Acquisition of the counting principles during the subset-knower stages: Insights from children's errors.

Studies on children's understanding of counting examine when and how children acquire the cardinal principle: the idea that the last word in a counted set reflects the cardinal value of the set. Using Wynn's (1990) Give-N Task, researchers classify children who can count to generate large sets as having acquired the cardinal principle (cardinal-principle-knowers) and those who cannot as lacking knowledge of it (subset-knowers). However, recent studies have provided a more nuanced view of number word acquisition. Here, we explore this view by examining the developmental progression of the counting principles with an aim to elucidate the gradual elements that lead to children successfully generating sets and being classified as CP-knowers on the Give-N Task. Specifically, we test the claim that subset-knowers lack cardinal principle knowledge by separating children's understanding of the cardinal principle from their ability to apply and implement counting procedures. We also ask when knowledge of Gelman & Gallistel's (1978) other how-to-count principles emerge in development. We analyzed how often children violated the three how-to-count principles in a secondary analysis of Give-N data (N = 86). We found that children already have knowledge of the cardinal principle prior to becoming CP-knowers, and that understanding of the stable-order and word-object correspondence principles likely emerged earlier. These results suggest that gradual development may best characterize children's acquisition of the counting principles and that learning to coordinate all three principles represents an additional step beyond learning them individually.

I know that voice! Mothers' voices influence children's perceptions of emotional intensity.

The ability to interpret others' emotions is a critical skill for children's socioemotional functioning. Although research has emphasized facial emotion expressions, children are also constantly required to interpret vocal emotion expressed at or around them by individuals who are both familiar and unfamiliar to them. The current study examined how speaker familiarity, specific emotions, and the acoustic properties that comprise affective prosody influenced children's interpretations of emotional intensity. Participants were 51 7- and 8-year-olds presented with speech stimuli spoken in happy, angry, sad, and nonemotional prosodies by both each child's mother and another child's mother unfamiliar to the target child. Analyses indicated that children rated their own mothers as more intensely emotional compared with the unfamiliar mothers and that this effect was specific to angry and happy prosodies. Furthermore, the acoustic properties predicted children's emotional intensity ratings in different patterns for each emotion. The results are discussed in terms of the significance of the mother's voice in children's development of emotional understanding.

Accelerated DNA Methylation Age: Associations With Posttraumatic Stress Disorder and Mortality.

OBJECTIVE: Recently developed indices of cellular age based on DNA methylation (DNAm) data, referred to as DNAm age, are being used to study factors that influence the rate of aging and the health correlates of these metrics of the epigenetic clock. This study evaluated associations between trauma exposure, posttraumatic stress disorder (PTSD) symptoms, and accelerated versus decelerated DNAm age among military veterans. We also examined whether accelerated DNAm age predicted mortality over the course of a 6.5-year medical record review period. METHODS: Three hundred thirty-nine genotype-confirmed white, non-Hispanic, middle-aged, trauma-exposed veterans underwent psychiatric assessment and genome-wide DNAm analysis. DNAm age was calculated using a previously validated algorithm. Medical records were available for a subset of 241 veterans and were reviewed approximately 6.5 years after DNA collection and PTSD assessment. RESULTS: PTSD hyperarousal symptoms were associated with accelerated DNAm age (ß = 0.20, p = .009) but trauma exposure and total PTSD severity were not. Accelerated DNAm age was also associated with 13% increased risk for all-cause mortality (hazard ratio = 1.13, 95% confidence interval = 1.01-1.26) during the medical record review period. CONCLUSIONS: Findings of this study replicate the association between PTSD and accelerated DNAm age and suggest that this effect may be specific to the hyperarousal symptom cluster. Results point to the potential utility of DNAm age algorithms for identifying individuals who are aging at an accelerated rate and for determining the factors that influence this process.

Stress-Generative Effects of Posttraumatic Stress Disorder: Transactional Associations Between Posttraumatic Stress Disorder and Stressful Life Events in a Longitudinal Sample.

Longitudinal studies have demonstrated transactional associations between psychopathology and stressful life events (SLEs), such that psychopathology predicts the occurrence of new SLEs, and SLEs in turn predict increasing symptom severity. The association between posttraumatic stress disorder (PTSD), specifically, and stress generation remains unclear. This study used temporally sequenced data from 116 veterans (87.9% male) to examine whether PTSD symptoms predicted new onset SLEs, and if these SLEs were associated with subsequent PTSD severity. The SLEs were objectively rated, using a clinician-administered interview and consensus-rating approach, to assess the severity, frequency, and personal dependence (i.e., if the event was due to factors that were independent of or dependent on the individual) of new-onset SLEs. A series of mediation models were tested, and results provided evidence for moderated mediation whereby baseline PTSD severity robustly predicted personally dependent SLEs, B = 0.03, p = .006, and dependent SLEs predicted increases in follow-up PTSD symptom severity, B = -0.04, p = .003, among participants with relatively lower baseline PTSD severity. After we controlled for baseline PTSD severity, personality traits marked by low constraint (i.e., high impulsivity) were also associated with an increased number of dependent SLEs. Our results provide evidence for a stress-generative role of PTSD and highlight the importance of developing interventions aimed at reducing the occurrence of personally dependent stressors.

Posttraumatic Stress Disorder Symptoms, Temperament, and the Pathway to Cellular Senescence.

Traumatic stress is thought to be associated with shortened telomere length (TL) in leukocytes, an age-related marker of increased risk for cellular senescence, although findings thus far have been mixed. We assessed associations between posttraumatic stress disorder (PTSD) symptom severity, temperament, and TL in a sample of 453 White, non-Hispanic, middle-aged, trauma-exposed male and female veterans and civilians. Given that prior research has suggested an association between PTSD and accelerated cellular age, we also examined associations between TL and an index of accelerated cellular age derived from DNA methylation data (DNAm age). Analyses revealed that, controlling for chronological age, PTSD was not directly associated with TL but rather this association was moderated by age, ß = -.14, p = .003, ΔR2 = .02. Specifically, PTSD severity evidenced a stronger negative association with TL among relatively older participants (≥ 55 years of age). In a subset of veterans with data pertaining to temperament (n = 150), positive emotionality, and, specifically, a drive toward achievement, ß = .26, p = .002, ΔR2 = .06, were positively associated with TL. There was no evidence of an association between age-adjusted TL and accelerated DNAm age. Collectively, these results indicate that older adults may be more vulnerable to the negative health effects of PTSD but that traits such as achievement, resilience, and psychological hardiness may be protective. These findings underscore the importance of identifying reliable biomarkers of cellular aging and senescence and of determining the biological mechanisms that contribute to stress-related disease and decline.

Contributions of polygenic risk for obesity to PTSD-related metabolic syndrome and cortical thickness.

BACKGROUND: Research suggests that posttraumatic stress disorder (PTSD) is associated with metabolic syndrome (MetS) and that PTSD-associated MetS is related to decreased cortical thickness. However, the role of genetic factors in these associations is unclear. This study evaluated contributions of polygenic obesity risk and PTSD to MetS and of MetS and polygenic obesity risk to cortical thickness. METHODS: 196 white, non-Hispanic veterans of the wars in Iraq and Afghanistan underwent clinical diagnostic interviews, physiological assessments, and genome-wide genotyping; 168 also completed magnetic resonance imaging scans. Polygenic risk scores (PRSs) for obesity were calculated from results of a prior genome-wide association study (Speliotes et al., 2010) and PTSD and MetS severity factor scores were obtained. RESULTS: Obesity PRS (ß=0.15, p=0.009) and PTSD (ß=0.17, p=0.005) predicted MetS and interacted such that the association between PTSD and MetS was stronger in individuals with greater polygenic obesity risk (ß=0.13, p=0.02). Whole-brain vertex-wise analyses suggested that obesity PRS interacted with MetS to predict decreased cortical thickness in left rostral middle frontal gyrus (ß=-0.40, p<0.001). CONCLUSIONS: Results suggest that PTSD, genetic variability, and MetS are related in a transactional fashion wherein obesity genetic risk increases stress-related metabolic pathology, and compounds the ill health effects of MetS on the brain. Genetic proclivity towards MetS should be considered in PTSD patients when prescribing psychotropic medications with adverse metabolic profiles. Results are consistent with a growing literature suggestive of PTSD-related accelerated aging.

Listening in: An Alternative Method for Measuring the Family Emotional Environment.

The family emotional environment influences children's development of emotion regulation in various ways. Children's difficulties with effectively regulating emotions, in turn, can contribute to the development of psychopathology. However, the pathways that explain how environmental emotion-including overheard emotion among family members-influences children's development of healthy or problematic emotion regulation are unclear. In this article, we briefly discuss the most common methods (e.g., questionnaires, laboratory observations) used to assess emotion in the family. We consider the benefits and limitations of these methods and discuss the need for objective measurement of the family emotional environment. We include a description of the Electronically Activated Recorder (EAR), which provides unobtrusive, extended sampling of the emotional tone of family interaction in the home. We present preliminary evidence of its use with 7- and 8-year-old and their families during one day at home. The method reveals that objectively assessed parent-to-parent interactions that are negatively toned, but not parental self-report of conflict or expressivity, are associated with children's self-reported emotional reactions to hearing independently recorded clips of their mothers' voices during simulated angry interactions. The finding suggests unique contributions of objective, unobtrusive, extended measurement of the family emotional environment to understanding aspects of children's emotional development that may not be captured with other commonly used methods. We discuss future directions that explore how EAR may be used to further our knowledge of the pathways between environmental emotion as a risk factor that influences children's emotional functioning and their psychological well-being.

Psychometric Properties of the Dissociative Subtype of PTSD Scale: Replication and Extension in a Clinical Sample of Trauma-Exposed Veterans.

The addition of the dissociative subtype of posttraumatic stress disorder (PTSD) to the DSM-5 has spurred investigation of its genetic, neurobiological, and treatment response correlates. In order to reliably assess the subtype, we developed the Dissociative Subtype of PTSD Scale (DSPS; Wolf et al., 2017), a 15-item index of dissociative features. Our initial investigation of the dichotomous DSPS lifetime items in a veteran epidemiological sample demonstrated its ability to identify the subtype, supported a three-factor measurement structure, distinguished the three subscales from the normal-range trait of absorption, and demonstrated the greater contribution of derealization and depersonalization symptoms relative to other dissociative symptomatology. In this study, we replicated and extended these findings by administering self-report and interview versions of the DSPS, and assessing personality and PTSD in a sample of 209 trauma-exposed veterans (83.73% male, 57.9% with probable current PTSD). Results replicated the three-factor structure using confirmatory factor analysis of current symptom severity interview items, and the identification of the dissociative subtype (via latent profile analysis). Associations with personality supported the discriminant validity of the DSPS and suggested the subtype was marked by tendencies towards odd and unusual cognitive experiences and low positive affect. Receiver operating characteristic curves identified diagnostic cut-points on the DSPS to inform subtype classification, which differed across the interview and self-report versions. Overall, the DSPS performed well in psychometric analyses, and results support the utility of the measure in identifying this important component of posttraumatic psychopathology.

Posttraumatic Stress Disorder as a Catalyst for the Association Between Metabolic Syndrome and Reduced Cortical Thickness.

BACKGROUND: Metabolic syndrome (MetS), defined by a constellation of cardiometabolic pathologies, is highly prevalent among veterans, especially veterans with posttraumatic stress disorder (PTSD), and poses a major risk for adverse health outcomes, including neurodegeneration and mortality. Given this, we evaluated 1) the association between MetS and neural integrity, indexed by cortical thickness; 2) the relationship between PTSD and MetS; and 3) whether PTSD was associated with cortical thickness indirectly through MetS. METHODS: The sample consisted of 346 U.S. military veterans (89.3% male; 71.4% white) who deployed to Iraq, Afghanistan, or both. Neuroimaging data were available for 274 participants. RESULTS: In whole-brain analyses, MetS was negatively associated with cortical thickness in two left and four right hemisphere regions, as follows: bilateral temporal lobe, including temporal pole, fusiform gyrus, and insula, and extending into occipital cortex (left hemisphere) and orbitofrontal cortex (right hemisphere); bilateral precuneus, posterior cingulate, calcarine, and occipital-parietal cortex; and right rostral anterior cingulate cortex and central sulcus/postcentral gyrus. Path models showed that PTSD predicted MetS (ß = .19, p < .001), which was associated with reduced cortical thickness (ß = -.29 to -.43, all p < .001). CONCLUSIONS: Results from this young veteran sample provide evidence that PTSD confers risk for cardiometabolic pathology and neurodegeneration and raise concern that this cohort may be aging prematurely and at risk for substantial medical and cognitive decline. This study highlights the need to identify the molecular mechanisms linking PTSD to MetS and effective interventions to reduce PTSD-related health comorbidities.