Stability, change, and heritability of borderline personality disorder traits from adolescence to adulthood: a longitudinal twin study

Abstract

Although personality disorders are best understood in the context of lifetime development, there is a paucity of work examining their longitudinal trajectory. An understanding of the expected course and the genetic and environmental contributions to these disorders is necessary for a detailed understanding of risk processes that lead to their manifestation. The current study examined the longitudinal course and heritability of borderline personality disorder (BPD) over a period of 10 years starting in adolescence (age 14) and ending in adulthood (age 24). In doing so, we built on existing research by using a large community sample of adolescent female twins, a sensitive dimensional measure of BPD traits, an extended follow-up period, and a longitudinal twin design that allowed us to investigate the heritability of BPD traits at four discrete ages spanning midadolescence to early adulthood. Results indicated that mean-level BPD traits significantly decline from adolescence to adulthood, but rank order stability remained high. BPD traits were moderately heritable at all ages, with a slight trend for increased heritability from age 14 to age 24. A genetically informed latent growth curve model indicated that both the stability and change of BPD traits are highly influenced by genetic factors and modestly by nonshared environmental factors. Our results indicate that as is the case for other personality dimensions, trait BPD declines as individuals mature from adolescence to adulthood, and that this process is influenced in part by the same genetic factors that influence BPD trait stability.

Figure 1

Note: Initial biometric growth model (all paths included) for initial BPD status and BPD change over time. BPD refers to borderline personality disorder traits. The model allows for BPD scores to be observed at four assessment points (age 14–17). Each assessment point is assumed to reflect an effect of initial status (intercept), change (slope), and assessment-specific additive genetic (A), shared environmental (C), and nonshared envoronmental effects (E). The intercept and slope effects are also decomposed into correlated additive genetic, shared environmental, and nonshared environmental effects. Subscripted numbers refer to age of measurement; numbers above the paths from initial level and slope to occasion-specific scores refer to years from initial assessment.

Figure 2

Note: Final biometric growth model after removal of non-significant paths for initial BPD status (level) and BPD change over time (slope). BPD refers to borderline personality disorder traits; A refers to genetic influence; C refers to shared environmental influence; E refers to nonshared environmental influence; subscripted numbers refer to age of measurement. Coefficients on the diagram are standardized variance component estimates (i.e., paths squared).