Weak and uneven associations of home, neighborhood, and school environments with stress hormone output across multiple timescales.

The progression of lifelong trajectories of socioeconomic inequalities in health and mortality begins in childhood. Dysregulation in cortisol, a stress hormone that is the primary output of the hypothalamus-pituitary-adrenal (HPA) axis, has been hypothesized to be a mechanism for how early environmental adversity compromises health. However, despite the popularity of cortisol as a biomarker for stress and adversity, little is known about whether cortisol output differs in children being raised in socioeconomically disadvantaged environments. Here, we show that there are few differences between advantaged and disadvantaged children in their cortisol output. In 8-14-year-old children from the population-based Texas Twin Project, we measured cortisol output at three different timescales: (a) diurnal fluctuation in salivary cortisol (n = 400), (b) salivary cortisol reactivity and recovery after exposure to the Trier Social Stress Test (n = 444), and (c) cortisol concentration in hair (n = 1210). These measures converged on two moderately correlated, yet distinguishable, dimensions of HPA function. We tested differences in cortisol output across nine aspects of social disadvantage at the home (e.g., family socioeconomic status), school (e.g., average levels of academic achievement), and neighborhood (e.g., concentrated poverty). Children living in neighborhoods with higher concentrated poverty had higher diurnal cortisol output, as measured in saliva; otherwise, child cortisol output was unrelated to any other aspect of social disadvantage. Overall, we find limited support for alteration in HPA axis functioning as a general mechanism for the health consequences of socioeconomic inequality in childhood.

Twin models of environmental and genetic influences on pubertal development, salivary testosterone, and estradiol in adolescence.

OBJECTIVE: Research on sources of variation in adolescent's gonadal hormone levels is limited. We sought to decompose individual differences in adolescent testosterone, estradiol, and pubertal status, into genetic and environmental components. DESIGN: A sample of male and female adolescent twins from the greater Austin and Houston areas provided salivary samples, with a subset of participants providing longitudinal data at 2 waves. PARTICIPANTS: The sample included 902 adolescent twins, 49% female, aged 13-20 years (M = 15.91) from the Texas Twin Project. Thirty-seven per cent of twin pairs were monozygotic; 30% were same-sex dizygotic (DZ) pairs; and 33% were opposite-sex DZ pairs. MEASUREMENTS: Saliva samples were assayed for testosterone and estradiol using chemiluminescence immunoassays. Pubertal status was assessed using self-report. Biometric decompositions were performed using multivariate quantitative genetic models. RESULTS: Genetic factors contributed substantially to variation in testosterone in males and females in the follicular phase of their menstrual cycle (h2  = 60% and 51%, respectively). Estradiol was also genetically influenced in both sexes, but was predominately influenced by nonshared environmental factors. The correlation between testosterone and estradiol was mediated by a combination of genetic and environmental influences for males and females. Genetic and environmental influences on hormonal concentrations were only weakly correlated with self-reported pubertal status, particularly for females. CONCLUSIONS: Between-person variability in adolescent gonadal hormones and their interrelationship reflects both genetic and environmental processes, with both testosterone and estradiol containing sizeable heritable components.

Hair and Salivary Testosterone, Hair Cortisol, and Externalizing Behaviors in Adolescents.

Although testosterone is associated with aggression in the popular imagination, previous research on the links between testosterone and human aggression has been inconsistent. This inconsistency might be because testosterone's effects on aggression depend on other moderators. In a large adolescent sample ( N = 984, of whom 460 provided hair samples), we examined associations between aggression and salivary testosterone, hair testosterone, and hair cortisol. Callous-unemotional traits, parental monitoring, and peer environment were examined as potential moderators of hormone-behavior associations. Salivary testosterone was not associated with aggression. Hair testosterone significantly predicted increased aggression, particularly at low levels of hair cortisol (i.e., Testosterone × Cortisol interaction). This study is the first to examine the relationship between hair hormones and externalizing behaviors and adds to the growing literature that indicates that androgenic effects on human behavior are contingent on aspects of the broader endocrine environment-in particular, levels of cortisol.

Genetic and environmental influences on testosterone in adolescents: evidence for sex differences.

The current study investigated genetic and environmental influences on salivary testosterone during adolescence, using data from 49 pairs of monozygotic twins and 68 pairs of dizygotic twins, ages 14-19 years (M = 16.0 years). Analyses tested for sex differences in genetic and environmental influences on testosterone and its relation to pubertal development. Among adolescent males, individual differences in testosterone were heritable (55%) and significantly associated with self-reported pubertal status (controlling for age) via common genetic influences. In contrast, there was minimal heritable variation in testosterone for females, and testosterone in females was not significantly associated with pubertal status after controlling for age. Rather, environmental influences shared by twins raised together accounted for nearly all of the familial similarity in female testosterone. This study adds to a small but growing body of research that investigates genetic influences on individual differences in behaviorally relevant hormones.

An in-laboratory stressor reveals unique genetic variation in child cortisol output.

Dysregulation of biological stress response, as measured by cortisol output, has been a primary candidate mechanism for how social experiences become biologically embedded. Cortisol is the primary output of the hypothalamic pituitary adrenal (HPA) axis. Cortisol levels vary systematically across the day and change in response to both sudden, acute stress experiences as well as prolonged exposure to environmental stress. Using data from 8- to 15-year-old twins in the Texas Twin Project, we investigate the extent to which genetic influences are shared across different measures of cortisol output: chronic cortisol accumulations in hair (n = 1,104), diurnal variation in salivary output (n = 488), and salivary response to a standardized, acute in-laboratory stressor (n = 537). Multivariate twin models indicate that genetic factors regulating cortisol response to the in-laboratory stressor are separable from those regulating baseline cortisol levels, naturally occurring diurnal variation in cortisol, and hair cortisol levels. These findings illustrate that novel environments can reveal unique genetic variation, reordering people in terms of their observed phenotype rather than only magnifying or mitigating preexisting differences. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

Socioeconomic Disadvantage and the Pace of Biological Aging in Children.

BACKGROUND AND OBJECTIVES: Children who grow up in socioeconomic disadvantage face increased burden of disease and disability throughout their lives. One hypothesized mechanism for this increased burden is that early-life disadvantage accelerates biological processes of aging, increasing vulnerability to subsequent disease. To evaluate this hypothesis and the potential impact of preventive interventions, measures are needed that can quantify early acceleration of biological aging in childhood. METHODS: Saliva DNA methylation and socioeconomic circumstances were measured in N = 600 children and adolescents aged 8 to 18 years (48% female) participating in the Texas Twin Project. We measured pace of biological aging using the DunedinPoAm DNA methylation algorithm, developed to quantify the pace-of-aging-related decline in system integrity. We tested if children in more disadvantaged families and neighborhoods exhibited a faster pace of aging as compared with children in more affluent contexts. RESULTS: Children living in more disadvantaged families and neighborhoods exhibited a faster DunedinPoAm-measured pace of aging (r = 0.18; P = .001 for both). Latinx-identifying children exhibited a faster DunedinPoAm-measured pace of aging compared with both White- and Latinx White-identifying children, consistent with higher levels of disadvantage in this group. Children with more advanced pubertal development, higher BMI, and more tobacco exposure exhibited faster a faster DunedinPoAm-measured pace of aging. However, DunedinPoAm-measured pace of aging associations with socioeconomic disadvantage were robust to control for these factors. CONCLUSIONS: Children growing up under conditions of socioeconomic disadvantage exhibit a faster pace of biological aging. DNA methylation pace of aging might be useful as a surrogate end point in evaluation of programs and policies to address the childhood social determinants of lifelong health disparities.

Hormones: empirical contribution. Cortisol reactivity and recovery in the context of adolescent personality disorder.

The present study examined whether the associations between stress responses and psychopathology were moderated by adolescent personality disorder (PD) traits. Participants were a community sample of 106 adolescents (47 male, Mage = 16.01) and their parents. Parents reported on adolescents' PD traits and behavioral problems. Changes in salivary cortisol were assessed in response to a laboratory-based stress induction. Moderated regression analyses revealed significant linear and quadratic interactions between cortisol recovery and PD traits in the prediction of behavioral problems. Although typically conceptualized as "adaptive," steeper poststressor recovery was associated with more behavioral problems when PD traits were high. These findings suggest that, in the presence of maladaptive personality traits, premature recovery from environmental stressors may indicate an inability to respond appropriately to negative environmental stimuli, thus reflecting a core disturbance in PD trait functioning. The results underscore the informative role that personality plays in illuminating the nature of hormone functioning in adolescents and are interpreted in a developmental psychopathology framework.