Adolescents' Personality Development - A Question of Psychosocial Stress.
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ABSTRACT:
SUBMITTER: Raufelder D
PROVIDER: S-EPMC8719601 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Objective: The aim of the current study was to examine the unique and joint contributions of iron deficiency, iron supplementation, and psychosocial stress in infancy and stress in adolescence to neurocognitive functioning in adolescence.Methods: The current study (N = 796; Mage = 14.4y) involved a prospective cohort of low- and middle-socioeconomic status adolescents in Santiago, Chile. As infants, they had participated in an iron supplementation trial. Infant iron status was assessed at 12-18 months, and mothers answered questions about family psychosocial stress at 6-12 months and in adolescence (maternal depressive symptoms, home support for child development, stressful life events, father absence, socioeconomic status, and parental education). Neurocognitive functioning was assessed in adolescence using the Balloon Analogue Risk Task, Stockings of Cambridge, Trail Making Test, Purdue Pegboard Test, and Wisconsin Card Sorting Test.Results: Greater psychosocial stress in infancy predicted less risk-taking, poorer planning abilities and fluid cognition, and slower processing speed in adolescence. Iron deficiency anemia in infancy predicted less risk-taking. Greater adolescent psychosocial stress predicted difficulties in set-shifting. There were no interactions between infant psychosocial stress and iron deficiency predicting adolescent neurocognitive functioning.Conclusion: These results suggest that interventions to reduce infant psychosocial stress may be more likely to prevent multiple neurocognitive deficits in adolescence than interventions to reduce infant iron deficiency.
| S-EPMC7007823 | biostudies-literature
Project description:Exposure to psychosocial stressors and ensuing stress physiology have been associated with spontaneous invasive mammary tumors in the Sprague-Dawley rat model of human breast cancer. Mammary gland (MG) development is a time when physiologic and environmental exposures influence breast cancer risk. However, the effect of psychosocial stress exposure on MG development remains unknown. Here, in the first comprehensive longitudinal study of MG development in nulliparous female rats (from puberty through young adulthood; 8-25 wks of age), we quantify the spatial gradient of differentiation within the MG of socially stressed (isolated) and control (grouped) rats. We then demonstrate that social isolation increased stress reactivity to everyday stressors, resulting in downregulation of glucocorticoid receptor (GR) expression in the MG epithelium. Surprisingly, given that chemical carcinogens increase MG cancer risk by preventing normal terminal end bud (TEB) differentiation, chronic isolation stress did not alter TEBs. Instead, isolation blunted MG growth and alveolobular differentiation and reduced epithelial cell proliferation in these structures. Social isolation also enhanced corpora luteal progesterone at all ages but reduced estrogenization only in early adulthood, a pattern that precludes modulated ovarian function as a sufficient mechanism for the effects of isolation on MG development. This longitudinal study of natural variation provides an integrated view of MG development and the importance of increased GR activation in nulliparous ductal growth and alveolobular differentiation. Thus, social isolation and its physiological sequelae disrupt MG growth and differentiation and suggest a contribution of stress exposure during puberty and young adulthood to the previously observed increase in invasive MG cancer observed in chronically socially-isolated adult Sprague-Dawley rats.
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Project description:BackgroundThe gonadal hormone testosterone not only regulates sexual behavior but is also involved in social behavior and cognition in both sexes. Changes in testosterone secretion in response to stress have been reported. In addition, stress associated mental disorders such as borderline personality disorder (BPD) and posttraumatic stress disorder (PTSD) are characterized by alterations in basal testosterone metabolism. However, testosterone changes to stress have not been investigated in mental disorders such as BPD and PTSD so far.MethodsIn the study described, we investigated testosterone reactivity to an acute psychosocial stressor, the Trier Social Stress Test (TSST). Our sample consisted of young adult women with BPD (n = 28), PTSD (n = 22) or both disorders (n = 22), and healthy control (n = 51). Based on previous studies on basal testosterone secretion in these disorders, we expected the stress-associated testosterone reactivity to be higher in the BPD group and lower in the PTSD group, when compared to the healthy control group.ResultsThe study could demonstrate an increase in testosterone after acute stress exposure across all groups and independent of BPD or PTSD status. Different possible explanations for the absence of a group effect are discussed.ConclusionsFrom the results of this study, we conclude that stress-related changes in testosterone release are not affected by BPD or PTSD status in a female patient population. This study expands the knowledge about changes in gonadal hormones and stress reactivity in these disorders.
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Project description:BACKGROUND:Nociceptin is a key regulator linking environmental stress and alcohol drinking. In a genome-wide methylation analysis, we recently identified an association of a methylated region in the OPRL1 gene with alcohol-use disorders. METHODS:Here, we investigate the biological basis of this observation by analysing psychosocial stressors, methylation of the OPRL1 gene, brain response during reward anticipation and alcohol drinking in 660 fourteen-year-old adolescents of the IMAGEN study. We validate our findings in marchigian sardinian (msP) alcohol-preferring rats that are genetically selected for increased alcohol drinking and stress sensitivity. RESULTS:We found that low methylation levels in intron 1 of OPRL1 are associated with higher psychosocial stress and higher frequency of binge drinking, an effect mediated by OPRL1 methylation. In individuals with low methylation of OPRL1, frequency of binge drinking is associated with stronger BOLD response in the ventral striatum during reward anticipation. In msP rats, we found that stress results in increased alcohol intake and decreased methylation of OPRL1 in the nucleus accumbens. CONCLUSIONS:Our findings describe an epigenetic mechanism that helps to explain how psychosocial stress influences risky alcohol consumption and reward processing, thus contributing to the elucidation of biological mechanisms underlying risk for substance abuse.
| S-EPMC5975104 | biostudies-literature
Project description:IntroductionsAvoidant personality disorder (AVPD) has excessive and pervasive anxiety and discomfort in social situations. The aims of this study were to explore the relationship between AVPD and physical and psychological stress and psychological tests.MethodsWe evaluated 93 AVPD patients and 355 nonpatient controls by salivary amylase and cortisol responses during exposure to the Trier Social Stress Test (TSST) and electrical stimulation stress. Spielberger state-trait anxiety inventory (STAI), Profile of Mood State (POMS), Beck Depression Inventory (BDI), Depression and Anxiety Cognition Scale (DACS), and Childhood Trauma Questionnaire (CTQ) were administered.ResultsFollowing electrical stimulation, salivary cortisol levels in female AVPD decreased significantly less than that in female's controls, but salivary cortisol levels did not show a difference between male AVPD patients and controls. Salivary alpha-amylase (sAA) levels did not show a difference between females or male AVPD patients and controls. Following TSST exposure, sAA levels did not show a difference between females or male AVPD patients and controls. Salivary cortisol levels did not show a difference between females or male AVPD patients and controls. In the AVPD patients, POMS scores were significantly higher compared with the controls. STAI, BDI, DACS scores, and CTQ significantly increased in the AVPD patients compared with the controls. LF in heart rate variability in AVPD significantly increased more compared with controls.ConclusionsThese results suggest that heightened sympathetic reactivity in female AVPD co-occurs with attenuated salivary cortisol responses to electric stimulation stress and there is a significant difference between AVPD and controls in mood, anxiety, social cognition, and automatic nerve systems.
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Project description:Prenatal maternal psychosocial stress might influence the development of childhood asthma. Evaluating paternal psychosocial stress and conducting a sibling comparison could provide further insight into the role of unmeasured confounding. We examined the associations of parental psychosocial stress during and after pregnancy with asthma at age 7 years in the Norwegian Mother and Child Cohort Study (n = 63,626; children born in 2000-2007). Measures of psychosocial stress included lifetime major depressive symptoms, current anxiety/depression symptoms, use of antidepressants, anxiolytics, and/or hypnotics, life satisfaction, relationship satisfaction, work stress, and social support. Childhood asthma was associated with maternal lifetime major depressive symptoms (adjusted relative risk (aRR) = 1.19, 95% confidence interval (CI): 1.09, 1.30), in addition to symptoms of anxiety/depression during pregnancy (aRR = 1.17, 95% CI: 1.06, 1.29) and 6 months after delivery (aRR = 1.17, 95% CI: 1.07, 1.28). Maternal negative life events during pregnancy (aRR = 1.10, 95% CI: 1.06, 1.13) and 6 months after delivery (aRR = 1.14, 95% CI: 1.11, 1.18) were also associated with asthma. These associations were not replicated when evaluated within sibling groups. There were no associations with paternal psychosocial stress. In conclusion, maternal anxiety/depression and negative life events were associated with offspring asthma, but this might be explained by unmeasured maternal background characteristics that remain stable across deliveries.
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Project description:The alternative dimensional model of personality disorder (PD) in the Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM-5; American Psychiatric Association, 2013), Section III, has two main criteria: impairment in personality functioning and one or more pathological personality traits. The former is defined as disturbances in self-functioning (viz., identity, self-direction), and/or interpersonal functioning (viz., empathy, intimacy). Distinguishing personality functioning and traits is important conceptually, because simply having extreme traits is not necessarily pathological. However, adding personality functioning to PD diagnosis represents an empirical challenge, because the constructs overlap conceptually. Further, there is debate regarding whether diagnosis of mental disorder requires either distress or disability, concepts that also overlap with maladaptive-range personality traits and personality dysfunction. We investigated interrelations among these constructs using multiple self-report measures of each domain in a mixed community-patient sample (N = 402). We examined the structures of functioning (psychosocial disability and personality) and personality traits, first independently, then jointly. The disability/functioning measures yielded the 3 dimensions we have found previously (Ro & Clark, 2013). Trait measures had a hierarchical structure which, at the 5-factor level, reflected neuroticism/negative affectivity (N/NA), (low) sociability, disinhibition, (dis)agreeableness, and rigid goal engagement. When all measures were cofactored, a hierarchical structure again emerged which, at the 5-factor level, included (a) internalizing (N/NA and self-pathology vs. quality-of-life/satisfaction); (b) externalizing (social/interpersonal dysfunction, low sociability, and disagreeableness); (c) disinhibition; (d) poor basic functioning; and (e) rigid goal engagement. Results are discussed in terms of developing an integrated PD diagnostic model.
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