Infant inhibited temperament in primates predicts adult behavior, is heritable, and is associated with anxiety-relevant genetic variation.
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ABSTRACT:
SUBMITTER: Fox AS
PROVIDER: S-EPMC8613309 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Maternal biological systems impact infant temperament as early as the prenatal period, though the mechanisms of this association are unknown. Using a prospective, longitudinal design, we found that maternal (N = 89) amplitudes of the late positive potential (LPP) in response to negative stimuli during the second, but not the third, trimester of pregnancy predicted observed and physiological indices of temperamental reactivity in infants at age 4 months. Maternal LPP was positively associated with observed infant fear and negatively associated with frontal EEG asymmetry and cortisol reactivity in infants at age 4 months. Results identify a putative mechanism, early in pregnancy, for the intergenerational transmission of emotional reactivity from mother to infant.
| S-EPMC7316194 | biostudies-literature
Project description:Recent models of psychopathology suggest the presence of a general factor capturing the shared variance among all symptoms along with specific psychopathology factors (e.g., internalizing and externalizing). However, few studies have examined predictors that may serve as transdiagnostic risk factors for general psychopathology from early development. In the current study we examine, for the first time, whether observed and parent-reported infant temperament dimensions prospectively predict general psychopathology as well as specific psychopathology dimensions (e.g., internalizing and externalizing) across childhood. In a longitudinal cohort (N = 291), temperament dimensions were assessed at 4 months of age. Psychopathology symptoms were assessed at 7, 9, and 12 years of age. A bifactor model was used to estimate general, internalizing, and externalizing psychopathology factors. Across behavioral observations and parent-reports, higher motor activity in infancy significantly predicted greater general psychopathology in mid to late childhood. Moreover, low positive affect was predictive of the internalizing-specific factor. Other temperament dimensions were not related with any of the psychopathology factors after accounting for the general psychopathology factor. The results of this study suggest that infant motor activity may act as an early indicator of transdiagnostic risk. Our findings inform the etiology of general psychopathology and have implications for the early identification for children at risk for psychopathology.
| S-EPMC8273182 | biostudies-literature
Project description:Parent emotion socialization refers to the process by which parents impart their values and beliefs about emotion expressivity to their children. Parent emotion socialization requires attention as a construct that develops in its own right. The socialization of child worry, in particular, has implications for children's typical socioemotional development, as well as their maladaptive development towards anxiety outcomes. Existing theories on emotion socialization, anxiety, and parent-child relationships guided our investigation of both maternal anxiety and toddler inhibited temperament as predictors of change in mothers' unsupportive (i.e., distress, punitive, and minimizing) responses to toddler worry across 1 year of toddlerhood. Participants included 139 mother-toddler dyads. Mothers reported on their own anxiety and their emotion socialization responses to toddler worry. We assessed toddler inhibited temperament through a mother-report survey of shyness and observational coding of dysregulated fear. Maternal anxiety but not child inhibited temperament predicted distress reactions and punitive responses, whereas maternal anxiety and toddler dysregulated fear both uniquely predicted minimizing responses. These results support continued investigation of worry socialization as a developmental outcome of both parent and child characteristics.
| S-EPMC8340527 | biostudies-literature
Project description:ObjectiveBehavioral inhibition (BI) is a temperament identified in early childhood that is a risk factor for later social anxiety. However, mechanisms underlying the development of social anxiety remain unclear. To better understand the emergence of social anxiety, longitudinal studies investigating changes at behavioral neural levels are needed.MethodBI was assessed in the laboratory at 2 and 3 years of age (N = 268). Children returned at 12 years, and an electroencephalogram was recorded while children performed a flanker task under 2 conditions: once while believing they were being observed by peers and once while not being observed. This methodology isolated changes in error monitoring (error-related negativity) and behavior (post-error reaction time slowing) as a function of social context. At 12 years, current social anxiety symptoms and lifetime diagnoses of social anxiety were obtained.ResultsChildhood BI prospectively predicted social-specific error-related negativity increases and social anxiety symptoms in adolescence; these symptoms directly related to clinical diagnoses. Serial mediation analysis showed that social error-related negativity changes explained relations between BI and social anxiety symptoms (n = 107) and diagnosis (n = 92), but only insofar as social context also led to increased post-error reaction time slowing (a measure of error preoccupation); this model was not significantly related to generalized anxiety.ConclusionResults extend prior work on socially induced changes in error monitoring and error preoccupation. These measures could index a neurobehavioral mechanism linking BI to adolescent social anxiety symptoms and diagnosis. This mechanism could relate more strongly to social than to generalized anxiety in the peri-adolescent period.
| S-EPMC5975216 | biostudies-literature
Project description:Early theorists (Freud and Darwin) speculated that extremely shy children, or those with anxious temperament, were likely to have anxiety problems as adults. More recent studies demonstrate that these children have heightened responses to potentially threatening situations reacting with intense defensive responses that are characterized by behavioral inhibition (BI) (inhibited motor behavior and decreased vocalizations) and physiological arousal. Confirming the earlier impressions, data now demonstrate that children with this disposition are at increased risk to develop anxiety, depression, and comorbid substance abuse. Additional key features of anxious temperament are that it appears at a young age, it is a stable characteristic of individuals, and even in non-threatening environments it is associated with increased psychic anxiety and somatic tension. To understand the neural underpinnings of anxious temperament, we performed imaging studies with 18-fluoro-deoxyglucose (FDG) high-resolution Positron Emission Tomography (PET) in young rhesus monkeys. Rhesus monkeys were used because they provide a well validated model of anxious temperament for studies that cannot be performed in human children. Imaging the same animal in stressful and secure contexts, we examined the relation between regional metabolic brain activity and a trait-like measure of anxious temperament that encompasses measures of BI and pituitary-adrenal reactivity. Regardless of context, results demonstrated a trait-like pattern of brain activity (amygdala, bed nucleus of stria terminalis, hippocampus, and periaqueductal gray) that is predictive of individual phenotypic differences. Importantly, individuals with extreme anxious temperament also displayed increased activity of this circuit when assessed in the security of their home environment. These findings suggest that increased activity of this circuit early in life mediates the childhood temperamental risk to develop anxiety and depression. In addition, the findings provide an explanation for why individuals with anxious temperament have difficulty relaxing in environments that others perceive as non-stressful.
| S-EPMC2430534 | biostudies-literature
Project description:BackgroundAutonomic hyperarousal has been proposed as a dispositional risk factor for anxiety disorders (ADs). Therefore, we studied physiological arousal in offspring of fathers and mothers with and without ADs and whether infant hyperarousal predicts subsequent fearful temperament.MethodsInfants (N = 128; age = 4 months) did a novel stimuli task (exposure to visual, olfactory, and acoustic stimuli and an unfamiliar male) and a habituation task (exposure to a repeated acoustic stimulus). Heart rate (HR) and heart rate variability (HRV) were measured during baseline, stimuli and post-stimuli rest. Parents' AD status and severity were measured using a diagnostic interview and their fearful temperament using a questionnaire. Child fearful temperament was measured at 4 months, 1 year and 2.5 years with observations during structured tasks.ResultsParents' fearful temperament (significant in the habituation task), AD status (significant in the novel stimuli task) and AD severity (significant in both tasks) predicted a higher HR in their infants. Infants' higher HR reactivity to novel stimuli and diminished HR recovery at 4 months predicted a more fearful temperament during infancy and toddlerhood. Infants' higher HR at 4 months predicted a more fearful temperament at 2.5 years.ConclusionsParental prenatal anxiety (disorders) predicted infants' autonomic arousal, which in turn predicted later fearful temperament in children. Outcomes suggest that autonomic hyperarousal is a dispositional risk factor of ADs.
| S-EPMC7687129 | biostudies-literature
Project description:Telomere length (TL) is considered an important biomarker of whole-organism health and aging. Across humans and other vertebrates, short telomeres are associated with increased subsequent mortality risk, but the processes responsible for this correlation remain uncertain. A key unanswered question is whether TL-mortality associations arise due to positive effects of genes or early-life environment on both an individual's average lifetime TL and their longevity, or due to more immediate effects of environmental stressors on within-individual TL loss and increased mortality risk. Addressing this question requires longitudinal TL and life history data across the entire lifetimes of many individuals, which are difficult to obtain for long-lived species like humans. Using longitudinal data and samples collected over nearly two decades, as part of a long-term study of wild Soay sheep, we dissected an observed positive association between TL and subsequent survival using multivariate quantitative genetic models. We found no evidence that telomere attrition was associated with increased mortality risk, suggesting that TL is not an important marker of biological aging or exposure to environmental stress in our study system. Instead, we find that among-individual differences in average TL are associated with increased lifespan. Our analyses suggest that this correlation between an individual's average TL and lifespan has a genetic basis. This demonstrates that TL has the potential to evolve under natural conditions, and suggests an important role of genetics underlying the widespread observation that short telomeres predict mortality.
| S-EPMC8053994 | biostudies-literature
Project description:It is currently unknown whether differences in neural responsiveness to infant cues observed in postpartum affective disturbance are specific to depression/anxiety or are better attributed to a common component of internalizing distress. It is also unknown whether differences in mothers' brain response can be accounted for by effects of past episodes, or if current neural processing of her child may serve as a risk factor for development of future symptoms. Twenty-four mothers from a community-based sample participated in an fMRI session viewing their 3-month- old infant during tasks evoking positive or negative emotion. They were tracked across the ensuing 15 months to monitor changes in affective symptoms. Past and current episodes of depression and anxiety, as well as future symptoms, were used to predict differences in mothers' hemodynamic response to their infant in positive compared to negative emotion contexts. Lower relative activation in largely overlapping brain regions involving frontal lobe structures to own infant positive vs. negative emotion was associated with concurrent (3-month) depression diagnosis and prospective (3-18 month) depression and anxiety symptoms. There was little evidence for impacts of past psychopathology (more limited effect of past anxiety and nonsignificant effect of past depression). Results suggest biased maternal processing of infant emotions during postpartum depression and anxiety is largely accounted for by a shared source of variance (internalizing distress). Furthermore, differential maternal responsiveness to her infant's emotional cues is specifically associated with the perpetuation of postpartum symptoms, as opposed to more general phenotypic or scarring effects of past psychopathology.
| S-EPMC8078806 | biostudies-literature
Project description:In this functional magnetic resonance imaging (fMRI) study we examined neural processing of infant faces associated with a happy or a sad temperament in nulliparous women. We experimentally manipulated adult perception of infant temperament in a probabilistic learning task. In this task, participants learned about an infant's temperament through repeated pairing of the infant face with positive or negative facial expressions and vocalizations. At the end of the task, participants were able to differentiate between "mostly sad" infants who cried often and "mostly happy" infants who laughed often. Afterwards, brain responses to neutral faces of infants with a happy or a sad temperament were measured with fMRI and compared to brain responses to neutral infants with no temperament association. Our findings show that a brief experimental manipulation of temperament can change brain responses to infant signals. We found increased amygdala connectivity with frontal regions and the visual cortex, including the occipital fusiform gyrus, during the perception of infants with a happy temperament. In addition, amygdala connectivity was positively related to the post-manipulation ratings of infant temperament, indicating that amygdala connectivity is involved in the encoding of the rewarding value of an infant with a happy temperament.
| S-EPMC5548834 | biostudies-other
Project description:BACKGROUND:An early-life anxious temperament (AT) is a risk factor for the development of anxiety, depression, and comorbid substance abuse. We validated a nonhuman primate model of early-life AT and identified the dorsal amygdala as a core component of AT's neural circuit. Here, we combine RNA sequencing, viral-vector gene manipulation, functional brain imaging, and behavioral phenotyping to uncover AT's molecular substrates. METHODS:In response to potential threat, AT and brain metabolism were assessed in 46 young rhesus monkeys. We identified AT-related transcripts using RNA-sequencing data from dorsal amygdala tissue (including central nucleus of the amygdala [Ce] and dorsal regions of the basal nucleus). Based on the results, we overexpressed the neurotrophin-3 gene, NTF3, in the dorsal amygdala using intraoperative magnetic resonance imaging-guided surgery (n = 5 per group). RESULTS:This discovery-based approach identified AT-related alterations in the expression of well-established and novel genes, including an inverse association between NTRK3 expression and AT. NTRK3 is an interesting target because it is a relatively unexplored neurotrophic factor that modulates intracellular neuroplasticity pathways. Overexpression of the transcript for NTRK3's endogenous ligand, NTF3, in the dorsal amygdala resulted in reduced AT and altered function in AT's neural circuit. CONCLUSIONS:Together, these data implicate neurotrophin-3/NTRK3 signaling in the dorsal amygdala in mediating primate anxiety. More generally, this approach provides an important step toward understanding the molecular underpinnings of early-life AT and will be useful in guiding the development of treatments to prevent the development of stress-related psychopathology.
| S-EPMC6999854 | biostudies-literature