Concurrent and prospective associations between family socioeconomic status, social support and salivary diurnal and hair cortisol in adolescence.

BACKGROUND: Exposure to socioeconomic adversity is hypothesized to impact hypothalamic-pituitary-adrenal (HPA) axis activity and cortisol secretion, but existing evidence is inconsistent. Yet, few studies have investigated this association using a developmental approach that considers potential protective contextual factors. This study examined the role of stability and changes in family socioeconomic status (SES) in the prediction of multiple cortisol indicators and tested whether social support moderated these associations. METHODS: Participants were part of a population-based sample of twin pairs recruited at birth. Family SES was assessed in early childhood (ages 0-5) and mid-adolescence (age 14). Social support was assessed at ages 14 and 19. Diurnal cortisol (n = 569) was measured at age 14 at awakening, 30 min later, in the afternoon and evening over four non-consecutive days. Hair cortisol concentration (HCC, n = 704) was measured at age 19. All data were collected before the pandemic and multilevel regression models were conducted to account for the nested data structure. RESULTS: Youth exposed to lower family SES levels in childhood and mid-adolescence had a flatter diurnal slope and higher HCC compared with those who experienced upward socioeconomic mobility in mid-adolescence. Contrastingly, mid-adolescence SES showed no association with the diurnal slope or HCC for youth from higher-SES households in early childhood. Moreover, youth raised in higher-SES families in early childhood had a higher CAR in mid-adolescence if they reported greater social support in mid-adolescence. Social support also moderated the SES-cortisol association in mid-adolescence, with higher-SES youth showing higher awakening cortisol secretion when reporting more social support. CONCLUSIONS: Our findings support the hypothesis that early socioeconomic adversity sensitizes HPA axis activity to later socioeconomic disadvantage, which may bear consequences for socioemotional and behavioral functioning.

Reconsidering the failure model: Using a genetically controlled design to assess the spread of problems from reactive aggression to internalizing symptoms through peer rejection across the primary school years.

According to the failure model (Patterson & Capaldi, 1990), peer rejection is the intermediary link between problem behaviors and internalizing symptoms. The present study tested the model with 464 monozygotic and same-sex dizygotic twin pairs (234 female, 230 male dyads). Teacher-reported reactive aggression and internalizing symptoms, and peer-reported peer rejection were collected at ages 6, 7, and 10 (from 2001 to 2008). Support for the failure model emerged in conventional non-genetically controlled analyses, but not twin-difference score analyses (which remove shared environmental and genetic contributions). Univariate biometric models attributed minimal variance in failure model variables to shared environmental factors, suggesting that genetic factors play an important unacknowledged role in developmental pathways historically ascribed to nonshared experiences in the failure model.

Does early child negative emotionality moderate the association between maternal stimulation and academic readiness and achievement?

We investigated whether child temperament (negative emotionality, 5 months) moderated the association between maternal stimulation (5 months-2½ years) and academic readiness and achievement (vocabulary, mathematics, and reading). We applied structural equation modeling to the data from the Quebec Longitudinal Study of Child Development (N = 1121-1448; mostly Whites; 47% girls). Compared to children with low negative emotionality, those with high negative emotionality had higher levels of academic readiness (6 years) and mathematics achievement (7 years) when exposed to high levels of maternal stimulation (ß = 3.17, p < .01 and ß = 2.91, p < .01, respectively). The results support the differential susceptibility model whereby highly emotionally negative children were more susceptible to the influences of low and high levels of maternal stimulation in academic readiness and mathematics achievement's developments.

Genetic and phenotypic evidence of the predictive validity of preschool parent reports of hyperactivity/impulsivity and inattention.

To determine the validity of parent reports (PRs) of ADHD in preschoolers, we assessed hyperactivity/impulsivity (HI) and inattention (IN) in 1114 twins with PRs at 1.5, 2.5, 4, 5, 14, 15, and 17 years, and teacher-reports at 6, 7, 9, 10, and 12. We examined if preschool PRs (1) predict high HI/IN trajectories, and (2) capture genetic contributions to HI/IN into adolescence. Group-based trajectory analyses identified three 6-17 years trajectories for both HI and IN, including small groups with high HI (N = 88, 10.4%, 77% boys) and IN (N = 158, 17.3%, 75% boys). Controlling for sex, each unit of HI PRs starting at 1.5 years and at 4 years for IN, increased more than 2-fold the risk of belonging to the high trajectory, with incremental contributions (Odds Ratios = 2.5-4.5) at subsequent ages. Quantitative genetic analyses showed that genetic contributions underlying preschool PRs accounted for up to a quarter and a third of the heritability of later HI and IN, respectively. Genes underlying 1.5-year HI and 4-year IN contributed to 6 of 8 later HI and IN time-points and largely explained the corresponding phenotypic correlations. Results provide phenotypic and genetic evidence that preschool parent reports of HI and IN are valid means to predict developmental risk of ADHD.

Perinatal and early-life factors associated with stable and unstable trajectories of psychopathic traits across childhood.

BACKGROUND: This study aimed to identify perinatal and early-life factors associated with trajectories of psychopathic traits across childhood. METHODS: Participants were 1631 children (51.5% girls) from the Quebec Longitudinal Study of Child Development. A wide range of perinatal and early-life factors were assessed from pregnancy to age 2.5 years using medical files and mothers' reports. Psychopathic traits were assessed via teachers' reports at ages 6, 7, 8, 10, and 12 years. Latent class growth analyses and multinomial logistic regressions controlling for child sex were conducted. Two-way interaction effects between perinatal/early-life factors and child sex were explored. RESULTS: Four trajectories of psychopathic traits were identified: High-stable (4.48%), Increasing (8.77%), Decreasing (11.46%), and Low-stable (75.29%). A few perinatal factors and most child-level and family-level early-life factors significantly increased the odds of following the High-stable v. the Low-stable trajectory. Higher levels of psychotropic exposures during pregnancy, socioeconomic adversity, child's physical aggression, child's opposition, mother's depressive symptoms, and hostile parenting increased the likelihood of following the Increasing instead of the Low-stable trajectory. Higher socioeconomic adversity, mother's depressive symptoms, and inconsistent parenting were associated with membership to the High-stable instead of the Decreasing trajectory. Most associations were not moderated by child sex. CONCLUSIONS: These results shed light on the perinatal and early-life factors that are associated with specific pathways of psychopathic traits during childhood and suggest that different factors could be targeted to prevent the exacerbation (v. low and stable levels) or the stability at high levels (v. attenuation) of these traits.

Mental health comorbidities following peer victimization across childhood and adolescence: a 20-year longitudinal study.

BACKGROUND: Peer victimization is associated with a wide range of mental health problems in youth, yet few studies described its association with mental health comorbidities. METHODS: To test the association between peer victimization timing and intensity and mental health comorbidities, we used data from 1216 participants drawn from the Quebec Longitudinal Study of Child Development, a population-based birth cohort. Peer victimization was self-reported at ages 6-17 years, and modeled as four trajectory groups: low, childhood-limited, moderate adolescence-emerging, and high-chronic. The outcomes were the number and the type of co-occurring self-reported mental health problems at age 20 years. Associations were estimated using negative binomial and multinomial logistic regression models and adjusted for parent, family, and child characteristics using propensity score inverse probability weights. RESULTS: Youth in all peer victimization groups had higher rates of co-occurring mental health problems and higher likelihood of comorbid internalizing-externalizing problems [odds ratios ranged from 2.06, 95% confidence interval (CI) 1.52-2.79 for childhood-limited to 4.34, 95% CI 3.15-5.98 for high-chronic victimization] compared to those in the low victimization group. The strength of these associations was highest for the high-chronic group, followed by moderate adolescence-emerging and childhood-limited groups. All groups also presented higher likelihood of internalizing-only problems relative to the low peer victimization group. CONCLUSIONS: Irrespective of timing and intensity, self-reported peer victimization was associated with mental health comorbidities in young adulthood, with the strongest associations observed for high-chronic peer victimization. Tackling peer victimization, especially when persistent over time, could play a role in reducing severe and complex mental health problems in youth.

Medical conditions and Attention-Deficit/Hyperactivity Disorder symptoms from early childhood to adolescence.

The comorbidity between physical and mental health conditions is challenging and frequently goes unrecognized in practice. Associations between Attention-Deficit/Hyperactivity Disorder (ADHD) and physical conditions have been reported in youth. However, prior research failed to: (1) address the patterns of associations in early childhood, middle childhood, and adolescence within the same population sample; (2) consider a large set of physical disorders at the same time; (3) take confounders into account. Our goal was to assess the associations between ADHD symptoms and a broad set of physical conditions across developmental periods. This birth cohort study (n = 2057) is the first to explore the associations between ADHD and a wide range of medical conditions by encompassing the whole early development from 5 months to 17 years in the same sample and relying on innovative network analyses. We found significant associations between ADHD symptoms and several physical conditions, some of which were observed in early childhood, middle childhood, and adolescence (e.g., asthma, sleep problems) or were confounded by socioeconomic status or psychiatric comorbidities (e.g., body mass index, dental caries). The study calls for an effective integrated care model encompassing mental and general healthcare across the developmental period.

Risk of total metachronous advanced neoplasia at surveillance colonoscopy after detection of serrated lesions: a matched case-cohort study.

BACKGROUND : Serrated lesions are potential colorectal cancer precursors. This study evaluated the presence of total metachronous advanced neoplasia (T-MAN) at follow-up in patients with index serrated lesions compared with a matched cohort without serrated lesions. METHODS : Patients aged 45-74 years with serrated lesions were matched 2:1 by sex, age, synchronous polyps, and timing of index colonoscopy, to patients without serrated lesions. The primary outcome was T-MAN (advanced adenoma or high-risk serrated lesion) at follow-up. Secondary outcomes included presence of T-MAN stratified by synchronous polyps and serrated lesion characteristics. RESULTS : 1425 patients were included (475 patients, 642 serrated lesions; 950 controls; median follow-up 2.9 versus 3.6 years). Patients with serrated lesions had greater risk of T-MAN than those without (hazard ratio [HR] 6.1, 95 %CI 3.9-9.6). Patients with serrated lesions and high-risk adenoma (HRA) had higher risk of T-MAN than those with HRA alone (HR 2.6, 95 %CI 1.4-4.7); similarly, patients with serrated lesions plus low-risk adenoma (LRA) had higher risk than those with LRA alone (HR 7.0, 95 %CI 2.8-18.4), as did patients with serrated lesions without adenoma compared with no adenoma (HR 14.9, 95 %CI 6.5-34.0). Presence of proximal sessile serrated lesion (SSL; HR 9.3, 95 %CI 5.4-15.9), large SSL (HR 17.8, 95 %CI 7.4-43.3), and proximal large SSL (HR 25.0, 95 %CI 8.8-71.3), but not distal SSL, were associated with greater risk for T-MAN. CONCLUSION : Patients with serrated lesions had higher risk for T-MAN regardless of synchronous adenomas. Patients with serrated lesions and HRA, and those with large or proximal SSLs, were at greatest risk.

Polygenic risk score and peer victimisation independently predict depressive symptoms in adolescence: results from the Quebec Longitudinal Study of Children Development.

BACKGROUND: Peer victimisation has been associated with depressive symptoms during adolescence, however not all peer victimised adolescents will exhibit such symptoms. This study tested whether having a genetic predisposition to developing depression increased the risk of experiencing depressive symptoms in peer victimised youth. To date, no study has explored such gene-environment interaction using a polygenic risk score for depression (PRS-depression) in the context of peer victimisation and depressive symptoms in adolescence. METHODS: The sample included 748 participants born in 1997/98 from the Quebec Longitudinal Study of Child Development with genotype data and prospectively collected information on peer victimisation (12-13 years) obtained from both self- and teacher-reports, as well as self-reported depressive symptoms (15-17 years). The PRS-depression was based on the genome-wide association meta-analysis of broad depression by Howard et al. (2019). RESULTS: Self- and teacher-reported peer victimisation in early adolescence were both associated with depressive symptoms in adolescence (ß = 0.34, p < .001; ß = 0.14, p = .001 respectively), and this association remained significant when accounting for PRS-depression (ß = 0.33, p < .001; ß = 0.13, p = .002 respectively). PRS-depression was independently associated with depressive symptoms, but there was no significant PRS-depression by peer victimisation interaction (self-reported and teacher-reported). PRS-depression was correlated with self-reported, but not teacher-reported, peer victimisation. CONCLUSIONS: Our findings suggested that a partial measure of an individual's genetic predisposition to depression, as measured by PRS-depression, and being exposed to peer victimisation (self- and teacher-reported) were independently associated with depressive symptoms in adolescence. Furthermore, PRS-depression did not exacerbate the risk of depressive symptoms among adolescents who had been peer victimised. Lastly, we found evidence of a gene-environment correlation between PRS-depression and self-reported peer victimisation. Future studies are needed to replicate this finding and to further understand the role of genetic predispositions in experiencing depressive symptoms following peer victimisation.

Nocturnal sleep duration trajectories in early childhood and school performance at age 10 years.

Sleep plays a fundamental role in brain development and resultant functions. The aim was to verify whether nocturnal sleep duration during early childhood has long-term associations with academic achievement at age 10 years. The present study is part of the Quebec Longitudinal Study of Child Development, a representative cohort of infants born in 1997-1998 in the province of Quebec, Canada. Children with known neurological conditions were excluded from this cohort. Four trajectories of parent-reported nocturnal sleep duration at ages 2.5, 3, 4, 5 and 6 years were determined using a SAS procedure named PROC TRAJ. Sleep duration at age 10 years was also reported. Teachers provided data on academic performance when the children were age 10 years. These data were available for 910 children (430 boys, 480 girls; 96.6% Caucasians). Univariate and multivariable logistic regressions were performed using SPSS. Children who slept less than 8 hr per night at 2.5 years but normalized later on (Traj1) had three-five times the odds of having grades below the class average in reading, writing, mathematics and science compared with children who slept sufficiently (Traj3-4: 10-11 hr per night). Children who slept about 9 hr per night throughout childhood (Traj2) had two-three times the odds of being below the class average in mathematics and science. Sleep duration at age 10 years was not correlated with the academic performance. These results point to the presence of a very important early period during which sufficient sleep is needed to fine-tune the functions necessary for academic achievement later on.

Prenatal and concurrent blood mercury concentrations and associations with IQ in canadian preschool children.

BACKGROUND: Prenatal and childhood mercury (Hg) exposures have been associated with negative impacts on child neurodevelopment. It is unclear if associations persist at the low Hg exposures typical in Western countries. OBJECTIVE: To examine associations between prenatal/childhood blood Hg concentrations and child IQ in Canadian male and female children while considering the potential modifying role of prenatal fish consumption. METHODS: We analyzed data from the Maternal-Infant Research on Environmental Chemicals study. Hg was measured in first trimester (n = 527), cord (n = 430), and child (at 3-4 years of age, n = 355) blood and examined sex-stratified associations between blood Hg and children's Full Scale IQ (FSIQ), Verbal IQ (VIQ), Performance IQ (PIQ), and General Language Composite (GLC) scores (assessed with WPPSI-III). Prenatal Hg analyses were further stratified by prenatal fish consumption (low: 0-2, moderate: 3-7, or high: ≥8 times/month). RESULTS: Higher cord blood Hg concentrations were associated with lower PIQ (ß = -3.27; 95%CI: 6.44, -0.09) in male children with the lowest prenatal fish consumption. Progressively stronger positive associations were observed with PIQ in male children for moderate (ß = 1.08; 95%CI: 0.10, 2.26) and high (ß = 3.07; 95%CI: 1.95, 4.19) prenatal fish consumption. Cord blood Hg concentrations were positively associated with female children's FSIQ (ß = 1.29; 95% CI: 0.77, 1.81) and PIQ (ß = 2.01; 95% CI: 1.19, 2.83); however, when stratified only in the highest fish consumption subgroup. Among female children, higher child blood Hg concentrations were associated with an approximately 1-point increase in FSIQ, VIQ, and GLC. CONCLUSIONS: Prenatal exposure to low levels of Hg was associated with lower PIQ scores in male children with low prenatal fish intake. Positive associations between cord and child blood Hg concentrations and IQ were primarily observed in female children and may be due to beneficial effects of prenatal fish intake.

Rates of synchronous advanced neoplasia and colorectal cancer in patients with colonic serrated lesions.

BACKGROUND AND AIMS: Serrated lesions (SL) have been associated with significant risks of developing colorectal cancer (CRC). Data on synchronous findings after SL detection during colonoscopy is limited. Study aim was to evaluate the rate of synchronous advanced neoplasia (S-AN) and synchronous CRC (S-CRC) in colonoscopies where SLs were detected. METHODS: We conducted a retrospective study of screening aged patients 45-74year with colorectal SL (sessile serrated polyp [SSP] or traditional serrated adenoma [TSA]) detected during an elective colonoscopy. Primary outcome was risk of S-AN in patients with SL. Secondary outcomes included risk of S-AN or S-CRC stratified by SL characteristics. RESULTS: The study included 1262 patients with 1649 SLs (1214 with SSPs and 48 with TSAs). 47.2% were female and 22.9% of exams were screening colonoscopies, 48.2% surveillance, 28.9% diagnostic. The overall rates of S-AN and S-CRC were 15.1% and 1.3%, respectively. Presence of SSPs ≥ 10 mm was associated with higher rates of S-AN, (18.1 vs. 12.2%, Odds-Ratio [OR] = 1.61 [95% Confidence Interval [CI] 1.17-2.23], p = 0.004). SSP dysplasia was predictive of S-AN, (30.3 vs 14.1%, OR = 2.68 [95%CI 1.24-5.78], p = 0.012) but not S-CRC. SSP number (≥ 3) and location (proximal) were not predictors of S-AN or S-CRC. CONCLUSION: Patients with SLs are at high-risk of S-AN and S-CRC. Findings of SSPs ≥ 10 mm and SSP dysplasia are associated with high-risk of S-AN. Endoscopists should exercise heightened vigilance for synchronous findings when SLs are detected, especially SSPs ≥ 10 mm or when bowel preparation is suboptimal. Studies contrasting synchronous risk of other polyp types are needed to confirm these results.

The phenotypic associations and gene-environment underpinnings of socioeconomic status and diurnal cortisol secretion in adolescence.

While converging evidence suggests that both environmental and genetic factors underlie variations in diurnal cortisol, the extent to which these sources of influence vary according to socioeconomic status (SES) has seldom been investigated, particularly in adolescence. To investigate whether a distinct genetic and environmental contribution to youth's diurnal cortisol secretion emerges according to family SES and whether the timing of these experiences matters. Participants were 592 twin pairs, who mostly came from middle-income and intact families and for whom SES was measured in childhood and adolescence. Diurnal cortisol was assessed at age 14 at awakening, 30 min later, in the afternoon and evening over four nonconsecutive days. SES-cortisol phenotypic associations were specific to the adolescence period. Specifically, higher awakening cortisol levels were detected in wealthier backgrounds, whereas higher cortisol awakening response (CAR) and diurnal changes were present at both ends of the SES continuum. Moreover, smaller genetic contributions emerged for awakening cortisol in youth from poorer compared to wealthier backgrounds. The results suggest that the relative contribution of inherited factors to awakening cortisol secretion may be enhanced or suppressed depending on the socio-family context, which may help to decipher the mechanisms underlying later adjustment.

Experiencing food insecurity in childhood: influences on eating habits and body weight in young adulthood.

OBJECTIVE: To examine how food insecurity in childhood up to adolescence relates to eating habits and weight status in young adulthood. DESIGN: A longitudinal study design was used to derive trajectories of household food insecurity from age 4·5 to 13 years. Multivariable linear and logistical regression analyses were performed to model associations between being at high risk of food insecurity from age 4·5 to 13 years and both dietary and weight outcomes at age 22 years. SETTING: A birth cohort study conducted in the Province of Quebec, Canada. PARTICIPANTS: In total, 698 young adults participating in the Québec Longitudinal Study of Child Development. RESULTS: After adjusting for sex, maternal education and immigrant status, household income and type of family, being at high risk (compared with low risk) of food insecurity in childhood up to adolescence was associated with consuming higher quantities of sugar-sweetened beverages (ßadj: 0·64; 95 % CI (0·27, 1·00)), non-whole-grain cereal products (ßadj: 0·32; 95 % CI (0·07, 0·56)) and processed meat (ßadj: 0·14; 95 % CI (0·02, 0·25)), with skipping breakfast (ORadj: 1·97; 95 % CI (1·08, 3·53)), with eating meals prepared out of home (ORadj: 3·38; 95 % CI (1·52, 9·02)), with experiencing food insecurity (ORadj: 3·03; 95 % CI (1·91, 4·76)) and with being obese (ORadj: 2·01; 95 % CI (1·12, 3·64)), once reaching young adulthood. CONCLUSION: Growing up in families experiencing food insecurity may negatively influence eating habits and weight status later in life. Our findings reinforce the importance of public health policies and programmes tackling poverty and food insecurity, particularly for families with young children.

Links between peer victimization, dating violence victimization and depression in adolescence: A genetically-informed study.

OBJECTIVE: The current study aimed to test if individuals with inherent dispositions to depression-related cognitions and behaviors are more at risk of experiencing relational difficulties, such as peer victimization and dating violence victimization. METHOD: This study used a genetically informed design with 806 twins (51.5% girls) to test 1) if at least part of the association between peer victimization in school and dating violence victimization in emerging adulthood can be explained by common underlying heritable factors. Participants provided repeated assessments of their peer victimization in school at ages 13 through 17, their depression symptoms at ages 13 through 19, as well as their victimization in dating relationships at age 19. RESULTS: A Cholesky decomposition based on structural equation modeling supported the hypotheses. Specifically, the association between peer victimization and dating violence victimization was to a significant extent explained by common underlying genetic vulnerabilities that were associated with depression symptoms. No sex moderation was found. CONCLUSIONS: The findings highlight the importance of addressing early indicators of vulnerability toward depression symptoms to prevent victimization by peers or dating partners.

Childhood psychopathic traits and mental health outcomes in adolescence: compensatory and protective effects of positive relationships with parents and teachers.

We identified mental health outcomes associated with specific developmental trajectories of psychopathic traits across childhood and tested whether positive relationships with parents and teachers have compensatory or protective effects. Participants were 1401 children (52.82% girls) from the Quebec Longitudinal Study of Child Development with available data on teacher-reported psychopathic traits (ages 6-12 years) and self-reported mental health outcomes (ages 15-17 years). Parents and teachers reported their levels of positive relationship with the child (ages 6-8 and 10-12 years). Trajectories of psychopathic traits (High-stable, Increasing, Decreasing, and Low-stable) were included as predictors of mental health outcomes (e.g., conduct disorder, anxiety) in structural equation models controlling for child sex, family SES, and earlier psychopathology. Compensatory effects were tested via main effects of positive relationships and protective effects were tested via their interactive effects with trajectories memberships. When compared to the Low-stable trajectory of psychopathic traits, the High-stable, Increasing, and Decreasing trajectories were associated with distinct sets of mental health outcomes, with children from the Increasing trajectory being at higher risk for both externalizing and internalizing psychopathology. Positive relationships with parents and teachers only partially compensated for these effects. Findings suggest that clinicians cannot expect the detrimental effects associated with psychopathic traits to be entirely prevented by children's positive relationships with parents and/or teachers. This study reinforces the importance of providing intensive preventive interventions to elementary school children with high levels of psychopathic traits to prevent the long-term negative consequences associated with these traits.

Developmental Patterns of Gambling Participation and Substance use Throughout Adolescence in a Population Birth Cohort.

This study investigated adolescents' single and co-occurring developmental patterns of gambling participation and substance use and their association with gambling and substance use-related issues at age 17, controlling for confounders. Multiple assessments from age 12 to 17 were conducted in a population-based cohort (N=1594, 51.2% boys). Latent growth modeling was used to analyze developmental patterns and Generalized linear models to examine their association with age-17 gambling and substance use-related problems, types and variety of activities, and substance abuse. Results revealed six developmental patterns, including Low- or Non-substance Users or Gamblers (24.2% sample), two trajectory-classes of Later-Onset Increasing (to a moderate level) substance users, either with or without gambling participation (7.8% and 45.5%, respectively), two trajectory-classes of Early-Onset Increasing (to a higher level) substance users, either with or without gambling participation (6.2% and 12.7%, respectively), and a smaller trajectory-class of Slow-Increasing Substance Users and Early-Onset Gamblers, declining to non-gambling after age 13 (3.6%). Gambling participation and substance use did not appear to influence each other with regard to their onset and course throughout adolescence, and to age-17 types and variety of gambling activities or substances used, problems related to gambling participation or substance use, or substance abuse. These findings are consistent with the addictive syndrome model and with both common and individualized approaches to prevention and treatment for adolescent gamblers or substance users.

Link Between Peer Victimization in College and Cortisol Secretion: Roles of Genetic Vulnerabilities and Social Support.

It is unclear whether peer victimization in college interacts with genetic vulnerabilities or social support in predicting cortisol secretion. This issue was addressed using a sample of 162 Monozygotic and 237 Dizygotic twin pairs (54% females; 86% Whites, 6% Blacks, 6% Asians, 0.3% Native North Americans). At age 19, participants provided hair for cortisol extraction and reported about victimization in college and support by the mother, father, and best friend. Biometric modeling revealed that environmental influences on cortisol secretion were reduced and genetic influences exacerbated when victimization was high. Moderate to high maternal support mitigated the association between victimization and high cortisol secretion. The findings suggest that victimization in college contributes to physical "wear-and-tear", which may be counteracted by social support.

Childhood Overeating and Disordered Eating From Early Adolescence to Young Adulthood: A Longitudinal Study on the Mediating Role of BMI, Victimization and Desire for Thinness.

Eating disorders have early origins, and there could be a continuum between childhood eating behaviors, such as overeating, and long-term disordered eating, but this remains to be shown. BMI, desire for thinness and peer victimization could influence this continuum, but their interactions are unknown. To fill this gap, the study used data from the Quebec Longitudinal Study of Child Development (N = 1511; 52% girls), in which 30.9% of youth presented a trajectory associated with high disordered eating from 12 to 20 years. The results support an indirect association between overeating at age 5 and disordered eating trajectories, with different mediation processes observed between boys and girls. The findings underscore the importance of promoting healthy body images and eating behaviors among youths.

Changing genetic architecture of body mass index from infancy to early adulthood: an individual based pooled analysis of 25 twin cohorts.

BACKGROUND: Body mass index (BMI) shows strong continuity over childhood and adolescence and high childhood BMI is the strongest predictor of adult obesity. Genetic factors strongly contribute to this continuity, but it is still poorly known how their contribution changes over childhood and adolescence. Thus, we used the genetic twin design to estimate the genetic correlations of BMI from infancy to adulthood and compared them to the genetic correlations of height. METHODS: We pooled individual level data from 25 longitudinal twin cohorts including 38,530 complete twin pairs and having 283,766 longitudinal height and weight measures. The data were analyzed using Cholesky decomposition offering genetic and environmental correlations of BMI and height between all age combinations from 1 to 19 years of age. RESULTS: The genetic correlations of BMI and height were stronger than the trait correlations. For BMI, we found that genetic correlations decreased as the age between the assessments increased, a trend that was especially visible from early to middle childhood. In contrast, for height, the genetic correlations were strong between all ages. Age-to-age correlations between environmental factors shared by co-twins were found for BMI in early childhood but disappeared altogether by middle childhood. For height, shared environmental correlations persisted from infancy to adulthood. CONCLUSIONS: Our results suggest that the genes affecting BMI change over childhood and adolescence leading to decreasing age-to-age genetic correlations. This change is especially visible from early to middle childhood indicating that new genetic factors start to affect BMI in middle childhood. Identifying mediating pathways of these genetic factors can open possibilities for interventions, especially for those children with high genetic predisposition to adult obesity.