Differential susceptibility in youth: evidence that 5-HTTLPR x positive parenting is associated with positive affect ‘for better and worse’

Abstract

Positive affect has been implicated in the phenomenological experience of various psychiatric disorders, vulnerability to develop psychopathology and overall socio-emotional functioning. However, developmental influences that may contribute to positive affect have been understudied. Here, we studied youths' 5-HTTLPR genotype and rearing environment (degree of positive and supportive parenting) to investigate the differential susceptibility hypothesis (DSH) that youth carrying short alleles of 5-HTTLPR would be more influenced and responsive to supportive and unsupportive parenting, and would exhibit higher and lower positive affect, respectively. Three independent studies tested this gene–environment interaction (GxE) in children and adolescents (age range 9–15 years; total N=1874). In study 1 (N=307; 54% girls), positive/supportive parenting was assessed via parent report, in study 2 (N=197; 58% girls) via coded observations of parent–child interactions in the laboratory and in study 3 (N=1370; 53% girls) via self report. Results from all the three studies showed that youth homozygous for the functional short allele of 5-HTTLPR were more responsive to parenting as environmental context in a ‘for better and worse' manner. Specifically, the genetically susceptible youth (that is, S'S' group) who experienced unsupportive, non-positive parenting exhibited low levels of positive affect, whereas higher levels of positive affect were reported by genetically susceptible youth under supportive and positive parenting conditions. These GxE findings are consistent with the DSH and may inform etiological models and interventions in developmental psychopathology focused on positive emotion, parenting and genetic susceptibility.

Testing the Temporal Relationship Between Maternal and Adolescent Depressive and Anxiety Symptoms in a Community Sample

“…Although the autoregressive parameters in the model account for the influence of preexisting depression that may have been influenced by genetic and environmental factors that may have been set in motion in early childhood, it does not necessarily account for ongoing interaction of genetic vulnerability and environmental factors. Related lines of research have found support for specific cognitive processes, such as rumination (Flancbaum, et al, 2011) and depressive inferential styles (Abela, Skitch, Adams, & Hankin, 2006; Abela, et al, 2009), as well gene x environment interactions (Hankin, et al, 2011) that may account for the associations between maternal and offspring depression.…”

5‐HTTLPR Moderates Naltrexone and Psychosocial Treatment Responses in Heavy Drinking Men Who Have Sex with Men

“…A growing body of work suggests that S allele carriers, while more sensitive to stress, may also be more responsive to supportive environments or treatment interventions to reduce the impact of environmental stressors (Kaufman et al, 2004, Hankin et al, 2011). It has been hypothesized that the S allele is a “plasticity factor” rather than simply a risk factor following exposure to adverse environment (e.g., Kuepper et al, 2012).…”

Emotion regulation moderates the risk associated with the 5-HTT gene and stress in children.

“…The link between high stress and depression appears to be further exacerbated in people who carry a short allele in the serotonin transporter polymorphism (5-HTTLPR, linked to serotonin function) (Caspi, Hariri, Holmes, Uher, & Moffitt, 2010; Caspi et al, 2003; Kim et al, 2007; Lesch et al, 1996; Manuck & McCaffery, 2014; Uher & McGuffin, 2010), a group that represents approximately 40–70% of the general population (Kim et al, 2007). These individuals – compared to those without a short allele – appear to be particularly sensitive to the quality of their environment, such that experiencing negative environments is associated with significantly worse psychological health (Belsky & Pluess, 2009; Hankin et al, 2011; Taylor et al, 2006). Given that genes and stressful environments are not always modifiable, how can people with this risky combination avoid depression?…”