Self-Compassion and Parenting in Mothers and Fathers with Depression.

Depression in parents impairs parenting and increases the risk of psychopathology among their children. Prevention and intervention could be informed by knowledge of the mechanisms that break the inter-generational transmission of psychopathology and build resilience in both parents and their children. We used data from two independent studies to examine whether higher levels of self-compassion were associated with better parenting and fewer emotional and behavioral problems in children of parents with a history of depression. Study 1 was a pilot trial of mindfulness-based cognitive therapy that included 38 parents with recurrent depression. Study 2 was a longitudinal study that consisted of 160 families, including 50 mothers and 40 fathers who had a history of depression. Families were followed up approximately 16 months after the first assessment (time 2; n = 106 families). In both studies, self-compassion was assessed with the Self-Compassion Scale. Parents reporting higher levels of self-compassion were more likely to attribute the cause of their children's behavior to external factors, were less critical, and used fewer distressed reactions to cope with their children's emotions. Parents' self-compassion was longitudinally associated with children's internalizing and externalizing problems, but these associations became nonsignificant after controlling for child gender, parent education, and depressive symptoms. Future larger scale and experimental designs need to examine whether interventions intended to increase self-compassion might reduce the use of negative parenting strategies and thereby the inter-generational transmission of psychopathology.

Does father-child conflict mediate the association between fathers' postnatal depressive symptoms and children's adjustment problems at 7 years old?

BACKGROUND: Paternal depressive symptoms are associated with children's emotional and behavioural problems, which may be mediated by negative parenting. But there is no research on the influence of paternal depressive symptoms on children's emotion regulation and limited literature investigating fathers' parenting as a mediator in the pathway between paternal depressive symptoms and children's externalizing and internalizing problems. We aimed to investigate the mediating role of father-child conflict (at 3 years) in the association between postnatal paternal depressive symptoms (at 9 months) and children's emotional and behavioural problems (at 7 years) (aim 1). We also examined whether mediation pathways were more pronounced for boys or for girls (aim 2). METHOD: Secondary data analysis was conducted on the Millennium Cohort Study, when children were 9 months, 3 years and 7 years old (n = 3520). Main study variables were measured by self-report questionnaires. Fathers completed the Rutter Scale (depressive symptoms) and the Parent-Child Relationship Questionnaire (father-child conflict), while mothers completed the Strengths and Difficulties Questionnaire and the Social Behaviour Questionnaire (child emotional and behavioural problems, emotion regulation). We used structural equation modelling to estimate direct, indirect and total effects of paternal depressive symptoms on child outcomes, mediated by father-child conflict whilst adjusting for relevant covariates (maternal depressive symptoms, child temperament, marital conflict, and socio-economic factors such as poverty indicator and fathers' education level). Multi-group and interaction analysis was then conducted to determine the differential effect by gender of the association between paternal depressive symptoms on child outcomes via father-child conflict. RESULTS: Father-child conflict mediated the association between paternal depressive symptoms and emotion regulation problems [standardized indirect effect (SIE) 95% confidence interval (CI) -0.03 to -0.01, p < 0.001; standardized total effect (STE) 95% CI -0.05 to -0.01, p < 0.05] (aim 1). Father-child conflict mediated a larger proportion of the effect in boys (SIE 95% CI -0.03 to -0.01, p < 0.001; STE 95% CI -0.05 to 0.00, p = 0.063) than it did in girls (SIE 95% CI -0.02 to -0.01, p < 0.001; STE 95% CI -0.04 to 0.01, p = 0.216) (aim 2). CONCLUSIONS: Father-child conflict may mediate the association between postnatal paternal depressive symptoms and children's emotion regulation problems. Paternal depressive symptoms and father-child conflict resolution may be potential targets in preventative interventions.

Why do depressed individuals have difficulties in their parenting role?

Although existing research has shown that depression in parents has a negative effect on parent-child interactions, the mechanisms underpinning impaired parenting are still unknown. In this editorial, we review core difficulties that have been noted in depressed individuals including reduced positive and increased negative affect, poor emotion regulation, executive function deficits, reduced motivation and rumination, and discuss how each of these can alter parenting. We suggest that these causal processes are inter-related and can interact with one another in affecting parenting. We conclude that an improved understanding of these processes will have implications for the development of more specific and potentially more effective treatments that have the potential to break the intergenerational transmission of psychopathology.

Expressed emotion as an assessment of family environment with mothers and fathers of 1-year-old children.

BACKGROUND: High levels of expressed emotion (EE) in parents have been found to put children at risk for emotional and behavioural problems. However, the majority of existing studies have focused on mothers of school-aged children and adolescents rather than younger children, and have only rarely included fathers. METHODS: The present study examined the reliability of EE in mothers and fathers of 1-year old children. It also investigated whether depression and marital problems in the postnatal period predicted EE toward the child at 12 months. EE was assessed with the Preschool Five Minute Speech Sample in 163 families. RESULTS: The rater-interrater and code-recode reliability was high for most EE dimensions. Mothers and fathers were found to display quite similar EE scores. Regression analyses showed that depression and couple relationship significantly predicted EE in mothers, but not fathers. CONCLUSIONS: The findings suggest that EE provides a reliable and useful assessment of the family environment in families of young children.

Co-transmission of conduct problems with attention-deficit/hyperactivity disorder: familial evidence for a distinct disorder.

Common disorders of childhood and adolescence are attention-deficit/hyperactivity disorder (ADHD), oppositional defiant disorder (ODD) and conduct disorder (CD). For one to two cases in three diagnosed with ADHD the disorders may be comorbid. However, whether comorbid conduct problems (CP) represents a separate disorder or a severe form of ADHD remains controversial. We investigated familial recurrence patterns of the pure or comorbid condition in families with at least two children and one definite case of DSM-IV ADHDct (combined-type) as part of the International Multicentre ADHD Genetics Study (IMAGE). Using case diagnoses (PACS, parental account) and symptom ratings (Parent/Teacher Strengths and Difficulties [SDQ], and Conners Questionnaires [CPTRS]) we studied 1009 cases (241 with ADHDonly and 768 with ADHD + CP), and their 1591 siblings. CP was defined as > or =4 on the SDQ conduct-subscale, and T > or = 65, on Conners' oppositional-score. Multinomial logistic regression was used to ascertain recurrence risks of the pure and comorbid conditions in the siblings as predicted by the status of the cases. There was a higher relative risk to develop ADHD + CP for siblings of cases with ADHD + CP (RRR = 4.9; 95%CI: 2.59-9.41); p < 0.001) than with ADHDonly. Rates of ADHDonly in siblings of cases with ADHD + CP were lower but significant (RRR = 2.9; 95%CI: 1.6-5.3, p < 0.001). Children with ADHD + CP scored higher on the Conners ADHDct symptom-scales than those with ADHDonly. Our finding that ADHD + CP can represent a familial distinct subtype possibly with a distinct genetic etiology is consistent with a high risk for cosegregation. Further, ADHD + CP can be a more severe disorder than ADHDonly with symptoms stable from childhood through adolescence. The findings provide partial support for the ICD-10 distinction between hyperkinetic disorder (F90.0) and hyperkinetic conduct disorder (F90.1).

A high-density SNP linkage scan with 142 combined subtype ADHD sib pairs identifies linkage regions on chromosomes 9 and 16.

As part of the International Multi-centre ADHD Genetics project we completed an affected sibling pair study of 142 narrowly defined Diagnostic and Statistical Manual of Mental Disorders, fourth edition combined type attention deficit hyperactivity disorder (ADHD) proband-sibling pairs. No linkage was observed on the most established ADHD-linked genomic regions of 5p and 17p. We found suggestive linkage signals on chromosomes 9 and 16, respectively, with the highest multipoint nonparametric linkage signal on chromosome 16q23 at 99 cM (log of the odds, LOD=3.1) overlapping data published from the previous UCLA (University of California, Los Angeles) (LOD>1, approximately 95 cM) and Dutch (LOD>1, approximately 100 cM) studies. The second highest peak in this study was on chromosome 9q22 at 90 cM (LOD=2.13); both the previous UCLA and German studies also found some evidence of linkage at almost the same location (UCLA LOD=1.45 at 93 cM; German LOD=0.68 at 100 cM). The overlap of these two main peaks with previous findings suggests that loci linked to ADHD may lie within these regions. Meta-analysis or reanalysis of the raw data of all the available ADHD linkage scan data may help to clarify whether these represent true linked loci.

Inhibitory deficits in attention-deficit/hyperactivity disorder are independent of basic processing efficiency and IQ.

BACKGROUND: A substantial proportion of children with attention-deficit/hyperactivity disorder (ADHD) show deficits on inhibitory control tests. However, questions remain about (i) the extent of these deficits across different inhibitory domains, (ii) their relationship to deficits in non-executive processes and (iii) whether they extend into adolescence. METHODS: Seventy-seven children and adolescents with ADHD and 50 non-ADHD controls completed three inhibitory tasks, a simple two choice RT task (2CR) and an IQ assessment. RESULTS: ADHD was moderately associated with deficits on all tasks (effect sizes d=0.5-0.9). Deficits were equally marked in childhood and adolescence. Inhibitory deficits were not associated with IQ and, although reduced substantially, remained significant after performance on a simple reaction time task was controlled for statistically. DISCUSSION: In highlighting the significant, but limited, role of inhibitory deficits in ADHD, these results are consistent with recent accounts that emphasize the neuropsychological heterogeneity of this condition.

The analysis of 51 genes in DSM-IV combined type attention deficit hyperactivity disorder: association signals in DRD4, DAT1 and 16 other genes.

Attention deficit hyperactivity disorder (ADHD) is a common neurodevelopmental disorder, starting in early childhood and persisting into adulthood in the majority of cases. Family and twin studies have demonstrated the importance of genetic factors and candidate gene association studies have identified several loci that exert small but significant effects on ADHD. To provide further clarification of reported associations and identify novel associated genes, we examined 1,038 single-nucleotide polymorphisms (SNPs) spanning 51 candidate genes involved in the regulation of neurotransmitter pathways, particularly dopamine, norepinephrine and serotonin pathways, in addition to circadian rhythm genes. Analysis used within family tests of association in a sample of 776 DSM-IV ADHD combined type cases ascertained for the International Multi-centre ADHD Gene project. We found nominal significance with one or more SNPs in 18 genes, including the two most replicated findings in the literature: DRD4 and DAT1. Gene-wide tests, adjusted for the number of SNPs analysed in each gene, identified associations with TPH2, ARRB2, SYP, DAT1, ADRB2, HES1, MAOA and PNMT. Further studies will be needed to confirm or refute the observed associations and their generalisability to other samples.