Intergenerational transmission of psychopathology: An examination of symptom severity and directionality

Abstract

The present study examined the intergenerational transmission of internalizing and externalizing symptom severity, which indexes comorbidity, and symptom directionality, which indicates differentiation toward externalizing versus internalizing problems. Data are from 854 male and female, same-sex adult twin pairs born between 1926 and 1971 (32-60 years old, M = 44.9 years, SD = 4.9 years) from the Twin and Offspring Study in Sweden and their adolescent offspring (11-22 years old, M = 15.7 years, SD = 2.4 years, 52% female). Children-of-twins models revealed additive (9%) and dominant (45%) genetic and nonshared environmental (47%) influences on twins' symptom severity, and additive genetic (39%) and nonshared environmental (61%) influences on twins' symptom directionality. Both comorbid problems and preponderance of symptoms of a particular - internalizing versus externalizing - spectrum were correlated across parent and child generations, although associations were modest especially for directionality (i.e., transmission of specific symptom type). By interpreting findings alongside a recent study of adolescent twins, we demonstrate that the intergenerational transmission of symptom severity and symptom directionality are both unlikely to be attributable to genetic transmission, are both likely to be influenced by direct phenotypic transmission and/or nonpassive rGE, and the intergenerational transmission of symptom severity is also likely to be influenced by passive rGE.

Keywords: children-of-twins; comorbidity; directionality; externalizing; intergenerational transmission; internalizing; severity.

Figure 1.

Data visualization of symptom severity and directionality scores

Figure 2.

Children-of-twins Model rA and rD are the average correlations between twin 1 and 2 expected by quantitative genetic theory that would indicate additive and dominant genetic influences, respectively, for MZ/DZ twin families. A_T = additive genetic influences of twin parents on their own phenotype, E_T = nonshared environmental influences of twin parents on their own phenotype, D_T = dominant genetic influences of twin parents on their own phenotype, C_T = shared environmental influences of twin parents on their own phenotype. c_ta = extended family effect (also called c1’ or cp in various places). Only one type of dashed line (Dotted – estimating d_t or dashed – estimating c_t and c_ta) can be included in the model. p = phenotypic direct association. a_ta = genetic transmission (also called a1’ or ap in the broader literature) A_A = additive genetic influences of adolescent offspring on their own phenotype, A_TA = genetic transmission, E_A = nonshared environmental influences of adolescent offspring on their own phenotype. This model (with the current sample size and sibling type complement) has insufficient power to estimate C_A (shared environmental influences of adolescent offspring on their own phenotype).