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Descriptors:
Psychopathology; Risk; Public Health; Diagnostic Tests; Attention Deficit Hyperactivity Disorder; Genetics; Pervasive Developmental Disorders; Body Weight; Siblings; Prenatal Influences; Environmental Influences; Correlation; Attribution Theory; Molecular Structure; Autism; Hazardous Materials; Disadvantaged Environment; Intervention; Drug Therapy

Abstract:
Background: Attention deficit hyperactivity disorder (ADHD) and its possible causes still attract controversy. Genes, pre and perinatal risks, psychosocial factors and environmental toxins have all been considered as potential risk factors. Method: This review (focussing on literature published since 1997, selected from a search of PubMed) critically considers putative risk factors with a focus on genetics and selected environmental risks, examines their relationships with ADHD and discusses the likelihood that these risks are causal as well as some of the main implications. Results: No single risk factor explains ADHD. Both inherited and noninherited factors contribute and their effects are interdependent. ADHD is familial and heritable. Research into the inherited and molecular genetic contributions to ADHD suggest an important overlap with other neurodevelopmental problems, notably, autism spectrum disorders. Having a biological relative with ADHD, large, rare copy number variants, some small effect size candidate gene variants, extreme early adversity, pre and postnatal exposure to lead and low birth weight/prematurity have been most consistently found as risk factors, but none are yet known to be definitely causal. There is a large literature documenting associations between ADHD and a wide variety of putative environmental risks that can, at present, only be regarded as correlates. Findings from research designs that go beyond simply testing for association are beginning to contest the robustness of some environmental exposures previously thought to be ADHD risk factors. Conclusions: The genetic risks implicated in ADHD generally tend to have small effect sizes or be rare and often increase risk of many other types of psychopathology. Thus, they cannot be used for prediction, genetic testing or diagnostic purposes beyond what is predicted by a family history. There is a need to consider the possibility of parents and siblings being similarly affected and how this might impact on engagement with families, influence interventions and require integration with adult services. Genetic contributions to disorder do not necessarily mean that medications are the treatment of choice. We also consider how findings might influence the conceptualisation of ADHD, public health policy implications and why it is unhelpful and incorrect to dichotomise genetic/biological and environmental explanations. It is essential that practitioners can interpret genetic and aetiological research findings and impart informed explanations to families. (Contains 2 tables and 1 figure.) Note:The following two links are not-applicable for text-based browsers or screen-reading software. Show Hide Full Abstract

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Descriptors:
Grade Point Average; Genetics; Social Environment; Depression (Psychology); Interaction; Body Weight; Twins; Children; Environmental Influences; Correlation; Birth; Nutrition; Delinquency; Prenatal Influences

Abstract:
Numerous studies report gene-environment interactions, suggesting that specific alleles have different effects on social outcomes depending on environment. In all these studies, however, environmental conditions are potentially endogenous to unmeasured genetic characteristics. That is, it could be that the observed interaction effects actually reflect underlying genetic tendencies that lead individuals into certain environments. What is critical to move this literature forward is random environmental variation that we know is not correlated with innate characteristics of subjects. We exploit a natural experiment that randomizes a particular stressor--birth weight discordance within twin pairs--to address this challenge and ask: Do random differences in early environment (prenatal nutrition) moderate genetic effects on depression, delinquency, or GPA? Using Add Health data, the only consistently significant allele-birth weight interaction we reveal works in the opposite direction of Caspi et al.'s classic finding regarding the interaction of maltreatment with genetic variation in the serotonin transporter promoter. Less robust interactions found for "DRD2" and "MAOA" are consistent with this pattern that reverses prior findings. These results do not necessarily overturn existing research but support our methodological point that gene-environment research must address endogeneity. (Contains 6 tables, 1 figure and 9 notes.) Note:The following two links are not-applicable for text-based browsers or screen-reading software. Show Hide Full Abstract

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Descriptors:
Pregnancy; Well Being; Depression (Psychology); Mothers; Fathers; Nurses; Prediction; Children; Mental Health; Physical Health; Prenatal Influences; Measures (Individuals); Behavior Problems; Risk; Health Services; Symptoms (Individual Disorders); Preadolescents; Foreign Countries; Therapy; Help Seeking

Abstract:
In a prospective population-based study, mothers and fathers of 1,247 children reported their physical and mental health during pregnancy, after delivery, within the child's first 18 months of life, and at 12 years. Additionally, maternal health clinic nurses rated parents' well-being and perceived need for support. At age 12, child outcomes were also measured using CBCL and YSR externalizing and internalizing scales. Results indicate that both ante- and postnatal maternal distress predicted future externalizing problems in offspring. Conversely, fathers' postnatal distress predicted subsequent internalizing problems. Furthermore, mother's depressed mood in the first trimester best predicted the child's externalizing problems at age 12. Nurses's ratings of mother's antenatal and perinatal need for support, perinatal distress, and family's need for support were associated with both internalizing and externalizing problems at age 12. Maternal antenatal distress increases the risk of offspring's externalizing problems in preadolescense, and postnatal distress in either parent increases the risk of internalizing problems. Parental self-reports and indirect ratings from health care providers during pregnancy and infancy may therefore reliably recognize offspring at risk for subsequent psychiatric symptomatology. Note:The following two links are not-applicable for text-based browsers or screen-reading software. Show Hide Full Abstract

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Pregnancy; Developmental Delays; Genetics; Autism; Communicable Diseases; Prenatal Influences; At Risk Persons; Children

Abstract:
We analyzed data from case groups of 538 children with autism spectrum disorders (ASD) and 163 with developmental delays (DD), and from 421 typically developing controls to assess associations with maternal influenza or fever during pregnancy. Exposure information was obtained by telephone interviews, and outcomes were clinically confirmed. Though neither ASD nor DD was associated with influenza, both were associated with maternal fever during pregnancy: OR's (odds ratios) were 2.12 (95% CI 1.17, 3.84) and 2.50 (95% CI 1.20, 5.20) respectively. However, the fever-associated ASD risk was attenuated among mothers who reported taking antipyretic medications (OR = 1.30, 95% CI 0.59, 2.84), but remained elevated for those who did not (OR = 2.55, 95% CI 1.30, 4.99). Note:The following two links are not-applicable for text-based browsers or screen-reading software. Show Hide Full Abstract

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Descriptors:
Mothers; Infants; Young Children; Pregnancy; Body Composition; Prenatal Influences; Child Behavior; Personality; Behavior Problems; Psychopathology; Foreign Countries

Abstract:
Recent research suggests that fetal exposure to increased maternal body mass index (BMI) during pregnancy may be associated with psychopathology later in life. When this link first emerges, and if it is due to intrauterine exposures or confounding variables is not known. We therefore assessed associations between maternal pre-pregnancy BMI and: (1) temperament at 1 year of age, and (2) Child Behavior Checklist internalizing and externalizing scales at age 2 in the 2900 mothers and infants enrolled in the Western Australian Pregnancy Study. Pre-pregnancy BMI was positively associated with externalizing scores ([beta] = 0.131, 95 % CI 0.013-0.249) at age 2, even after adjustment for confounders, but not with internalizing scores or an increased risk of difficult temperament. These data suggest that fetal exposure to increased maternal BMI is associated with elevated levels of behavior problems as early as age 2, and that this may be linked to the intrauterine environment. Note:The following two links are not-applicable for text-based browsers or screen-reading software. Show Hide Full Abstract

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Descriptors:
Pregnancy; Self Efficacy; Addictive Behavior; Smoking; Anxiety; Depression (Psychology); Regression (Statistics); Reinforcement; Symptoms (Individual Disorders); Recidivism; Mothers; Prenatal Influences; Predictor Variables; Social Support Groups; Questionnaires

Abstract:
Objective: Based on conceptual models of addiction and affect regulation, this study examined the mechanisms linking current major depressive syndrome (MDS) and anxiety syndrome (AS) to postpartum smoking relapse. Method: Data were collected in a randomized clinical trial from 251 women who quit smoking during pregnancy. Simple and multiple mediation models of the relations of MDS and AS with postpartum relapse were examined using linear regression, continuation ratio logit models, and a bootstrapping procedure to test the indirect effects. Results: Both MDS and AS significantly predicted postpartum smoking relapse. After adjusting for MDS, AS significantly predicted relapse. However, after adjusting for AS, MDS no longer predicted relapse. Situationally based self-efficacy, expectancies of controlling negative affect by means other than smoking, and various dimensions of primary and secondary tobacco dependence individually mediated the effect of both MDS and AS on relapse. In multiple mediation models, self-efficacy in negative/affective situations significantly mediated the effect of MDS and AS on relapse. Conclusions: The findings underscore the negative impact of depression and anxiety on postpartum smoking relapse and suggest that the effects of MDS on postpartum relapse may be largely explained by comorbid AS. The current investigation provided mixed support for affect regulation models of addiction. Cognitive and tobacco dependence-related aspects of negative and positive reinforcement significantly mediated the relationship of depression and anxiety with relapse, whereas affect and stress did not. The findings emphasize the unique role of low agency with respect to abstaining from smoking in negative affective situations as a key predictor of postpartum smoking relapse. (Contains 1 figure and 4 tables.) Note:The following two links are not-applicable for text-based browsers or screen-reading software. Show Hide Full Abstract

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Descriptors:
Pregnancy; Emotional Development; Anxiety; Emotional Problems; Interaction; Environmental Influences; Psychiatry; Prenatal Influences; Perinatal Influences; Genetics; Mothers; Symptoms (Individual Disorders); Toddlers; Parent Influence; At Risk Persons; Child Development

Abstract:
Objective: First, we give an overview of child psychiatric research in the Generation R Study, a population-based cohort from fetal life forward. Second, we examine within Generation R whether the functional polymorphism (5-HTTLPR) in the promoter of the serotonin transporter gene interacts with prenatal maternal chronic difficulties, prenatal maternal anxiety or postnatal maternal anxiety to influence child emotional development. Method: A total of 2,136 northern European children were genotyped for 5-HTTLPR and rs25531. Mothers reported chronic difficulties and anxiety symptoms at 20 weeks' pregnancy and when the child was 3 years old. Child emotion recognition was observed at 3 years, and child emotional problems were assessed with the CBCL/1 1/2-5 at 5 years. Results: There were consistent main effects of maternal difficulties and anxiety on child emotional problems, but no main effect of 5-HTTLPR. Moreover, children with the s allele were at increased risk for emotional problems if their mothers reported prenatal anxiety symptoms (beta = 2.02, p less than 0.001) or postnatal anxiety symptoms (beta = 1.64, p less than 0.001). Also, in children of mothers with prenatal anxiety symptoms, the s allele was associated with less accurate emotion-matching (beta = -0.11, p = 0.004). Conclusions: This population-based study shows that vulnerability due to 5-HTTLPR is not specific for certain adverse exposures or severe events, but suggests that the small effects of gene-environment interaction on emotional development become manifest early in life. (Contains 10 tables and 3 figures.) Note:The following two links are not-applicable for text-based browsers or screen-reading software. Show Hide Full Abstract

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Descriptors:
Pregnancy; Autism; Screening Tests; Symptoms (Individual Disorders); Prenatal Influences; Pervasive Developmental Disorders; Young Adults; Correlation

Abstract:
An existing randomised controlled trial was used to investigate whether multiple ultrasound scans may be associated with the autism phenotype. From 2,834 single pregnancies, 1,415 were selected at random to receive ultrasound imaging and continuous wave Doppler flow studies at five points throughout pregnancy (Intensive) and 1,419 to receive a single imaging scan at 18 weeks (Regular), with further scans only as indicated on clinical grounds. There was no significant difference in the rate of Autism Spectrum Disorder between the Regular (9/1,125, 0.8%) and Intensive (7/1,167, 0.6%) groups, nor a difference between groups in the level of autistic-like traits in early adulthood. There is no clear link between the frequency and timing of prenatal ultrasound scans and the autism phenotype. (Contains 2 figures, 3 tables, and 1 footnote.) Note:The following two links are not-applicable for text-based browsers or screen-reading software. Show Hide Full Abstract

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Descriptors:
Pregnancy; Risk; Smoking; Teaching Methods; Foreign Countries; Control Groups; International Schools; Prenatal Influences; Mothers; Behavior Problems; Correlation; Elementary School Students; Questionnaires; Measures (Individuals); Scores; Prevention; Health Promotion

Abstract:
This retrospective cross-sectional paper examines the relationship between maternal smoking during pregnancy and children's behavioural problems at 9 years of age independent of a wide range of possible confounders. The final sample comprised 7,505 nine-year-old school children participating in the first wave of the Growing Up in Ireland study. The children were selected through the Irish national school system using a 2-stage sampling method and were representative of the nine-year population. Information on maternal smoking during pregnancy was obtained retrospectively at 9 years of age via parental recall and children's behavioural problems were assessed using the Strengths and Difficulties Questionnaire across separate parent and teacher-report instruments. A quasi-experimental approach using propensity score matching was used to create treatment (smoking) and control (non-smoking) groups which did not differ significantly in their propensity to smoke in terms of 16 observed characteristics. After matching on the propensity score, children whose mothers smoked during pregnancy were 3.5 % (p less than 0.001) and 3.4 % (p less than 0.001) more likely to score in the problematic range on the SDQ total difficulties index according to parent and teacher-report respectively. Maternal smoking during pregnancy was more strongly associated with externalising than internalising behavioural problems. Analysis of the dose-response relationship showed that the differential between matched treatment and control groups increased with level of maternal smoking. Given that smoking is a modifiable risk factor, the promotion of successful cessation in pregnancy may prevent potentially adverse long-term consequences. Note:The following two links are not-applicable for text-based browsers or screen-reading software. Show Hide Full Abstract

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Descriptors:
Genetics; Autism; Neonates; Intelligence Quotient; Incidence; Screening Tests; Scientific Research; Language Impairments; Risk; Child Development; Individual Differences; Clinical Diagnosis; Prenatal Influences

Abstract:
Most people have 23 pairs of chromosomes; one set from the mother and one from the father. However, nondisjunction errors during meiosis can lead to a case of trisomy, where there are three rather than two chromosomes. Although such events are not uncommon, they are usually lethal, and account for a high proportion of spontaneous abortions. There is surprisingly little research on sex chromosome trisomies: The explanation is largely due to the mild impact of the trisomy, which means that many people who have a sex chromosome trisomy would not be aware of their status. Most of the information about prevalence and consequences of sex chromosome trisomies comes from a set of studies carried out in the 1960-1970s in which newborn babies underwent chromosome screening. Findings from the newborn screening studies were summarized in a systematic review by Leggett, Jacobs, Nation, Scerif, and Bishop (2010), who noted a reduction in IQ in XXX, XXY and XYY groups, with both groups of males showing evidence of disproportionate verbal impairments. The report by Lee et al. makes a unique contribution by extending the study of the impact of supernumerary sex chromosomes to include rare cases of children with four or five sex chromosomes. They demonstrate a clear "dosage" effect, whereby the more chromosomes, the greater the negative impact on IQ and development. The study by Lee et al. (2012) has important clinical implications, as well as theoretical importance, because parental choices can be influenced by what they are told about the likely outcome of the child. It is important to emphasise that although there is an increased risk of both structural language problems and autistic features in children with additional sex chromosomes, there is wide individual variation. Some children with trisomies do not have any difficulties, and only a minority merit a diagnosis of autistic disorder (Bishop et al., 2011; Ross et al., 2012). Note:The following two links are not-applicable for text-based browsers or screen-reading software. Show Hide Full Abstract

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