXTR methylation at birth and (iii) OXTR methylation levels were more stable across time (birth-age 9). In contrast, for youth with high internalizing problems, CU were associated with prenatal risks of an interpersonal nature (that is, intimate partner violence, family conflict) but not OXTR methylation. Findings support the existence of distinct developmental pathways to CU.


Assuntos
Transtorno da Conduta/epidemiologia , Transtorno da Conduta/genética , Receptores de Ocitocina/genética , Meio Social , Criança , Vítimas de Crime , Metilação de DNA , Família/psicologia , Feminino , Humanos , Recém-Nascido , Estudos Longitudinais , Masculino , Gravidez , Estudos Prospectivos , Risco
3.
Mol Psychiatry ; 12(5): 432-42, 2007 May.
Artigo em Inglês | MEDLINE | ID: mdl-17453060

RESUMO

Family studies have demonstrated genetic influences on environmental exposure: the phenomenon of gene-environment correlation (rGE). A few molecular genetic studies have confirmed the results, but the identification of rGE in studies that measure genes and environments faces several challenges. Using examples from studies in psychology and psychiatry, we integrate the behavioral and molecular genetic literatures on rGE, describe challenges in identifying rGE and discuss the implications of molecular genetic findings of rGE for future research on gene-environment interplay and for attempts to prevent disease by reducing environmental risk exposure. Genes affect environments indirectly, via behavior and personality characteristics. Associations between individual genetic variants and behaviors are typically small in magnitude, and downstream effects on environmental risk are further attenuated by behavioral mediation. Genotype-environment associations are most likely to be detected when the environment is behaviorally modifiable and highly specified and a plausible mechanism links gene and behavior. rGEs play an important causal role in psychiatric illness. Although research efforts should concentrate on elucidating the genetic underpinnings of behavior rather than the environment itself, the identification of rGE may suggest targets for environmental intervention even in highly heritable disease. Prevention efforts must address the possibility of confounding between rGE and gene-environment interaction (G x E).


Assuntos
Meio Ambiente , Predisposição Genética para Doença , Transtornos Mentais/etiologia , Transtornos Mentais/prevenção & controle , Medicina Baseada em Evidências , Humanos , Transtornos Mentais/genética
4.
J Child Psychol Psychiatry ; 42(6): 803-15, 2001 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-11583253

RESUMO

This prospective study of a birth cohort addressed three questions. Which individual and family-of-origin characteristics predict the age at which young men make the transition to fatherhood? Do these same characteristics predict how long young men live with their child? Are individual differences in the amount of time fathers spend living with their child associated with the father's psychosocial characteristics in young adulthood? In this unique study, it was found that by age 26, 19% of the 499 study men had become fathers. Individual and family-of-origin characteristics were assessed from birth until age 15 and contemporaneous characteristics were assessed at age 26. Young men who experienced a stressful rearing environment and a history of conduct problems were more likely to become fathers at an early age and to spend less time living with their child. Of those who experienced none of the risk factors, fewer than 10% had become fathers by age 26 compared to more than 60% of those who experienced five risk factors. Fathers who lived apart from their child reported the most social and psychological difficulties in young adulthood. These findings point to individual and family-of-origin characteristics that might be targeted in order to delay fatherhood and increase levels of paternal involvement. However, given their troubled life histories and poor social-psychological adjustment in young adulthood, some absent fathers might have difficulties providing positive parenting and partnering unless policy initiatives to promote intact families also support young fathers.


Assuntos
Relações Pai-Filho , Pai/psicologia , Idade Paterna , Adolescente , Adulto , Fatores Etários , Humanos , Masculino , Estudos Prospectivos , Fatores de Risco , Fatores Socioeconômicos
6.
J Urol ; 101(2): 191, 1969 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-5765480
7.
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