Gordon Thomas Harold

The evidence for a neurobiological model of childhood antisocial behavior.

Children with persistent antisocial and aggressive behavior are diagnosed as having disruptive behavior disorder. The authors review evidence that antisocial children, and especially those who persist with this behavior as they grow older, have a range of neurobiological characteristics. It is argued that serotonergic functioning and stress-regulating mechanisms are important in explaining individual differences in antisocial behavior. Moreover, low fear of punishment and physiological underactivity may predispose antisocial individuals to seek out stimulation or take risks and may help to explain poor conditioning and socialization. The authors propose a theoretical model highlighting the interplay between neurobiological deficits and cognitive and emotional functioning as mediators of the link between early adversity and antisocial behavior problems in childhood. Implications for intervention programs are discussed.

Marital Satisfaction and Depression: Different Causal Relationships for Men and Women?:

A sample of 150 recently married couples provided data egarding marital satisfaction and depressive symptoms Approximatey 18 months later, 116 of these couples provided complete information on marital satisfaction and depression once again The data were examined using three sets of causal models, which yielded converging results For men, causal paths emerged from depression to marital satisfaction, whereas for women causal paths were from satisfaction to depression The results are discussed in relation to the marital discord model of depression

The genetic aetiology of childhood depression: a review

BACKGROUND We review the evidence for the familiality of major depressive disorder (MDD) and the genetic aetiology of depressive symptoms in children and adolescents. METHODS Databases and reference lists were searched for family, twin and adoption studies of childhood MDD and childhood depressive symptoms. Data from independent family studies that fulfilled specified inclusion criteria were pooled and odds ratios were calculated for top-down and bottom-up family studies. RESULTS Estimates of familial risk differ by control group and by study design (odds ratio range 1.70, 3.98). Twin studies show that depressive symptoms in young people are heritable although rater and measurement issues are important. Adoption studies show little evidence for a genetic influence on depressive symptoms. CONCLUSIONS MDD in young people is familial although control group and study design affect the magnitude of the familial risk. Estimates of heritability from twin and adoption studies vary widely and few firm conclusions can be made regarding the genetic aetiology of depressive symptoms in childhood. Areas that require future work include the examination of rater effects, measurement issues, the effects of age and comorbidity and reasons for the discrepancy between twin and adoption findings.

Prenatal smoking might not cause attention-deficit/hyperactivity disorder: evidence from a novel design

Background It is widely considered that exposure to maternal cigarette smoking in pregnancy has risk effects on offspring attention-deficit/hyperactivity disorder (ADHD). This view is supported by consistent observations of association. It is, however, impossible to be certain of adequate control for confounding factors with observational designs. We use a novel “natural experiment” design that separates prenatal environmental from alternative inherited effects. Methods The design is based on offspring conceived with Assisted Reproductive Technologies recruited from 20 fertility clinics in the United Kingdom and United States who were: 1) genetically unrelated, and 2) related to the woman who underwent the pregnancy. If maternal smoking in pregnancy has true risk effects, association will be observed with ADHD regardless of whether mother and offspring are related or unrelated. Data were obtained from 815 families of children ages 4 years–11 years with parent questionnaires and antenatal records. Birth weight was used as a comparison outcome. The key outcome considered was child ADHD symptoms. Results Association between smoking in pregnancy and lower birth weight was found in unrelated and related mother-offspring pairs, consistent with a true risk effect. However, for ADHD symptoms, the magnitude of association was significantly higher in the related pairs (β = .102, p < .02) than in the unrelated pairs (β= −.052, p > .10), suggesting inherited effects. Conclusions Our findings highlight the need to test causal hypotheses with genetically sensitive designs. Inherited confounds are not necessarily removed by statistical controls. The previously observed association between maternal smoking in pregnancy and ADHD might represent an inherited effect.

Pathways to Violence in the Children of Mothers Who Were Depressed Postpartum

The impact of postnatal depression on a childs risk for violent behavior was evaluated in an urban British community sample (N=122 families). Mothers were interviewed during pregnancy, at 3 months postpartum, and when the child was 1, 4, and 11 years of age. Mothers, teachers, and children reported on violent symptoms at age 11. Structural equation modeling revealed that the childs violence was predicted by the mothers postnatal depression even when her depression during pregnancy, her later history of depression, and family characteristics were taken into account. Violence was associated with symptoms of attention-deficit/hyperactivity disorder and problems with anger management. Children were most violent if mothers had been depressed at 3 months and at least once thereafter.

Archival ReportPrenatal Smoking Might Not Cause Attention-Deficit/Hyperactivity Disorder: Evidence from a Novel Design

Background It is widely considered that exposure to maternal cigarette smoking in pregnancy has risk effects on offspring attention-deficit/hyperactivity disorder (ADHD). This view is supported by consistent observations of association. It is, however, impossible to be certain of adequate control for confounding factors with observational designs. We use a novel “natural experiment” design that separates prenatal environmental from alternative inherited effects. Methods The design is based on offspring conceived with Assisted Reproductive Technologies recruited from 20 fertility clinics in the United Kingdom and United States who were: 1) genetically unrelated, and 2) related to the woman who underwent the pregnancy. If maternal smoking in pregnancy has true risk effects, association will be observed with ADHD regardless of whether mother and offspring are related or unrelated. Data were obtained from 815 families of children ages 4 years–11 years with parent questionnaires and antenatal records. Birth weight was used as a comparison outcome. The key outcome considered was child ADHD symptoms. Results Association between smoking in pregnancy and lower birth weight was found in unrelated and related mother-offspring pairs, consistent with a true risk effect. However, for ADHD symptoms, the magnitude of association was significantly higher in the related pairs (β = .102, p < .02) than in the unrelated pairs (β= −.052, p > .10), suggesting inherited effects. Conclusions Our findings highlight the need to test causal hypotheses with genetically sensitive designs. Inherited confounds are not necessarily removed by statistical controls. The previously observed association between maternal smoking in pregnancy and ADHD might represent an inherited effect.

Assessing the effects of age, sex and shared environment on the genetic aetiology of depression in childhood and adolescence

BACKGROUND Depressive symptoms and disorder are experienced by a significant proportion of young people and have long-lasting deleterious effects. The aims of the current investigation were to examine the aetiology of depressive symptoms using a twin design. In particular to examine the effects of sex, age, maternal depression and anxiety symptoms and to examine the aetiology of high depression scores. METHODS Questionnaires were sent to the families of a population-based sample of twins aged between 8 and 17 years. Parents and children over the age of 11 were asked to complete the Mood and Feelings Questionnaire and Hospital Anxiety and Depression Scale (mothers only). Responses were obtained from 1463 families and data were analysed using genetic model fitting and DeFries and Fulker regression analysis. RESULTS Depressive symptoms, particularly when self-rated, were significantly genetically influenced. There was evidence of significant heterogeneity according to age, with shared environmental factors more important and genetic factors less important for children aged 8 to 10 than for adolescents aged 11 to 17 years. Some but not all of the shared environmental influences on parent-rated depressive symptoms were accounted for by maternal symptoms of depression and anxiety. There was a significant effect of gender for self-rated depressive symptoms. For boys, genetic factors were of greater importance and common environmental influences of less importance than for girls. Shared environmental effects had a substantial influence on high self-rated depression scores. Adolescents who scored highly on self-rated depression questionnaires experienced significantly more shared life events and their mothers had significantly higher internalising symptoms than adolescents who scoredwithin the normal range. CONCLUSIONS The results of this study add to the evidence that the aetiology of depressive symptoms differs by age, with genetic factors becoming more important from childhood to adolescence. Some but not all of the shared environmental effect observed for mother-rated depression scores is due to maternal depression and anxiety symptoms. For self-rated depressive symptoms, the importance of genetic and environmental factors may also differ by sex, with genetic influences more important for boys. The aetiology of high depression symptom scores, when self-rated, appears to differ from scores within the normal range in that shared environmental factors appear to be more important. Further research is needed to identify these shared environmental factors using longitudinal models that test genetic and environmental mediation.

Adolescent clinical outcomes for young people with attention-deficit hyperactivity disorder.

BACKGROUND Attention-deficit hyperactivity disorder (ADHD) is recognised as a common, disabling condition. Little information is available regarding the long-term outcomes for individuals with ADHD in the UK. AIMS To examine the 5-year outcome for a UK cohort of children with diagnosed, treated ADHD and identify whether maternal and social factors predict key outcomes. METHOD One hundred and twenty-six school-aged children (mean age 9.4 years, s.d. = 1.7) diagnosed with ADHD were reassessed 5 years later during adolescence (mean age 14.5 years, s.d. = 1.7) for ADHD, conduct disorder and other antisocial behaviours. RESULTS Most adolescents (69.8%) continued to meet full criteria for ADHD, were known to specialist services and exhibited high levels of antisocial behaviour, criminal activity and substance use problems. Maternal childhood conduct disorder predicted offspring ADHD continuity; maternal childhood conduct disorder, lower child IQ and social class predicted offspring conduct disorder symptoms. CONCLUSIONS The treatment and monitoring of ADHD need to be intensified as outcomes are poor especially in offspring of mothers with childhood conduct disorder symptoms.

Depressive symptoms in children and adolescents: changing aetiological influences with development

BACKGROUND Evidence suggests that depressive symptoms become increasingly heritable as children grow into adolescence. However, the literature is not entirely consistent in this respect and existing longitudinal twin studies have examined changes within adolescence only. METHOD Parent and self-report questionnaire data were used to examine the genetic and environmental influences on depressive symptoms in a UK sample of 670 twin pairs aged 5-17. Age effects were examined cross-sectionally and longitudinally using data collected over a 3-year period. RESULTS Cross-sectional analyses showed that shared environmental effects had significant influence in younger children but not in adolescence, when depression scores were significantly more heritable. The results of these cross-sectional analyses were supported when two waves of parent-report data collected over three years were analysed. Significant new genetic influences emerged in adolescence but no new shared environmental influences. Some sex differences were found, with girls showing greater genetic influence than boys, but only from parent-report data. CONCLUSIONS These findings support and extend earlier work which has shown increasing genetic influence on depressive symptoms as children grow into adolescence.

Interparental conflict, negative parenting, and children's adjustment: bridging links between parents' depression and children's psychological distress

Pathways linking parental depressive symptoms, adult relationship insecurity, interparental conflict, negative parenting, and childrens psychological adjustment (internalizing symptoms and externalizing problems) were assessed using a 3-wave longitudinal research design. Two-parent families (N = 352) with 11- to 13-year-old children (179 boys, 173 girls) participated in the study. Maternal and paternal depressive symptoms were associated with insecurity in adult close relationships assessed 12 months later, which was concurrently related to heightened levels of interparental conflict. Controlling for childrens initial symptom levels, interparental conflict was related to child appraisals of father and mother rejection assessed an additional 12 months later, which were related to childrens internalizing symptoms and externalizing problems, respectively. Results are discussed with regard to the implications for understanding the complex interplay between adult depressive symptoms, attributions in close adult relationships, interparental conflict, negative parenting, and childrens psychological adjustment.