Symptoms In Offspring Research Articles

Prenatal tobacco exposure and the risk of conduct disorder symptoms in offspring at the age of 14 years: Findings from the Raine Study

BackgroundEmerging epidemiological evidence suggests that offspring born to mothers who smoked tobacco during pregnancy may have elevated risk of developing conduct disorder (CD) symptoms. We examined associations between maternal and paternal tobacco smoking during pregnancy and CD symptoms in offspring at the age of 14 years. MethodsWe obtained data from the Raine Study, a multi-generational cohort study based in Western Australia. DSM-oriented scale of the Child Behavior Checklist (CBCL) was used to measure CD symptoms in offspring. Negative binomial regression was used to estimate the rate ratio (risks) (RR) of CD symptoms in offspring. We also produced the E-values to investigate the extent of unmeasured confounding. Paternal smoking during pregnancy was used as a proxy for environmental tobacco smoke exposure. ResultsComplete data were available for 1747 mother-offspring and 1711 father-offspring pairs. After adjusting for potential confounders, we found elevated risks (rates) of CD symptoms in offspring born to mothers smoking tobacco during the first trimester [RR 1.52 (95 % CI: 1.24–1.87)], third trimester [RR 1.36 (95 % CI: 1.09–1.69)] and during both trimesters of pregnancy [RR 1.50 (95 % CI: 1.19–1.90)]. The rates of CD symptoms in offspring increased with the level of exposure to maternal smoking during pregnancy. However, we noted insufficient statistical evidence for an association between paternal smoking during pregnancy and CD symptoms in offspring. ConclusionThe associations we found for maternal but not paternal smoking may suggest a biological mechanism for intrauterine tobacco exposure on the risk of CD symptoms in offspring. Early interventions assisting pregnant mothers to quit tobacco smoking, or avoid smoking initiation, have potential to contribute health benefits to both mothers and their offspring.

Maternal immune activation generates anxiety in offspring: A translational meta-analysis

AimsMaternal immune activation (MIA) during pregnancy is recognized as an etiological risk factor for various psychiatric disorders, such as schizophrenia, major depressive disorder, and autism. Prenatal immune challenge may serve as a “disease primer” into an altered trajectory of fetal brain development that, in combination with other genetic and environmental factors, may ultimately result in the emergence of different psychiatric conditions. However, the association between MIA and the offspring's chances of developing anxiety disorders is less clear. To examine the effect of MIA on offspring anxiety, a systematic review and meta-analysis of the preclinical literature was conducted.MethodA systematic search of the PubMed, Web of Science, PsycINFO, and Cochrane Library electronic databases was performed using the PRISMA and WHO methodologies for systematic reviews. Studies that investigated if MIA during rodent's pregnancy could cause anxiety symptoms in offspring were included.ResultOverall, the meta-analysis showed that MIA induced anxiety behavior in offspring. The studies provide strong evidence that prenatal immune activation impacts specific molecular targets, synapse formation and function, and a disbalance in neurotransmission that could be related to the generation of offspring anxiety. Future research should further explore the role of MIA in anxiety endophenotypes.ConclusionAccording to this meta-analysis, MIA plays an important role in the pathophysiological mechanisms of anxiety disorders and provides a promising therapeutic target.

Maternal posttraumatic stress and FKBP5 Genotype interact to predict trauma-related symptoms in preschool-age offspring

BackgroundChildren of parents with posttraumatic stress (PTS) face heightened risk for developing emotional and behavioral problems, regardless of whether they experience a traumatic event themselves. The current study investigates whether child FKBP5, a stress relevant gene shown to interact with child trauma exposure to increase risk for PTS, also moderates the well-established link between maternal PTS and child symptoms. MethodsData are derived from a longitudinal lab-based study for which 205 dyads of trauma-exposed mothers and their preschool-age children from a sample enriched for violence exposure provided DNA samples and completed measures of maternal and child trauma-related symptoms. Hypotheses tested whether child FKBP5 rs1360780 SNP genotype interacts with child trauma exposure and maternal PTS to predict child trauma-related symptoms. ResultsHypotheses were partially supported, with maternal PTS predicting increased child symptoms for children carrying the minor T-allele (CT/TT), but not those homozygous for the major C-allele. LimitationsStudy results may not generalize to lower-risk or non-clinical populations, did not assess between-group differences in race/ethnicity, and do not consider other genes that may interact with FKBP5 or contribute to genetic risk for trauma-related impairment. ConclusionsThese findings provide the first evidence that the robust gene x environment interaction involving FKBP5 and child trauma exposure extends to other environmental perturbations, including maternal PTS. Our results highlight the importance of efforts to address trauma-related psychopathology in caregivers, which may disrupt intergenerational risk processes and improve outcomes for children.

Mother’s PCOS Diagnosis Is Not Associated With Behavioral Symptoms in Offspring at 4-5 years

Introduction: Variation in prenatal sex steroid concentrations has been linked to child behavioral problems, with higher maternal total and free testosterone associated with child internalizing and externalizing symptoms. Polycystic Ovary Syndrome (PCOS) is a hyperandrogenic disorder that results in elevated testosterone levels during pregnancy among affected women. Population-based analyses suggest a higher risk of depression and anxiety diagnosis in children of women with PCOS. Animal models of prenatal hyperandrogenism further support an association with increased anxiety in offspring. Within the context of a multi-center U.S. pregnancy cohort, we examined early childhood behavioral and social responsiveness in children born to mothers with and without PCOS. Methods: Pregnant women were recruited in their first trimester for The Infant Development and Environment Study (TIDES). PCOS status was determined by maternal reports of PCOS diagnosis or history of hirsutism/oligomenorrhea. Women who reported neither a history of PCOS or symptoms of hirsutism or oligomenorrhea served as a comparison group. When participating children were age 4, mothers completed the Behavioral Assessment System for Children, 2nd Edition (BASC-2), a measure of child behavior problems, and the Social Responsiveness Scale, 2nd Edition (SRS-2), a measure of social impairment consistent with autistic traits. We fit linear regression models considering three outcomes: (1) BASC-2 externalizing composite score (e.g., hyperactivity, aggression); (2) BASC internalizing composite score (e.g., anxiety, depression, somatization); and (3) SRS-2 total score, adjusting for covariates, maternal age, child age, race, study center, income, education, alcohol and tobacco use, child sex, maternal depression. For all outcomes, higher scores indicate more problematic behaviors. Results: A total of 360 mother/child pairs completed the 4-year assessment and were included in this analysis. This included 81 mothers with PCOS (37 male, 44 female) and 279 comparison mothers (132 male, 147 female). Mean maternal age at delivery was 30.7 years (±4.7) for PCOS cases and 31.9 years (±5.4) for comparison mothers. Interaction terms indicated no effect modification by child sex. In analyses combining both sexes, maternal PCOS was not associated with externalizing behaviors (β=1.81; 95% CI: ‐2.37, 6.0; p=0.40), internalizing behaviors (β=2.20; 95% CI: ‐2.14, 6.53; p=0.32), or social impairment (β=-0.34; 95% CI: ‐3.34, 2.65; p=0.82). Conclusions: In this prospective evaluation, we observed no association between maternal PCOS and neurobehavioral symptoms in children at age 4. Given that prior literature using population databases suggested increased behavioral symptoms in school-aged and older children of PCOS mothers, these symptoms may become more apparent with development and continued assessment is warranted.

Maternal Stress Predicts Dentate Gyrus Microstructure, Dentate Gyrus-Orbitofrontal Functional Connectivity, Decreased Cognitive Flexibility, Increased Rumination and Depressive Symptoms in Adult Offspring

Maternal Stress Predicts Dentate Gyrus Microstructure, Dentate Gyrus-Orbitofrontal Functional Connectivity, Decreased Cognitive Flexibility, Increased Rumination and Depressive Symptoms in Adult Offspring

Psychological distress among greek parents of children with an autism spectrum disorder: Is there a link to anxiety symptoms in neurotypical offspring?

IntroductionParents of children with an autism spectrum disorder (ASD) are at higher risk of suffering from mental health problems (MHP) than parents of children with other developmental disabilities. Research on the general population documented that MHP in parents contributes as a significant risk factor for maladjustment outcomes in their offspring, while parental anxiety disorders in particular have been associated with a higher prevalence of anxiety disorders in the offspring. However, evidence concerning possible associations between parent-offspring psychological problems in the case of ASD-families is scarce and inconsistent.This study forms a part of a larger PhD study and some preliminary findings have been partially discussed in previous work.ObjectivesTo investigate any association between anxiety symptoms in neurotypical offspring (ASD-siblings) with parental MHP.Methods118 parent-child-dyads from ASD-families that fulfilled inclusion criteria participated in this study and answered a demographic questionnaire. Parents were administered the GHQ-28, while the children answered the STAIC-A-Trait. A hierarchical multiple regression was performed to test the hypothesis.ResultsParticipating parents demonstrating poorer mental health, with 53 (44.9%) of them considered as suffering from psychological distress according to the score of GHQ-28. Furthermore, hierarchical regression showed that STAIC-(A-Trait) total score of ASD-siblings was associated with parental anxiety (std beta=0.292; p=0.29;model 1) and this association persisted after demographics entered the model (std beta=0.300; p=0.029; model 2).ConclusionsThis study shows a significant association between parental psychological distress and anxiety in the neurotypical offspring in ASD-families, highlighting the need to provide all members of ASD-families with the appropriate services.DisclosureNo significant relationships.

Risk of conduct and oppositional defiant disorder symptoms in offspring of parents with mental health problems: Findings from the Raine Study

BackgroundEpidemiological data indicate that paternal and maternal mental health difficulties are predictors of conduct disorder (CD) and oppositional defiant disorder (ODD) in offspring. We tested the association between maternal anxiety and depressive symptoms and paternal emotional problems with CD and ODD symptoms in adolescent offspring aged 17. MethodsData was from the Raine Study, a birth cohort study based in Western Australia. Offspring CD and ODD symptoms at age 17 years were measured using the DSM-oriented scales of the Child Behavior Checklist (CBCL). Depression, Anxiety, and Stress Scale (DASS) was used to assess maternal depressive and anxiety symptoms, and a self-reported questionnaire measured paternal emotional problems when the offspring was 10 years. Negative binomial regression model was used to explore associations. ResultsAdjusting for potential confounding factors, we found an increased risk of CD symptoms in the offspring of mothers with anxiety [RR = 1.76 (95%CI; 1.08–2.86)], depressive [RR = 1.40 (95%CI; 1.01–1.95)], and comorbid anxiety and depressive symptoms [RR = 2.24 (95%CI 1.35–3.72)]. We also found an increased risk of ODD symptoms in offspring of mothers with depressive [RR = 1.24 (95%CI 1.02–1.52)], but not anxiety symptoms [RR = 1.23 (95%CI 0.92–1.67)]. No associations were seen with paternal emotional problems. ConclusionOur study showed that adolescents whose mothers reported anxiety, depressive, and comorbid anxiety and depressive symptoms had a higher risk of CD and ODD symptoms at age 17. The findings have implications for preventive strategies.

Interpersonal Problems in Parents and Adolescent Borderline Personality Disorder Features.

Research shows that parental personality pathology is associated with borderline personality disorder features and internalizing/externalizing symptoms in offspring. However, studies have been limited by DSM-IV-based assessments of parental personality pathology. The authors leveraged evidence that interpersonal problems described by the Interpersonal Circumplex align with Criterion A of the DSM-5 Alternative Model for Personality Disorders and therefore used a measure of interpersonal problems to capture parental personality pathology. The authors hypothesized that parental interpersonal problems would be associated with a latent variable of borderline features in adolescent offspring. They also examined whether this relation with offspring borderline features existed above and beyond relations with offspring internalizing/externalizing symptoms, age, and gender. The sample included 524 inpatient adolescents (Mage = 15.31, 62.4% female) and their parents (80.5% female). Parental interpersonal problems demonstrated unique relationships with adolescent borderline features and externalizing symptoms, but not internalizing symptoms. Implications of the results, limitations, and future directions are discussed.

Systematic Review and Meta-analysis of Genetically Informed Research: Associations Between Parent Anxiety and Offspring Internalizing Problems

ObjectiveParent anxiety is associated with offspring internalizing problems (emotional problems related to anxiety and depression). This may reflect causal processes, whereby exposure to parent anxiety directly influences offspring internalizing (and/or vice versa). However, parent–offspring associations could also be attributable to their genetic relatedness. A systematic review and meta-analysis were conducted to investigate whether exposure to parent anxiety is associated with offspring internalizing after controlling for genetic relatedness.MethodA literature search across 5 databases identified 429 unique records. Publications were retained if they used a quasi-experimental design in a general population sample to control for participant relatedness in associations between parent anxiety and offspring internalizing outcomes. Publications were excluded if they involved an experimental exposure or intervention. Studies of prenatal and postnatal anxiety exposure were meta-analyzed separately. Pearson’s correlation coefficient estimates (r) were pooled using multilevel random-effects models.ResultsEight publications were retained. Data were drawn from 4 population cohorts, each unique to a quasi-experimental design: adoption, sibling-comparison, children-of-twins or in vitro fertilization. Cohorts were located in northern Europe or America. Families were predominantly of European ancestry. Three publications (Nfamilies >11,700; offspring age range, 0.5–10 years) showed no association between prenatal anxiety exposure and offspring internalizing outcomes after accounting for participant relatedness (r = .04; 95% CI: −.07, .14). Six publications (Nfamilies >12,700; offspring age range, 0.75–22 years) showed a small but significant association between concurrent symptoms in parents and offspring after accounting for participant relatedness (r = .13; 95% CI: .04, .21).ConclusionInitial literature, derived from homogeneous populations, suggests that prenatal anxiety exposure does not cause offspring internalizing outcomes. However, postnatal anxiety exposure may be causally associated with concurrent offspring internalizing via nongenetic pathways. Longitudinal stability, child-to-parent effects, and the role of moderators and methodological biases require attention.

Does maternal psychopathology bias reports of offspring symptoms? A study using moderated non-linear factor analysis.

Mood-state biases in maternal reports of emotional and behavioral problems in their children have been a major concern for the field. However, few studies have addressed this issue from a measurement invariance perspective. Using data from baseline assessment of the Adolescent Brain Cognitive Development (ABCD) study (n=8,507 mother-child dyads; youth aged 9-11years), we examined how dimensions of maternal psychopathology, including internalizing problems, were associated with indices of bias in reports of their children's dimensions of internalizing, externalizing, neurodevelopmental, detachment, somatoform psychopathology using moderated non-linear factor analysis. Moderated non-linear factor analyses examined multiple potential biases in maternal reports of youth psychopathology. Across analyses, we found very small magnitudes of associations between dimensions of maternal psychopathology and biases in reports of child emotional and behavioral problems. Based on these results, we find little psychometric evidence for maternal psychopathology biasing reports of child behavior problems.

Maternal depressive and anxiety symptoms and the risk of attention deficit hyperactivity disorder symptoms in offspring aged 17: Findings from the Raine Study

BackgroundWhile previous studies have suggested that maternal anxiety and depressive symptoms are associated with increased risk of attention-deficit/hyperactivity disorder (ADHD) in their offspring in early and late childhood, studies exploring the risk in late adolescence are however lacking. This study aims to examine the association between maternal anxiety and depressive symptoms and the risk of ADHD symptoms in late adolescence (at age 17). MethodsWe used data from the Raine Study. Maternal depressive and anxiety symptoms were measured when the child was 10 years of age using the Depression, Anxiety, and Stress Scale (DASS). Offspring ADHD symptoms at age 17 were assessed using the DSM-oriented scales of the child behavior checklist (CBCL). Log-binomial regression was used to explore the associations. ResultsWe found an increased risk of ADHD symptoms in offspring of mothers with comorbid anxiety and depressive symptoms when compared with offspring of mothers with no symptoms [RR 5.60 (95%CI 3.02-10.37)]. There was a nearly three-fold increase in the risk of ADHD symptoms in offspring of mothers with increased anxiety symptoms compared with offspring of mothers who were in the normal range [RR 2.84 (95%CI 1.18-6.83)]. No association was observed with maternal depressive symptoms. ConclusionThis study found an increased risk of ADHD symptoms in the offspring of mothers with anxiety as well as comorbid anxiety and depressive symptoms but not among the offspring of mothers with depressive symptoms. Early screening and intervention for ADHD symptoms in offspring with maternal anxiety and comorbid anxiety and depressive symptoms are warranted.

Maternal and paternal mental health problems and the risk of offspring depression in late adolescence: findings from the Raine study

Background There are limited studies on the risk of depressive symptoms in adolescent offspring exposed to parental mental health problems in middle childhood. Aim We investigated the association between parental mental health problems, particularly paternal emotional problems and maternal symptoms of anxiety and depression, and the risk of depressive symptoms in adolescent offspring aged 17. Methods The study included 995 parent-offspring pairs from the 1989–91 birth cohort (the Raine Study) in Western Australia. Log-binomial regression was used to assess the associations. Results An increased risk of depression symptoms was observed in the adolescent offspring of mothers with depressive [RR 1.45, 95% CI 1.13–1.86] as well as anxiety symptoms [RR 1.43, 95% CI 1.09–1.87].Compared to those non-exposed, offspring whose mothers reported comorbid anxiety and depressive symptoms were more likely to have developed depressive symptoms by late adolescence [RR 1.63, 95%CI 1.11–2.38]. An increased risk of depressive symptoms was also seen in the offspring of fathers with emotional problems [RR 1.29, 95%CI 1.01–1.53]. Conclusion Our findings suggest an increased risk of depressive symptoms in the adolescent offspring of parents with mental health problems, specifically paternal emotional problems (29%) and maternal anxiety (43%), depression (45%), as well as comorbid anxiety and depressive symptoms (63%).

Parental Family Violence and Mental Health among parents and their offspring in the Southern Province, Rwanda

Background
 Children who witness violence between parents have an elevated risk of developing mental disorders as well as being victims or perpetrator of family violence (FV) in their future relationships when compared with children from non-violent family.
 Objectives
 To assess links between both parental FV and mental disorders, and mental disorders in their offspring.
 Methods
 One hundred and thirty eight (138) participants dispatched in two categories: spouses/partners (N: 89; 40 Males) and offspring (N: 49; 20 Males) have been recruited from eight District Police Unities (DPU) of the Rwandan Southern Province to participate in this cross-sectional study during a 7 months period. This study used the student “t” to examine the links between parental FV and mental disorders in offspring.
 Results
 Parental FV was linked with PTSD, psychopathic and addiction behavior symptoms in offspring. Parental anxious attachment was linked with anxiety and addiction behavior symptoms in offspring and the risk of being perpetrator or victims of FV. Parental avoidant attachment was linked with depression symptoms in offspring. Further, both parental low self-esteem and PTSD were linked with depression and PTSD symptoms in offspring.
 Conclusion 
 The results indicate that FV and mental disorders experienced by parents seem to affect offspring’s mental health and generate specific mental disorders. Therefore, the intervention programs should focus on the treatment of both parental and children mental disorders.
 Rwanda J Med Health Sci 2020;3(3):291-314

Agmatine improves the behavioral and cognitive impairments associated with chronic gestational ethanol exposure in rats

Chronic maternal ethanol exposure leads to poor intelligence, impaired cognition and array of neurological symptoms in offsprings and commonly referred as fetal alcohol spectrum disorder (FASD). Despite high prevalence and severity, the neurochemical basis of FASD remains largely unexplored. The present study evaluated the pharmacological effects of agmatine in cognitive deficits associated with FAS in rat’s offsprings prenatally exposed to alcohol. Pregnant rats received ethanol in liquid modified diet during the entire gestational period of 21 days. Offsprings were treated with agmatine (20–80 mg/Kg, i.p.) during early postnatal days (PND: 21–35) and subsequently evaluated for anxiety in elevated plus maze (EPM), depression in forced swim test (FST) and learning and memory in Morris’s water maze (MWM) during post adolescent phase. Hippocampal agmatine, BDNF, TNF-α and IL-6 levels were also analyzed in prenatally ethanol exposed pups. Offsprings prenatally exposed to ethanol demonstrated delayed righting reflex, reduced exploratory behavior along with anxiety, depression-like behavior and impaired memory. These behavioral abnormalities were correlated with a significant reduction in hippocampal agmatine and BDNF levels and elevation in TNF-α and IL-6 immunocontent. Chronic agmatine (40 and 80 mg/Kg, i.p.) administration for 15 days (PND: 21–35), improved entries and time spent in open arm of EPM, decreased immobility time in FST. It also reduced latency to reach the platform location; increased the number of entries, time spent in platform quadrant and also number of crossing over platform quadrant when subjected to MWM test in prenatally ethanol exposed offsprings. This study provides functional evidences for the therapeutic potential of agmatine in cognitive impairment and other neurological complications associated with FASD.

Cord Serum Cytokines at Birth and Children’s Anxiety-Depression Trajectories From 3 to 8 Years: The EDEN Mother–Child Cohort

BackgroundRecent research suggests that immune dysregulation in pregnancy could be a risk factor for anxiety and depression symptoms in offspring. Whereas animal studies have demonstrated the importance of the link between perinatal cytokines and abnormal behaviors in offspring, human epidemiological studies in this area remain limited. The objectives of the study were to describe the network of cord serum cytokines at birth and test whether they are associated with subsequent anxiety and depression symptom trajectories in offspring. MethodsWe used data and biological samples from 871 mother–child pairs followed up from pregnancy to 8 years of age and participating in the French mother–child cohort EDEN (a study on the pre- and early postnatal determinants of child health and development). Cord serum cytokines were measured at birth. Children’s symptoms of anxiety and depression were assessed with the emotional difficulties subscore of the Strength and Difficulties Questionnaire at ages 3, 5, and 8 years, from which trajectories of anxiety-depression symptoms were derived. ResultsResults showed a significant association between cord serum interleukin-7 at birth and the trajectories of children’s anxiety-depression symptoms between ages 3 to 8 years (adjusted odds ratio, 0.73; 95% confidence interval, 0.57–0.93). The associations considered relevant confounders, including prenatal maternal depressive symptoms. ConclusionsEarly immune changes may contribute to subsequent anxiety and depression symptoms in childhood. Beyond the understanding of mechanisms underlying the occurrence of emotional difficulties in children, our findings open avenues for future research in human and animals.

Dietary Quality and Dietary Inflammatory Potential During Pregnancy and Offspring Emotional and Behavioral Symptoms in Childhood: An Individual Participant Data Meta-analysis of Four European Cohorts

BackgroundThe impact of maternal diet during pregnancy on child neurodevelopment is of public health and clinical relevance. We evaluated the associations of dietary quality based on the Dietary Approaches to Stop Hypertension (DASH) score and dietary inflammatory potential based on the energy-adjusted Dietary Inflammatory Index (E-DII) score during pregnancy with emotional and behavioral symptoms of offspring at 7 to 10 years of age. MethodsIndividual participant data for 11,870 mother–child pairs from four European cohorts participating in the ALPHABET project were analyzed. Maternal antenatal DASH and E-DII scores were generated from self-completed food frequency questionnaires. Symptoms of depression and anxiety, aggressive behavior, and attention-deficit/hyperactivity disorder in children were assessed using mother-reported tests and classified within the normal or borderline/clinical ranges using validated cutoffs. Adjusted odds ratios were determined by multivariable logistic regression models and aggregated by the two-level individual participant data meta-analysis method. ResultsHigher maternal DASH scores (indicating better dietary quality) were associated with lower risk of depressive and anxiety symptoms, aggressive behavior symptoms, and attention-deficit/hyperactivity disorder symptoms within the borderline/clinical ranges: odds ratio [OR] 0.97, 95% confidence interval [CI], 0.95–0.99; OR 0.97, 95% CI, 0.94–0.99; OR 0.97, 95% CI, 0.95–0.98, per one-unit DASH score increase, respectively. For depression and anxiety, aggressive behavior, and attention-deficit/hyperactivity disorder symptoms, a one-unit increase in E-DII scores (a more proinflammatory diet) was associated with a 7% increased risk of all three analyzed emotional and behavioral symptoms: OR 1.07, 95% CI, 1.03–1.11; OR 1.07, 95% CI, 1.02–1.13; OR 1.07, 95% CI, 1.01–1.13, respectively. ConclusionsOur findings suggest that a maternal low-quality and proinflammatory diet may increase the risk of emotional and behavioral symptoms in children.

Maternal Ferritin Levels during Pregnancy and ADHD Symptoms in 4-Year-Old Children: Results from the INMA-INfancia y Medio Ambiente (Environment and Childhood) Prospective Birth Cohort Study.

Ferritin status during prenatal brain development may influence the risk of attention deficit and hyperactivity disorder (ADHD) symptoms in childhood. We investigated the association of maternal ferritin in pregnancy and ADHD-like symptoms in offspring. A total of 1095 mother-child pairs from three birth cohorts of the INMA Project (Spain) were studied. Maternal plasma ferritin in pregnancy was measured at 11.57 weeks of gestation. Children′s ADHD-like symptoms at ages 4–5 years were assessed using the ADHD Rating Scale-IV. The count model of the zero-inflated Poisson regression model showed a significant inverse association between ferritin (continuous variable) and inattention, β = −0.19 (−0.32, −0.07), for boys. Comparing ferritin level by tertiles, significant differences were observed between the first tertile ([1.98, 20.92]) and the second ([20.92, 38.79]) and third tertiles ([38.79, 216.5]) (mg/L).The number of symptoms was lower for those in the third tertile, β = −0.3 (−0.55, −0.5), and for those in the second one, β = −0.37 (−0.6, −0.14). The model stratification by sex also showed this inverse association for boys only, β = −0.21 (−0.34, −0.08). No associations were found between ferritin level and hyperactivity or total ADHD symptoms. High ferritin levels during pregnancy show a protective association with child inattentive-type ADHD symptoms.

Preventing the Onset of Anxiety Disorders in Offspring of Anxious Parents: A Six-Year Follow-up.

This study examined the effects of a family-based intervention Coping and Promoting Strength (CAPS) relative to a control condition, information-monitoring (IM), to prevent the onset of anxiety disorders in offspring of anxious parents sixyears after their initial assessment. One hundred thirty six families participated in the original randomized trial; 113 (83%) completed the one time follow-up assessment. Presence of anxiety disorders and severity of symptoms in offspring were assessed by masked evaluators using the Anxiety Disorders Interview Schedule; parents and offspring also completed questionnaires assessing offspring anxiety. Using the intentionto treat sample from the original trial, Cox regression models showed significant intervention main effects in the rate of onset of anxiety disorders from baseline to follow-up (anxiety disorder: hazard ratio (HR) = 2.55, 95% CI: 1.54, 4.21) but growth curves suggest effects occurred within the first year after program completion. No group differences were found in the cumulative incidence of anxiety disorders at the six-year follow-up. Additional intervention appears needed to maintain the initial positive effects long-term to reduce the risk for downstream disability.Clinical Trials Registration: NCT00847561.

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.

Intergenerational Transmission of Parental Neuroticism to Emotional Problems in 8-Year Old Children: Genetic and Environmental Mechanisms

Background: 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) vs. to shared genetic risk. Methods: This study is based on data from the Norwegian Mother, Father and Child Cohort Study. We used data from 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). Outcomes: After accounting for assortative mating in parents (phenotypic r=0.26), genetic transmission of maternal neuroticism accounted for 16% of the correlation with offspring neuroticism (mother-child r=0.31), 18% of the association with offspring depressive symptoms (r=0.31), and 0% of the association with offspring anxiety symptoms (r=0.16). Intergenerational transmission of genes associated with paternal neuroticism accounted for ~40% 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 was explained by maternal influences through assortative mating. Interpretations: These results are consistent with direct effects between maternal and offspring neuroticism and between maternal neuroticism and offspring symptoms of anxiety and depression, suggesting that interventions targeted at family functioning could benefit the children. Funding Statement: This work was supported by the Research Council of Norway (RCN) (262177). E.M.E. and L.C.G. were funded by the RCN (262177). E.Y. was funded by the RCN (288083 and 262177). A.H. was supported by the South-Eastern Norway Regional Health Authority (2018059 and 2020022). T.A.McA. was supported by a Sir Henry Dale Fellowship, jointly funded by the Wellcome Trust and the Royal Society (107706/Z/15/Z) and the RCN (288083). L.J.H. was supported by funding from the SouthEastern Norway Regional Health Authority (2018058). F.A.T. was supported by the RCN (300668). This work was partly supported by the RCN through its Centres of Excellence funding scheme, project number 262700. Declaration of Interests: The authors have declared that they have no competing or potential conflicts of interest. Ethics Approval Statement: The establishment of MoBa and initial data collection was based on a license from the Norwegian Data protection agency and approval from The Regional Committees for Medical and Health Research Ethics. The MoBa cohort is based on regulations based on the Norwegian Health Registry Act. The current study was approved by The Regional Committees for Medical and Health Research Ethics.