Carer's Attachment Anxiety, Stressful Life-Events and the Risk of Childhood-Onset Type 1 Diabetes.
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ABSTRACT:
SUBMITTER: Turin A
PROVIDER: S-EPMC8205563 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Brain-derived neurotrophic factor (BDNF) polymorphisms have been examined for their contribution toward depression with equivocal results. More homogeneous phenotypes might be used to improve our understanding of genetic liability to depression. The aim of our study was to (a) test for an association between the BDNF Val66Met polymorphism and childhood-onset melancholic depression and (b) to examine the interactive effects of stressful life events (SLE) and the Val66Met polymorphism on the risk of childhood-onset melancholic depression.A total of 583 depressed probands were involved in this study (162 of the melancholic subtype). Diagnoses were derived through the Interview Schedule for Children and Adolescents - Diagnostic Version and life event data were collected using an Intake General Information Sheet.Overall, 27.8% of the participants fulfilled the criteria for melancholy. In the melancholic group, the proportion of females was higher (53.1%), although there were more males in the overall depressed sample. We detected no significant differences in genotype or allele frequency between the melancholic and the nonmelancholic depressed group. The BDNF Val66Met polymorphism and SLE interaction was not significantly associated with the melancholy outcome.In our study, females were more prone to developing the early-onset melancholic phenotype. To our knowledge, this is the first study to investigate the differentiating effect of the genotype and the G×E interaction on the melancholic phenotype in a large sample of depressed young patients. We did not find an association between the melancholic subtype of major depression and the BDNF genotype and SLE interaction in this sample, which is representative of the Hungarian clinic-referred population of depressed youths.
| S-EPMC4714603 | biostudies-literature
Project description:BackgroundStressful life events (SLEs) and adverse childhood experiences (ACEs) have been reported to be associated with perinatal depression (PND) or perinatal anxiety (PNA) alone; however, in most cases, majority of PND and PNA coexist and could lead to more serious health consequences. The independent effect of recent SLEs and their joint effects with ACEs on perinatal comorbid anxiety and depression (CAD) remain inadequately explored.MethodsBased on a longitudinal study, 1082 participants receiving prenatal care in Ma'anshan, China were included. Women were recruited in the first trimester (T1: ≤14+ 6 weeks) and followed up at 15 ~ 27 weeks (T2), 28 ~ 40 weeks (T3), and postpartum (T4). Depression and anxiety status were assessed at all time points, while recent SLEs and ACEs were measured at T1. Logistic regression was conducted to examine the associations of SLEs with the risks of CAD at different time points, as well as their joint effects with ACEs on CAD.ResultsApproximately 38.5% of women experienced at least one SLE, which was significantly associated with higher risks of CAD at all time points (p < 0.05). As the number of SLEs increased, the risk of CAD increased (p for trend < 0.05). Specific types of SLEs were associated with CAD in different periods, while only interpersonal events were consistently associated with risks of CAD throughout the whole perinatal period. The joint effects of SLEs with ACEs on CAD were identified throughout the perinatal period, with the highest observed in the first trimester (aOR = 7.47, 95% CI: 3.73-14.95; p for trend < 0.001).ConclusionOur study demonstrated independent associations of recent SLEs and their joint effects with ACEs with risks of perinatal CAD. SLEs combined with ACEs should be recognized as a major risk factor for perinatal CAD and managed at the earliest time to prevent and control CAD.
| S-EPMC9847044 | biostudies-literature
Project description:BackgroundThe aim of the study was to estimate the effect of the accumulation of major life events (MLE) in childhood and adulthood, in both the private and working domains, on risk of type 2 diabetes mellitus (T2DM). Furthermore, we aimed to test the possible interaction between childhood and adult MLE and to investigate modification of these associations by educational attainment.MethodsThe study was based on 4,761 participants from the Copenhagen City Heart Study free of diabetes at baseline and followed for 10 years. MLE were categorized as 0, 1, 2, 3 or more events. Multivariate logistic regression models adjusted for age, sex, education and family history of diabetes were used to estimate the association between MLE and T2DM.ResultsIn childhood, experiencing 3 or more MLE was associated with a 69% higher risk of developing T2DM (Odds Ratio (OR) 1.69; 95% Confidence Interval (CI) 1.60, 3.27). The accumulation of MLE in adult private (p-trend = 0.016) and work life (p-trend = 0.049) was associated with risk of T2DM in a dose response manner. There was no evidence that experiencing MLE in both childhood and adult life was more strongly associated with T2DM than experiencing events at only one time point. There was some evidence that being simultaneously exposed to childhood MLE and short education (OR 2.28; 95% C.I. 1.45, 3.59) and work MLE and short education (OR 2.86; 95% C.I. 1.62, 5.03) was associated with higher risk of T2DM, as the joint effects were greater than the sum of their individual effects.ConclusionsFindings from this study suggest that the accumulation of MLE in childhood, private adult life and work life, respectively, are risk factors for developing T2DM.
| S-EPMC4578856 | biostudies-literature
Project description:Introduction: Borderline personality disorder (BPD) in adolescents is characterized by emotional dysregulation, insecure attachment, a history of stressful life events (SLEs) as well as dysfunctional parent-child interactions. The respective contribution of each of these factors on BPD affective symptoms is not yet clear. The purpose of this study is to assess the distinct impact of parental adversity and SLEs on BPD affective symptoms and the role of attachment and alexithymia in such emotional processes. Method: This study explored parental dysfunction and SLEs as predictors of affective symptoms of BPD and of attachment insecurity in BPD adolescents (n = 85) and healthy controls (n = 84) aged 13-19 years from the European Research Network on BPD. The links between adversity and BPD symptoms were also investigated by emotional dysregulation assessment, as measured by alexithymia and hopelessness. Results: Dysfunctional parental interactions were linked to affective symptoms, hopelessness, and anxious attachment in healthy controls but not in BPD. Cumulative SLEs were positively correlated with affective symptoms and avoidant attachment in the control group but negatively correlated with both these variables in BPD. Multivariate regression analysis revealed that, in BPD, affective symptoms were independent of dysfunctional parenting but depended on attachment, whereas in controls, a maternal affectionless control style directly predicted affective symptoms. Moreover, increasing numbers of SLEs reduced affective symptoms in BPD, independently of parental interactions or attachment, and were associated with growing use of operative thinking. Discussion: BPD patients showed paradoxical emotional reactions: there was no increase of hopelessness and affective symptoms with an increased parental dysfunction, but a decrease in affective symptoms and hopelessness with cumulative SLE. Two pathways arose, one involving attachment as an emotional dysregulation process for parent-child interactions and a second one for SLE, with a more direct pathway to affective symptoms, independent of attachment but dependent on early interactions, and involving alexithymia. In summary, adversity factors have distinct effects in BPD, and attachment is partly accountable for affective symptoms independently of adversity. Our results suggest that in highly insecure conditions, cumulative adversity may produce paradoxical effects, including a lesser expression of affective symptoms and hopelessness.
| S-EPMC8566741 | biostudies-literature
Project description:BACKGROUND:A few prospective studies suggest an association between maternal smoking during pregnancy and lower risk of type 1 diabetes. However, the role of unmeasured confounding and misclassification remains unclear. METHODS:We comprehensively evaluated whether maternal smoking in pregnancy predicts lower risk of childhood-onset type 1 diabetes in two Scandinavian pregnancy cohorts (185,076 children; 689 cases) and a Norwegian register-based cohort (434,627 children; 692 cases). We measured cord blood cotinine as an objective marker of nicotine exposure during late pregnancy in 154 cases and 476 controls. We also examined paternal smoking during pregnancy, in addition to environmental tobacco smoke exposure the first 6 months of life, to clarify the role of characteristics of smokers in general. RESULTS:In the pregnancy cohorts, maternal smoking beyond gestational week 12 was inversely associated with type 1 diabetes, pooled adjusted hazard ratio (aHR) 0.66 (95% CI = 0.51, 0.85). Similarly, in the Norwegian register-based cohort, children of mothers who still smoked at the end of pregnancy had lower risk of type 1 diabetes, aHR 0.65 (95% CI = 0.47, 0.89). Cord blood cotinine ?30 nmol/L was also associated with reduced risk of type 1 diabetes, adjusted odds ratio 0.42 (95% CI = 0.17, 1.0). We observed no associations of paternal smoking during pregnancy, or environmental tobacco smoke exposure, with childhood-onset type 1 diabetes. CONCLUSION:Maternal sustained smoking during pregnancy is associated with lower risk of type 1 diabetes in children. This sheds new light on the potential intrauterine environmental origins of the disease.
| S-EPMC6169737 | biostudies-literature
Project description:OBJECTIVE:To determine the relation between stressful life events and difficulties and the onset of breast cancer. DESIGN:Case-control study. SETTING:3 NHS breast clinics serving west Leeds. PARTICIPANTS:399 consecutive women, aged 40-79, attending the breast clinics who were Leeds residents. MAIN OUTCOME MEASURES:Odds ratios of the risk of developing breast cancer after experiencing one or more severe life events, severe difficulties, severe 2 year non-personal health difficulties, or severe 2 year personal health difficulties in the 5 years before clinical presentation. RESULTS:332 (83%) women participated. Women diagnosed with breast cancer were no more likely to have experienced one or more severe life events (adjusted odds ratio 0.91, 95% confidence interval 0.47 to 1. 81; P=0.79); one or more severe difficulties (0.86, 0.41 to 1.81; P=0.69); a 2 year severe non-personal health difficulty (0.53, 0.12 to 2.31; P=0.4); or a 2 year severe personal health difficulty (2.73, 0.68 to 10.93; P=0.16) than women diagnosed with a benign breast lump. CONCLUSION:These findings do not support the hypothesis that severe life events or difficulties are associated with onset of breast cancer.
| S-EPMC28252 | biostudies-literature
Project description:BackgroundRecurrent aphthous stomatitis (RAS) is a common and painful oral mucosal disease. Possible etiologies include genetics, vitamin deficiencies, trauma, immune dysfunction, and stress. The goal of this study was to examine the relationship between the occurrence, type, and magnitude of stressful events and the onset and duration of RAS episodes.MethodsOne hundred and sixty subjects with a history of RAS completed a weekly phone survey for up to 1 year, providing data on the occurrence of RAS episodes and details of any stressful events they experienced during the previous week. During RAS episodes, subjects also completed daily paper diaries that recorded incidence and duration of the RAS episode. Stressful events were quantified using the validated Recent Life Changes Questionnaire (RLCQ) and were classified as mental or physical stressors.ResultsStressful life events were significantly associated with the onset of RAS episodes (P < 0.001), however, not with the duration of the RAS episodes. Experiencing a stressful life event increased the odds of an RAS episode by almost three times (OR = 2.72; 95% CI = 2.04-3.62). When controlled for each other, mental stressors had a larger effect (OR = 3.46, 95% CI = 2.54-4.72) than physical stressors (OR = 1.44; 95% CI = 1.04-1.99) on the occurrence of RAS episodes. RAS episodes did not occur more frequently or last longer with increasing stress severity.ConclusionsIn patients with a history of RAS, stressful events may mediate changes involved in the initiation of new RAS episodes. Mental stressors are more strongly associated with RAS episodes than physical stressors.
| S-EPMC3323121 | biostudies-literature
Project description:Background and purposeUnexpected stressful life events may alter immune function and affect susceptibility to autoimmune diseases including multiple sclerosis (MS). Current results from epidemiological investigations examining the role of stress in MS remain inconsistent. The aim was to conduct the hitherto largest population-based case-control study on this topic.MethodsExtensive questionnaire information collected on lifestyle environmental factors available for 2930 incident MS cases and 6170 controls were used to assess the association of 10 major life events that had occurred before disease onset with the risk of MS by unconditional logistic regressions, adjusting for potential confounders. Stratified analyses were also performed by sex and time.ResultsCompelling evidence was found for a link between major life events and risk of MS - most events significantly increased disease risk by 17%-30%. It was further observed that women were affected to a greater extent than men under certain stressful scenarios, and that most events that happened recently (≤5 years prior to MS onset) had significant effects on MS, indicating a critical window in disease development.ConclusionStressful life events may have an adverse effect on the risk of MS. Research into the mechanisms of this observation may give important clues to triggering pathogenetic events in MS.
| S-EPMC7692913 | biostudies-literature
Project description:IMPORTANCE The study provides novel data to inform the mechanisms by which poverty negatively impacts childhood brain development. OBJECTIVE To investigate whether the income-to-needs ratio experienced in early childhood impacts brain development at school age and to explore the mediators of this effect. DESIGN, SETTING, AND PARTICIPANTS This study was conducted at an academic research unit at the Washington University School of Medicine in St Louis. Data from a prospective longitudinal study of emotion development in preschool children who participated in neuroimaging at school age were used to investigate the effects of poverty on brain development. Children were assessed annually for 3 to 6 years prior to the time of a magnetic resonance imaging scan, during which they were evaluated on psychosocial, behavioral, and other developmental dimensions. Preschoolers included in the study were 3 to 6 years of age and were recruited from primary care and day care sites in the St Louis metropolitan area; they were annually assessed behaviorally for 5 to 10 years. Healthy preschoolers and those with clinical symptoms of depression participated in neuroimaging at school age/early adolescence. EXPOSURE Household poverty as measured by the income-to-needs ratio. MAIN OUTCOMES AND MEASURES Brain volumes of children's white matter and cortical gray matter, as well as hippocampus and amygdala volumes, obtained using magnetic resonance imaging. Mediators of interest were caregiver support/hostility measured observationally during the preschool period and stressful life events measured prospectively. RESULTS Poverty was associated with smaller white and cortical gray matter and hippocampal and amygdala volumes. The effects of poverty on hippocampal volume were mediated by caregiving support/hostility on the left and right, as well as stressful life events on the left. CONCLUSIONS AND RELEVANCE The finding that exposure to poverty in early childhood materially impacts brain development at school age further underscores the importance of attention to the well-established deleterious effects of poverty on child development. Findings that these effects on the hippocampus are mediated by caregiving and stressful life events suggest that attempts to enhance early caregiving should be a focused public health target for prevention and early intervention. Findings substantiate the behavioral literature on the negative effects of poverty on child development and provide new data confirming that effects extend to brain development. Mechanisms for these effects on the hippocampus are suggested to inform intervention.
| S-EPMC4001721 | biostudies-literature
Project description:BackgroundAlthough stressful life events (SLEs) predict subsequent risk of developing a major depressive episode (MDE), limited information exists on whether or not race and gender alters the predictive role of SLE on risk of MDE over a long-term period. The current study explored race and gender differences in the long-term predictive role of SLE at baseline (1986) on subsequent risk of MDE 25 years later (2011) in a nationally representative cohort in the United States.MethodsUsing a life course epidemiological approach, this longitudinal study borrowed data from the Americans' Changing Lives (ACL) Study 1986-2011. Main predictor of interest was baseline SLE over the last 3?years measured at 1986. Main outcome was risk of MDE [Composite International Diagnostic Interview (CIDI)] 25 years later (2011). Covariates included demographics, socioeconomics, depressive symptoms [Center for Epidemiological Studies-Depression Scale (CES-D)], chronic medical conditions, and health behaviors measured at baseline (1986). Gender and race were the focal moderators. We employed logistic regressions in the pooled sample, and specific to race and gender, to test whether or not SLE?×?race and SLE?×?gender interactions are significant.ResultsIn the pooled sample, baseline SLE (1986) predicted risk of MDE 25 years later (2011). We also found a gender by SLE interaction, suggesting a stronger predictive role of SLE for subsequent clinical depression for men compared to women. Race did not modify the predictive role of SLE on subsequent risk of MDE 25 years later.ConclusionHow SLE predicts MDE 25 years later differs for men and women, with a stronger predictive role for men compared to women. More research is needed to better understand the complex links between gender, sex, stress, and depression.
| S-EPMC4805579 | biostudies-literature