Early risk for child externalising symptoms: Examining genetic, prenatal, temperamental and parental influences.

This study utilized the Early Growth and Development Study (N = 561 adoptive children; 57.2% male, 55.3% White), a study of children adopted at birth, to examine heritable (birth parent psychopathology) and prenatal risk (prenatal maternal distress and smoking during pregnancy), infant negative affectivity, adoptive parent over-reactivity and warmth as independent predictors of childhood externalizing symptoms. The current study evaluated if: (1) infant negative affectivity and over-reactive parenting are candidate mediators for the effects of heritable and prenatal risk on externalizing symptoms and (2) parental warmth weakens the influence of heritable risk, prenatal risk, negative affectivity, and over-reactive parenting on externalizing symptoms. There were main effects of heritable risk, infant negative affectivity, and over-reactive parenting on child externalizing symptoms. The study found no support for the hypothesized mediation and moderation effects, suggesting that targeting parental over-reactivity rather than warmth would be more effective in reducing risk for childhood externalizing symptoms.

Prenatal programming of developmental trajectories for obesity risk and early pubertal timing.

The thrifty phenotype and fetal overnutrition hypotheses are two developmental hypotheses that originated from the developmental origins of health and disease (DOHaD) perspective. The DOHaD posits that exposures experienced prenatally and early in life may influence health outcomes through altering form and function of internal organs related to metabolic processes. Obesity risk and early pubertal timing might be influenced by similar mechanisms. The thrifty phenotype hypothesis is primarily characterized by experiencing a deprivation of nutrients during gestation paired with an energy rich postnatal environment. The fetal overnutrition hypothesis says that obesity experienced prenatally will be associated with increased lifetime risk of obesity in the offspring. Both hypotheses were tested by examining developmental pathways from genetic and prenatal risk through early growth trajectories (birth to 7 years) to pubertal timing at age 11 years. Participants included 361 children adopted at birth (57% male; 57% non-Hispanic White, 11% Black, 9% Hispanic; adoptive family income Mdn = $70,000-$100,000, birth family income Mdn = < $15,000). Associations between boys' childhood body mass index (BMI) and pubertal timing were confounded by genetics, prenatal risk, and early growth. The thrifty phenotype hypothesis was partially supported for boys' childhood BMI (at ages 4 to 7 years). Both hypotheses were partially supported for girls' childhood BMI but not pubertal timing. A novel Gene × Prenatal Risk interaction showed that genetic risk predicted girls' childhood BMI most strongly at adequate compared with at excessive levels of gestational weight gain. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

Analysis of Early-Life Growth and Age at Pubertal Onset in US Children.

Importance: Earlier pubertal onset may be associated with an increased risk of chronic diseases. However, the extent to which growth in the first 5 years of life-an important developmental life stage that lays the foundation for later health outcomes-is associated with pubertal onset remains understudied. Objective: To assess whether changes in weight, length or height, and body mass index (BMI, calculated as weight in kilograms divided by height in meters squared) during the first 5 years of life are associated with earlier pubertal onset. Design, Setting, and Participants: This cohort study used data from 36 cohorts participating in the Environmental Influences on Child Health Outcomes program from January 1, 1986, to December 31, 2015. Participant inclusion required at least 1 anthropometric measure in the first 5 years of life and at least 1 measure of pubertal onset. Data were analyzed from January 1 to June 30, 2021. Exposures: Standardized velocities of weight, length or height, and BMI gain in early infancy (0-0.5 years), late infancy (0.5-2 years), and early childhood (2-5 years). Main Outcomes and Measures: Markers of pubertal onset for boys and girls, including age at peak height velocity (APHV), time to puberty score greater than 1, time to Tanner pubic hair stage greater than 1, and time to menarche. Multivariable regression models were used to estimate mean differences in APHV by growth periods. Results: Of 7495 children included in the study, 3772 (50.3%) were girls, 4505 (60.1%) were White individuals, and 6307 (84.1%) were born during or after the year 2000. Girls had a younger APHV (10.8 vs 12.9 years) than boys. In boys, faster weight gain (per 1-SD increase) in early infancy (ß, -0.08 years; 95% CI, -0.10 to -0.06), late infancy (ß, -0.10 years; 95% CI, -0.12 to -0.08), and early childhood (ß, -0.07 years; 95% CI, -0.08 to -0.05) was associated with younger APHV after adjusting for the child's birth year, race, and Hispanic ethnicity as well as maternal age at delivery; educational level during pregnancy; annual household income during pregnancy; prenatal cigarette smoking; whether the mother was nulliparous; whether the mother had gestational diabetes, hypertension, or preeclampsia; mode of delivery; prepregnancy BMI; gestational weight gain; and gestational age at delivery. Similar associations were observed for length or height and BMI gains during the same age periods. In girls, faster gains (per 1-SD increase) in weight (ß, -0.03 years; 95% CI, -0.05 to -0.01) and height (ß, -0.02 years; 95% CI, -0.04 to 0.00) in early childhood were associated with younger APHV. Faster BMI gain in late infancy was associated with earlier time to menarche, whereas faster BMI gain in early childhood was associated with earlier time to Tanner pubic hair stage greater than 1. Conclusions and Relevance: This cohort study found that faster gains in weight, length or height, or BMI in early life were associated with earlier pubertal onset. The results suggest that children who experience faster early growth should be monitored closely for earlier onset of puberty and referred as appropriate for supportive services.

Surviving winter on the Qinghai-Tibetan Plateau: Pikas suppress energy demands and exploit yak feces to survive winter.

The Qinghai-Tibetan Plateau, with low precipitation, low oxygen partial pressure, and temperatures routinely dropping below -30 °C in winter, presents several physiological challenges to its fauna. Yet it is home to many endemic mammalian species, including the plateau pika (Ochotona curzoniae). How these small animals that are incapable of hibernation survive the winter is an enigma. Measurements of daily energy expenditure (DEE) using the doubly labeled water method show that pikas suppress their DEE during winter. At the same body weight, pikas in winter expend 29.7% less than in summer, despite ambient temperatures being approximately 25 °C lower. Combined with resting metabolic rates (RMRs), this gives them an exceptionally low metabolic scope in winter (DEE/RMRt = 1.60 ± 0.30; RMRt is resting metabolic rate at thermoneutrality). Using implanted body temperature loggers and filming in the wild, we show that this is achieved by reducing body temperature and physical activity. Thyroid hormone (T3 and T4) measurements indicate this metabolic suppression is probably mediated via the thyroid axis. Winter activity was lower at sites where domestic yak (Bos grunniens) densities were higher. Pikas supplement their food intake at these sites by eating yak feces, demonstrated by direct observation, identification of yak DNA in pika stomach contents, and greater convergence in the yak/pika microbiotas in winter. This interspecific coprophagy allows pikas to thrive where yak are abundant and partially explains why pika densities are higher where domestic yak, their supposed direct competitors for food, are more abundant.

Assay validation of hair androgens across the menstrual cycle.

INTRODUCTION: Saliva is a common noninvasive biofluid for measuring stress and sex hormones, yet one pressing limitation is that salivary hormones fluctuate momentarily, daily, and (for girls) across the menstrual cycle. Hair steroid assays are thought to provide a cumulative index which collapses across hormonal variability, potentially eliminating the confound of daily and menstrual cyclicity and thereby reflecting individual differences in average hormone levels. Here we seek to validate a hair bioassay methodology and test whether hair androgens accurately measure long-term, stable androgen levels in emerging adult women across two menstrual cycles. METHODS: Hair samples were collected at the end of each menstrual cycle for two cycles, and saliva samples were collected in the morning once per week across two menstrual cycles (N = 11 women). Hair samples were segmented by 1 cm for the first 4 cm to reflect the hormone levels of the past four serial months. Hair samples were assayed using commercially-available enzyme-immuno-assays for testosterone and DHEA. RESULTS: Hair androgen concentrations were significantly correlated with averaged saliva hormone levels (DHEA: r = .75, p < .05; Testosterone: r = .67, p < .05). With respect to hair hormone stability, there were significant correlations for almost all the pairs of two 1 cm hair segments collected in two months that corresponded to the same time period. Hair androgens in one segment were significantly correlated with those in next segment. Regarding salivary androgen stability, the intra-class correlation across the weekly saliva samples indicated that for DHEA 59% of the total variance was within person and 41% was between person; and for testosterone 91% of the total variance was between person, and only 9% within person. DISCUSSION: Results suggest that a one-time measure of hair provides a valid and reliable estimate of average steroid levels across two months. Moreover, whereas saliva measures of androgen levels capture week-to-week fluctuations in steroids, hair samples provide information on individual differences in average exposure to steroids, across long periods of time, such as months. Results are encouraging that hair DHEA and testosterone reflects the cumulative hormonal concentration and can be used as a stable hormonal index. Results also indicate that it is feasible to collect the first 3-4 centimeters of hair for studies of stable hormone levels.