Neonatal anxiety and depression and breastfeeding cessation are significant public health problems. There is an association between maternal symptoms of anxiety and depression and early breastfeeding ...cessation. In earlier studies, the causality of this association was interpreted both ways; symptoms of anxiety and depression prepartum significantly impacts breastfeeding, and breastfeeding cessation significantly impacts symptoms of anxiety and depression.First, we aimed to investigate whether breastfeeding cessation is related to an increase in symptoms of anxiety and depression from pregnancy to six months postpartum. Second, we also investigated whether the proposed symptom increase after breastfeeding cessation was disproportionately high for those women already suffering from high levels of anxiety and depression during pregnancy.
To answer these objectives, we examined data from 42 225 women in the Norwegian Mother and Child Cohort Study (MoBa). Subjects were recruited in relation to a routine ultra-sound examination, and all pregnant women in Norway were eligible. We used data from the Medical Birth Registry of Norway and questionnaires both pre and post partum. Symptoms of anxiety and depression at six months postpartum were predicted in a linear regression analysis by WHO-categories of breastfeeding, symptoms of anxiety and depression prepartum (standardized score), and interaction terms between breastfeeding categories and prepartum symptoms of anxiety and depression. The results were adjusted for cesarean sections, primiparity, plural births, preterm births, and maternal smoking.
First, prepartum levels of anxiety and depression were related to breastfeeding cessation (β 0.24; 95% CI 0.21-0.28), and breastfeeding cessation was predictive of an increase in postpartum anxiety and depression ( β 0.11; 95%CI 0.09-0.14). Second, prepartum anxiety and depression interacted with the relation between breastfeeding cessation and postpartum anxiety and depression ( β 0.04; 95% CI 0.01-0.06). The associations could not be accounted for by the adjusting variables.
Breastfeeding cessation is a risk factor for increased anxiety and depression. Women with high levels of anxiety and depression during pregnancy who stop breastfeeding early are at an additional multiplicative risk for postpartum anxiety and depression.
Diet quality is related to the risk for depression and anxiety in adults and adolescents; however, the possible impact of maternal and early postnatal nutritional exposures on children's subsequent ...mental health is unexplored.
The large prospective Norwegian Mother and Child Cohort Study recruited pregnant women between 1999 and 2008. Data were collected from mothers during pregnancy and when children were 6 months and 1.5, 3, and 5 years of age. Latent growth curve models were used to model linear development in children's internalizing and externalizing problems from 1.5 to 5 years of age as a function of diet quality during pregnancy and at 1.5 and 3 years. Diet quality was evaluated by dietary pattern extraction and characterized as "healthy" or "unhealthy." The sample comprised 23,020 eligible women and their children. Adjustments were made for variables including sex of the child, maternal depression, maternal and paternal age, maternal educational attainment, household income, maternal smoking before and during pregnancy, mothers' parental locus of control, and marital status.
Higher intakes of unhealthy foods during pregnancy predicted externalizing problems among children, independently of other potential confounding factors and childhood diet. Children with a high level of unhealthy diet postnatally had higher levels of both internalizing and externalizing problems. Moreover, children with a low level of postnatal healthy diet also had higher levels of both internalizing and externalizing problems.
Among this large cohort of mothers and children, early nutritional exposures were independently related to the risk for behavioral and emotional problems in children.
To estimate the association between maternal use of acetaminophen during pregnancy and of paternal use before pregnancy with attention-deficit/hyperactivity disorder (ADHD) in offspring while ...adjusting for familial risk for ADHD and indications of acetaminophen use.
Diagnoses were obtained from the Norwegian Patient Registry for 112 973 offspring from the Norwegian Mother and Child Cohort Study, including 2246 with ADHD. We estimated hazard ratios (HRs) for an ADHD diagnosis by using Cox proportional hazard models.
After adjusting for maternal use of acetaminophen before pregnancy, familial risk for ADHD, and indications of acetaminophen use, we observed a modest association between any prenatal maternal use of acetaminophen in 1 (HR = 1.07; 95% confidence interval CI 0.96-1.19), 2 (HR = 1.22; 95% CI 1.07-1.38), and 3 trimesters (HR = 1.27; 95% CI 0.99-1.63). The HR for more than 29 days of maternal acetaminophen use was 2.20 (95% CI 1.50-3.24). Use for <8 days was negatively associated with ADHD (HR = 0.90; 95% CI 0.81-1.00). Acetaminophen use for fever and infections for 22 to 28 days was associated with ADHD (HR = 6.15; 95% CI 1.71-22.05). Paternal and maternal use of acetaminophen were similarly associated with ADHD.
Short-term maternal use of acetaminophen during pregnancy was negatively associated with ADHD in offspring. Long-term maternal use of acetaminophen during pregnancy was substantially associated with ADHD even after adjusting for indications of use, familial risk of ADHD, and other potential confounders.
Emerging evidence suggests that prenatal stress does not solely undermine child functioning but increases developmental plasticity to both negative and positive postnatal experiences. Here we test ...this proposition using the Norwegian Mother and Child Cohort study while implementing an extreme-group (i.e., high vs. low prenatal stress) design (n = 27,889 children for internalizing and n = 27,892 for externalizing problems). To measure prenatal stress, mothers reported on depressive and anxiety symptoms at gestational weeks 17 and 30 and of stressful life events at gestational week 30. We then evaluated whether, collectively, such prenatal stress amplified the effect of mothers' postnatal depressive and anxiety symptoms on children's internalizing and externalizing behavior problems at age 5 years. Results showed prenatal stress amplified effects of postnatal maternal depression/anxiety on child internalizing but not externalizing behavior, with some indication that this Prenatal-Stress-×-Postnatal-Maternal-Depression interaction proved more consistent with differential susceptibility than diathesis stress thinking: Children exposed to prenatal stress evinced greater internalizing problems if exposed to more postnatal maternal depressive/anxiety symptoms and, somewhat less strongly, displayed less internalizing problems if they experienced lower postnatal maternal depressive/anxiety symptoms. However, analyses using the whole sample instead of extreme groups yielded opposing results with children exposed to the least prenatal stress evincing greater sensitivity to postnatal maternal depressive/anxiety symptoms with regards to externalizing and internalizing behavior. Taken together, it appears that prenatal stress may have differing effects on plasticity depending on prenatal stress severity.
Sleep and depression are interlinked throughout the lifespan, but very few studies have examined the directionality of the sleep–depression link in children. The aim of the current study was to ...prospectively examine the bidirectional association between sleep problems and internalizing problems and depressive symptoms in toddlers and children aged 1.5 and 8 years. Data stem from the large ongoing population‐based longitudinal study, the Norwegian Mother, Father and Child Cohort Study, recruited from October 1999 to July 2009. A total of 35,075 children were included. Information on sleep duration, nocturnal awakenings and internalizing problems (Child Behaviour Checklist) was provided by the mothers at 1.5 years, whereas data on sleep duration and depressive symptoms (Short Mood and Feelings Questionnaire) were provided by the mothers when the children were 8 years old. Odds ratios (ORs) were calculated using logistic regression analyses. After accounting for previous internalizing problems, short sleep duration (≤10 hr) and frequent (≥3) nightly awakenings at 1.5 years predicted the development of depressive symptoms at 8 years of age (adjusted OR = 1.28; 95% confidence interval CI 1.08–1.51, and adjusted OR = 1.27, 95% CI 1.08–1.50, respectively). Also, internalizing problems at 1.5 years predicted onset of later short sleep duration (adjusted OR = 1.83, 95% CI 1.32–2.54) after accounting for early sleep problems. This prospective study demonstrated a bidirectional association between sleep and internalizing/depressive symptoms from toddlerhood to middle childhood. Intervention studies are needed to examine whether targeting either of these problems at this early age may prevent onset of the other.
Epidemiological studies have shown that long-term exposure to paracetamol during pregnancy is associated with attention-deficit/hyperactivity disorder (ADHD). The mechanism by which paracetamol may ...modulate the increased risk of developing ADHD is currently unknown. We have conducted an epigenome-wide association study (
= 384 cord blood samples) and investigated whether prenatal exposure to paracetamol is associated with DNA methylation in children diagnosed with ADHD.
Analyses identified significant differences in DNA methylation (
= 6211 CpGs) associated with prenatal exposure to paracetamol for more than 20 days in children diagnosed with ADHD compared to controls. In addition, these samples were differentially methylated compared to samples with ADHD exposed to paracetamol for less than 20 days (
= 2089 CpGs) and not exposed to paracetamol (
= 193 CpGs). Interestingly, several of the top genes ranked according to significance and effect size have been linked to ADHD, neural development, and neurotransmission. Gene ontology analysis revealed enrichment of pathways involved in oxidative stress, neurological processes, and the olfactory sensory system, which have previously been implicated in the etiology of ADHD.
These initial findings suggest that in individuals susceptible to ADHD, prenatal long-term exposure to paracetamol is associated with DNA methylation differences compared to controls.
Many studies detect associations between parent behaviour and child symptoms of anxiety and depression. Despite knowledge that anxiety and depression are influenced by a complex interplay of genetic ...and environmental risk factors, most studies do not account for shared familial genetic risk. Quantitative genetic designs provide a means of controlling for shared genetics, but rely on observed putative exposure variables, and require data from highly specific family structures.
The intergenerational genomic method, Relatedness Disequilibrium Regression (RDR), indexes environmental effects of parents on child traits using measured genotypes. RDR estimates how much the parent genome influences the child indirectly via the environment, over and above effects of genetic factors acting directly in the child. This 'genetic nurture' effect is agnostic to parent phenotype and captures unmeasured heritable parent behaviours. We applied RDR in a sample of 11,598 parent-offspring trios from the Norwegian Mother, Father and Child Cohort Study (MoBa) to estimate parental genetic nurture separately from direct child genetic effects on anxiety and depression symptoms at age 8. We tested for mediation of genetic nurture via maternal anxiety and depression symptoms. Results were compared to a complementary non-genomic pedigree model.
Parental genetic nurture explained 14% of the variance in depression symptoms at age 8. Subsequent analyses suggested that maternal anxiety and depression partially mediated this effect. The genetic nurture effect was mirrored by the finding of family environmental influence in our pedigree model. In contrast, variance in anxiety symptoms was not significantly influenced by common genetic variation in children or parents, despite a moderate pedigree heritability.
Genomic methods like RDR represent new opportunities for genetically sensitive family research on complex human traits, which until now has been largely confined to adoption, twin and other pedigree designs. Our results are relevant to debates about the role of parents in the development of anxiety and depression in children, and possibly where to intervene to reduce problems.
Background
An individual's overall burden of behavioural and emotional problems across childhood is associated with increased likelihood of later mental health conditions. However, the relative ...extent of behavioural versus emotional problems ‐ that is, the extent to which the domains are differentiated from one another ‐ may provide additional information about who is at risk of developing a mental health condition. Here, we seek to validate differentiation as an independent predictor of later mental health conditions, and to explore its aetiology.
Methods
We analysed data from ~79,000 children in the population‐based Norwegian Mother, Father, and Child Cohort Study, and linked health‐care registries. In preregistered analyses, we modelled the extent and rate of differentiation of behavioural and emotional problems between ages 1.5–5 years, and estimated associations with later symptoms (age 8) and diagnoses (after age 8). We also explored the aetiology of differentiation by estimating associations with early life exposures and, in a subset of 23,945 full siblings, assessing the impact of accounting for unobserved familial confounding.
Results
Differentiation of behavioural and emotional problems was associated with later symptoms and diagnoses of mental health conditions, independent of total problems. Maternal at‐risk drinking (β = 0.04 0.02, 0.06) and parental relationship problems (β = 0.04 0.02, 0.05) were associated with higher behavioural relative to emotional problems at age 5. Maternal prenatal distress (|β| = 0.04 0.03, 0.06), concurrent distress (|β| = 0.04 0.02, 0.06) and parental education (|β| = 0.05 0.04, 0.07) predicted higher emotional relative to behavioural problems at age 5. Estimates for maternal prenatal distress and at‐risk drinking were consistent across both unadjusted and adjusted analyses accounting for unobserved familial risk.
Conclusions
Differentiation of behavioural and emotional problems in early childhood represents a valid source of inter‐individual variability linked to the later emergence of psychopathology and may be relevant for early detection and prevention strategies for mental health.
Background
Fundamental questions about the roles of genes, environments, and their interplay in developmental psychopathology have traditionally been the domain of twin and family studies. More ...recently, the rapidly growing availability of large genomic datasets, composed of unrelated individuals, has generated novel insights. However, there are major stumbling blocks. Only a small fraction of the total genetic influence on childhood psychopathology estimated from family data is captured with measured DNA. Moreover, genetic influence identified using DNA is often confounded with indirect genetic effects of relatives, population stratification and assortative mating.
Methods
The goal of this paper is to review how combining DNA‐based genomic research with family‐based quantitative genetics helps to address key issues in genomics and push knowledge further.
Results
We focus on three approaches to obtaining more accurate and novel genomic findings on the developmental aetiology of psychopathology: (a) using knowledge from twin and family studies, (b) triangulating with twin and family studies, and (c) integrating data and methods with twin and family studies.
Conclusion
We support the movement towards family‐based genomic research, and show that developmental psychologists are particularly well‐placed to contribute hypotheses, analysis tools, and data.
There are major stumbling blocks in the genomics of psychopathology. This review shows how more accurate and novel genomic findings on the developmental aetiology of psychopathology can be obtained by (a) using knowledge from twin and family studies, (b) triangulating with twin and family studies, and (c) integrating data and methods with twin and family studies.
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.
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