We cannot be certain whether our young adult self-report SRS and ADHD items truly measure the same problems as ratings by outside observers; however, the genetic structure of our self-report SRS and ADHD scores is basically consistent with studies of SRS (Constantino & Todd, 2003
) and ADHD (Faraone et al., 2005
) symptoms reported by parents of minors. Our heritability estimates for SRS and ADHD in adults are somewhat lower than those reported for youth, but our study confirms at least moderate heritability for each trait.
In the preferred model from a prior study by Constantino, Hudziak, and Todd, the genetic factors affecting SRS and ADHD symptoms were separate, and reciprocal causation within individuals accounted for the correlation between SRS and ADHD symptoms (Constantino et al., 2003
). We did not test a reciprocal causation model using the current dataset because the small sample size and similar genetic structure for the two phenotypes make it impossible to reliably distinguish between our bivariate model and a reciprocal causation model. The expected covariance structure for these two types of models is identical in cases where the A and E variance components for the two phenotypes are the same (Duffy & Martin, 1994
). Our findings indicate that pleiotropy (shared genes affecting both SRS and ADHD symptoms) could explain the association between SRS and ADHD symptoms. However, it is still possible that the association between SRS and ADHD symptoms is partly due to measurement overlap or interaction of SRS and ADHD symptoms within individuals (reciprocal causation).
Although different measures of ADHD symptoms and autistic traits were used in our study, our results are remarkably similar to those of Ronald and colleagues(Ronald et al., 2008
). Their study of child twins reported somewhat higher heritability for Autistic and ADHD symptoms. They also reported slightly lower rg
than our study, but their confidence intervals for rg
overlap with ours. Their reported estimates for re
were also very similar to ours. Considering both studies, it appears that there is evidence of substantial genetic overlap between ADHD and autistic symptoms in both children and young adults.
This study has some limitations. We did not include DSM-IV hyperactive symptoms in our measure of self-report ADHD symptoms due to limitations on the size of the total survey. However, hyperactive symptoms are less stable than inattentive symptoms from childhood to adulthood (Todd et al., 2008
), so inclusion of hyperactive symptoms may not have been very helpful in this age group. Also, our previous study of Missouri twins found that unlike those with inattentive or combined type ADHD, children with the hyperactive-impulsive subtype did not have statistically significant SRS score elevations (Reiersen et al., 2007
). Although we did not find significant evidence for common environment effects, genetic dominance, or sex limitation effects, it is possible that our sample size was not large enough to detect these. Also, there are additional types of bivariate models that we did not perform because our sample size provides insufficient power to justify more complex analysis at this stage. We will consider evaluating more complex twin models once a larger sample is available for analysis. Of note, the DZ covariance for ADHD was negative for males in our study. This suggests the possibility of negative sibling interaction effects in males. However, given the small size of the male DZ group, this negative covariation could be due to random factors, and we did not have a large enough sample size to reliably assess for sibling interaction.
Recently we have demonstrated marked gene-environment interaction between prenatal exposure to cigarette smoke and genotype at the DRD4, DAT, and CHRNA4 loci for combined type ADHD (Neuman et al., 2007
; Todd & Neuman, 2007
). This is the ADHD subtype that is most strongly associated with elevated SRS scores in children (Reiersen et al., 2007
). Such gene-environment interaction could result in overestimation of A and underestimation of C in our models. Also, our high estimates for E could be partially due to non-response bias, variable decrease in ADHD symptoms with age, inaccurate self-report, or other forms of error variance. Despite these limitations, we found strong evidence for shared genetic influences on autistic and ADHD symptoms which supports continued study of the association between ADHD and autism.
In future studies, it may be fruitful to search for specific genes that influence both ADHD and autism. Given that the genetic correlation for SRS and ADHD was higher than the environmental correlation, it may be that some genes predispose to both types of symptoms but that environmental factors determine whether individuals have autistic traits, ADHD or both. In further support of this possibility, we have found an association between clinically elevated SRS score and the DRD4 7-repeat allele in Missouri twin subjects with latent-class derived severe combined type ADHD (OR 3.27, p=0.016), but there was no main or interaction effect of prenatal maternal smoking in predicting high SRS score in these children (Reiersen et al., 2008
). So, although prenatal maternal smoking appears to interact with genotype to produce severe combined type ADHD, it does not appear that this environmental factor influences SRS score in these children.
In conclusion, our findings indicate that self-reported inattentive/impulsive ADHD symptoms and autistic traits tend to co-occur in adults. This co-occurrence of ADHD and autistic symptoms may be due to substantial overlap of the genetic influences leading to these two types of symptoms. It may be important to assess for autistic features in adult patients with ADHD and measure both autistic traits and ADHD symptoms in studies of either disorder.