5-HTTLPR polymorphism is associated to differences in behavioral response and HPA reactivity to a social stressor in 4-month-old infants

BACKGROUND It is well-known that young infants react to physical stress with increased secretion of cortisol by the hypothalamic-pituitary-adrenal (HPA) axis (Gunnar et al 2009). Recently, it has been suggested that a serotonin transporter polymorphism, 5-HTTLPR, modulates early individual differences in stress reactivity to heel-prick (Mueller et al 2010). 5-HTTLPR might express in short (S) or long (L) allele version, resulting in three possible genotypes: LL, LS or SS (Canli et al 2007). S-carriers show altered HPA functioning (Gotlib et al 2008) and adverse developmental outcomes (Caspi et al 2003; Sen et al 2004). Infants are also very sensitive to social stress and previous studies using Still-Face paradigm (SF, Tronick et al 1978) documented that, when faced with an unresponsive mother, they show increased negative emotionality, decreased social-positive engagement (Weinberg et al 1999), and heightened cortisol secretion (Haley et al 2003). Although several studies suggest that maternal engagement modulates infant reactivity to social stress (Gunnar et al 2002), recently there are claims about the role of specific polymorphisms in older infants (Frigerio et al 2009; Luijk et al 2011). Nonetheless little is known about such genetic contributions in the first months of life. In current study we test the hypotheses that cortisol reactivity and behavioral response to SF would be greater in S-carrier infants, controlling for mother’s engagement. METHOD 62 4-month-old infants and their mothers took part to a modified version of SF procedure which includes a double “still-reunion” exposure (Haley et al 2003). The SF paradigm was videotaped and mothers’ and infants’ behavior was subsequently coded through ICEP (Tronick et al 2003). Two samples (T1, T2) of salivary cortisol were collected prior to SF (mean value set as baseline value) and three samples at 10 (T3 – early reactivity), 20 (T4 – late reactivity), 30 (T5 – recovery) minutes after SF ended. Epithelial cells using an oral brush were collected for genotyping. Non-parametric statistics were carried among 5-HTTLPR for association with infants’ behavioral response, HPA reactivity, and maternal engagement. RESULTS 5-HTTLPR was distributed among infants as follows: 19 LL, 35 LS and 8 SS. Behavioral response: Social Monitoring was significantly lower (p < .05) in SS infants during both Reunion episodes, compared to LLs and LSs. HPA reactivity: no differences were found for baseline value, late reactivity and recovery. However, SS infants had the highest early reactivity (p < .05) compared to other groups. Maternal engagement: no between-group differences were found. CONCLUSIONS Findings suggest a “double-risk” pattern associated to 5-HTTLPR SS genotype: overburdening the HPA axis in immediate reactivity and SS infants appear less capable to access maternal regulation of their own distress. Indications for future research and clinical practice are entailed.