Elsevier

Clinical Psychology Review

Volume 31, Issue 7, November 2011, Pages 1209-1223
Clinical Psychology Review

Genetic and environmental influences on impulsivity: A meta-analysis of twin, family and adoption studies

https://doi.org/10.1016/j.cpr.2011.07.005Get rights and content

Abstract

A meta-analysis of twin, family and adoption studies was conducted to estimate the magnitude of genetic and environmental influences on impulsivity. The best fitting model for 41 key studies (58 independent samples from 14 month old infants to adults; N = 27,147) included equal proportions of variance due to genetic (0.50) and non-shared environmental (0.50) influences, with genetic effects being both additive (0.38) and non-additive (0.12). Shared environmental effects were unimportant in explaining individual differences in impulsivity. Age, sex, and study design (twin vs. adoption) were all significant moderators of the magnitude of genetic and environmental influences on impulsivity. The relative contribution of genetic effects (broad sense heritability) and unique environmental effects were also found to be important throughout development from childhood to adulthood. Total genetic effects were found to be important for all ages, but appeared to be strongest in children. Analyses also demonstrated that genetic effects appeared to be stronger in males than in females. Method of assessment (laboratory tasks vs. questionnaires), however, was not a significant moderator of the genetic and environmental influences on impulsivity. These results provide a structured synthesis of existing behavior genetic studies on impulsivity by providing a clearer understanding of the relative genetic and environmental contributions in impulsive traits through various stages of development.

Highlights

► Meta-analyses on 41 key studies examining the heritability of impulsivity. ► Genetic and unique environmental effects were found to be equally important. ► Total genetic effects appeared to be strongest in children. ► Total genetic effects appeared to be stronger in males than in females.

Introduction

Impulsivity is one of the most researched behavioral traits, and has captured the interest of researchers and clinicians spanning the fields of psychology, neuroscience, neurogenetics and psychiatry (Cloninger et al., 1993, Congdon and Canli, 2008, Costa and McCrae, 1992, Evenden, 1999, Eysenck, 1967, Eysenck and Eysenck, 1977, Tellegen, 1982). Indeed, impulsivity is of key importance for psychopathology, including antisocial and aggressive behaviors, pathological gambling and attention deficit hyperactivity disorder (ADHD). Thus, researchers have been motivated to attain a deeper understanding of this multidimensional construct and its underlying genetic and environmental etiology. Although numerous twin and adoption studies have investigated the roots of individual differences in impulsivity, it has been difficult to draw clear conclusions given the fact that impulsivity has been described and measured in various ways in the literature. Current framework considers impulsivity to be comprised of several distinct dimensions including a sense of urgency, lack of planning, lack of persistence (or perseverance), and sensation seeking (Fischer et al., 2008, Whiteside and Lynam, 2001). However, there is yet to exist a comprehensive review of genetic and environmental influences on impulsivity and how these vary across the different facets (or dimensions) and definitions. Twin and family/adoption studies have the distinct ability to unravel genetic and environmental influences and to estimate their simultaneous contributions to individual differences in impulsivity. Thus, the purpose of the present review is to synthesize and consolidate the existing behavior genetic literature on impulsivity and its various methods of assessment and definition. Understanding the genetic and environmental etiology of impulsivity may also help further the understanding of this important multidimensional construct.

To provide a context for the current review, we begin with a summary of the various constructs and definitions of impulsivity as used in clinical and research settings, and its role in personality theory and psychopathology. A review of potential moderators of the genetic and environmental influences in impulsivity measures across studies is also provided as background to the meta-analysis.

Recent work has demonstrated that ‘impulsivity’ embodies a range of traits that are only moderately (co)related (Cyders and Smith, 2007, Whiteside and Lynam, 2001). One favorable attempt to identify and define the specific constructs rooted within impulsivity was a factor analysis of various measures of impulsivity by Whiteside and Lynam (2001). Instead of the non-operational (uni)- dimensional approach and definition to impulsive traits, Whiteside and Lynam (2001) identified four (etiologically) distinct constructs of impulsivity namely, (1) urgency or negative urgency, (2) lack of planning, (3) lack of perseverance, and (4) sensation seeking. To date, this four-factor structure of impulsivity has been confirmed on several, independent samples (Lynam et al., 2007, Smith et al., 2007).

Based on several lines of research, personality theorists have drawn several conclusions regarding impulsivity including, the fact that there seems to be a fundamental or underlying personality foundation in impulsive behaviors and traits. Personality researchers have also recognized and demonstrated numerous different representations of what that personality root or foundation is; and lastly, researchers have noted that various constructs or traits have been included under the broader realm of ‘impulsivity’ (or impulsive behaviors) (Barratt & Patton 1983; Depue & Collins, 1999; Evenden, 1999, Eysenck et al., 1985, Fischer et al., 2008, Smith et al., 2007, Tellegen, 1982, Whiteside and Lynam, 2001, Zuckerman, 1979).

The role of impulsivity in personality has stemmed from benchmark research conducted by Eysenck et al., 1985, Tellegen, 1982, Barratt and Patton, 1983. In their research, these personality theorists captured different manifestations of impulsivity using both narrow (psychoticism, venturesomeness, sensation seeking) and broad (extraversion and constraint) definitions employing three, four and five-factor models of personality (Cloninger et al., 1993, Costa and McCrae, 1992, Eysenck et al., 1985, Patton and Barratt, 1995, Tellegen, 1982, Whiteside and Lynam, 2001). The proper placement of impulsivity within these different personality models is one example of how personality theorists have struggled with the intricacy of this multidimensional construct. Additionally, some three-factor models including those formulated by Costa and McCrae, 1992, Tellegen, 1982, Cloninger et al., 1993 have even considered impulsivity as a compilation of different factors or components (Evenden, 1999). For example, Cloninger defined impulsivity as a combination of low harm avoidance and high novelty seeking (Cloninger et al., 1993). As a result, there has been a lack of consensus about how to properly define and structure impulsivity as a fundamental trait (Congdon & Canli, 2008).

Impulsivity has also played a significant role in theories of antisocial and criminal behavior (Whiteside & Lynam, 2001). For example, individuals who score high on personality measures of impulsivity have been found to be more antisocial and commit more recidivistic criminal acts compared to those who score low (White et al., 1994). It is possible that deficits in impulse control may produce antisocial behavior by interfering with an individual's ability to control their behavior as well as to think of the future consequences of their antisocial acts (Moffitt et al., 2001, White et al., 1994). Lack of impulse-control may manifest itself in numerous ways in a wide range of traits and behaviors, including risk taking (Barratt & Patton, 1983), sensation seeking (Zuckerman, 1979), novelty seeking (Cloninger et al., 1993), and aggression (Coccaro, Bergeman, & McClearn, 1993), which are all related to antisocial and criminal behavior.

In addition to its substantial role in the realm of personality and antisocial behavior, impulsivity has played a significant role in numerous psychiatric disorders in both children and adults (American Psychiatric Association, 2004). In its extreme form, impulsivity has been associated with a wide range of mental disorders, one example being attention deficit hyperactivity disorder (ADHD; Avila, Cuenca, Felix, Parcet, & Miranda, 2004; Barkley, 1997). ADHD is characterized by pervasive and impairing symptoms of inattention, hyperactivity and impulsivity. Specifically, ADHD encompasses a pattern of behavior in which a child has difficulty waiting for turns, intrudes in on or interrupts conversations, and/or blurts out answers before questions have been completed. Other disorders and behaviors where impulsivity is a major component include conduct disorder (Plutchik & Van Praag, 1995), borderline personality disorder (Conrod et al., 2000, Fossati et al., 2004, Links et al., 1999), substance use and abuse (Sher, Bartholow, & Wood, 2000), suicidal behavior (Dougherty et al., 2004, Esposito and Spirito, 2003, Swann et al., 2004), and various impulse control disorders e.g., pathological gambling, kleptomania, and pyromania. Impulsivity has been one of the defining characteristics of these disorders, which has affected a large percentage of the general population (Congdon & Canli, 2008).

Even though impulsivity is an important component in both normal varying personality, as well as pathological behaviors, it has not been consistently examined across phenotypic or behavioral genetic studies. Thus, there is a need to synthesize the existing behavior genetic literature on impulsivity with the aim of further elucidating the contributions of genetic and environmental influences on impulsivity.

To date, there have been more than a hundred published twin and family/adoption studies examining the genetic and environmental etiology of impulsivity. Results from the majority of these studies support the notion of a moderate additive genetic factor influencing impulsivity (e.g., Eaves et al., 2000, Hur and Bouchard, 1997). A smaller number of studies have demonstrated that impulsivity is influenced by non-additive or dominant genetic factors as well (Hur and Bouchard, 1997, Pedersen et al., 1988, Seroczynski et al., 1999).

While yielding valuable results, previous research has examined impulsivity in a variety of different ways employing different, perhaps even unrelated behaviors due to the multidimensionality of this complex construct. In addition, there is no gold standard for defining impulsivity or impulsive traits, which further accentuates the complexity of synthesizing the quantitative results obtained on this construct. Even with impulsivity's widespread significance in both normal varying personality, as well as pathological behaviors, it has not been consistently examined across phenotypic or behavioral genetic studies. This lack of integrative review thus motivated us to examine the genetic and environmental influences across a wide range of impulsivity measures and to investigate if results vary across them. The purpose of the current project is to synthesize the existing behavior genetic literature on impulsivity with the aim of further elucidating the contributions from genetic and environmental components on this important construct.

There are two major methods used to assess impulsivity: questionnaire measures and laboratory tasks. Self-report questionnaires have been by far the most commonly used technique for measuring impulsivity among young adolescents and adults. The number of questionnaires and surveys developed to measure impulsivity has been extensive to say the least (see Barratt and Patton, 1983, Patton and Barratt, 1995, Eysenck et al., 1985). A few examples include the Barratt Impulsiveness Scale (Patton et al., 1995), the Eysenck Impulsiveness Scale (Eysenck et al., 1985), the Zuckerman Sensation Seeking Scale (Zuckerman, 1979), and the Thurstone Temperament Schedule (Thurstone, 1950).

The second method of assessment, laboratory tasks, includes widely employed laboratory measures such as Continuous Performance Tasks (CPTs), the Go/NoGo task, the Iowa Gambling task, the Stop-Signal Paradigm and Delay of Gratification and Delay Discounting task(s). These tasks examine reaction time to responses as well as number of disinhibited or ‘impulsive’ errors committed. These tasks contrast the inhibition and execution of motor responses. Although somewhat distinct from one another, in the Go/NoGo and Stop-Signal tasks a successful performance requires the inhibition of a predominant response making it somewhat challenging. These tasks have been widely and effectively employed on a wide range of samples including children and adults in both clinical and healthy (normative) settings (Alderson et al., 2008, Aron and Poldrack, 2006, Moeller et al., 2001, Rubia, 2001, Rubia et al., 2003, Tamm et al., 2002). Consequently, results may vary across different measures given such a wide range of laboratory tasks that all aim to measure some form of (behavioral) disinhibition and impulsivity.

Method(s) of assessment may influence the outcome of results in behavior genetic studies (McCartney et al., 1990, Rhee and Waldman, 2002) and vary across measures. For instance in certain laboratory measures, external factors such as time of day and ambient temperature may affect variance estimates since these effectively increase measurement error and hence non-shared environmental effects (Boomsma & Gabrielli, 1985). Thus, in the present study, assessment method was used as a moderator comparing the magnitude of genetic and environmental influences in questionnaire measures of impulsivity to that of laboratory tasks of impulsive behaviors.

The influence of genetic and environmental factors may vary across development as well as across various traits (Loehlin, 1992, Plomin, 1976). Previous research has demonstrated that for different phenotypes there is a pattern of decrease in shared environment and a concomitant increase in heritability and non-shared environmental effects during development, particularly for personality traits and cognitive abilities (Loehlin, 1992, Miles and Carey, 1997, Scarr and McCartney, 1983). A possible explanation to the observed pattern of decreasing shared environmental effects as an individual grows older might be that they actively seek out environmental situations that are more closely matched to the his or her genotype, which in turn might increase the influence of non-shared environmental effects. In other words, as children grow older they are probably less supervised, become more independent and may select environments that are correlated with their phenotypes. Thus far, studies investigating developmental changes in the genetic and environmental influences on personality traits have yielded inconsistent and conflicting results (McCartney et al., 1990). As a result, it is important to examine whether the influence of genetic and environmental factors in impulsivity varies at different time points across development and age.

Thus far, twin studies have found no evidence of significant sex differences in the genetic and environmental etiology of psychopathology and normal personality (Bouchard and Loehlin, 2001, Jang, 2005) with the exception of antisocial behavior (Heiman et al., 2004, Moffitt et al., 2001, Tuvblad et al., 2006). There is also indication of sex differences in childhood disinhibition with boys showing higher mean disinhibition levels than girls (Galdstone, 2004). Given this sex difference on a phenotypic level, it is also important to examine whether the magnitude of genetic and environmental effects differs in males and females. Earlier behavior genetic studies have been inconsistent regarding sex differences in impulsivity, with some reporting significant sex differences in traits such as control and constraint (Finkel & McGue, 1997), and others reporting no significant differences in sex (McGue, Bacon, & Lykken, 1993). Thus, the present study examined whether sex is a significant moderator of impulsivity by comparing the results for males and females. Because of the unique relationship between opposite sex twins, including prenatal effects arising from a male and female sharing the womb, sex differences were examined for studies with and without opposite sex twins.

As twin and family/adoption studies rely on different methodological assumptions, the results from studies using these different study designs were also directly compared in the current analyses. The classical twin design compares the similarity of MZ twins to that of DZ twins and is recognized to be one of the most effective study designs for estimating the relative contribution of genes and environmental influences to human traits (Evans, Gillespie, & Martin, 2002). Perhaps one of the most criticized assumptions of the twin design is the equal environment assumption (EEA). In the twin design MZ twins who share all their genes, are compared to DZ twins who on average share half of their genes. If MZ twins are more similar than DZ twins on a particular trait, then that would indicate the importance of genetic effects. However, it has to be assumed that environmentally caused similarity is roughly the same for both types of twins. If this assumption is violated, higher correlations among MZ twins may be due to environmental factors, rather than genetic factors, and heritability estimate will be overestimated (Plomin, DeFries, McClearn, & McGuffin, 2001). Studies that have examined the EEA have generally shown that the assumption is fully justified (see for example, Jacobson, Prescott, & Kendler, 2002). The twin design also assumes random mating in the parent generation. Assortative mating tends to increase similarity between DZ twins, thereby biasing heritability estimates downward and the shared environmental estimates upward. For example, twin studies might overestimate the effects of shared environment if assortative mating is not taken into account. However, assortative mating for most personality traits has been found to be low in magnitude (Maes et al., 1998). Further, twins and singletons have generally been found to experience similar rates of psychiatric disorders and behavioral and emotional problems (Gjone and Novik, 1995, Moilanen et al., 1999, Simonoff et al., 1997, van den Oord et al., 1995). There are however, two ways in which twins differ from singletons: (i) lower birth weight and shorter gestational age (Plomin et al., 2001), and (ii) delayed language development (Rutter & Redshaw, 1991). These differences have however, been found to have a minor effect on traits and behavior later in life (Christensen et al., 2006).

As with the twin design, adoption studies also rely on several methodological assumptions. One important assumption in the adoption design is random placement. It is generally assumed that adoptive children are randomly placed into homes. However, that is seldom the case, since adoptive families are usually selected for similarities to biological parents (Evans et al., 2002). Adoptive parents also tend to be in good health and more affluent. Adoption designs are also subject to generalizability problems due to the fact that results from adopted individuals may not be representative of the greater population (Evans et al., 2002). Additionally, parent–offspring adoption studies might underestimate the influence of genetic effects if developmental changes are important to impulsivity, such that different genes may be important at different ages. Moreover, sibling adoption studies might overestimate shared environmental influences; previous adoption studies have found little to no genetic influences in temperament (Plomin, Coon, Carey, Defries, & Fulker, 1991). Therefore, due to the fact that twin and adoption/family studies rely on different methodological assumptions, it is important to investigate study design as a potential moderator.

Finally, the potential moderating effect of publication date was tested. That is, we examined whether studies published before 1985 differed from studies published after 1986. This cut-off was chosen because it seemed to be reasonable considering the fact that studies conducted before 1985 used different methods of reporting findings (such as not reporting twin correlations or effect sizes).

Although numerous studies have investigated the genetic and environmental influences on impulsivity, there have been no systematic reviews summarizing these results. The present study is therefore the first comprehensive and systematic review of the heritability and environmentality of impulsivity. We employed a meta-analysis to summarize and consolidate results obtained from twin, adoption, and family studies in order to better understand the genetic and environmental etiology of impulsivity and its underlying dimensions. With any systematic review or meta-analyses, it is useful to identify and determine the influence of different study and sample characteristics such as age and sex on the study results (Rosenthal, 1991). Thus, we also examined the influence of potential moderator variables on the genetic and environmental factors underlying impulsivity, including method of assessment, age, sex, study design, and publication date.

Section snippets

Search strategy

We searched for twin and family/adoption studies of impulsivity in the PsycInfo and Medline/PubMed [http://www.ncbi.nlm.nih.gov/sites/entrez] databases from January 1, 1970 to February 01, 2011. We limited our search to the year 1970 due to differences in assessment methods and low sample sizes in behavior genetic studies conducted before 1970. Search terms used included the following: ‘impulsivity’, ‘disinhibition’, ‘sensation seeking’, ‘novelty seeking’, ‘control’, ‘constraint’,

Determination of effect sizes

All of the adoption and twin studies included in the present study used a continuous variable as the measure of impulsivity and reported either intraclass or Pearson product–moment correlations, which were the effect sizes (r) used in the current analyses. These effect sizes were input and analyzed in a model-fitting program (Mx; Neale and Cardon, 1992, Neale et al., 2003) that estimates the relative contribution of genetic and environmental influences and tests alternative genetic or etiologic

Analyses of all data

The results from analyses including all samples that met inclusion criteria (41 studies; 58 independent samples; 153 data groups; 27,147 participants) are presented in Table 3. Briefly, the number of samples refers to the number of independent studies in the analyses, and the number of groups refers to the number of independently analyzed components (i.e., types of relatives) in the samples. The ADE model was the best fitting model compared to the other models as illustrated by the lowest AIC

Discussion

The present study is the first to systematically examine the heritability of impulsivity across studies of infants, children, adolescents and adults, analyzing over 27,000 individuals (or pairs of relatives) in 41 key studies. When all data from both twin and adoption/family studies that met inclusion criteria were analyzed, the overall results indicated important genetic and unique environmental influences on impulsivity. The magnitudes of the non-additive genetic influences were estimated in

Conclusions

In conclusion, the current study found substantial genetic and unique environmental effects on impulsivity with no common environmental influences. Data from large, methodologically sound twin and adoption studies have also demonstrated that traits including impulsivity are significantly heritable (Goldman, & Fishbein, 2000). Furthermore, the heritability of self-reported personality traits related to impulsiveness and irritability in twins reared together and apart showed heritability rates

Acknowledgments

This study was supported by grants to Serena Bezdjian from NIMH (F31 MH068953) and NIDA (T32 DA07313) and to Laura Baker from NIMH (R01 MH58354), and to Catherine Tuvblad from post-doctoral stipends from the Swedish Council for Working Life and Social Research (Project 2006–1501) and the Sweden–America Foundation.

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