Impulsivity is a multidimensional personality construct consisting of tendencies to act quickly and without thinking. It encompasses a broad set of behaviors including risk-taking, lack of planning, quick decision-making and inattention. Likewise, impulsive behaviors exhibit a wide range of consequences. While occasional spontaneity is normal and even advantageous, chronic impulsivity can be maladaptive, and poses a serious concern. Impulsivity underlies psychiatric conditions including conduct disorder, substance use disorder, Cluster B personality disorders, bipolar depression, autism, unipolar depression, and post-traumatic stress disorder (American Psychiatric Association 1994
; Moeller, et al. 2001
; Jensen, et al. 2007
). Cluster B personality disorders (the “dramatic”) are thought to be characterized by impulsive-aggression at their core; these disorders—borderline, antisocial, histrionic and narcissistic personality disorders—are severe manifestations of “action-oriented” behavior without concern for consequences (Fossati et al. 2005
). Impulsivity may also be a key risk factor for some forms of antisocial behavior in both children and adults, including reactive aggression (Coccaro 1989
; Raine et al. 2006
) and delinquency (White et al. 1994
). In adolescents, impulsive traits have also been linked to earlier and increased alcohol consumption, and earlier onset of recreational drug use (Verdejo-Garcia et al. 2007
That impulsivity predicts maladaptive behavior in children and adolescents as well as in adults highlights the importance of studying its development and etiology. Longitudinal studies of impulsivity, and particularly of the genetic and environmental influences on different facets of impulsivity, are rare in the literature. Because impulsive tendencies feature so prominently in a wide range of psychiatric disorders and antisocial behaviors across the span of development, it is imperative to investigate their genetic and environmental etiologies.
Impulsivity has been investigated using both laboratory tasks and self-report questionnaires, which encompass a variety of different facets and definitions. In personality research, impulsive behaviors include acting on the spur of the moment, excessively quick decision-making, risk-taking and sensation-seeking behaviors, and lack of planning (Eysenck and Eysenck 1977
). Some theories also consider the inability to focus attention to be another form or manifestation of impulsivity (Barratt 1959
; Patton et al. 1995
). As such, questionnaire measures of impulsivity typically include several of these facets, which are often moderately inter-correlated (Whiteside and Lynam 2001
), although the degree of overlap in their underlying genetic and environmental causes is not well understood. One of the most common self-report measures of impulsivity is the Barratt Impulsiveness Scale (BIS), which was developed for use in adults (Barratt 1959
), and later revised into its current form (Patton et al. 1995
). This 30-item scale yields a three-factor structure reflecting facets of Inattention, Non-planning and Motor Impulsivity (Patton et al. 1995
). BIS total scores are also often used. Moderate internal consistency has been shown for the BIS total score (Cronbach’s alpha = 0.78) (Patton et al. 1995
; Fossati et al. 2002
), but few studies have investigated the utility of this instrument and the fit of its factor structure in younger populations, including adolescents. To the best of our knowledge, Patton’s three-factor structure has not yet been replicated in adolescents. More importantly, there has been no examination of genetic and environmental influences on the subscales of the BIS, and the extent to which these influences may overlap.
Significant genetic contributions have been found for various measures of impulsivity. However, most studies utilize global measures that may reflect several different facets without distinguishing them, or examine genetic effects in specific individual facets without considering their relationship to other facets. For example, significant additive genetic influence has been found for risk-taking and lack of planning in twin studies of both adults and children (Eaves et al. 1977
; Saklofske and Eysenck 1983
; Pedersen et al. 1988
). However, none of these studies investigate commonality or difference in etiology between these different facets, or genetic overlap amongst them, a gap that the present study aims to fill. Other twin studies suggest significant non-additive genetic effects (Hur 2007
; Coccaro et al. 1993
; Seroczynski et al. 1999
). The effects of shared family environment (i.e., non-genetic influences that contribute to similarity within pairs of twins) have mostly been found to be negligible, and the effects of non-shared environment (i.e., experiences that make siblings dissimilar) are estimated to account for about 50% of variability in impulsive traits (Pedersen et al. 1988
; Seroczynski et al. 1999
). A recent meta-analysis of twin, adoption and family studies estimated overall 48% additive genetic, 7% non-additive genetic, and 45% non-shared environmental influence while averaging across various definitions of impulsivity using both laboratory and questionnaire measures (Bezdjian et al. 2011a
Although both genetic and non-shared environment are important to impulsivity across the lifespan, the review by Bezdjian et al. (2011a)
found that the relative importance of these effects appear to vary across development, with somewhat higher broad-sense heritability (i.e., combining additive and non-additive genetic effects) in infants (h2
= 0.53), children (h2
= 0.59) and adolescents (h2
= 0.54) than in adults (h2
Age differences in mean levels of impulsivity have also been studied, and results vary somewhat for different measures or facets. One form of impulsivity—risk-taking—appears to increase during adolescence compared to children and adults (Irwin 1989
; Spear 2000
; Trimpop et al. 1999
; Galvan et al. 2007
). However, another form of impulsivity—disinhibition—drops during adolescence from childhood levels, as cognitive control strengthens due to development of the frontal lobes (Casey et al. 2002
). Rates of NoGo errors, representative of failure to inhibit false responses, have also been found to decrease over the course of childhood and adolescence (Bezdjian et al. 2011b
), in support of the notion of increasing inhibitory control across development. Despite these findings concerning different trajectories for different facets of impulsivity, there has been little or no research into the extent to which genetic and environmental influences on impulsivity may change across development.
Impulsivity has been demonstrated to have some stability across development. For example, it has been found that hyperactivity, restlessness, and concentration problems in childhood predict impulsiveness in adulthood (Klinteberg et al. 1989
). Early childhood impulsivity predicts impulsivity in adolescence and young adulthood, such that rank ordering of individuals remains relatively stable over time (Caspi and Silva 1995
; Eysenck and Eysenck 1977
; Buss and Plomin 1975
). There is also evidence that childhood impulsivity may predict delinquency later in life, further strengthening the case for understanding the etiology of impulsive behavior. For example, cognitive and motor impulsive tendencies in 6–8 year old children were found to strongly predict externalizing adolescent behavior (Olson et al. 1999
). No study to our knowledge has examined impulsivity with the same instrument over time to investigate longitudinal stability in phenotypic levels as well as underlying genetic and environmental etiologies.
Sex differences in impulsivity and their underlying genetic and environmental influences have also been investigated. While some studies show little evidence of mean sex differences in impulsive traits in adolescence (De Fruyt et al. 2000
; McCrae et al. 2002
), other findings suggest significant sex differences in certain specific facets. For example, male adolescents exhibited more sensation seeking, and females a stronger sense of urgency, but no significant sex differences were found for lack of premeditation or lack of perseverance (d’Acremont and Van der Linder 2005
). Females have also been found to exhibit a slightly higher capacity for delaying gratification (Silverman 2003
). For the BIS—the instrument used in the present study—adolescent males scored slightly but significantly higher than adolescent females on total score (Fossati et al. 2002
). The meta-analysis of twin and adoption studies by Bezdjian et al. (2011a)
notably found no evidence of sex difference in genetic and environmental influences on overall impulsivity when combining studies using a variety of measures. It remains unknown, however, whether sex differences in genetic and environmental effects may vary across different facets.
In spite of the widely accepted view of impulsivity as a multifaceted construct, and findings that its various facets are genetically influenced, we have little understanding of how these effects may be distinct or overlapping for the different facets of impulsivity. Given the multifactorial nature of impulsivity, as well as the important developmental changes that occur particularly during adolescence, it is important to understand how genetic and environmental etiologies may overlap across different facets and how these influences may change through development.
The present study
The primary aim of the present study is to examine the genetic and environmental etiology of multiple aspects of impulsive behavior and their interrelationships in males and females across adolescence. Using data from an ongoing longitudinal twin study, we investigated the extent to which genes and environment affect variation and covariation among three facets of impulsivity measured on two separate occasions at age 11–13 and 14–16 years old. An adolescent version of the Barratt Impulsiveness Scale (BIS)—widely used to assess self-reported impulsive behaviors in adults—was developed specifically for this study, and thus the factor structure was also investigated and compared to that found in adults.