Preschool family irregularity and the development of sleep problems in childhood: a longitudinal study.

BACKGROUND: Previous studies have shown that poor family environments are related to more sleep problems; however, little is known about how family irregularity in early life affects the development of sleep problems over childhood using objective sleep measures. The current study tests the hypothesis that early family irregularity contributes to the development of sleep problems. METHODS: This population-based study comprises 5,443 children from the Generation R Study. Family irregularity was measured with seven maternal-reported questions on family routines when children were 2 and 4 years old. Mothers reported on sleep problems at child age 3, 6, and 10 years, whereas children completed questionnaires on sleep problems at age 10. Additionally, we used tri-axial wrist accelerometers for five nights in 851 children (mean age 11.7 years) to assess sleep objectively. RESULTS: Family irregularity was associated with more mother- and child-reported sleep problems at ages 3, 6, and 10 years as well as with a shorter sleep duration and later objective sleep onset, but not with sleep efficiency or waking time. The association between family irregularity and multi-informant subjective sleep problems at age 10 years was mediated by mother-reported child psychopathology at age 6 years. CONCLUSIONS: Our findings show a long-term robust association of preschool family irregularity with more sleep problems during childhood as well as shorter sleep duration and later sleep onset as measured objectively with actigraphy. In part, these sleep problems were associated with family irregularity by way of child psychopathology. These findings suggest that interventions improving preschool family irregularity, which are targeted to reduce child psychopathology, may also impact the development of sleep problems beneficially.

During day and night: Childhood psychotic experiences and objective and subjective sleep problems.

BACKGROUND: Psychotic experiences comprise auditory and visual perceptive phenomena, such as hearing or seeing things that are not there, in the absence of a psychotic disorder. Psychotic experiences commonly occur in the general pediatric population. Although the majority of psychotic experiences are transient, they are predictive of future psychotic and non-psychotic disorders. They have been associated with sleep problems, but studies with objective sleep measures are lacking. This study assessed whether psychotic experiences were associated with actigraphic sleep measures, symptoms of dyssomnia, nightmares, or other parasomnias. METHODS: This cross-sectional population-based study comprises 4149 children from the Generation R Study. At age 10 years, psychotic experiences including hallucinatory phenomena were assessed by self-report; dyssomnia and parasomnia symptoms were assessed by mother- and child-report. Additionally, at age 11 years, objective sleep parameters were measured using a tri-axial wrist accelerometer in N = 814 children, who wore the accelerometer for five consecutive school days. RESULTS: Psychotic experiences were not associated with objective sleep duration, sleep efficiency, arousal, or social jetlag. However, psychotic experiences were associated with self-reported dyssomnia (B = 2.45, 95%CI: 2.13-2.77, p < 0.001) and mother-reported parasomnia, specifically nightmares (ORadjusted = 3.59, 95%CI 2.66-4.83, p < 0.001). Similar results were found when analyses were restricted to hallucinatory phenomena. CONCLUSIONS: Childhood psychotic experiences were not associated with objective sleep measures. In contrast, psychotic experiences were associated with nightmares, which are a known risk indicator of psychopathology in pre-adolescence. More research is needed to shed light on the potential etiologic or diagnostic role of nightmares in the development of psychotic phenomena.

The bidirectional association between sleep problems and autism spectrum disorder: a population-based cohort study.

Background: Sleep difficulties are prevalent in children with autism spectrum disorder (ASD). The temporal nature of the association between sleep problems and ASD is unclear because longitudinal studies are lacking. Our aim is to clarify whether sleep problems precede and worsen autistic traits and ASD or occur as a consequence of the disorder. Methods: Repeated sleep measures were available at 1.5, 3, 6, and 9 years of age in 5151 children participating in the Generation R Study, a large prospective birth cohort in the Netherlands. Autistic traits were determined with the Pervasive Developmental Problems score (PDP) of the Child Behavior Checklist (CBCL) at 1.5 and 3 years and the Social Responsiveness Scale (SRS) at 6 years. This cohort included 81 children diagnosed with ASD. Results: Sleep problems in early childhood were prospectively associated with a higher SRS score, but not when correcting for baseline PDP score. By contrast, a higher SRS score and an ASD diagnosis were associated with more sleep problems at later ages, even when adjusting for baseline sleep problems. Likewise, a trajectory of increasing sleep problems was associated with ASD. Conclusions: Sleep problems and ASD are not bidirectionally associated. Sleep problems do not precede and worsen autistic behavior but rather co-occur with autistic traits in early childhood. Over time, children with ASD have an increase in sleep problems, whereas typically developing children have a decrease in sleep problems. Our findings suggest that sleep problems are part of the construct ASD.

Changes in face-specific neural processing explain reduced cuteness and approachability of infants with cleft lip.

The current study investigated whether changes in the neural processing of faces of infants with a facial abnormality - a cleft lip - mediate effects of the cleft lip on judgments of infant cuteness and approachability. Event-related potentials (ERPs) in response to pictures of faces of healthy infants and infants with a cleft lip, and ratings of cuteness and approachability of these infant faces, were obtained from 30 females. Infants with a cleft lip were rated as less attractive (less cute and approachable) than healthy infants, and both the N170 and P2 components of the ERP were of reduced amplitude in response to pictures of infants with a cleft lip. Importantly, decreased configural processing of infant faces with a cleft lip, as evidenced by reduced N170 amplitudes, mediated the reduced attractiveness ratings for infants with a cleft lip compared to healthy infants. Our findings help elucidate the mechanisms behind the less favorable responses to infants with a cleft lip, highlighting the role of face-specific rather than domain-general neural processes.

The dopamine D4 receptor gene, birth weight, maternal depression, maternal attention, and the prediction of disorganized attachment at 36 months of age: A prospective gene×environment analysis.

BACKGROUND: Efforts to understand the developmental pathways for disorganized attachment reflect the importance of disorganized attachment on the prediction of future psychopathology. The inconsistent findings on the prediction of disorganized attachment from the dopamine D4 receptor (DRD4) gene, birth weight, and maternal depression as well as the evidence supporting the contribution of early maternal care, suggest the importance of exploring a gene by environment model. METHODS: Our sample is from the Maternal Adversity, Vulnerability, and Neurodevelopment project; consisting of 655 mother-child dyads. Birth weight was cross-referenced with normative data to calculate birth weight percentile. Infant DRD4 genotype was obtained with buccal swabs and categorized according to the presence of the 7-repeat allele. Maternal depression was assessed with the Center for Epidemiologic Studies Depression Scale at the prenatal, 6-, 12-, and 24-month assessments. Maternal attention was measured at 6-months using a videotaped session of a 20-min non-feeding interaction. Attachment was assessed at 36-months using the Strange Situation Procedure. RESULTS: The presence of the DRD4 7-repeat allele was associated with less disorganized attachment, ß=-1.11, OR=0.33, p=0.0008. Maternal looking away frequency showed significant interactions with maternal depression at the prenatal assessment, ß=0.003, OR=1.003, p=0.023, and at 24 months, ß=0.004, OR=1.004, p=0.021, as at both time points, women suffering from depression and with frequent looking away behavior had an increased probability of disorganized attachment in their child, while those with less looking away behavior had a decreased probability of disorganized attachment in their child at 36 months. CONCLUSIONS: Our models support the contribution of biological and multiple environmental factors in the complex prediction of disorganized attachment at 36 months.

Mild perinatal adversities moderate the association between maternal harsh parenting and hair cortisol: Evidence for differential susceptibility.

It has been shown that following exposure to mild perinatal adversity, children have greater susceptibility to both the negative and positive aspects of their subsequent environment. In a large population-based cohort study (N = 1,776), we investigated whether mild perinatal adversity moderated the association between maternal harsh parenting and children's hair cortisol levels, a biomarker of chronic stress. Mild perinatal adversity was defined as late preterm birth (gestational age at birth of 34-37 weeks, 6 days) or small for gestational age (birth weight between the 2.5th and 10th percentile for full term gestational age). Harsh parenting was assessed by maternal self-report at 3 years. Children's hair cortisol concentrations were measured from hair samples collected at age 6. There were no significant bivariate associations between mild perinatal adversities and harsh parenting and hair cortisol. However, mild perinatal adversities moderated the association between maternal harsh parenting and hair cortisol levels. Children with mild perinatal adversity had lower cortisol levels if parented more harshly and higher cortisol levels in the absence of harsh parenting than children who did not experience mild perinatal adversity. These results provide further evidence that mild perinatal adversity is a potential marker of differential susceptibility to environmental influences.

Parent-child bed-sharing: The good, the bad, and the burden of evidence.

The practice of parent and child sharing a sleeping surface, or 'bed-sharing', is one of the most controversial topics in parenting research. The lay literature has popularized and polarized this debate, offering on one hand claims of dangers, and on the other, of benefits - both physical and psychological - associated with bed-sharing. To address the scientific evidence behind such claims, we systematically reviewed 659 published papers (peer-reviewed, editorial pieces, and commentaries) on the topic of parent-child bed-sharing. Our review offers a narrative walkthrough of the many subdomains of bed-sharing research, including its many correlates (e.g., socioeconomic and cultural factors) and purported risks or outcomes (e.g., sudden infant death syndrome, sleep problems). We found general design limitations and a lack of convincing evidence in the literature, which preclude making strong generalizations. A heat-map based on 98 eligible studies aids the reader to visualize world-wide prevalence in bed-sharing and highlights the need for further research in societies where bed-sharing is the norm. We urge for multiple subfields - anthropology, psychology/psychiatry, and pediatrics - to come together with the aim of understanding infant sleep and how nightly proximity to the parents influences children's social, emotional, and physical development.

Heritability and Genome-Wide Association Analyses of Sleep Duration in Children: The EAGLE Consortium.

STUDY OBJECTIVES: Low or excessive sleep duration has been associated with multiple outcomes, but the biology behind these associations remains elusive. Specifically, genetic studies in children are scarce. In this study, we aimed to: (1) estimate the proportion of genetic variance of sleep duration in children attributed to common single nucleotide polymorphisms (SNPs), (2) identify novel SNPs associated with sleep duration in children, and (3) investigate the genetic overlap of sleep duration in children and related metabolic and psychiatric traits. METHODS: We performed a population-based molecular genetic study, using data form the EArly Genetics and Life course Epidemiology (EAGLE) Consortium. 10,554 children of European ancestry were included in the discovery, and 1,250 children in the replication phase. RESULTS: We found evidence of significant but modest SNP heritability of sleep duration in children (SNP h2 0.14, 95% CI [0.05, 0.23]) using the LD score regression method. A novel region at chromosome 11q13.4 (top SNP: rs74506765, P = 2.27e-08) was associated with sleep duration in children, but this was not replicated in independent studies. Nominally significant genetic overlap was only found (rG = 0.23, P = 0.05) between sleep duration in children and type 2 diabetes in adults, supporting the hypothesis of a common pathogenic mechanism. CONCLUSIONS: The significant SNP heritability of sleep duration in children and the suggestive genetic overlap with type 2 diabetes support the search for genetic mechanisms linking sleep duration in children to multiple outcomes in health and disease.

Beyond main effects of gene-sets: harsh parenting moderates the association between a dopamine gene-set and child externalizing behavior.

BACKGROUND: In a longitudinal cohort study, we investigated the interplay of harsh parenting and genetic variation across a set of functionally related dopamine genes, in association with children's externalizing behavior. This is one of the first studies to employ gene-based and gene-set approaches in tests of Gene by Environment (G × E) effects on complex behavior. This approach can offer an important alternative or complement to candidate gene and genome-wide environmental interaction (GWEI) studies in the search for genetic variation underlying individual differences in behavior. METHODS: Genetic variants in 12 autosomal dopaminergic genes were available in an ethnically homogenous part of a population-based cohort. Harsh parenting was assessed with maternal (n = 1881) and paternal (n = 1710) reports at age 3. Externalizing behavior was assessed with the Child Behavior Checklist (CBCL) at age 5 (71 ± 3.7 months). We conducted gene-set analyses of the association between variation in dopaminergic genes and externalizing behavior, stratified for harsh parenting. RESULTS: The association was statistically significant or approached significance for children without harsh parenting experiences, but was absent in the group with harsh parenting. Similarly, significant associations between single genes and externalizing behavior were only found in the group without harsh parenting. Effect sizes in the groups with and without harsh parenting did not differ significantly. Gene-environment interaction tests were conducted for individual genetic variants, resulting in two significant interaction effects (rs1497023 and rs4922132) after correction for multiple testing. CONCLUSION: Our findings are suggestive of G × E interplay, with associations between dopamine genes and externalizing behavior present in children without harsh parenting, but not in children with harsh parenting experiences. Harsh parenting may overrule the role of genetic factors in externalizing behavior. Gene-based and gene-set analyses offer promising new alternatives to analyses focusing on single candidate polymorphisms when examining the interplay between genetic and environmental factors.

An epigenome-wide association meta-analysis of prenatal maternal stress in neonates: A model approach for replication.

Prenatal maternal stress exposure has been associated with neonatal differential DNA methylation. However, the available evidence in humans is largely based on candidate gene methylation studies, where only a few CpG sites were evaluated. The aim of this study was to examine the association between prenatal exposure to maternal stress and offspring genome-wide cord blood methylation using different methods. First, we conducted a meta-analysis and follow-up pathway analyses. Second, we used novel region discovery methods [i.e., differentially methylated regions (DMRs) analyses]. To this end, we used data from two independent population-based studies, the Generation R Study (n = 912) and the Avon Longitudinal Study of Parents and Children (ALSPAC, n = 828), to (i) measure genome-wide DNA methylation in cord blood and (ii) extract a prenatal maternal stress composite. The meta-analysis (ntotal = 1,740) revealed no epigenome-wide (meta P <1.00e-07) associations of prenatal maternal stress exposure with neonatal differential DNA methylation. Follow-up analyses of the top hits derived from our epigenome-wide meta-analysis (meta P <1.00e-04) indicated an over-representation of the methyltransferase activity pathway. We identified no Bonferroni-corrected (P <1.00e-06) DMRs associated with prenatal maternal stress exposure. Combining data from two independent population-based samples in an epigenome-wide meta-analysis, the current study indicates that there are no large effects of prenatal maternal stress exposure on neonatal DNA methylation. Such replication efforts are essential in the search for robust associations, whether derived from candidate gene methylation or epigenome-wide studies.

ASSOCIATION BETWEEN INFANT NIGHTTIME-SLEEP LOCATION AND ATTACHMENT SECURITY: NO EASY VERDICT.

We tested whether mother-infant bed-sharing is associated with increased secure infant-mother attachment, a previously unexplored association. Frequency of bed-sharing and mothers' nighttime comforting measures at 2 months were assessed with questionnaires in 550 Caucasian mothers from a population-based cohort. Attachment security was assessed with the Strange Situation Procedure (M.D.S. Ainsworth, M.C. Blehar, E. Waters, & S. Wall, 1978) at 14 months. When using a dichotomous variable, "never bed-sharing" (solitary sleepers) versus "any bed-sharing," the relative risk of being classified as insecurely attached for solitary-sleeping infants (vs. bed-sharers) was 1.21 (95% confidence interval: 1.05-1.40). In multivariate models, solitary sleeping was associated with greater odds of insecure attachment, adjusted odds ratio (OR): 1.50, 95% CI = 1.02-2.20) and, in particular, with greater odds of resistant attachment, adjusted OR = 1.74, 95% CI = 1.10-2.76); and with a lower attachment security score, ß = -0.12, t(495) = -2.61, p = .009. However, we found no evidence of a dose-response association between bed-sharing and secure attachment when using a trichotomous bed-sharing variable based on frequency of bed-sharing. Our findings demonstrate some evidence that solitary sleeping is associated with insecure attachment. However, the lack of a dose-response association suggests that further experimental study is necessary before accepting common notions that sharing a bed leads to children who are better or not better adjusted.

Genetic mechanisms of parenting.

This article is part of a Special Issue "Parental Care". The complexities of parenting behavior in humans have been studied for decades. Only recently did we begin to probe the genetic and epigenetic mechanisms underlying these complexities. Much of the research in this field continues to be informed by animal studies, where genetic manipulations and invasive tools allow to peek into and directly observe the brain during the expression of maternal behavior. In humans, studies of adult twins who are parents can suggest dimensions of parenting that might be more amenable to a genetic influence. Candidate gene studies can test specific genes in association with parental behavior based on prior knowledge of those genes' function. Gene-by-environment interactions of a specific kind indicating differential susceptibility to the environment might explain why some parents are more resilient and others are more vulnerable to stressful life events. Epigenetic studies can provide the bridge often necessary to explain why some individuals behave differently from others despite common genetic influences. There is a much-needed expansion in parenting research to include not only mothers as the focus-as has been the case almost exclusively to date-but also fathers, grandparents, and other caregivers.

A genome-wide approach to children's aggressive behavior: The EAGLE consortium.

Individual differences in aggressive behavior emerge in early childhood and predict persisting behavioral problems and disorders. Studies of antisocial and severe aggression in adulthood indicate substantial underlying biology. However, little attention has been given to genome-wide approaches of aggressive behavior in children. We analyzed data from nine population-based studies and assessed aggressive behavior using well-validated parent-reported questionnaires. This is the largest sample exploring children's aggressive behavior to date (N = 18,988), with measures in two developmental stages (N = 15,668 early childhood and N = 16,311 middle childhood/early adolescence). First, we estimated the additive genetic variance of children's aggressive behavior based on genome-wide SNP information, using genome-wide complex trait analysis (GCTA). Second, genetic associations within each study were assessed using a quasi-Poisson regression approach, capturing the highly right-skewed distribution of aggressive behavior. Third, we performed meta-analyses of genome-wide associations for both the total age-mixed sample and the two developmental stages. Finally, we performed a gene-based test using the summary statistics of the total sample. GCTA quantified variance tagged by common SNPs (10-54%). The meta-analysis of the total sample identified one region in chromosome 2 (2p12) at near genome-wide significance (top SNP rs11126630, P = 5.30 × 10(-8) ). The separate meta-analyses of the two developmental stages revealed suggestive evidence of association at the same locus. The gene-based analysis indicated association of variation within AVPR1A with aggressive behavior. We conclude that common variants at 2p12 show suggestive evidence for association with childhood aggression. Replication of these initial findings is needed, and further studies should clarify its biological meaning. © 2015 Wiley Periodicals, Inc.

Single Nucleotide Polymorphism Heritability of Behavior Problems in Childhood: Genome-Wide Complex Trait Analysis.

OBJECTIVE: Genetic factors contribute to individual differences in behavior problems. In children, genome-wide association studies (GWAS) have yielded the first suggestive results when aiming to identify genetic variants that explain heritability, but the proportion of genetic variance that can be attributed to common single nucleotide polymorphisms (SNPs) remains to be determined, as only a few studies have estimated SNP heritability, with diverging results. METHOD: Genomic-relationship-matrix restricted maximum likelihood (GREML) as implemented in the software Genome-Wide Complex Trait Analysis (GCTA) was used to estimate SNP heritability (SNP h(2)) for multiple phenotypes within 4 broad domains of children's behavioral problems (attention-deficit/hyperactivity symptoms, internalizing, externalizing, and pervasive developmental problems) and cognitive function. We combined phenotype and genotype data from 2 independent, population-based Dutch cohorts, yielding a total number of 1,495 to 3,175 of 3-, 7-, and 9-year-old children. RESULTS: Significant SNP heritability estimates were found for attention-deficit/hyperactivity symptoms (SNP h(2) = 0.37-0.71), externalizing problems (SNP h(2) = 0.44), and total problems (SNP h(2) = 0.18), rated by mother or teacher. Sensitivity analyses with exclusion of extreme cases and quantile normalization of the phenotype data decreased SNP h(2) as expected under genetic inheritance, but they remained statistically significant for most phenotypes. CONCLUSION: We provide evidence of the influence of common SNPs on child behavior problems in an ethnically homogenous sample. These results support the continuation of large GWAS collaborative efforts to unravel the genetic basis of complex child behaviors.

The magnificent seven: A quantitative review of dopamine receptor d4 and its association with child behavior.

A large volume of behavioral research has explored the variable number of tandem repeat (VNTR) polymorphism on the dopamine receptor D4 gene (DRD4). However, findings are inconsistent and there is no agreement about what constitutes "functional" and "less functional" variants at this locus. First, we systematically review studies exploring biological differences between DRD4 VNTRs (k=21). Second, we systematically review studies relating DRD4 variation to behavioral traits in population-based, non-clinical samples of children and adolescents (k=46; N=13,195), highlighting the various genotypic classifications previously used. Third, we use meta-analyses to examine associations of DRD4 VNTRs with five broadly-defined behavioral outcomes (externalizing and attention problems, executive function, social/emotional development, and "reactive" temperament). We identify a significant association of "longer" DRD4 variants with lower levels of executive function and social/emotional development, but not independent of the choice of genotypic classification. We suggest that until the functionality of DRD4 VNTRs is established, researchers should report all genotypic classifications to ensure full transparency and allow for further meta-analytic work.

Beyond the usual suspects: a multidimensional genetic exploration of infant attachment disorganization and security.

Although the environmental influences on infant attachment disorganization and security are well-studied, little is known about their heritability. Candidate gene studies have shown small, often non-replicable effects. In this study, we gathered the largest sample (N = 657) of ethnically homogenous, 14-month-old children with both observed attachment and genome-wide data. First, we used a Genome-Wide Association Study (GWAS) approach to identify single nucleotide polymorphisms (SNPs) associated with attachment disorganization and security. Second, we annotated them into genes (Versatile Gene-based Association Study) and functional pathways. Our analyses provide evidence of novel genes (HDAC1, ZNF675, BSCD1) and pathways (synaptic transmission, cation transport) associated with attachment disorganization. Similar analyses identified a novel gene (BECN1) but no distinct pathways associated with attachment security. The results of this first extensive, exploratory study on the molecular-genetic basis of infant attachment await replication in large, independent samples.

Differential susceptibility in a developmental perspective: DRD4 and maternal sensitivity predicting externalizing behavior.

This study is the first to investigate the longitudinal effects of gene-environment interplay between DRD4 genotype and maternal sensitivity on child externalizing behavior. Multiple measures of maternal sensitivity (14, 36, and 48 months) and externalizing behavior (18 months, 36 months, and 5 years) were assessed in a large cohort study (N = 548). Early maternal insensitivity (14 months) was associated with early externalizing behavior (18 months) in a for better and for worse manner, but only in children with at least one DRD4 7-repeat, consistent with a differential susceptibility model. Later insensitivity (48 months) predicted externalizing behavior at age 5 independent of DRD4 genotype. A structural equation model including all measures across time supported the differential susceptibility model: The overall effect of early maternal sensitivity on later externalizing behavior was significant only for children with a DRD4 7-repeat allele. The results highlight the importance of studying gene-environment interactions across development.

Is parent-child bed-sharing a risk for wheezing and asthma in early childhood?

Household crowding can place young children at risk for respiratory infections which subsequently provoke asthma symptoms. However, crowding might also protect against asthma, in accordance with the hygiene hypothesis. We tested if parent-infant bed-sharing, an important dimension of household crowding, increases or decreases the risk for asthma. In a population-based prospective cohort (N = 6160) we assessed bed-sharing at 2 and 24 months; wheezing between 1 and 6 years of age; and asthma at 6 years of age. Generalised estimating equation models were used to assess repeated measures of wheezing and asthma. We found no association between bed-sharing in early infancy and wheezing or diagnosis of asthma. By contrast, we found a positive association between bed-sharing in toddlerhood and both wheezing (OR 1.42, 95% CI 1.15-1.74) and asthma (OR 1.57, 95% CI 1.03-2.38). Wheezing was not associated with bed-sharing when using cross-lagged modelling. This study suggests that bed-sharing in toddlerhood is associated with an increased risk of asthma at later ages, and not vice versa. Further studies are needed to explore the underlying causal mechanisms.

Are boys more sensitive to sensitivity? Parenting and executive function in preschoolers.

During early childhood, girls outperform boys on key dimensions of cognitive functions, including inhibitory control, sustained attention, and working memory. The role of parenting in these sex differences is unknown despite evidence that boys are more sensitive to the effects of the early environment. In this study, we measured parental sensitivity at 14 and 36 months of age, and children's cognitive and executive functions (sustained attention, inhibitory control, and forward/backward memory) at 52 months of age, in a longitudinal cohort (N=752). Boys scored significantly lower than girls on inhibitory control (more Go/NoGo "commission errors") and short-term memory (forward color recall task), but boys did not differ from girls on attention (Go/NoGo "omission errors") or working memory (backward color recall task). In stratified analyses, parental sensitivity at 36 months of age was negatively associated with number of errors of commission (p=.05) and omission (p=.02) in boys, whereas child's age was the only significant predictor of commission and omission errors in girls. A combined analysis of both sexes confirmed an interaction between sex and parenting for omission errors (p=.03). The results indicate that sex differences in cognitive functions are evident in preschoolers, although not across all dimensions we assessed. Boys appear to be more vulnerable to early parenting effects, but only in association with omission errors (attention) and not with the other cognitive function dimensions.

Preschool children without 7-repeat DRD4 gene more likely to develop disorganized attachment style.

BACKGROUND: The current paper aimed to explore the effects of birth weight and the 7-repeat allele in Exon III of the dopamine D4 receptor (DRD4) gene on the development of disorganized attachment, a potential endophenotype of depression. Infants born with low birth weight have been shown to be at higher risk for later neurological impairments, psychological disorders or behavioural problems. The DRD4 gene is critical for the cognitive and emotional processes that are sub-served by neural circuits in the prefrontal cortex. This paper examined the main effect of birth weight and DRD4 on the development of disorganized attachment. METHODS: Data was used from the Maternal Adversity, Vulnerability and Neurodevelopment (MAVAN) project. The sample consisted of 251 mother-child dyads with complete data. Attachment style was assessed using the modified separation-reunion procedure. RESULTS: There was no main effect for birth weight on disorganized attachment, (b = -0.001, p = 0.998). There was, however, a main effect for the DRD4 7-repeat polymorphism on disorganized attachment (b = -1.120, p = 0.004). LIMITATIONS: Compared to studies of similar design, the sample size in this study was relatively small. Additionally, a significant number of subjects did not have complete data. CONCLUSIONS: Children without the DRD4 7-repeat allele were more likely to have disorganized attachment than children with the DRD4 7-repeat allele. This indicates that the 7-repeate allele of the DRD4 gene may actually serve as a protective factor against disorganized attachment.