In the current study, we used such ACE models to answer two questions regarding the etiology of executive functions: (1) How much of the individual differences in these executive functions are due to genetic and environmental influences?; and (2) Do genetic influences on these three executive functions operate at only the general level (i.e., common to all three executive functions) or at both general and specific levels?
A few previous twin studies have examined the first question at the level of individual tasks in adolescents or adults. These studies generally suggest moderate genetic (around 40% to 60% on average), virtually no significant shared environmental, and moderate nonshared environmental influences on individual tasks thought to tap Inhibiting, Updating, and Shifting abilities, such as the antisaccade task, working memory span tasks, and the Wisconsin Card Sorting Test (e.g., Ando, Ono, & Wright, 2001
; Anokhin, Heath, & Myers, 2004
; Anokhin, Heath, & Ralano, 2003
; Fan, Wu, Fossella, & Posner, 2001
; Luciano et al., 2001
; Malone & Iacono, 2002
, Posthuma, Mulder, Boomsma, & de Geus, 2002
; Wright et al., 2001
Although these studies provide preliminary evidence that executive functions may be somewhat genetically influenced, the task impurity problem complicates the interpretation of heritability estimates based on single complex executive function tasks, because it is unclear to what extent those results reflect nonexecutive variance. As discussed earlier, one fruitful method for circumventing this problem in behavioral and neuropsychological studies is to adopt a latent variable approach, but it has not been applied to multivariate genetic studies targeting specific executive function constructs. The use of latent variables in a genetic context is highly informative, because it enables separation of the genetic and environmental influences on each task into those influencing the target executive function and those influencing the nonexecutive components of the tasks. For example, if the heritability estimates for the individual tasks for a particular executive function reflect only the variance associated with nonexecutive requirements of those tasks, then the variance shared among these tasks should not be heritable at all. Perhaps a more likely possibility would be that the genetic influences on multiple executive function tasks overlap somewhat, which would result in some heritability of the latent variable, though there could also still be some genetic influences on the nonexecutive components of each task. As these examples illustrate, by conducting behavioral genetic analyses at the level of latent variables, the current study seeks to provide more precise estimates of the genetic and environmental influences on individual differences in executive functions than have to date been provided.
An examination of multiple executive functions at the level of latent variables also enables us to address the second research goal above, namely to specify the level (or levels) at which genetic influences on executive functions operate and thereby shed new light on the etiology of the unity and diversity of executive functions. For example, one plausible scenario is that executive functions are related because they share common genetic and environmental influences, but are separable purely because of environmental influences unique to individual executive functions. In this case, there would be only one level of genetic influences (the general level that is common to all three executive functions). Those influences could overlap considerably with those that affect g
, which is known to have moderate to large genetic (50% to 75%) as well as some environmental (mostly nonshared) influences by late adolescence (McGue et al., 1993
; Neisser et al., 1996
Another possible configuration that could explain the unity and diversity of executive functions is that the unity is due to shared genetic and environmental influences, as in the previous scenario, but the diversity is also due to genetic and environmental influences unique to the individual executive functions (rather than just environmental influences). In this case, there are two levels of genetic influences: one that operates at the general level, producing unity, and another that operates on specific executive functions, producing diversity. This configuration would be similar to that found for specific cognitive abilities, which seem to be related through genetic and environmental influences on g
, and separable because of large environmental and, in some cases, small genetic influences unique to particular cognitive abilities (Alarcón et al., 1999
; Petrill, 1997
Of course, many other combinations of genetic and environmental influences could logically explain the unity and diversity of executive functions. Hence, the “problem space” for understanding individual differences in executive functions is large. Reducing this space is important, because it will likely constrain what lines of research will be most productive for further understanding the nature of executive functions.
For example, a good deal of research on executive control has begun to incorporate genetic information with the aim of understanding the neurobiology of executive functions and, by extension, disorders often associated with impairments in executive control. This line of research has focused on finding specific genetic variants associated with executive control abilities and/or related disorders such as ADHD (e.g., Faraone et al., 2005
) and schizophrenia (e.g., Egan et al., 2001
). Although such genetic association studies have great potential for elucidating the genetic and biological bases of executive functions, the lack of a clear picture of the underlying genetic and environmental structure of executive functions limits their impact. In particular, most molecular genetic studies have focused on gross executive control ability as measured by individual neuropsychological tests such as the Wisconsin Card Sorting Test. However, the emerging evidence that there are separable executive functions and that those executive functions differentially relate to disorders of interest begs the question of whether such research should incorporate multiple executive functions and multiple tasks for each function. The answer to this question depends on whether there are genetic influences on executive functions at the level of latent variables and, if so, whether those influences operate at only the general level (i.e., common to all executive functions) or at both the general and specific levels.
In the current study, we took a latent variable approach to answer the two primary questions. To specify the etiology of executive functions, we estimated the ACE components of each executive function, measured as a latent variable. To specify the etiology of the unity and diversity of executive functions, we then used a multivariate ACE model of all three executive functions, estimating ACE components for both what is common to the three executive functions and what is unique to each executive function. Once we specified the genetic and environmental structure of these three executive functions, we tested two key alternative hypotheses regarding the unity of executive functions: that it primarily reflects the same genetic and/or environmental influences as speed or IQ. More specifically, in these secondary analyses, we examined to what extent executive function variance overlaps with variance in IQ and speed, respectively.