Affective intensity and lability: Heritability in adult male twins

Background ity to monitor and self-regulate heightened levels of affect lability and affect intensity is associated with a range of mood, anxiety, and personality disorders, psychosomatic symptoms and socially maladaptive behaviors. Despite the importance of these aspects of affective regulation, there are no twin study data to shed light on the genetic and environmental components of these constructs. s ive Lability Scale (ALS) and Affect Intensity Measure (AIM) questionnaires were administered to 796 male twins in the Vietnam Era Twin Registry and subjected to twin and model-fitting analyses. Complete data were available from 182 monozygotic and 119 dizygotic twin pairs. s rical genetic model-fitting estimates indicated that additive genetic influence accounted for 40% of the variance in affect intensity and 25% of the variance in the ALS subscale assessing anxiety-depression mood shifts. Nonadditive genetic influence was indicated for ALS subscales measuring shifts between normal mood and depression (29%) and anger (27%), respectively. There was negligible evidence of shared environmental influence on affect measures. In contrast, estimates of nonshared environmental influences ranged from 52% to 74%. tions were not included in this study due to the nature of the twin cohort. Data from subjects in a population cohort may not generalize to clinical populations. Measures of environment were not included. sions results provide evidence for moderate heritability of affect intensity and specific measures of affect lability. Individual differences in mood regulation may represent phenotypic variation in a core psychobiologic vulnerability (e.g., neurotransmitter systems).