These findings suggest that, at least in healthy young males, adverse childhood events are associated with changes in HPA-axis functioning. Longitudinal studies are needed to investigate whether the blunted cortisol response is a risk factor in the etiology of psychiatric disorders or rather reflects resiliency with regard to the development of psychopathology.

The development of biological markers of aging has primarily focused on adult samples. Epigenetic clocks are a promising tool for measuring biological age that show impressive accuracy across most tissues and age ranges. In adults, deviations from the DNA methylation (DNAm) age prediction are correlated with several age-related phenotypes, such as mortality and frailty. In children, however, fewer such associations have been made, possibly because DNAm changes are more dynamic in pediatric populations as compared to adults. To address this gap, we aimed to develop a highly accurate, noninvasive, biological measure of age specific to pediatric samples using buccal epithelial cell DNAm. We gathered 1,721 genome-wide DNAm profiles from 11 different cohorts of typically developing individuals aged 0 to 20 y old. Elastic net penalized regression was used to select 94 CpG sites from a training dataset (n = 1,032), with performance assessed in a separate test dataset (n = 689). DNAm at these 94 CpG sites was highly predictive of age in the test cohort (median absolute error = 0.35 y). The Pediatric-Buccal-Epigenetic (PedBE) clock was characterized in additional cohorts, showcasing the accuracy in longitudinal data, the performance in nonbuccal tissues and adult age ranges, and the association with obstetric outcomes. The PedBE tool for measuring biological age in children might help in understanding the environmental and contextual factors that shape the DNA methylome during child development, and how it, in turn, might relate to child health and disease.

Early life factors can shape the development of hypothalamic pituitary adrenal (HPA) axis. Maternal prenatal stress might constitute such an early environmental factor. As little is known about the relation between maternal prenatal stress and cortisol reactivity in human offspring, we performed a longitudinal study including four assessments of infant cortisol reactivity to stressful events in a non-clinical population. General and pregnancy-related feelings of stress and anxiety, as well as circadian cortisol levels, were measured in 173 mothers in the last trimester of pregnancy. Infant cortisol reactivity was measured at 5 weeks to a bathing session, at 8 weeks to a vaccination, at 5 months to a stressful mother-infant interaction (still face procedure), and at 12 months to a maternal separation (strange situation procedure). Maternal prenatal fear of bearing a handicapped child was a consistent predictor of infant cortisol reactivity. Although the effects were mild, higher fear was significantly related to higher salivary cortisol reactivity to the bathing session and to decreased cortisol reactivity to vaccination and maternal separation. Thus, pregnancy-specific anxieties predict infant cortisol reactivity in the first year of life, but the direction of the effect depends on infant age and/or the nature of the stressor. While this specific anxiety was a better predictor than stress experience or maternal cortisol concentrations, the underlying mechanisms of these associations remain unclear. Future studies should try to incorporate multiple measures of HPA-axis reactivity during development when studying the long-term consequences of maternal prenatal stress.

BackgroundProlonged cardiac activity that exceeds metabolic needs can be detrimental for somatic health. Psychological stress could result in such “additional cardiac activity.”PurposeIn this study, we examined whether prolonged additional reductions in heart rate variability (AddHRVr) can be measured in daily life with an algorithm that filters out changes in HRV that are purely due to metabolic demand, as indexed by movement, using a brief calibration procedure. We tested whether these AddHRVr periods were related to worry, stress, and negative emotions.MethodsMovement and the root of the mean square of successive differences (RMSSD) in heart rate were measured during a calibration phase and the subsequent 24 h in 32 participants. Worry, stress, explicit and implicit emotions were assessed hourly using smartphones. The Levels of Emotional Awareness Scale and resting HRV were used to account for individual differences. During calibration, person-specific relations between movement and RMSSD were determined. The 24-h data were used to detect prolonged periods (i.e., 7.5 min) of AddHRVr.ResultsAddHRVr periods were associated with worrying, with decreased explicit positive affect, and with increased tension, but not with the frequency of stressful events or implicit emotions. Only in people high in emotional awareness and high in resting HRV did changes in AddHRVr covary with changes in explicit emotions.ConclusionsThe algorithm can be used to capture prolonged reductions in HRV that are not due to metabolic needs. This enables the real-time assessment of episodes of potentially detrimental cardiac activity and its psychological determinants in daily life.

Mental illness is highly prevalent and runs in families. Mental disorders are considered to enhance the risk for the development of psychopathology in the offspring. This heightened risk is related to the separate and joint effects of inherited genetic vulnerabilities for psychopathology and environmental influences. The early years of life are suggested to be a key developmental phase in the intergenerational psychopathology transmission. Available evidence supports the idea that early exposure to parental psychopathology, during the pregnancy and first postpartum year, may be related to child psychological functioning beyond the postpartum period, up to adulthood years. This not only highlights the importance of intervening early to break the chain of intergenerational transmission of psychopathology but also raises the question of whether early interventions targeting parental mental disorders in this period may alleviate these prolonged adverse effects in the infant offspring. The current article focuses on the specific risk of psychopathology conveyed from mentally ill parents to the offspring during the pregnancy and first postpartum year. We first present a summary of the available evidence on the associations of parental perinatal mental illness with infant psychological outcomes at the behavioral, biological, and neurophysiological levels. Next, we address the effects of early interventions and discuss whether these may mitigate the early intergenerational transmission of risk for psychopathology. The summarized evidence supports the idea that psychopathology-related changes in parents’ behavior and physiology in the perinatal period are related to behavioral, biological, and neurophysiological correlates of infant psychological functioning in this period. These alterations may constitute risk for later development of child and/or adult forms of psychopathology and thus for intergenerational transmission. Targeting psychopathology or mother-infant interactions in isolation in the postnatal period may not be sufficient to improve outcomes, whereas interventions targeting both maternal psychopathology and mother-infant interactions seem promising in alleviating the risk of early transmission.

a b s t r a c tBackground: While acute cortisol administration has been found to impair retrieval of emotional memories in healthy subjects, the duration of this memory impairment is still unknown. Propranolol, on the other hand, may impair the reconsolidation of emotional memories during reactivation, although human studies examining such effects are scarce. The present investigation was therefore undertaken to examine the immediate and prolonged effects of a single administered dose of cortisol or propranolol on memory retrieval in a double-blind placebo controlled design. Methods: Eighty-five healthy male participants were asked to retrieve previously learned emotional and neutral information after ingestion of 35 mg cortisol, 80 mg propranolol or placebo. After a washout period of 1 week, recall was again tested. Results: Memory retrieval of neutral and emotional information was impaired by a single dose of cortisol compared to placebo. The memory impairment due to cortisol remained, even after a washout period of 1 week. No immediate or prolonged effects of propranolol on memory retrieval were found, despite significant reductions in sympathetic arousal. Conclusions: These results lend support to the hypothesis that cortisol is able to attenuate (emotional) memory recall in men over longer time spans and may therefore augment the treatment of disorders like post-traumatic stress disorder and phobias, but do not clarify the mechanism(s) through which propranolol exerts its therapeutic effects.

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Oxytocin increases orienting of attention in response to emotional gaze cues, both for happy and fearful expressions. Replication is needed in female and clinical populations. Effects of oxytocin on early, automatic processing levels should be studied in relation to previously found pro-social and behavioral effects of oxytocin.