Practitioner Review: Differential susceptibility theory: might it help in understanding and treating mental health problems in youth?

Diathesis-stress models conceptualise individual differences in propensity for psychopathology as an interaction between environmental risk factors and intra-individual vulnerabilities. In contrast, the differential susceptibility theory and related frameworks view intra-individual differences as variations in sensitivity to the environments rather than merely vulnerability to them. Specifically, they suggest that more sensitive individuals are more affected by the quality of their context, whether positive or negative, than others who are less sensitive. Empirical research over the last two decades has found support for this notion in that greater sensitivity is associated with a greater risk of psychopathology in adverse contexts, but also with lower risk in positive environments. However, despite growing academic and public interest in this field, it is currently unclear to what extent the differential susceptibility model is relevant, or applicable, to clinical practice. The purpose of this review is to focus on the differential susceptibility theory as an alternative explanation of individual differences in mental health and examine its relevance in the treatment of mental health problems in young people. We provide an overview of differential susceptibility and related theories, and current relevant research in the field. We identify potential implications of differential susceptibility models for understanding and treating mental health problems in young people, whilst also highlighting important gaps in research that limit their application at present. Finally, we suggest directions for future research that will assist in the translation of differential susceptibility theories into clinical practice

Exploring the association between anxiety and conduct problems in a large sample of twins aged 2-4

Anxiety and conduct problems covary, yet studies have not explored the genetic and environmental origins of this association.We analyzed parent-reported anxiety and conduct problems in 6,783 pairs of twins at 2-, 3-, and 4-years of age. As anxiety and conduct problems were fairly stable across the three ages (average 1-year correlation was .53), ratings from all three were combined. The aggregate anxiety and conduct ratings correlated .33 for boys and .30 for girls. Bivariate genetic analyses indicated fairly low genetic correlations (.31 for boys, .16 for girls), and high shared environmental correlations (1.0 for boys and 0.99 for girls) between anxiety and conduct problems. Most of the phenotypic correlation was accounted for by shared environmental mediation (65% for boys and 94% for girls), indicating that many of the same family environmental factors are responsible for the development of both anxiety and conduct problems

Developmental change in the association between adolescent depressive symptoms and the home environment: results from a longitudinal, genetically informative investigation

Background: Depression is already highly prevalent by late adolescence, indicating that research into its developmental emergence should consider earlier risk factors and environmental contexts. The home environment is a key context for children and adolescents throughout development. However, the nature of relationships that exist between aspects of the home environment and the development of depressive symptoms cannot be assumed. Genetically informative studies have been used to provide insights about the aetiology of such relationships, often finding them to be partly confounded by the influence of children's genes. Here, we investigate developmental change in the aetiology of the association between aspects of the home environment and depressive symptoms at the onset of adolescence. Methods: We used longitudinal child‐ and parent‐report data from >5,000 twin pairs enrolled in the UK‐representative Twins Early Development Study. Multivariate, genetically sensitive structural equation models were used to decompose latent variance and covariance in depressive symptoms (measured at 12 and 16 years) and aspects of the home environment (at 9 and 14 years) into genetic and environmental influences. Results: Going from childhood to adolescence, genetic influences accounted for an increasing proportion of the association [30% (16–42) of r = .44 in childhood; 40% (25–61) of r = .43 in adolescence], at the expense of shared environmental influences, which decreased from 70% (58–83) to 48% (29–62). Unique environmental influences accounted for a significant proportion of the association in adolescence only [12% (06–18)]. Developmental changes could largely be attributed to subtle shifts in the relative importance of stable aetiological factors, rather than the emergence of influences unique to adolescence. Conclusions: These findings emphasise the importance of developmental and aetiological context in interpreting associations between aspects of the home environment and child emotional outcomes

Finding gene-environment interactions for Phobias

Phobias are common disorders causing a great deal of suffering. Studies of gene-environment interaction (G × E) have revealed much about the complex processes underlying the development of various psychiatric disorders but have told us little about phobias. This article describes what is already known about genetic and environmental influences upon phobias and suggests how this information can be used to optimise the chances of discovering G × Es for phobias. In addition to the careful conceptualisation of new studies, it is suggested that data already collected should be re-analysed in light of increased understanding of processes influencing phobias

Adolescent Irritability: Phenotypic Associations and Genetic Links With Depressed Mood

OBJECTIVE: Irritability has been proposed to underlie the developmental link between oppositional problems and depression. However, little is known about the genetic and environmental influences on irritability and its overlap with depression. This paper tests the hypothesis that the association between irritability and depression is accounted for by genetic factors. As such, it draws on the notion of “generalist genes” i.e., genes of general effect that underlie phenotypic overlap between disorders. METHOD: The G1219 study, a UK-based twin sample (N=2651), was used in a cross-sectional and longitudinal design. Irritable and headstrong/hurtful dimensions of oppositional behavior were derived using factor analysis. Regression was used to estimate the association between depression and delinquency. Multivariate genetic analyses were used to estimate the genetic overlap between irritability versus headstrong/hurtful behaviors with depression and delinquency respectively. RESULTS: Irritability showed a significantly stronger phenotypic relationship with depression than delinquency, whereas headstrong/hurtful behaviors were more strongly related to delinquency than depression. In multivariate genetic analyses, the genetic correlation between irritability and depression (0.70; CI: 0.59-0.82) was significantly higher than that between irritability and delinquency (0.57; CI: 0.45-0.69); conversely, the genetic correlation between headstrong/hurtful behaviors and delinquency (0.80; CI: 0.72-0.86) was significantly higher than that between headstrong/hurtful behaviors and depression (0.46; CI: 0.36-0.57). In longitudinal models, the phenotypic association between irritability at Time 1 and depression at Time 2 was accounted for by the genetic association between irritability and depression at Time1. CONCLUSIONS: The findings are consistent with the theory that genes with general effects underlie the relationship between irritability and depression

Understanding the genetic and environmental specificity and overlap between well-being and internalizing symptoms in adolescence

Moderate inverse correlations are typically found between well-being and mental illness. We aimed to investigate the role of genes and environments in explaining the relationships between two aspects of well-being and two measures of internalizing symptoms. Altogether, 4700 pairs of 16-year-old twins contributed data on subjective happiness and life satisfaction, as well as symptoms of depression and emotional problems. Well-being was moderately correlated with internalizing symptoms (range = 0.45, 0.58). Multivariate twin model-fitting indicated both genetic and environmental overlap. Life satisfaction and happiness demonstrated different patterns of overlap, with stronger genetic links between life satisfaction and depression. Non-shared environmental influences were largely specific to each trait. This study supports the theory of mental health and illness being partly (but not entirely) correlated dimensions. There are also significant genetic and environmental factors to identify for well-being that go beyond the absence of mental illness. It is therefore possible that different interventions are needed for treating mental illness and promoting mental health

Etiological influences on perceptions of parenting: A longitudinal, multi-informant twin study

Children and their parents often differ in their perception of the relationship they share. As this relationship changes developmentally, the nature of these differences may also change. Longitudinal genetic designs can be used to investigate the developmental etiologies of shared and distinct perceptions. In this study, we used longitudinal psychometric models to analyze child and parent reports of negative parenting for 6417 twin pairs from the Twins Early Development Study at ages 9, 12 and 14 years. Within-time cross-reporter correlations, indicating the degree to which children and parents perceived negative parenting behaviors similarly at each age, were moderate (r = .44 − .46). Longitudinal genetic analyses revealed these shared perceptions to be relatively stable during the transition into adolescence, with this stability driven by a combination of children’s genetic factors and family-wide environmental factors. In contrast, child- and parent-specific perceptions of parenting were predominantly age-specific, a developmental pattern underpinned by child genetic factors and a combination of family-wide and unique environmental influences. These results and their implications are discussed in the context of interplay between reciprocal interactions, subjective insight and developmental behavioral change in the parent–child relationship

Associations between attentional bias and interpretation bias and change in school concerns and anxiety symptoms during the transition from primary to secondary school

The transition from primary to secondary school is often associated with a period of heightened anxiety and worry. For most children, any feelings of anxiety subside relatively quickly but for a small minority, emotional difficulties can continue into the first year of secondary school and beyond. This study recruited 109 children and measured their anxiety symptoms and school concerns toward the end of primary school and again at the end of their first term of secondary school. We investigated for the first time whether pre-transition measures of attentional and interpretation bias, and the magnitude of change in attentional bias toward and away from threat stimuli were associated with pre- and post-transition measures of anxiety and school concerns, and the change in these measures over time. Over 50% of the current sample exceeded clinical levels of anxiety at pre-transition. However, anxiety symptoms and school concerns had significantly reduced by post-transition. Higher levels of pre-transition anxiety or school concerns, and a greater magnitude of change in attentional bias towards threat stimuli predicted a larger reduction in anxiety symptoms and school concerns across the transition period. A greater interpretation bias toward threat was associated with higher pre-transition anxiety symptoms and school concerns but not post-transition scores, or the change in these scores. While many children experience heightened anxiety prior to school transition, this appears to be largely temporary and self-resolves. Nonetheless, the current findings highlight the importance of monitoring children’s anxiety and concerns, and related cognitive processes during this important transition period

Heart-beat perception, panic/somatic symptoms and anxiety sensitivity in children

There is considerable evidence implicating heart-beat perception (HBP) accuracy and anxiety sensitivity (AS) in the development of panic in adults. However, to date there have been no studies exploring the association between HBP, AS and childhood panic/somatic symptoms. Seventy-nine children aged 8 to 11 years completed a mental tracking paradigm (Psychophysiology 18 (1981) 483) to assess HBP, the Children’s Anxiety Sensitivity Index (J Clin Chil Psychol 20 (1991) 162) and the Screen for Childhood Anxiety Related Emotional Disorders (J Am Acad Child Adoles Psych 38 (1999) 1230). Those with good HBP (n = 7, 9%) had significantly higher panic/somatic symptoms (t = -1.71, P < 0.05), and AS (t = -2.16, P < 0.02) than those with poor HBP. There were no effects of age, sex or BMI on HBP. Those with high levels of panic/somatic symptoms were seven times more likely to have good HBP and had AS scores 1 S.D. higher than the remainder of the sample. Multivariate analyses revealed that these two phenotypes had independent associations with high panic/somatic symptoms. These results extend the literature on HBP and panic and suggest that in children, as in adults, increased panic/somatic symptoms are associated with enhanced ability to perceive internal physiological cues, and fear of such sensations

Polymorphisms in the circadian expressed genes PER3 and ARNTL2 are associated with diurnal preference and GNβ3 with sleep measures

Sleep and circadian rhythms are intrinsically linked, with several sleep traits, including sleep timing and duration, influenced by both sleep homeostasis and the circadian phase. Genetic variation in several circadian genes has been associated with diurnal preference (preference in timing of sleep), although there has been limited research on whether they are associated with other sleep measurements. We investigated whether these genetic variations were associated with diurnal preference (Morningness-Eveningness Questionnaire) and various sleep measures, including: the global Pittsburgh Sleep Quality index score; sleep duration; and sleep latency and sleep quality. We genotyped 10 polymorphisms in genes with circadian expression in participants from the G1219 sample (n = 966), a British longitudinal population sample of young adults. We conducted linear regressions using dominant, additive and recessive models of inheritance to test for associations between these polymorphisms and the sleep measures. We found a significant association between diurnal preference and a polymorphism in period homologue 3 (PER3) (P < 0.005, recessive model) and a novel nominally significant association between diurnal preference and a polymorphism in aryl hydrocarbon receptor nuclear translocator-like 2 (ARNTL2) (P < 0.05, additive model). We found that a polymorphism in guanine nucleotide binding protein beta 3 (GNβ3) was associated significantly with global sleep quality (P < 0.005, recessive model), and that a rare polymorphism in period homologue 2 (PER2) was associated significantly with both sleep duration and quality (P < 0.0005, recessive model). These findings suggest that genes with circadian expression may play a role in regulating both the circadian clock and sleep homeostasis, and highlight the importance of further studies aimed at dissecting the specific roles that circadian genes play in these two interrelated but unique behaviours