Symptoms In Offspring Research Articles

Like father like daughter: sex-specific parent-of-origin effects in the transmission of liability for psychotic symptoms to offspring.

Children of parents with major mood and psychotic disorders are at increased risk of psychopathology, including psychotic symptoms. It has been suggested that the risk of psychosis may be more often transmitted from parent to opposite-sex offspring (e.g., from father to daughter) than to same-sex offspring (e.g., from father to son). To test whether sex-specific transmission extends to early manifestations of psychosis, we examined sex-specific contributions to psychotic symptoms among offspring of mothers and fathers with depression, bipolar disorder and schizophrenia. We assessed psychotic symptoms in 309 offspring (160 daughters and 149 sons) aged 8-24 years (mean=13.1, s.d.=4.3), of whom 113 had a mother with schizophrenia, bipolar disorder or major depression and 43 had a father with schizophrenia, bipolar disorder or major depression. In semi-structured interviews, 130 (42%) offspring had definite psychotic symptoms established and confirmed by psychiatrists on one or more assessments. We tested the effects of mental illness in parents on same-sex and opposite-sex offspring psychotic symptoms in mixed-effect logistic regression models. Psychotic symptoms were more prevalent among daughters of affected fathers and sons of affected mothers than among offspring of the same sex as their affected parent. Mental illness in the opposite-sex parent increased the odds of psychotic symptoms (odds ratio (OR)=2.65, 95% confidence interval (CI) 1.43-4.91, P=0.002), but mental illness in the same-sex parent did not have a significant effect on psychotic symptoms in offspring (OR=1.13, 95% CI 0.61-2.07, P=0.697). The opposite-sex-specific parent-of-origin effects may suggest X chromosome-linked genetic transmission or inherited chromosomal modifications in the etiology of psychotic symptoms.

The role of prenatal maternal stress in the development of childhood anxiety symptomatology: The QF2011 Queensland Flood Study.

It is possible that findings suggesting a link between prenatal maternal stress (PNMS) and anxiety symptoms in offspring are confounded by postnatal and/or shared mother-child heritability effects. Following exposure to a natural disaster, the Queensland Flood Study investigated the unique and additive effects of various types of disaster-related PNMS (objective hardship, cognitive appraisal, and subjective distress) on childhood anxiety symptomatology (internalizing and/or anxiety symptom measures). Timing of flood exposure during pregnancy and child sex were examined as potential moderators. After controlling for maternal psychosocial factors, greater objective hardship as a result of the floods was significantly associated with greater anxiety symptoms (N = 114) and marginally associated with greater internalizing behaviors (N = 115). Earlier timing of the flood in pregnancy was associated with greater anxiety symptoms. No such associations were found between any PNMS measure and teacher-rated child internalizing behaviors (N = 90). Sex and timing did not moderate associations. Our findings suggest that, in isolation, increased maternal hardship due to exposure to an independent stressor, during pregnancy, may have a programming effect on childhood anxiety symptoms.

Do Parental Psychiatric Symptoms Predict Outcome in Children With Psychiatric Disorders? A Naturalistic Clinical Study

Parental psychiatric symptoms can negatively affect the outcome of children's psychopathology. Studies thus far have mainly shown a negative effect of maternal depression. This study examined the associations between a broad range of psychiatric symptoms in mothers and fathers and the child's outcome. Internalizing and externalizing psychiatric symptoms were assessed in 742 mothers, 440 fathers, and their 811 children at the first evaluation in 3 child and adolescent psychiatric outpatient clinics and at follow-up (on average 1.7 years later). Predictions of child's symptoms scores were tested at follow-up by parental symptom scores at baseline, parental scores at follow-up, and offspring scores at baseline. Children whose mother or father scored above the (sub)clinical threshold for psychiatric symptoms at baseline had higher symptom scores at baseline and at follow-up. Offspring follow-up scores were most strongly predicted by offspring baseline scores, in addition to parental psychiatric symptoms at follow-up. Offspring symptom scores at follow-up generally were not predicted by parental scores at baseline. Maternal and paternal associations were of similar magnitude. Higher symptom scores at follow-up in children of parents with psychopathology were mainly explained by higher symptom scores at baseline. Continuing parent-offspring associations could be a result of reciprocal effects, ie, parental symptoms influencing offspring symptoms and offspring symptoms influencing parental symptoms. Nevertheless, the results show that these children are at risk for persisting symptoms, possibly indicating the need to treat maternal and paternal psychopathology.

Reduced reward responsiveness moderates the effect of maternal depression on depressive symptoms in offspring: evidence across levels of analysis.

Reduced reward responsiveness (RR) may contribute to depression vulnerability. At the neurophysiological level, RR is reliably and validly assessed using the reward positivity (RewP) event-related potential component. We previously identified a blunted RewP in 9-year-old children at high risk for depression due to maternal depression, but the role of RR in pathways from parental history to the development of depressive symptoms has not been examined. At age 9, never-depressed children (N=369) completed a task in which RewP was measured in response to monetary reward and loss feedback. Parental history of depression was assessed using semistructured interviews, and children reported on their depressive symptoms. At age 12, youth depressive symptoms were reassessed, along with a self-report measure of RR. We tested RR as a moderator of the effects of parental depression on depressive symptoms at age 12, using both neurophysiological and self-report measures and controlling for age 9 symptoms. Main effects of RR and interactions with maternal depression were significant. Maternal depression predicted greater depressive symptoms in youth with blunted and average RewP but was not a significant predictor in youth with an enhanced RewP. A similar pattern was observed for self-reported RR. The two measures of RR were not correlated with each other and accounted for unique variance in symptoms. Interactions between RR and paternal depression were not significant. Reduced RR, as measured by neurophysiology and self-report, moderates the effects of maternal depression on depressive symptoms in offspring. Assessment of RR along with risk factors such as parental depression may aid in identifying children at greatest risk and enhancing RR could be a potential target for prevention. Results highlight the utility of multimethod approaches for advancing understanding of depression risk.

Memantine rescues prenatal citalopram exposure-induced striatal and social abnormalities in mice

Prenatal exposure to citalopram (CTM), an antidepressant drug, has been associated with altered behavior, including autism-like symptoms in both human and rodent offspring. However, the neurological basis underlying these abnormal behaviors is not well understood. Here, we examined behavioral, morphological, and biochemical alterations in the male and female offspring of C57BL/6 mouse mothers that had been exposed to CTM during the last trimester of gestation. We observed abnormal behavior such as anxiety, altered locomotion and disordered social interactions in 2–5 months old offspring with prenatal CTM exposure. Using Golgi-Cox staining, we found that CTM caused significantly reduced dendritic length and number of dendritic branches in striatal neurons, as well as altered subunit levels of N-methyl-d-aspartate receptors (NMDARs) and calcium/calmodulin-dependent protein kinase II (CaMKII). Memantine, a selective NMDAR antagonist, improved prenatal CTM-induced abnormal protein levels and social interaction deficits. These results highlight potential mechanisms underlying the abnormal behavior observed in children who are prenatally exposed to CTM.

F33. MATERNAL AND PATERNAL CANNABIS USE DURING PREGNANCY AND RISK OF PSYCHOTIC SYMPTOMS IN THE OFFSPRING

BackgroundCannabis use has repeatedly been associated with psychotic symptoms, with persistent risks beyond the direct effects of exogenous cannabinoids. However, it remains unknown whether cannabis use during pregnancy is a causal risk factor for psychotic symptoms in the offspring, or whether this relationship is explained by shared etiological factors, such as genetic and environmental vulnerabilities. More innovative study designs are needed to address this question. Here, we examined the adverse effects of cannabis exposure during pregnancy on psychotic symptoms in pre-adolescent offspring. Such a method would help causal inference as comparisons can be made between the observed associations of maternal versus paternal cannabis use during pregnancy and the risk of psychotic symptoms in the offspring. If the association between cannabis use and psychotic symptoms is causal, early intra-uterine exposure to cannabis could potentially affect neurodevelopment and, hence, contribute to the pathogenesis of psychotic phenomena in children who have not yet used cannabis themselves.MethodsThis study used data from the Generation R Study, a prospective population-based birth cohort from Rotterdam, the Netherlands. Participants were included if data on maternal cannabis use during pregnancy of offspring psychotic-like symptoms at age ten years were available (N = 3692). To determine cannabis exposure, we used prospective maternal self-reports during pregnancy and cannabis metabolite levels from urine. Paternal cannabis use during pregnancy was obtained through maternal report. At age ten years, children were queried regarding psychotic symptoms. Ordinal logistic regression was conducted to investigate whether maternal and paternal cannabis use were associated with offspring psychotic symptoms. In a secondary analysis, a distinction was made between maternal cannabis use exclusively before versus continued maternal cannabis use during pregnancy. All models were adjusted for covariates that were previously associated with cannabis use in this cohort.ResultsMaternal cannabis use was associated with an increased risk for psychotic symptoms in their offspring (n = 183, ORadjusted=1.38 [95% CI 1.03–1.85]). Estimates were comparable for cannabis use exclusively before pregnancy versus continued cannabis during pregnancy (cannabis use before pregnancy: n = 98, ORadjusted=1.39 [95% CI 0.94–2.06]; continued cannabis use during pregnancy: n = 85, ORadjusted=1.37 [95% CI 0.90–2.08]). Paternal cannabis use was significantly associated with offspring psychotic symptoms (n = 297, ORadjusted=1.44 [95% CI 1.14–1.82]).DiscussionUsing data from a large population-based birth cohort, we demonstrated that maternal and paternal cannabis use were each associated with offspring psychotic symptoms at age ten years, well before the risk period of adolescent cannabis use initiation. Notably, estimates were similar for maternal cannabis use exclusively before pregnancy versus continued cannabis use during pregnancy. Moreover, estimates were comparable for maternal versus paternal cannabis use during pregnancy. This suggests that common etiologies, rather than solely causal intra-uterine mechanisms, underlie the association between parental cannabis use and offspring psychotic symptoms, shedding potential new light on the debated causal path from cannabis use to psychosis. Our findings indicate that diagnostic screening and preventative measures need to be adapted for young people at risk for severe mental illness, and that these programs need to offer a family-focused approach.

Prenatal diet and children's trajectories of hyperactivity-inattention and conduct problems from 3 to 8years: the EDEN mother-child cohort.

Evidence shows that diet contributes substantially to lifelong physical and mental health. Although dietary exposure during gestation and early postnatal life is critical, human epidemiological data are limited regarding its link with children's subsequent externalizing issues. The aim of this study was to investigate the role of maternal diet during pregnancy in offspring's symptoms of hyperactivity-inattention and conduct problems from ages 3 to 8years. We used data of 1,242 mother-child pairs from a French cohort followed up from pregnancy until the children were 8years of age. Dietary patterns (DP) of the mother during pregnancy were assessed with food frequency questionnaires. Children's externalizing behavior was assessed with the Strength and Difficulties Questionnaire at ages 3, 5, and 8years, from which trajectories of hyperactivity-inattention symptoms and conduct problems were derived. We conducted multivariable logistic models to study associations adjusted for a range of potential confounders. Results showed significant relationships between maternal 'low Healthy diet' (adjusted Odds Ratio (aOR)=1.61; IC 95%: 1.09-2.37) and 'high Western diet' (aOR=1.67; IC 95%: 1.13-2.47) during pregnancy and children's trajectories of high symptoms of hyperactivity-inattention. The associations took into account relevant confounders such as DP of the children at age 2years, maternal stress and depression, gestational diabetes, and socioeconomic variables. Maternal diet during pregnancy was independently associated with children's hyperactivity-inattention symptoms but not with conduct problems. Early prevention addressing lifestyle should specifically target diet in pregnant women.

Maternal protein malnutrition induces autism-like symptoms in rat offspring

Objective: We tested the correlation between maternal protein malnutrition and autistic-like symptoms using behavioral tests in rodents that measure main behavioral characteristics observed in humans with autism spectrum disorder (ASD).Methods: Pregnant female rats were fed a normal diet or a hypoproteic diet during gestation and lactation periods. The litters were weighed every 3 days during lactation, and the offspring were tested in behavioral tasks during infancy (postnatal day (PND) 5: quantification of ultrasonic vocalizations; PND 13: homing behavior test) and adolescence (PND 30–32: open field, hole-board, play social behavior, and object recognition tests) in order to capture the prevalence of some of the core and associated symptoms of ASD.Results: Litters of the hypoproteic diet group had a lesser weight gain during lactation. In addition, pups of dams fed with a hypoproteic diet vocalized less compared to those fed with a normal diet, and they showed impaired social discrimination abilities in the homing behavior test. In adolescence, both male and female offspring of the hypoproteic diet group showed no impairment in locomotor activity; however, they exhibited stereotypic behavior in the hole-board test and a decrease in social play behaviors. Male offspring showed increased interest in exploring a familiar object rather than a novel object.Conclusion: Our results show that maternal protein malnutrition in rats causes offspring behaviors that resemble core and associated ASD symptoms.

Repercussões da Conjugalidade em Sintomas Internalizantes e Externalizantes em Filhos Adolescentes

Resumo A conjugalidade dos cuidadores reverbera no desenvolvimento dos filhos, entretanto, especificidades nessa relação ainda necessitam estudos nacionais. Investigou-se a percepção de adolescentes sobre o relacionamento conjugal de seus cuidadores e quais dimensões da conjugalidade repercutem em sintomas internalizantes e externalizantes dos mesmos. Realizou-se uma pesquisa quantitativa e explicativa. 115 adolescentes responderam ao Familiograma, FBQ, CTS2 e YSR. Verificou-se correlação positiva e significativa entre percepção de conflito e violência conjugal com os sintomas, bem como correlação negativa e significativa de afetividade e aliança parental com sintomas. Violência psicológica conjugal, cometida pela mãe, foi preditora de sintomas internalizantes e externalizantes dos filhos e a aliança parental foi preditora de sintomas externalizantes. Ressalta-se a necessidade de atuação preventiva em núcleos familiares com violência.

The effect of paternal depression on depressive symptoms in adolescent offspring

The effect of paternal depression on depressive symptoms in adolescent offspring

Treatment of psychiatric symptoms among offspring of parents with bipolar disorder.

Bipolar disorder is highly familial and has a protracted and diagnostically confusing prodrome. This review critically evaluates recently published literature relevant to the treatment of psychiatric symptoms in high-risk offspring of parents with Bipolar Disorder. Non-pharmacological treatment options including psychotherapy, resilience promotion through good sleep, diet, and exercise hygiene, and omega-3 fatty acid supplementation are important first line interventions for high-risk offspring. There has been some success in treating this population with open-label trials with mood stabilizers and atypical antipsychotics; however, these results have not been replicated in randomized controlled trails. Despite some progress in early identification of symptoms in offspring of parents with Bipolar Disorder, there is scarce evidence supporting the treatment of these high-risk youth to prevent psychiatric symptoms from progressing to threshold bipolar or other psychiatric disorders. There is a need for prospective and randomized trials and research that identifies reliable biomarkers to individualize treatments for these youth.

3.30 Parent-Child Agreement in Assessment of Anxiety, Mood, and Sleep Disorder Symptoms in Offspring of Bipolar Parents

3.30 Parent-Child Agreement in Assessment of Anxiety, Mood, and Sleep Disorder Symptoms in Offspring of Bipolar Parents

Perinatal Exposure to the Cyanotoxin β-N-Méthylamino-L-Alanine (BMAA) Results in Long-Lasting Behavioral Changes in Offspring-Potential Involvement of DNA Damage and Oxidative Stress.

We recently demonstrated that perinatal exposure to the glutamate-related herbicide, glufosinate ammonium, has deleterious effects on neural stem cell (NSC) homeostasis within the sub-ventricular zone (SVZ), probably leading to ASD-like symptoms in offspring later in life. In the present study, we aimed to investigate whether perinatal exposure to another glutamate-related toxicant, the cyanobacterial amino acid β-N-methylamino-L-alanine (BMAA), might also trigger neurodevelopmental disturbances. With this aim, female mice were intranasally exposed to low doses of BMAA, 50mgkg-1 three times a week from embryonic days 7-10 to postnatal day 21. Behavioral analyses were performed during the offspring's early life and during adulthood. Developmental analyses revealed that perinatal exposure to BMAA hastened the appearance of some reflexes and communicative skills. BMAA-exposed offspring displayed sex-dependent changes in emotional cognition shortly after exposure. Later in life, the female offspring continued to express emotional defects and to display abnormal sociability, while males were less affected. To assess whether early exposure to BMAA had deleterious effects on NSC homeostasis, we exposed mice NSCs to 1 and 3mM BMAA during 24h. We found that BMAA-exposed NSCs produced high levels of ROS, highlighting the ability of BMAA to induce oxidative stress. We also showed that BMAA exposure increased the number of γH2AX/53BP1 foci per nucleus, suggesting that BMAA-induced DNA damage in NSCs. Collectively, this data strongly suggests that perinatal exposure to the cyanobacteria BMAA, even at low doses, results in neurobehavioral disturbances during both the postnatal period and adulthood. This is considered to be underpinned at the cellular level through dysregulation of NSC homeostasis in the developing brain.

Maternal body mass index: Relation with infant respiratory symptoms and infections.

Maternal obesity is increasingly prevalent in many westernized countries. Many studies report associations between maternal obesity and childhood wheeze or asthma but few have considered maternal obesity in relation to respiratory infections or symptoms other than wheeze during infancy. This study assesses the relationship between maternal BMI and reported wheeze, cough and respiratory infections during the first year of life. In 2799 mother-child pairs, we examined the relations between maternal pre-pregnancy BMI and pregnancy weight gain and reported offspring wheeze, prolonged cough, lower respiratory tract infection, croup, and ear infection before age 1 year, along with reported diarrhea or vomiting. Maternally reported paternal BMI was included in the models as a proxy for unmeasured confounding by shared familial factors. Higher maternal BMI was associated with increased risks of offspring wheeze, prolonged cough and lower respiratory tract infection (relative risks (95%CI) per 5 kg/m2 1.09 (1.05-1.13), 1.09 (1.03-1.14), and 1.13 (1.07-1.20), respectively). These associations remained after adjusting for maternally reported paternal BMI. No associations were found with croup, ear infection, or diarrhea or vomiting. Pregnancy weight gain was not associated with any of the offspring symptoms or illnesses. Higher maternal BMI is associated with increased risk of wheeze, cough, and maternally reported lower respiratory tract infection in infancy. These associations were independent of maternally reported paternal BMI. These observations might be explained by intrauterine effects of maternal obesity upon respiratory or immune development.

Attenuated psychotic symptoms in children and adolescent offspring of patients with schizophrenia

ObjectiveTo compare the offspring of patients with SZ (SZoff) with those of a community control group (CC-off) to determine the variables associated with attenuated psychotic symptoms (APS), general symptomatology and functioning that may help to differentiate those at genetic risk for SZ. Methods41 SZ-off and 107 CC-off aged 6–17years were included. The Structured Interview for Prodromal Symptoms (SIPS), scored on the Scale of Prodromal Symptoms (SOPS), was administered by a child psychiatrist blinded to parental diagnoses, together with other clinical and functional scales. ResultsThe SZ-off group presented higher scores in positive (p=0.000), negative (p=0.012), and disorganized (p=0.009) subscale scores, as well as in the total score (p=0.001) on the SOPS when compared with the CC-off group. Other scales indicated significant emotional (p=0.028), behavioral (p=0.000) and peer-related problems (p=0.025), lower performance at school (p=0.025) and increased dysfunction score (p=0.005) in the SZ-off group. Logistic regression analysis revealed lower socioeconomic statuses (OR: 0.92, 95%CI: 0.87–0.97) and higher SOPS positive subscale scores (OR: 2.41, 95%CI: 1.31–4.42) in the SZ-off group. ConclusionsSZ-off presented significantly more APS and higher mean scores in psychopathological scales than CC-off, together with increased dysfunction scores. These early warning signs and follow-up for those at genetic high risk for schizophrenia will provide useful information about symptom progression, facilitating early intervention to improve short and long-term outcomes in youths with a positive family history.

Maternal infection and stress during pregnancy and depressive symptoms in adolescent offspring

Maternal infection during pregnancy has been linked to increased risk of offspring depression. Additionally, maternal stress during pregnancy has been consistently linked with adverse offspring outcomes associated with depression. Relatedly, stress has been associated with increased risk of infection; however no study has investigated stress-infection interactions during pregnancy and risk for offspring depression. Participants were drawn from the Child Health and Development Studies (CHDS), a prospective, longitudinal study that enrolled pregnant women from 1959 to 1966. Maternal health and birth outcome information were collected, as well as open-ended interviews about worrisome events during pregnancy. The present study included participants from a subsample of women whose offspring (n = 1711) completed self-reports of depressive symptoms during adolescence. Results indicated that maternal infection during only the second trimester was associated with higher scores on adolescent offspring depressive symptoms, while controlling for maternal education at birth, adolescent age, and maternal depressive symptoms at adolescence. Maternal experiences of daily stress during pregnancy moderated this association, such that mothers diagnosed with second trimester infection and who experienced daily stress had offspring with significantly higher depression scores than mothers of adolescents diagnosed with an infection alone. Findings have potential implications for prevention and intervention strategies.

Transgenerational trauma in a post-conflict setting: Effects on offspring PTSS/PTSD and offspring vulnerability in Cambodian families

We assessed transgenerational effects of maternal traumatic exposure, posttraumatic stress symptoms and posttraumatic stress disorder on trauma-related symptoms in Cambodian offspring born after the genocidal Khmer Rouge Regime. We conducted a randomized cross-sectional study. N=378 mothers from 4 provinces of the country and one of each of their grown-up children were interviewed. Lifetime traumatic exposure was determined using a context-adapted event list. Present posttraumatic stress symptoms and a potential posttraumatic stress disorder were assessed using the civilian version of the Posttraumatic Stress Disorder Checklist. We found no indication of transgenerational effects that were directly related to maternal traumatic exposure, posttraumatic stress symptoms or posttraumatic stress disorder. Instead, a gender-specific moderating effect was found. Individual traumatic exposure had a stronger effect on posttraumatic stress symptoms in daughters, the higher the mother's lifetime traumatic exposure. There is evidence of an interaction between lifetime traumatic exposure of mothers and their offspring that can be interpreted as an increased vulnerability to symptoms of posttraumatic stress in daughters. The mechanisms of transgenerational trauma in the Cambodian context require further research, as learning from previous conflicts will be instructive when addressing the pressing humanitarian needs of today's world.

Is there a link between biological parents' insight into their offspring's schizophrenia and their cognitive functioning, expressed emotion and knowledge about disorder?

BackgroundRecent studies suggest that parents' awareness of their offspring's schizophrenia could influence their offspring's insight. Low patient insight is linked to impairment of specific cognitive abilities, and biological parents of schizophrenia patients have impaired capacities in these same domains. However, little is known about what specific socio-demographic, affective or cognitive factors may influence biological parents' awareness of their offspring's disease. MethodData were drawn from 41 patient–parent dyads. Insight was assessed with a modified version of Amador's Scale to assess Unawareness of Mental Disorders, exploring dimensions of parents' awareness and attribution of their offspring's illness and symptoms. ResultsHigher educational levels, better working memory and executive functioning of parents were associated with better attribution of their offspring's symptoms to schizophrenia. ConclusionsParents' insight into their offspring's schizophrenia is associated with cognitive abilities. This must be taken into account when developing family interventions.

Maternal hypothyroxinaemia in early pregnancy and problem behavior in 5-year-old offspring

IntroductionThere is evidence, though not consistent, that offspring born to mothers with subtle decreases in thyroid function early in their pregnancies may be at risk of cognitive impairments and attention problems. However, other types of problem behavior have not been addressed thus far. We tested whether maternal thyroid function in early pregnancy is associated with several types of problem behavior in offspring at age 5–6 years. MethodsThis was a longitudinal study that included the data of 2000 mother-child pairs from the Amsterdam Born Children and their Development study. At a median gestational age of 12.9 (interquartile range: 11.9–14.1) weeks, maternal blood was sampled for assessment of free T4 and TSH. Overall problem behavior, hyperactivity/inattention, conduct problems, emotional problems, peer relationship problems and prosocial behavior were measured at age 5–6 years using the Strengths and Difficulties Questionnaire, which was filled out by both parents and teachers. ResultsMaternal hypothyroxinaemia <5th percentile was associated with a 1.70 (95% confidence interval (CI): 1.01–2.86) increased odds of teacher-reported hyperactivity/inattention after adjustment for confounders. By increasing the cut-off level to <10th percentile, the odds ratio became 1.47 (95% CI: 0.99–2.20). There were no associations between maternal thyroid function parameters and hyperactivity/inattention as reported by parents, nor with teacher or parent reports of other types of problem behavior. ConclusionsOur results partially confirm previous observations, showing that early disruptions in the maternal thyroid hormone supply may be associated with ADHD symptoms in offspring. Our study adds that there is no evidence for an effect on other types of problem behavior.

Fish and seafood consumption during pregnancy and the risk of asthma and allergic rhinitis in childhood: a pooled analysis of 18 European and US birth cohorts.

It has been suggested that prenatal exposure to n-3 long-chain fatty acids protects against asthma and other allergy-related diseases later in childhood. The extent to which fish intake in pregnancy protects against child asthma and rhinitis symptoms remains unclear. We aimed to assess whether fish and seafood consumption in pregnancy is associated with childhood wheeze, asthma and allergic rhinitis. We pooled individual data from 60 774 mother-child pairs participating in 18 European and US birth cohort studies. Information on wheeze, asthma and allergic rhinitis prevalence was collected using validated questionnaires. The time periods of interest were: infancy (0-2 years), preschool age (3-4 years), and school age (5-8 years). We used multivariable generalized models to assess associations of fish and seafood (other than fish) consumption during pregnancy with child respiratory outcomes in cohort-specific analyses, with subsequent random-effects meta-analyses. The median fish consumption during pregnancy ranged from 0.44 times/week in The Netherlands to 4.46 times/week in Spain. Maternal fish intake during pregnancy was not associated with offspring wheeze symptoms in any age group nor with the risk of child asthma [adjusted meta-analysis relative risk (RR) per 1-time/week = 1.01, 95% confidence interval 0.97-1.05)] and allergic rhinitis at school age (RR = 1.01, 0.99-1.03). These results were consistently found in further analyses by type of fish and seafood consumption and in sensitivity analyses. We found no evidence supporting a protective association of fish and seafood consumption during pregnancy with offspring symptoms of wheeze, asthma and allergic rhinitis from infancy to mid childhood.