Figure 2 - uploaded by C. W. O'Neal
Content may be subject to copyright.
Developmental processes leading to young adult obesity and genetic amplifications. Unstandardized coefficients are shown with standardized coefficients in parentheses. Only statistically significant paths are included. *p p p
Source publication
Although previous research has documented the adverse influence of early socioeconomic disadvantage on youths' physical health outcomes and the increase in health inequalities over the early life course, little is known about genetically informed sequential life course developmental processes leading to health outcomes. Consistent with the life cou...
Contexts in source publication
Context 1
... approximate percentages for each precocious transition event were: 23.8 % for early sex, 9.3 % for early preg- nancy, 28 % for early marriage, 27 % for leaving home early, 11 % for joining the work force prematurely, and 13.2 % for high school drop outs. Figure 2 illustrates the full model assessing early socioeconomic adversities, subsequent adverse developmental processes, and amplifi- cation of these effects by genetic polymorphisms as well as the interactions of these genes with age-graded social contexts (G 9 E). ...
Context 2
... shown in Fig. 2, we found evidence that cumulative socioeconomic adversity at Wave 1 (1995) may create a ''chain of risks'' influencing young adults' BMI ( Wave 4, 2008) after controlling for race/ethnicity, gender, and lag- ged BMI ( Wave 2, 1995). More specifically, cumulative socioeconomic adversity was associated with parental rejection (B = .16), ...
Similar publications
Background
Youth trauma exposure is associated with syndemic HIV risk. We measured lifetime prevalence, type, and correlates of trauma experience by gender among adolescents living in the HIV hyper-endemic setting of Soweto, South Africa. Methods
Using data from the Botsha Bophelo Adolescent Health Survey (BBAHS), prevalence of “ever” experiencing...
Many researches have identified that adverse childhood experiences (ACEs) are associated with non-suicidal self-injury (NSSI) and suicidality. However, most studies have been restricted to a few types of ACEs. This study aims to investigate associations of 13 common types of ACEs with NSSI, suicidal ideation (SI) and suicide attempt (SA), as well a...
Background:
The global health community is devoting considerable attention to adolescents and young people, but risk of death in this population is poorly measured. We aimed to reconstruct global, regional, and national mortality trends for youths aged 15-24 years between 1990 and 2019.
Methods:
In this systematic analysis, we used all publicly...
Context: Bullying has been identified as an important adolescent health problem. Objective: This study aimed to examine the relationship between being involved in bullying either as a bully, a victim or a provocative-victim with stature and health-related quality of life (HRQoL). Design: Cross-sectional study. Results: Data were collected from a na...
Citations
... The longitudinal study of Wickrama et al. [23] showed that adolescents with more depressive symptoms and those with more genetic risk alleles, in general, had a higher BMI compared with adolescents with fewer depressive symptoms and risk alleles. Similarly, the population-based study of Schwartz et al. [24] showed that children who had experienced at least one depressive event had a higher average BMI than children without such an experience; the older the children, the stronger the association. ...
... Two out of three cross-sectional declared no association between depression and obesity [20,21], while one study concluded that depressive symptoms explained a significant amount of the variance in BMI [22]. All six longitudinal studies identified a positive association between depressive symptoms and BMI [23][24][25][26][27]. Only one recent meta-analysis [28] revealed that there is no association between overweight or obesity and the risk of depression. ...
One of the most critical factors that affects or leads to obesity is depression. However, another point of view is that obesity leads to depression. This systematic review estimates evidence arising from observational and systematic studies concerning the association between obesity and depression in children and adolescents. Moreover, the role of the family environment is investigated in this review. A systematic literature search was performed for research conducted between 2014 and 2021 on PubMed. The basic inclusion criteria were the language, study issue and type, and age of the participants. Studies that examined non-healthy populations, or were not related, or with no access were excluded. Titles and abstracts were screened independently, and full-text manuscripts meeting inclusion criteria were extracted. Finally, twenty-seven studies were retained. Most of them highlighted a positive association between obesity and depression. However, it is not clear whether obesity leads to depression or vice versa. Our review also revealed that the role of the family in this association has not been well studied and understood, since only one study addressed the issue. The evidence from our review emphasizes major public health issues; therefore, appropriate health policies should be developed. Moreover, additional research is required to fully understand the role of the family environment in the association between depression and obesity in childhood.
... Possible sources of individual differences could include positive caregiving relationships or access to community resources or high-quality food (Campbell et al., 2014;Larsen et al., 2015;Schwarzenberg & Georgieff, 2018;Wilkinson et al., 2018). Potential individual genetic characteristics might also be investigated as sources of individual differences (Wickrama et al., 2014). In addition, we did not test all possible pathways from early adversity to later BMI in our analyses. ...
Childhood adversity is associated with higher adult weight, but few investigations prospectively test mechanisms accounting for this association. Using two socioeconomically high-risk prospective longitudinal investigations, the Minnesota Longitudinal Study of Risk and Adaptation (MLSRA; N = 267; 45.3% female) and the Fragile Families and Child Wellbeing Study (FFCWS; n = 2,587; 48.5% female), pathways between childhood adversity and later body mass index (BMI) were tested using impulsivity, emotion dysregulation, and overeating as mediators. Childhood adversity from 0 to 5 years included four types of adversities: greater unpredictability, threat/abuse, deprivation/neglect, and low socioeconomic status. Parents reported on child impulsivity, emotion dysregulation, and overeating. Height and weight were self-reported and measured at 32 and 37 years in MLSRA and at 15 years in FFCWS. FFCWS results indicated that threat, deprivation, and low socioeconomic status predicted greater impulsivity and emotion dysregulation at 5 years, which in turn predicted greater overeating at 9 years and higher BMI z-score at 15 years. Early unpredictability in FFCWS predicted higher BMI through greater impulsivity but not emotion dysregulation at age 5. MLSRA regression results replicated the threat/abuse → emotion dysregulation → overeating → higher BMI pathway. These findings suggest that different dimensions of early adversity may follow both similar and unique pathways to predict BMI.
... Diatheses-stress models (Goforth, Pham, and Carlson 2011) posit that developmental outcomes (e.g., youth behavior) are the result of an interaction between genetic predisposition vulnerability and stressful experiences. Accordingly, previous research has shown that the negative associations of some "vulnerability genes" (e.g., BMIrelated PGS) with developmental outcomes are amplified by socioeconomic adversity (Wickrama, O'Neal, and Oshri 2014). Similarly, the beneficial association of specific genes (e.g., educational PGS) can be weakened by socioeconomic adversity (Bolyard and Savelyev, 2021). ...
... Precocious transitions, such as dropping out of school, early parenthood, and independent living during adolescence, limit the acquisition of human and social capital (Hagan & Foster, 2001) and increase the likelihood of negative consequences for individual and family wellbeing. Those transitions often create stressful life contexts that are maladaptive as adolescents are not equipped with the cognitive or emotional skills and competencies to handle these role changes (Foster, Hagan, & Brooks-Gunn, 2008;Oshri, Rogosch, Burnette, & Cicchetti, 2011;Wickrama, Conger, Lorenz, & Jung, 2008;Wickrama, O'Neal, & Oshri, 2014). Furthermore, those who experience precocious transitions often struggle with the emotional, social (e.g., familial), and financial demands of adulthood, which are atypical to adolescence (Hatch, 2005;Wickrama, Conger, Wallace, & Elder, 2003). ...
Growing evidence suggests that maltreatment is reproduced across generations as victims of maltreatment are at an increased risk for maltreatment perpetration. Unfortunately, little information about mediating pathways exists to provide an explanation for why maltreatment begets maltreatment. We use the number of types of maltreatment experienced to predict later maltreatment perpetration and then examine two developmental pathways that may serve as bridges between maltreatment victimization and perpetration: adolescent problem behaviors and precocious transitions to adulthood. With prospective, longitudinal data from the Rochester Youth Development Study, we assess the relevance of these pathways for the number of maltreatment experiences as well as the number of maltreatment victimization experiences by developmental period (i.e., childhood and adolescence). Our results demonstrate a significant relationship between maltreatment victimization and maltreatment perpetration. Adolescent delinquency and two precocious transitions, dropping out of school and independent living, as well as the accumulation of precocious transitions and problem behaviors, serve as mediators of this intergenerational relationship. Furthermore, the relationship between the number of types of maltreatment and subsequent perpetration is primarily driven by experiences of maltreatment during adolescence. We discuss the implications of these results and set an agenda for the development of programs and policies to interrupt the cycle of maltreatment.
... Because the main purposes of our study were to identify the heterogeneity in transition patterns and to investigate the associations between early cumulative adversities, race and gender, we did not examine these potential interaction effects. Finally, research suggests that non-observed biomarker components and contextual effects (e.g., gene-environment interaction) may multiplicatively influence the timing of transition events, particularly precocious development (Wickrama et al., 2014). Consequently, biomarker information may be also associated with transition patterns in the current study. ...
The purposes of the present study are to investigate: (1) the heterogeneity in life transition patterns of youth from adolescence to young adulthood (ages 18-30) involving the timing and sequence of four transition events (college graduation, full-time employment, marriage, and parenthood), (2) the influence of early socioeconomic adversity on life transition patterns from adolescence to young adulthood, and (3) the influence of gender and race/ethnicity on these transition patterns. Using a multivariate discrete-time mixture survival model with a sample of 14,503 adolescents from the National Longitudinal Study of Adolescent to Adult Health (Add Health), the study identified four life transition patterns and found that early socioeconomic adversity shapes disrupted life transition patterns from adolescence to young adulthood. Gender and race/ethnicity differences are discussed. These results highlight the need for prevention and intervention programs that selectively target at-risk youth beginning in adolescence and continuing through subsequent transition periods.
... Previous research suggests that stressful life experiences in early years may proliferate over the life course, leading to health problems in young adulthood (Pearlin and Skaff 1996;Wickrama et al. 2014). For instance, parent-child disconnection in behavioral (e.g., lack of joint activities), cognitive (e.g., lack of mutuality in decision-making), and emotional (e.g., lack of acceptance of the child, feeling of closeness with the child) dimensions creates an unsupportive and isolated family environment for youth. ...
... Parent-child disconnection was assessed using relationship measures from both parents' and adolescents' reports (Crosnoe and Elder 2004). First, lack of bonding with adolescents was assessed with parental reports (Wickrama et al. 2014). Mothers responded to five items assessing their relationships with the target adolescents at Wave 1 (1995). ...
Previous studies have documented that early stressful family relationships influence subsequent stressful life circumstances and health outcomes over the life course. Less is known, however, about whether stressful parent-child relationships increase the influence of proximal stressors on youth health operating as a stress-sensitizing life context, and individual genetic variations have effects on these developmental processes. Informed by life course stress process theory, which focuses on the proliferation, accumulation, and interactions of stressors over the life course as health risks, we examined whether (a) parent–child disconnection influences the occurrence of stressful life events in young adulthood, (b) parent–child disconnection potentiates the impact of stressful life events on young adults’ health, or (c) potential health impact is intensified further by individual genotype. Using longitudinal data from a nationally representative sample of 11,290 adolescents (Mean age 15.5 years, 53% female) over a period of 13 years, we found parent–child disconnection influenced young adults’ stressful life events and amplified the impact of stressful life events on cardio-metabolic disease risk. We also found the association between stressful life events and cardio-metabolic disease risk was further intensified by the 5-HTTLPR polymorphism. Our findings demonstrate that stressful family relationships not only initiate stress processes over the early life course, but also sensitize youth to stressors, and that 5-HTTLPR polymorphism interacts with stressful life experiences to predict heightened disease risk.
... However, very little has been done to examine the interaction between PRS and childhood adversity in predicting psychiatric disorders. Those studies that do exist have explored this interaction in relation to risk of depression [19,20], health problems and alcohol use [21,22], and smoking behaviour [23], and the findings consistently support the presence of a GxE interaction. However, no studies to date have explored whether a PRS modifies the association between childhood adversity and onset of psychotic disorders. ...
... Polygenic risk scores for schizophrenia did not increase exposure to, or reporting of, childhood adversity in cases and controls. This is in line with previous findings which showed no statistically significant correlations between PRS and childhood adverse events in both clinical and non-clinical samples [19,21]. Similar findings come from studies on candidate gene associations with history of childhood adversity in psychosis. ...
Background: A history of childhood adversity is associated with psychotic disorder, with an increase in risk according to number or severity of exposures. However, it is not known why only some exposed individuals go on to develop psychosis. One possibility is preexisting genetic vulnerability. Research on gene–environment interaction in psychosis has primarily focused on candidate genes, although the genetic effects are now known to be polygenic. This pilot study investigated whether the effect of childhood adversity on psychosis is moderated by the polygenic risk score for schizophrenia (PRS).
Methods: Data were utilized from the Genes and Psychosis (GAP) study set in South London, United Kingdom. The GAP sample comprises 285 first-presentation psychosis cases and 256 unaffected controls with information on childhood adversity. We studied only white subjects (80 cases and 110 controls) with PRS data, as the PRS has limited predictive ability in patients of African ancestry. The occurrence of childhood adversity was assessed with the Childhood Experience of Care and Abuse Questionnaire (CECA.Q) and the PRS was based on genome-wide meta-analysis results for schizophrenia from the Psychiatric Genomics Consortium.
Possible interaction between childhood adversity and PRS was investigated using an additive model to test interaction as departure from additivity. This means that the combined effect of PRS and environment differs from the sum of their individual effects.
Results: First-presentation psychosis patients were more than two times more likely to report exposure to two or more childhood adversities compared with controls (P = .003). In fact, a score test for trend provided evidence for a linear trend (z = 4.97, P < .001), indicating a dose–response effect for repeated adverse experiences. Furthermore, higher polygenic scores significantly predicted psychosis case status in this subsample (adjusted b = 7.68, 95% CI 3.69–11.66, P < .001).
Nevertheless, no evidence was found for interaction as departure from additivity, indicating that the effect of polygenic risk scores on psychosis was not increased in the presence of a history of childhood adversity (P = .918).
Conclusion: These findings are compatible with a multifactorial threshold model in which both genetic liability and exposure to environmental risk contribute to the etiology of psychosis.
... Parental Rejection At Wave I, a parent of the participant (most of the time it was the mother) answered five questions (among others) about their relationship with the participant (e.g.,''You just do not understand him/her''; Wickrama, O'Neal, & Oshri, 2014). An average was computed such that higher scores represent more rejection from the parent (Cronbach's a = 0.64). ...
A number of studies have indicated that gay men tend to be shorter, on average, than heterosexual men. Less evidence exists that lesbian women are taller, on average, than heterosexual women. The most popular explanation of the association between sexual orientation and height involves prenatal factors, such that, for example, gay men may have been exposed to lower than typical androgens during fetal development, which impacts their height and sexual orientation as adults. An alternative explanation involves stress, given that stress has been associated with sexual minority identification and with lower height. Another alternative explanation involves nutrition, although its relationship is less clear with sexual minority identification. Using the Add Health data, which is a large, nationally representative and longitudinal sample of American adolescents (n = 14,786), we tested a mediation model, such that sexual orientation → pubertal stress/nutrition → height. Within men, we found that gay men (n = 126) were shorter, on average, than heterosexual men (n = 6412). None of the 24 pubertal stress-related and 15 pubertal nutrition-related variables assessed in the Add Health data mediated the relationship between sexual orientation and height in men. Within women, lesbians (n = 75) did not differ significantly in stature compared to heterosexual women (n = 6267). Thus, prenatal mechanisms (e.g., hormones, maternal immune response) are likely better candidates for explaining the height difference between gay men and heterosexual men.
... However, very little has been done to examine the interaction between PRS and childhood adversity in predicting psychiatric disorders. Those studies that do exist have explored this interaction in relation to risk of depression [19,20], health problems and alcohol use [21,22], and smoking behaviour [23], and the findings consistently support the presence of a GxE interaction. However, no studies to date have explored whether a PRS modifies the association between childhood adversity and onset of psychotic disorders. ...
... Polygenic risk scores for schizophrenia did not increase exposure to, or reporting of, childhood adversity in cases and controls. This is in line with previous findings which showed no statistically significant correlations between PRS and childhood adverse events in both clinical and non-clinical samples [19,21]. Similar findings come from studies on candidate gene associations with history of childhood adversity in psychosis. ...
A history of childhood adversity is associated with psychotic disorder, with an increase in risk according to number or severity of exposures. However, it is not known why only some exposed individuals go on to develop psychosis. One possibility is pre-existing genetic vulnerability. Research on gene-environment interaction in psychosis has primarily focused on candidate genes, although the genetic effects are now known to be polygenic. This pilot study investigated whether the effect of childhood adversity on psychosis is moderated by the polygenic risk score for schizophrenia (PRS). Data were utilised from the Genes and Psychosis (GAP) study set in South London, UK. The GAP sample comprises 285 first-presentation psychosis cases and 256 unaffected controls with information on childhood adversity. We studied only white subjects (80 cases and 110 controls) with PRS data, as the PRS has limited predictive ability in patients of African ancestry. The occurrence of childhood adversity was assessed with the Childhood Experience of Care and Abuse Questionnaire (CECA.Q) and the PRS was based on genome-wide meta-analysis results for schizophrenia from the Psychiatric Genomics Consortium. Higher schizophrenia PRS and childhood adversities each predicted psychosis status. Nevertheless, no evidence was found for interaction as departure from additivity, indicating that the effect of polygenic risk scores on psychosis was not increased in the presence of a history of childhood adversity. These findings are compatible with a multifactorial threshold model in which both genetic liability and exposure to environmental risk contribute independently to the etiology of psychosis.
... monitoring, and that are unsupportive have been linked to adverse adolescent health outcomes, such as unhealthy body mass index values (Wickrama, O'Neal, & Oshri, 2014) and depressive symptoms (Wickrama et al., 2013). Conversely, adolescents who perceive more positive parenting quality display fewer depressive symptoms, increased self-efficacy, and more positive social connections (Mancini et al., 2015;Repetti et al., 2002). ...
Parents' early life stressful experiences have lifelong consequences, not only for themselves but also for their children. The current study utilized a sample of military families (n = 266) including data from both active-duty and civilian parents and their adolescent children. Hypotheses reflecting principles of persistence, transmission, and proximity as pertaining to parents and their children were examined. The impact of parents' childhood experiences on their functioning later in life and, consequently, their adolescent children's well-being were examined. Adults who encountered more stressful childhood experiences, including relatively prevalent and less severe adversities (e.g., verbal conflict between parents) experienced poorer functioning than adults who encountered little early stress. Civilian parents' current functioning was related to adolescent children's well-being, whereas the functioning of active-duty parents was generally not related to children's well-being. Persistence, transmission, and proximity hypotheses were generally supported but with variations attributable to whether an adult was a military member. (PsycINFO Database Record
