The main goals of the present study were to (1) evaluate the feasibility of a twin approach to investigate genetic contributions to a laboratory-based anhedonic phenotype, (2) provide preliminary heritability estimates for reward responsiveness and perceived stress, and (3) assess the genetic and environmental correlation between perceived stress and reward responsiveness.
The present findings provide initial evidence that both reward responsiveness and perceived stress are heritable and influenced by individual-specific environmental factors. Consistent with previous literature assessing components of hedonic capacity (e.g., Loas, 1996
) findings revealed that additive genetic factors and individual-specific environment/measurement error contributed to 46% and 54% of the variance in reward responsiveness, respectively. Moreover, replicating prior findings (Federenko et al. 2006
), heritability estimates suggested that additive genetic factors contributed to 44% of the variance in stress perception while individual-specific environment contributed to the remainder. Of note, the genetic correlation between GDD and reward responsiveness was modest (ra
=0.29). This finding is in line with conceptualizations suggesting that low positive affect and high negative affect are separate components of depression, with the former uniquely differentiating depression from anxiety and general negative affectivity being a nonspecific factor linked to both disorders (Watson et al. 1995
). More generally, this finding highlights the heterogeneity of depression and provides support for the endophenotypic research conceptualization (e.g. Hasler et al. 2004
). In contrast to GDD and reward responsiveness, the genetic overlap between perceived stress and GDD was large (ra
=0.67); this overlap may be the result of robust associations between neuroticism, stress perception, and depression (e.g., Federenko, et al. 2006
; Kendler et al. 2006
Critically, this study suggests substantive overlap between genetic and individual-specific environmental factors influencing stress perception and reward responsiveness. Thus, genes that enhance perceived stress also increase reward responsiveness (ra
=0.72); conversely, individual-specific environmental factors that enhance perceived stress decrease reward responsiveness (re
=−0.43). Genetic overlap between stress perception and reward responsiveness is intriguing, particularly when considering a large body of animal and human work emphasizing links between increased stress sensitivity and vulnerability to addiction, including evidence that stress can enhance the rewarding properties of addictive drugs (Hyman et al. 2006
; Kreek et al. 2005
). The negative correlations between environmental factors influencing perceived stress and reward responsiveness, on the other hand, raises the possibility that life stressors increasing stress perception might have deleterious consequences on the ability to modulate behavior as a function of reinforcers. Although speculative, this interpretation is consistent with prior findings of (1) a negative relationship between perceived stress and reward responsiveness (Pizzagalli et al. 2007
) and (2) increased anhedonia when facing laboratory (Bogdan & Pizzagalli, 2006
) and naturalistic (Berenbaum & Connelly, 1996) stressors. The positive genetic correlation and negative environment correlation between stress perception and reward responsiveness may account for the lack of a phenotypic correlation in the present study.
The limitations of this study warrant attention. First, although comparable to some prior twin studies (e.g., Berenbaum et al. 1990
; Kendler et al. 1991
; Mathews et al.
2007), the small sample size limited our statistical power; this is evidenced by large 95% confidence intervals. Second, data were collected outside controlled laboratory settings, which may have contributed to measurement error. However, MZ and DZ correlations were similar to those reported from other studies with larger samples (e.g., Federenko et al.
2005; Hay et al. 2001
), and the general pattern of behavioral performance was comparable to prior independent samples tested with the same reward task in the laboratory.4
Unlike prior studies using this paradigm, however, no significant correlations emerged between the behavioral task and depressive measures, highlighting an important limitation of this study.
Despite these limitations, this is the first twin study, to our knowledge, that assesses: 1) hedonic capacity with an objective behavioral measure, and 2) genetic and environmental correlations between general depression, reward responsiveness and perceived stress. The findings of this study extend prior research using this probabilistic reward task in which reduced reward responsiveness has been associated with 1) elevated depressive (particularly anhedonic) symptoms (Pizzagalli et al. 2005
) and a clinical diagnosis of depression (Pizzagalli et al. in press
); 2) acute laboratory-induced stress (Bogdan & Pizzagalli, 2006
) and elevated perceived stress (Pizzagalli et al. 2007
); and 3) pharmacologically induced reduction of dopaminergic transmission (Pizzagalli et al. 2008
). Collectively, these findings indicate that laboratory-based assessments of quantifiable aspects of depressive phenotypes might provide a powerful tool for parsing the heterogeneity characteristic of this complex and debilitating disease. In addition to replicating the present findings, molecular genetic approaches will be required to test the potential contributions of various candidate genes to hedonic capacity (e.g., Bogdan et al. 2006
; Noble, 2003
) and perceived stress (e.g., Otte et al. 2007
), which promise to provide critical insights into the etiology of depression.