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the public about ADHD in Adults
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Program Committee: Stephen V. Faraone, PhD, Program Director;
Lenard Adler, MD, David Goodman, MD, Co-Chairs, APSARD Education Committee;
Jonathan Marx, MBA, Media and Marketing Director

The Familial Relationship Between Attention Deficit Hyperactivity Disorder and Substance Use Disorders

While it has been well documented that attention deficit hyperactivity disorder (ADHD) and substance use disorders (SUD) commonly co-occur, little is known about the reasons for this association.  Since both disorders are highly heritable one hypothesis is the high co-occurrence may be due to common genes.  One way to assess for a genetic relationship between ADHD and SUD is through a familial risk analysis.  Familial risk analysis compares the prevalence of an illness in relatives of individuals with a given disorder based on the presence or absence of the same illness in relatives.  Since both ADHD and SUD are known familial illnesses, we can expect relatives of individuals with ADHD and SUD to have a higher prevalence of the same disorders.   

The way in which these two disorders aggregate in families can provide insight as to the nature of the association between the disorders.  If ADHD and SUD are independent disorders we would expect that different relatives of affected individuals with each condition would be affected with the same disorder.  For example, an individual with ADHD would have many relatives with ADHD and an individual with SUD would have many relatives with SUD.  Another possibility is that the genes that produce one disorder (ADHD or SUD) would express both risks in relatives.  For example, an individual with ADHD would have many relatives with ADHD or SUD afflicting different relatives.  A third possibility is that an individual with co-occurring ADHD and SUD would have many relatives who also have co-occurring ADHD and SUD.  This latter scenario is known as co-segregation and it usually suggests that the combined condition is driven by closely linked genes that are inherited together.  

Through the Massachusetts General Hospital longitudinal family studies of boys and girls with and without ADHD and their first-degree relatives we were able to test these hypotheses and examine the nature of the relationship between ADHD and SUD.  These children were first assessed in childhood and followed prospectively onto young adult years (“grown-up child”) through the peak period of risk for the development of addictions.  Our sample consisted of 404 subjects with a mean age of 22 years and their 1,336 relatives.  All individuals who participated in the study were systematically assessed with structured diagnostic interviews. Our findings showed that SUD in a grown-up child significantly increased the risk for SUD in relatives irrespective of having ADHD, and that ADHD in the grown-up child significantly increased the risk for SUD in relatives irrespective of whether or not the grown-up child had a SUD.   Our results also showed that grown-up children with both ADHD and SUD co-occurring together had an excess of relatives in which both conditions were present in the same relative (co-segregation).  Furthermore, we found the risk for SUD was not specific to alcohol or drug dependence indicating that what it is inherited is a general increased risk to develop a SUD. Finally, we documented that these risks were equally operant in boys and girls indicating that these risks are due to ADHD and not the sex of the affected individual.

Taken together, these patterns of familial aggregation point to three overlapping risks for the development of SUD in ADHD that include common familial etiological factors due to genes associated with ADHD, genes associated with SUD, and genes associated with their combined presence.  This triple risk may explain why the risk for SUD is so high in individuals with ADHD.

While these findings support the hypothesis that genetic influences are involved in mediating the risk for SUD in ADHD, we were also interested in examining familial environmental influences such as parental modeling of substance use through exposure to a parent with an active SUD. Our findings revealed that exposure to maternal SUD, but not paternal SUD, during adolescent years was associated with a modest increased risk for SUD in offspring (Yule 2013).  Taken together, these findings suggest that genetic influences are an important determinant of risk for SUD in children with ADHD.  Although modest, exposure to active maternal SUD also has a detrimental effect in moderating the risk for SUD in their adolescent offspring.

Our findings have clinical and public health implications.   Clinically, when a youth presents for treatment of ADHD clinicians should screen for SUD in the child and the family.  When a youth presents for the management of SUD, clinicians should also screen the youth and their family members for ADHD.  Since ADHD typically onsets years before the onset of substance use, ADHD children could benefit for early intervention strategies aimed at mitigating the risk for subsequent SUD.  For example, treatment for ADHD has also been shown to be an important intervention to decrease risk for SUD among youth with ADHD (Biederman 1999).          

In summary, the bidirectional association between ADHD and SUD seems to be due to strong genetic links between the two disorders.  All children within families with ADHD should be closely monitored for SUD.



Yule, A. M., Martleon, M., Faraone, S., Carrellas, N., Wilens, T. E., & Biederman, J. (2017). Examining the association between attention deficit hyperactivity disorder and substance use disorders: A familial risk analysis. Journal of Psychiatric Research(85), 49-55.


Yule, A. (2013). The Impact of Exposure to Parental Substance Use Disorders on Substance Use Disorder Risk in Growing-Up Boys and Girls. Poster presented at the American Academy of Child and Adolescent Psychiatry, Orlando, FL.

Biederman, J., Wilens, T., Mick, E., Spencer, T., & Faraone, S. (1999). Pharmacotherapy of attention-deficit/hyperactivity disorder reduces risk for substance use disorder. Pediatrics, 104(2), e20.