Offspring Depressive Symptoms Research Articles

Prenatal maternal Inflammation, childhood cognition and adolescent depressive symptoms

BackgroundAccumulating evidence indicates that higher prenatal maternal inflammation is associated with increased depression risk in adolescent and adult-aged offspring. Prenatal maternal inflammation (PNMI) may increase the likelihood for offspring to have lower cognitive performance, which, in turn, may heighten risk for depression onset. Therefore, this study explored the potential mediating role of childhood cognitive performance in the relationship between PNMI and adolescent depressive symptoms in offspring. MethodsParticipants included 696 mother-offspring dyads from the Child Health and Development Studies (CHDS) cohort. Biomarkers of maternal inflammation [interleukin (IL)-6, IL-8, IL-1 receptor antagonist (IL-1RA) and soluble TNF receptor-II (sTNF-RII)] were assayed from first (T1) and second trimester (T2) sera. Childhood (ages 9–11) cognitive performance was assessed via standardized Peabody Picture Vocabulary Test (PPVT), a measure of receptive vocabulary correlated with general intelligence. Adolescent (ages 15–17) depressive symptoms were assessed via self-report. ResultsThere were no significant associations between T1 biomarkers and childhood PPVT or adolescent depressive symptoms. Higher T2 IL1-RA was directly associated with lower childhood PPVT (b = -0.21, SE = 0.08, t = -2.55, p = 0.01), but not with adolescent depressive symptoms. T2 IL-6 was not directly associated with childhood PPVT, but higher T2 IL-6 was directly associated at borderline significance with greater depressive symptoms in adolescence (b = 0.05, SE = 0.03, t = 1.96, p = 0.05). Lower childhood PPVT predicted significantly higher adolescent depressive symptoms (b = -0.07, SE = 0.02, t = -2.99, p < 0.01). There was a significant indirect effect of T2 IL-1RA on adolescent depressive symptoms via childhood PPVT (b = 0.03, 95 % CI = 0.002–0.03) indicating a partially mediated effect. No significant associations were found with T2 sTNF-RII nor IL-8. ConclusionsLower childhood cognitive performance, such as that indicated by a lower PPVT score, represents a potential mechanism through which prenatal maternal inflammation contributes to adolescent depression risk in offspring.

Microglial function interacts with the environment to affect sex-specific depression risk

There is a two-fold higher incidence of depression in females compared to men with recent studies suggesting a role for microglia in conferring this sex-dependent depression risk. In this study we investigated the nature of this relation. Using GWAS enrichment, gene-set enrichment analysis and Mendelian randomization, we found minimal evidence for a direct relation between genes functionally related to microglia and sex-dependent genetic risk for depression. We then used expression quantitative trait loci and single nucleus RNA-sequencing resources to generate polygenic scores (PGS) representative of individual variation in microglial function in the adult (UK Biobank; N = 54753–72682) and fetal (ALSPAC; N = 1452) periods. The adult microglial PGS moderated the association between BMI (UK Biobank; beta = 0.001, 95 %CI 0.0009 to 0.003, P = 7.74E-6) and financial insecurity (UK Biobank; beta = 0.001, 95 %CI 0.005 to 0.015, P = 2E-4) with depressive symptoms in females. The fetal microglia PGS moderated the association between maternal prenatal depressive symptoms and offspring depressive symptoms at 24 years in females (ALSPAC; beta = 0.04, 95 %CI 0.004 to 0.07, P = 0.03). We found no evidence for an interaction between the microglial PGS and depression risk factors in males. Our results illustrate a role for microglial function in the conferral of sex-dependent depression risk following exposure to a depression risk factor.

Intergenerational continuity of loneliness and potential mechanisms: Young Finns Multigenerational Study

Evidence on the intergenerational continuity of loneliness and on potential mechanisms that connect loneliness across successive generations is limited. We examined the association between loneliness of (G0) parents (859 mothers and 570 fathers, mean age 74 years) and their children (G1) (433 sons and 558 daughters, mean age 47 years) producing 991 parent–offspring pairs and tested whether these associations were mediated through subjective socioeconomic position, temperament characteristics, cognitive performance, and depressive symptoms. Mean loneliness across parents had an independent effect on their adult children’s experienced loneliness (OR = 1.72, 95% CI 1.23–2.42). We also found a robust effect of mothers’ (OR = 1.64, 95% CI 1.17–2.29), but not of fathers’ loneliness (OR = 1.47, 95% CI 0.96–2.25) on offspring’s experienced loneliness in adulthood. The associations were partly mediated by offspring depressive (41–54%) and anxiety (29–31%) symptoms. The current findings emphasize the high interdependence of loneliness within families mediated partly by offspring’s mental health problems.

Sex-Specific Pathways From Prenatal Maternal Inflammation to Adolescent Depressive Symptoms

Prenatal maternal inflammation has been associated with major depressive disorder in offspring in adulthood as well as with internalizing and externalizing symptoms in childhood; however, the association between prenatal inflammation and offspring depression in adolescence has yet to be examined. To determine whether maternal levels of inflammatory biomarkers during pregnancy are associated with depressive symptomatology in adolescent-aged offspring and to examine how gestational timing, offspring sex, and childhood psychiatric symptoms impact these associations. This was an observational study of a population-based birth cohort from the Child Health and Development Studies (CHDS), which recruited almost all mothers receiving obstetric care from the Kaiser Foundation Health Plan (KFHP) in Alameda County, California, between June 1959 and September 1966. Pregnancy data and blood sera were collected from mothers, and offspring psychiatric symptom data were collected in childhood (ages 9-11 years) and adolescence (ages 15-17 years). Mother-offspring dyads with available maternal prenatal inflammatory biomarkers during first and/or second trimesters and offspring depressive symptom data at adolescent follow-up were included. Data analyses took place between March 2020 and June 2023. Levels of inflammatory biomarkers (interleukin 6 [IL-6], IL-8, IL-1 receptor antagonist [IL-1RA], and soluble tumor necrosis factor receptor-II) assayed from maternal sera in the first and second trimesters of pregnancy. Self-reported depressive symptoms at adolescent follow-up. A total of 674 mothers (mean [SD] age, 28.1 [5.9] years) and their offspring (350 male and 325 female) were included in this study. Higher second trimester IL-6 was significantly associated with greater depressive symptoms in offspring during adolescence (b, 0.57; SE, 0.26); P = .03). Moderated mediation analyses showed that childhood externalizing symptoms significantly mediated the association between first trimester IL-6 and adolescent depressive symptoms in male offspring (b, 0.18; 95% CI, 0.02-0.47), while childhood internalizing symptoms mediated the association between second trimester IL-1RA and adolescent depressive symptoms in female offspring (b, 0.80; 95% CI, 0.19-1.75). In this study, prenatal maternal inflammation was associated with depressive symptoms in adolescent-aged offspring. The findings of the study suggest that pathways to adolescent depressive symptomatology from prenatal risk factors may differ based on both the timing of exposure to prenatal inflammation and offspring sex.

Dentate Gyrus Microstructure Is Associated With Resilience After Exposure to Maternal Stress Across Two Human Cohorts

BackgroundMaternal stress (MS) is a well-documented risk factor for impaired emotional development in offspring. Rodent models implicate the dentate gyrus (DG) of the hippocampus in the effects of MS on offspring depressive-like behaviors, but mechanisms in humans remain unclear. Here, we tested whether MS was associated with depressive symptoms and DG micro- and macrostructural alterations in offspring across 2 independent cohorts. MethodsWe analyzed DG diffusion tensor imaging–derived mean diffusivity (DG-MD) and volume in a three-generation family risk for depression study (TGS; n = 69, mean age = 35.0 years) and in the Adolescent Brain Cognitive Development (ABCD) Study (n = 5196, mean age = 9.9 years) using generalized estimating equation models and mediation analysis. MS was assessed by the Parenting Stress Index (TGS) and a measure compiled from the Adult Response Survey from the ABCD Study. The Patient Health Questionnaire-9 and rumination scales (TGS) and the Child Behavior Checklist (ABCD Study) measured offspring depressive symptoms at follow-up. The Schedule for Affective Disorders and Schizophrenia–Lifetime interview was used to assign depression diagnoses. ResultsAcross cohorts, MS was associated with future symptoms and higher DG-MD (indicating disrupted microstructure) in offspring. Higher DG-MD was associated with higher symptom scores measured 5 years (in the TGS) and 1 year (in the ABCD Study) after magnetic resonance imaging. In the ABCD Study, DG-MD was increased in high-MS offspring who had depressive symptoms at follow-up, but not in offspring who remained resilient or whose mother had low MS. ConclusionsConverging results across 2 independent samples extend previous rodent studies and suggest a role for the DG in exposure to MS and offspring depression.

Within-person pathways among maternal depressive symptoms and offspring internalizing problems from early childhood through adolescence.

The report examined reciprocal within-person associations among maternal depressive symptoms and offspring depressive, anxiety and irritability symptoms from early childhood to adolescence using a random intercept cross-lagged panel model (RI-CLPM). Participants were 609 mother-child dyads participating in the Stony Brook Temperament Study. Child and maternal internalizing symptoms were assessed every 3 years from ages 3 to 15 using maternal report on the Child Behavior Checklist (CBCL) and Diagnostic Inventory for Depression, respectively. At the between-person level, maternal depressive symptoms, and child depressive, anxiety, and irritability symptoms were all positively associated with one another. At the within-person level, greater within-person child anxiety symptoms at age 3 predicted both greater child anxiety and depressive symptoms at age 15 via greater child anxiety from ages 6 to 12, and greater within-person child irritability at age 3 predicted greater maternal depressive symptoms at age 15 via greater child irritability from ages 6 to 12. Findings reveal novel within-person developmental pathways from early childhood internalizing problems to later internalizing problems in both the child and mother. Intervention and prevention efforts should thus focus on early identification and prevention of childhood internalizing symptoms to reduce negative effects on both child and parent symptoms.

Do environmental effects indexed by parental genetic variation influence common psychiatric symptoms in childhood?

Parental genes may indirectly influence offspring psychiatric outcomes through the environment that parents create for their children. These indirect genetic effects, also known as genetic nurture, could explain individual differences in common internalising and externalising psychiatric symptoms during childhood. Advanced statistical genetic methods leverage data from families to estimate the overall contribution of parental genetic nurture effects. This study included up to 10,499 children, 5990 mother–child pairs, and 6,222 father–child pairs from the Norwegian Mother Father and Child Study. Genome-based restricted maximum likelihood (GREML) models were applied using software packages GCTA and M-GCTA to estimate variance in maternally reported depressive, disruptive, and attention-deficit hyperactivity disorder (ADHD) symptoms in 8-year-olds that was explained by direct offspring genetic effects and maternal or paternal genetic nurture. There was no strong evidence of genetic nurture in this sample, although a suggestive paternal genetic nurture effect on offspring depressive symptoms (variance explained (V) = 0.098, standard error (SE) = 0.057) and a suggestive maternal genetic nurture effect on ADHD symptoms (V = 0.084, SE = 0.058) was observed. The results indicate that parental genetic nurture effects could be of some relevance in explaining individual differences in childhood psychiatric symptoms. However, robustly estimating their contribution is a challenge for researchers given the current paucity of large-scale samples of genotyped families with information on childhood psychiatric outcomes.

Transactional Relations Between Peer Victimization and Depressive Symptoms Among Youth at Risk of Developing Depression: Evidence for Gender Differences.

Offspring of mothers with a history of major depressive disorder (MDD) are at high risk of developing the disorder themselves, yet specific mechanisms of risk remain unclear. One hypothesized mechanism is interpersonal stress, which has been shown to be elevated in offspring of mothers with a history of MDD. The goal of this study was to examine the role of a specific form of interpersonal stress, peer victimization (overt and relational). In doing so, we not only examined the impact of peer victimization on changes in youth depression, but also youth depression on changes in peer victimization, consistent with stress generation models. Participants were 251 mothers with (n = 129) or without (n = 122) a history of MDD and their child (aged 8-14 years at baseline) who were assessed every six months for two years. Using random intercepts cross-lagged panel models (RI-CLPM), we were able to separate between-subject effects (mother MDD group differences in average levels of peer victimization and offspring depressive symptoms) and within-subject effects (transactional influences between within-subject fluctuations in peer victimization and depressive symptoms among offspring over time). Overall, these effects were stronger for relational victimization than for overt victimization and stronger for girls than boys. These results support the role of peer victimization, particularly relational victimization, as a risk factor among offspring of mothers with MDD, particularly girls, and highlight transactional relations between relational victimization and depressive symptoms in girls over time, which may create a vicious cycle of risk.

Maternal adherence to healthy lifestyle and risk of depressive symptoms in the offspring: mediation by offspring lifestyle.

Adherence to healthy lifestyles can be beneficial for depression among adults, but the intergenerational impact of maternal healthy lifestyles on offspring depressive symptoms is unknown. In total, 10 368 mothers in Nurses' Health Study II and 13 478 offspring in the Growing Up Today Study were paired. Maternal and offspring healthy lifestyles were defined as a composite score including a healthy diet, normal body mass index (BMI), never-smoking, light-to-moderate consumption of alcohol, and regular moderate-to-vigorous physical activity. Maternal lifestyles were assessed during their offspring's childhood. Offspring depressive symptoms were repeatedly assessed five times using the Center for Epidemiological Studies Depression Scale-10 (CESD-10); the offspring were between the ages of 14 and 30 when the first CESD-10 was assessed. Covariates included maternal variables (age at baseline, race/ethnicity, antidepressant use, pregnancy complications, etc.) and offspring age and sex. Children of mothers with the healthiest lifestyle had significantly fewer depressive symptoms (a 0.30 lower CESD-10 score, 95% confidence interval (CI) 0.09-0.50) in comparison with children of mothers with the least healthy lifestyle. The association was only found significant in female offspring but not in males. For individual maternal lifestyle factors, a normal BMI, never-smoking, and adherence to regular physical activity were independently associated with fewer depressive symptoms among the offspring. The association between maternal healthy lifestyles and offspring depressive symptoms was mediated by offspring's healthy lifestyles (mediation effect: 53.2%, 95% CI 15.8-87.3). Our finding indicates the potential mechanism of intergenerational transmission of healthy lifestyles to reduce the risk of depressive symptoms in offspring.

A transactional mediation model of risk for the intergenerational transmission of depression: The role of maternal criticism.

In this study, we sought to combine two lines of research to better understand risk for the intergenerational transmission of depression. The first focuses on the role of maternal criticism as a potential mechanism of risk for depression in youth while the second builds from interpersonal and stress generation models regarding the potential impact of youth depression on future escalations in maternal criticism. Specifically, we examined the role of maternal criticism within a transactional mediation model using data from a multi-wave study. Participants were 251 mother-offspring pairs consisting of mothers with (n = 129) and without (n = 122) a history of major depressive disorder (MDD) during their child's lifetime who completed assessments every 6 months for 2 years. We found support for the hypothesized transactional mediational model in which maternal expressed emotion-criticism (EE-Crit) mediated the link between maternal history of MDD and residual change in youth's depressive symptoms over the previous 6 months and, reciprocally, youth depressive symptoms mediated the relation between maternal MDD history and residual change in EE-Crit 6 months later. These results indicate that maternal criticism and offspring depressive symptoms may contribute to a vicious cycle of depression risk, which should be considered for interventions targeted toward youth at risk of developing MDD.

The association between the romantic relationships of parents and offspring depressive symptoms: Mediating effects of offspring communication patterns and romantic relationships.

This study investigated a conceptual model by testing how parental romantic relationships influenced the depressive symptoms of grown-up children and whether the constructive communication patterns of grown-up children and romantic relationships played mediation effects within it. A total of 421 Chinese participants were enrolled in the study. The level of depressive symptoms, romantic relationship satisfaction and closeness, couple communication patterns, and parental romantic relationships were measured via self-report questionnaires. According to the results, the structural equation modeling analysis verified that the severity of participants’ depressive symptoms was negatively associated with the parental romantic relationship and that the association was mediated by participants’ constructive communication patterns and their own romantic relationships. Furthermore, compared with nondepressed participants, depressed participants were less satisfied with their parental romantic relationships, exhibited fewer constructive communication patterns, and were more distant and unsatisfied with current romantic relationships.

Father absence and trajectories of offspring mental health across adolescence and young adulthood: Findings from a UK-birth cohort

BackgroundHigh prevalence of parental separation and resulting biological father absence raises important questions regarding its impact on offspring mental health across the life course. We specifically examined whether these relationships vary by sex and the timing of exposure to father absence (early or middle childhood). MethodsThis study is based on up to 8409 children from the Avon Longitudinal Study of Parents and Children (ALSPAC). Participants provided self-reports of depression (Clinical Interview Schedule-Revised) at age 24 years and depressive symptoms (Short Mood and Feelings Questionnaire) between the ages of 10 and 24 years. Biological father absence in childhood was assessed through maternal questionnaires at regular intervals from birth to 10 years. We estimated the association between biological father absence and trajectories of depressive symptoms using multilevel growth-curve modelling. ResultsEarly but not middle childhood father absence was strongly associated with increased odds of offspring depression and greater depressive symptoms at age 24 years. Early childhood father absence was associated with higher trajectories of depressive symptoms during adolescence and early adulthood compared with father presence. Differences in the level of depressive symptoms between middle childhood father absent and father present groups narrowed into adulthood. LimitationsThis study could be biased by attrition and residual confounding. ConclusionsWe found evidence that father absence in childhood is persistently associated with offspring depression in adolescence and early adulthood. This relationship varies by sex and timing of father's departure, with early childhood father absence emerging as the strongest risk factor for adverse offspring mental health trajectories Further research is needed to identify mechanisms that could inform preventative interventions to reduce the risk of depression in children who experience father absence.

The risk of depressive symptoms in offspring exposed to prenatal alcohol and tobacco use: evidence from a population-based longitudinal study

IntroductionEvidence from epidemiological studies indicated that intrauterine exposure to alcohol and tobacco is linked with a number of adverse outcomes in offspring. However, few studies have linked prenatal alcohol and tobacco exposures to offspring depressive symptoms with mixed results.ObjectivesThe objective of this study was to examine the link between maternal prenatal alcohol and tobacco exposures and depressive symptoms in offspring.MethodsUsing data from the Raine Study, a prospective multigenerational observational study, we examined the associations between maternal prenatal alcohol and tobacco use and the risk of depressive symptoms in offspring at age 17 years (N=1168). Depressive symptoms in offspring were measured using the Beck Depression Inventory for Youth. Log-binomial regression was used to estimate relative risk (RR) for associations between exposures and outcome. To better investigate the role of potential confounders, risk factors were sequentially added as adjustment variables in separate models.ResultsAfter adjustment for potential confounders, depressive symptoms in offspring remained related to maternal alcohol use of six or more standard drinks per week during the first trimester of pregnancy [RR 1.59 (95% CI: 1.11-2.26)]. Further, the risk of depressive symptoms was 50% higher for offspring exposed to prenatal tobacco use when compared to non-exposed. The Associations did not appear to be mediated by the effects of prenatal alcohol and tobacco use on adverse pregnancy outcomes.ConclusionsEarly screening and prevention of these exposures could possibly reduce depressive symptoms in offspring. Moreover, future examinations such as Mendelian Randomization that allow a stronger causal inference is warranted.DisclosureNo significant relationships.

Maternal postnatal depression and anxiety and the risk for mental health disorders in adolescent offspring: Findings from the Avon Longitudinal Study of Parents and Children cohort.

The impacts of postnatal psychiatric disorders on different types of mental health problems in offspring are unclear. We investigated the prospective associations of maternal postnatal depression, and anxiety, with offspring depression, anxiety, psychotic-like experiences and Borderline Personality Disorder symptoms, in adolescence, and examined whether these were independent of each other. Data were obtained from the Avon Longitudinal Study of Parents and Children (ALSPAC) birth cohort. Maternal postnatal depression and anxiety at 8 weeks were measured using the Edinburgh Postnatal Depression Scale and Crown-Crisp Index, respectively. Offspring mental health outcomes were measured at 10-13 years old, using a variety of questionnaire-based and interview assessments. Logistic regression analyses were used to assess the associations between maternal postnatal risk factors and offspring mental health, and path analysis was used to investigate the pathways of maternal postnatal factors to adolescent offspring outcomes. Data were available for 14,054 mothers with information reported on postnatal depression and 13,892 on postnatal anxiety. Logistic regression analyses found significant associations between maternal postnatal depression and offspring anxiety at 10 years old (odds ratio = 1.039, 95% confidence interval = [1.005, 1.073], p = 0.022) and between maternal postnatal anxiety and offspring psychotic experiences at 12/13 years old (odds ratio = 1.042, 95% confidence interval = [1.008, 1.077], p = 0.016). These significant associations remained after applying path analyses, when we controlled for potential offspring psychopathological overlay. These findings suggest that mothers with postnatal depression are more likely to have offspring with anxiety at 10 years old, and that mothers with postnatal anxiety are more likely to have offspring with psychotic experiences at 12/13 years old. Our findings suggest specific pathways in the association between postnatal anxiety/depression and offspring mental health and contribute to the importance of identifying mothers and their offspring with increased vulnerability to adverse outcomes resulting from postnatal mental health disorders.

Intergenerational transmission of mastery between mothers and older offspring: Considering direct, moderated, and mediated effects.

Mastery involves a sense of having control over one's surroundings and an ability to accomplish meaningful goals and determine important meaningful outcomes across situations. Mastery is a dynamic, learned resource that has implications for mental health. Although mastery is known to be influenced by exposure to family members (i.e., parental socialization, parenting styles; provided opportunities for autonomy and choice) there remain few long-term considerations of intergenerational transmission of mastery within families and the enduring implications for offspring's mental health and adjustment. Using a nationally representative sample from the National Longitudinal Survey of Youth, the current study addresses the longitudinal effects of mothers' early sense of mastery on adolescent and adult offspring's mastery and well-being. In considering mothers' reports between 1987 and 1992 and offspring's ongoing reports between 1994 and 2012; this study addressed questions about direct, moderated, and mediated mother effects on longitudinal offspring outcomes. Mother mastery and mother self-esteem predicted offspring's respective reports, but only mother mastery predicted offspring depressive symptoms. Effects of mother mastery, but not mother self-esteem, were moderated by offspring age. Older offspring of high mastery mothers showed the largest benefits for reported mastery. Older offspring of low mastery mothers reported the greatest concerns with depressive symptoms. Last, effects of mother mastery on offspring depressive symptoms were mediated by offspring mastery and self-esteem. We discuss the fit of these findings with existing theories and empirical work on intergenerational transmission. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

Intergenerational transmission of parental neuroticism to emotional problems in 8-year-old children: Genetic and environmental influences.

Children of parents with high levels of neuroticism tend to have high neuroticism themselves as well as increased risk of experiencing symptoms of anxiety and depression. It is not yet clear how much of this link is attributable to a potential effect of parent on child (e.g., via a socializing effect) versus to shared genetic risk. We aimed to determine whether there is an intergenerational association after accounting for genetic transmission and assortative mating. We used data from the Norwegian Mother, Father and Child Cohort Study including 11,088 sibling pairs in the parental generation, their partners (N=22,176) and their offspring (N=26,091). Exposures were maternal and paternal neuroticism (self-reported), and the outcomes were neuroticism, symptoms of depression, and symptoms of anxiety in 8-year-old children (mother-reported). After accounting for assortative mating in parents (phenotypic r=0.26) and genetic transmission (explaining 0%-18% of the mother-offspring correlations), potential maternal effects explained 80% (95% CI=47-95) of the association with offspring neuroticism (mother-child r=0.31), 78% (95% CI=66-89) of the association with offspring depressive symptoms (r=0.31), and 98% (95% CI=45-112) of the association with offspring anxiety symptoms (r=0.16). Intergenerational transmission of genetic variants associated with paternal neuroticism accounted for ∼40% (CI=22%-58%) of the father-offspring correlations with neuroticism and symptoms of depression (r=0.13 and 0.13, respectively) but none with offspring symptoms of anxiety (r=0.05). The remaining father-offspring correlations were explained by maternal influences through assortative mating. These results are consistent with direct effects between maternal and offspring neuroticism and between maternal neuroticism and offspring symptoms of anxiety and depression. Further understanding of these intergenerational processes will require an adequate model of how these constructs (neuroticism, anxiety and depression) relate to each other within generations.

Maternal and paternal depression and child mental health trajectories: evidence from the Avon Longitudinal Study of Parents and Children.

The relationships between offspring depression profiles across adolescence and different timings of parental depression during the perinatal period remain unknown. To explore different timings of maternal and paternal perinatal depression in relation to patterns of change in offspring depressive mood over a 14 year period. Data were obtained from the Avon Longitudinal Study of Parents and Children (ALSPAC). Parental antenatal depression (ANTD) was assessed at 18 weeks gestation, and postnatal depression (PNTD) at 8 weeks postpartum. Population-averaged trajectories of offspring depressive symptoms were estimated using the Short Mood and Feelings Questionnaire (SMFQ) on nine occasions between 10 and 24 years of age. Full data were available for 5029 individuals. Offspring exposed to both timings of maternal depression had higher depressive symptoms across adolescence compared with offspring not exposed to ANTD or PNTD, characterised by higher depressive symptoms at age 16 (7.07 SMFQ points (95% CI = 6.19, 7.95; P < 0.001)) and a greater rate of linear change (0.698 SMFQ points (95% CI = 0.47, 0.93; P = 0.002)). Isolated maternal ANTD and to a lesser extent PNTD were also both associated with higher depressive symptoms at age 16, yet isolated maternal PNTD showed greater evidence for an increased rate of linear change across adolescence. A similar pattern was observed for paternal ANTD and PNTD, although effect sizes were attenuated. This study adds to the literature demonstrating that exposure to two timings of maternal depression (ANTD and PNTD) is strongly associated with greater offspring trajectories of depressive symptoms.

Joint associations of parental personality traits and socio-economic position with trajectories of offspring depression: Findings from up to 6925 families in a UK birth cohort.

Parental personality may influence the course of offspring depression but epidemiological evidence for associations is lacking. It is also unknown whether associations between parental personality and offspring depression differ by socio-economic position (SEP). Our aims were to describe the trajectories of depressive symptoms across adolescence of offspring of parents with and without maladaptive personality traits and to test for effect modification by SEP. A longitudinal study in the Avon Longitudinal Study of Parents and Children birth cohort (ns=3054-7046). Exposures were binary measures of maladaptive maternal and paternal personality traits. The outcome was depressive symptoms measured over nine occasions (ages 11-24) using the short mood and feelings questionnaire (SMFQ; range: 0-26). Effect modifiers were parental education and self-reported material hardship. Multilevel growth curve models were used to estimate trajectories. offspring of mothers with high (vs. low) maladaptive traits showed higher levels of depressive symptoms at multiple ages of adolescence, the greatest of which was observed at age 22 (predicted SMFQ difference age 10=0.66, 95% confidence intervals [CIs]: 0.25 to 1.28; age 22=1.00, CI: 0.51 to 1.50). There was weaker and inconsistent evidence of an association between paternal maladaptive personality and offspring depressive symptoms (SMFQ difference age 10=0.21, CI:-0.58 to 0.99; age 22=0.02, CI: -0.94 to 0.90). Lower SEP was also associated with higher offspring depressive symptoms (SMFQ difference material hardship vs. no hardship age 10=0.79, 95% CI: 0.46 to 1.13; age 22=0.96, CI: 0.56 to 1.36). There was minimal statistical evidence for effect modification. The offspring of mothers with high levels of maladaptive personality traits show evidence of greater depressive symptoms throughout adolescence although the absolute increase in symptoms is small. Evidence for the associations with fathers' personality was weaker. Socio-economic position and maladaptive personality traits appear to be independent risk factors for offspring depressive symptoms.

Hippocampal subregion volume in high-risk offspring is associated with increases in depressive symptoms across the transition to adolescence

BackgroundThe hippocampus has been implicated in the pathophysiology of depression. This study examined whether youth hippocampal subregion volumes were differentially associated with maternal depression history and youth's depressive symptoms across the transition to adolescence. Methods74 preadolescent offspring (Mage=10.74+/-0.84 years) of mothers with (n = 33) and without a lifetime depression history (n = 41) completed a structural brain scan. Youth depressive symptoms were assessed with clinical interviews and mother- and youth-reports prior to the neuroimaging assessment at age 9 (Mage=9.08+/-0.29 years), at the neuroimaging assessment, and in early adolescence (Mage=12.56+/-0.40 years). ResultsMaternal depression was associated with preadolescent offspring's reduced bilateral hippocampal head volumes and increased left hippocampal body volume. Reduced bilateral head volumes were associated with offspring's increased concurrent depressive symptoms. Furthermore, reduced right hippocampal head volume mediated associations between maternal depression and increases in offspring depressive symptoms from age 9 to age 12. LimitationsThis study included a modest-sized sample that was oversampled for early temperamental characteristics, one neuroimaging assessment, and no correction for multiple comparisons. ConclusionsFindings implicate reductions in hippocampal head volume in the intergenerational transmission of risk from parents to offspring.

Prenatal alcohol and tobacco use and the risk of depression in offspring at age of 17 years: findings from the Raine Study

BackgroundPrenatal alcohol and tobacco exposures have been associated with adverse mental health consequences in offspring. The objective of this study was to test the associations between maternal prenatal alcohol and tobacco exposures and depressive symptoms in the offspring, adjusting for a wide range of potential confounders. MethodsWe used data from 1168 mother-offspring pairs from the Raine Study based in Perth, Western Australia. Depressive symptoms at age 17 years were measured using the Beck Depression Inventory for Youth (BDI-Y). Associations between prenatal alcohol and tobacco use and the risk of depressive symptoms in offspring were estimated by risk ratios (RR) derived with multivariable log-binomial regression. ResultsAmong offspring who were assessed for depressive symptoms, 5% were born to mothers who consumed six or more standard drinks of alcohol per week during pregnancy and 20% were exposed to prenatal tobacco. After adjustment for confounders, depressive symptoms at the age of 17 years remained associated with maternal alcohol use of six or more standard drinks per week [RR 1.59 (95% CI: 1.11-2.26)] and any tobacco use [RR 1.36 (95% CI: 1.05-1.79)] during the first trimester of pregnancy. ConclusionOffspring exposed to prenatal alcohol and tobacco use had greater risks of depressive symptoms compared with unexposed offspring, suggesting early screening and prevention of these exposures could possibly reduce depressive symptoms in offspring.