Tarnow Articles

ADHD and Substance Abuse 

The relationship between ADHD and Substance Use Disorders (SUD) is complex and controversial. This issue is a frequent cause of concern for individuals with ADHD and for their parents and/or families. Generally, there are two over-riding concerns with which people struggle regarding this topic. One concern is whether children are at an increased risk for developing SUD simply because of the impact of ADHD on the child's psychosocial development. The other general concern is whether the treatment of ADHD with stimulants increases the risk of later SUD by, in effect, "priming the pump" for later substance use and dependence.

Studies suggest that about 71% of children do not outgrow ADHD symptoms in adolescence and that about 66% of adults still demonstrate at least one of the major "disabling" symptoms of childhood ADHD. Although most ADHD adults show fairly good outcomes, about 40% to 50% have a comorbid disorder, including mood disorders, substance abuse, and antisocial behaviors.

Oppositional behavior, aggression, and antisocial behavior are the psychiatric symptoms that most frequently co-occur with ADHD, followed by mood disorders (MD) such as depression, bi-polar disorder, and dysthymia . About half of ADHD children will meet criteria for oppositional defiant disorder (ODD) or conduct disorder (CD). Mood Disorders co-occur with ADHD at a rate of about 20%-40%.

In order to understand the impact that ADHD can have on developmental processes that can subsequently lead to an increased risk of SUD, one must have a basic understanding of theory underlying ADHD. First, there is no clear, unequivocal cause of ADHD (or any other mental disorder, for that matter). However, mounting evidence suggests that ADHD is a neurobiological-neurodevelopmental disorder that includes biologically and/or genetically based brain structure and function abnormalities. These brain abnormalities can lead to ineffective and maladaptive interactions with the person's environment. These problematic interactions then may result in increased psychosocial difficulties, leading to more negative feedback from the environment, creating a self-perpetuating cycle of maladaptive functioning and negative environmental responding. Many believe the main culprit responsible for the cluster of symptoms identified with ADHD is behavioral disinhibition.

The desired opposite of behavioral disinhibition is behavioral inhibition. Behavioral inhibition is the primary "executive" function of the brain that is believed to promote the ability to resist (1) responding to a highly desirable or reinforcing circumstance, (2) to stop an ongoing response to an event, (3) to create a delay in responding so that one can effectively problem-solve and exercise good decision-making, and (4) to protect that delay period from disruption by competing events. If one is able to successfully engage in behavioral inhibition, then one is more likely to engage in key subsequent "executive" functions that promote adaptive development and positive life-long adjustment.

A host of potential difficulties associated with behavioral disinhibition may manifest themselves through various developmental problems, which in turn, can lead to psychosocial impairment and conduct disorders that predict an increased risk of SUD.

For example, during the first year of life, a bonding or attachment process occurs between parent and child. This foundational process directly influences the growth of brain structures that mediate self-regulation. It is during this time that a child either gains a deep sense that the world is a trustworthy place where needs are responded to in timely and effective fashion or that the world is an unsafe, unresponsive place. The attachment relationship is so important because it is within this relationship that the ability to self-soothe and self-calm develops. This developmental ability, in turn, allows a toddler to begin exploring and interacting with the world, forming a sense of self apart from the parent, and developing feelings of competence and confidence.

Impaired development of attachment and self-soothing processes can have a profound impact on subsequent developmental processes. The attachment and self-soothing process relies in part on the child's ability to construct mental and verbal representations of the parent, internalize the parent's soothing talk, and develop the ability to self-instruct. If impaired behavioral inhibition disrupts these functions and thereby hinders the attachment and self-calming processes, then numerous other developmental difficulties can occur that extend from infancy through adulthood.

When this progression of developmental process go awry, numerous negative outcomes tend to occur, many of which are associated with an increased risk for SUD, including;

  • academic failure, low self-esteem, poor peer relationships and an expectation of rejection by others
  • a sense of "learned helplessness" where the person comes to believe there is no positive relationship between effort and outcome
  • opposition, defiance, negativity, hostility
  • aggression against people and/or property
  • resistance to authority and following rules
  • increased levels of depression and anxiety

Research suggests that, except for tobacco smoking, it may be this developmental pathway that increases the risk of developing a comorbid CD and this, in turn appears to increase the risk of SUD for children with ADHD. Currently, research indicates that ADHD alone predisposes an individual to a higher risk of smoking tobacco. Otherwise, it appears that ADHD+CD and ADHD+MD children appear to have very different long-term outcomes relative to children with ADHD alone, including an increased risk for SUD. For example, in one study (Biederman et al., 1997) 140 ADHD children and 120 controls were followed for four years, then SUD levels were assessed. Results indicated:

  • No differences in the rates of SUD between the groups – 15% of the subjects in both the ADHD and the control groups had SUD
  • However, ADHD+CD and ADHD+MD children were more likely to develop SUD than were children in either the control or ADHD only groups
  • ADHD subjects who did abuse alcohol and drugs, even those with ADHD only, showed a much shorter time period between onset of abuse and dependence compared to controls (1.2 years vs. 3 years)
  • There was no difference in the type of drug that was abused and both the ADHD and control groups tended to use alcohol and marijuana.

While ADHD children as a group may not be at risk for SUD during childhood greater than that of the rest of the population, those children who continue to meet criteria for ADHD as late teens and adults may not be so fortunate. Another recent study (Wilens et al., 1997) compared 120 adults with ADHD to 268 non-ADHD controls. Results indicated:

  • ADHD was associated with earlier onset of SUD regardless of whether or not there was a comorbid psychiatric disorder
  • CD and MD in juveniles conferred a significantly increased risk of early onset SUD independent of ADHD
  • ADHD without CD or MD increased the risk of early onset SUD
  • ADHD with CD and MD predicted a very early onset of SUD

In addition, Biederman et al. (1997) compared lifetime rates of SUD in 239 ADHD adults vs. 268 non-ADHD, healthy adult controls. Results indicated:

  • ADHD was associated with nearly a twofold increased risk for SUD (27% vs. 55%)
  • ADHD subjects were more likely to make the transition from an alcohol use disorder to a drug use disorder and were significantly more likely to continue to abuse substances following a period of dependence
  • Age of onset of SUD in ADHD subjects averaged three years earlier than controls (late adolescence vs. early adulthood)
  • ADHD only was a significant risk factor for developing SUD
  • The greatest risk for SUD was associated with CD whether or not ADHD was also present

Taken together, these results suggest that, as ADHD children develop and move into later childhood and adolescence, they are at an increased to develop a CD or MD. This results in an increased risk for SUD in late adolescence and early adulthood. Unfortunately, this often is the time when these young people are leaving home, going to college, and trying to establish careers and significant relationships.

ADHD also appears to have a relevant impact on the course and treatment of substance abuse. For example, Wilens, Biederman, and Mick (1998) compared the course of SUD between 130 ADHD adults and 71 non-ADHD adults, all of whom had a lifetime history of SUD. The rate of onset was significantly earlier for those diagnosed with ADHD. Although the rate of SUD remitted in 80% of both groups, the rate of remission and duration of the SUD was different for the ADHD vs. the non-ADHD subjects. The duration of the SUD was 37.2 months longer in the ADHD vs. the non-ADHD group. The median time to SUD remission was more than twice as long in ADHD than in control subjects (144 vs. 60 months, respectively). Thus, ADHD appears to be associated with an earlier onset of SUD, a longer duration, and a significantly slower remission rate.

The use of stimulants in the treatment of ADHD has raised concern as to whether children are inadvertently being primed to develop a SUD, including the abuse of their stimulant medication. The National Institute of Mental Health and the Department of Education recently completed a Multimodal Treatment Study of Children with ADHD (MTA). This was a 14-month, multicentered study of children ages 7 to 9 years with a diagnosis of ADHD combined type. Results indicate that a treatment protocol that combines pharmacotherapy with behavioral treatment achieved the best results, compared to those on medication only, behavioral treatment only, or community care (control group). Medication was found to be the most effective single mode of treatment. This is not surprising. Based on extensive research over several years, it is clear that stimulant medication is the pharmacotherapy treatment of choice. In over 155 studies that examined populations from children to adults, the average response rate to stimulants was 70%. Stimulants improved the core symptoms of ADHD, which in turn often led to improved social and academic functioning.

Research indicates that stimulant treatment of ADHD in childhood is not associated with a higher prevalence of substance abuse in adulthood. More importantly, recent research data (Biederman et al., 1999) have emerged to confirm that pharmacological treatment of ADHD significantly lowers the risk for SUD in the high-risk, mid-adolescent age group. This study compared the overall rate of SUD between 45 unmedicated ADHD adolescents, 117 medicated adolescents, and 344 non-ADHD controls. The results were as follows:

  • unmedicated ADHD subjects were at significantly greater lifetime risk for SUD compared with the medicated ADHD and control groups (33% vs. 13% vs. 10%, respectively)
  • there was no significant increase in SUD risk with the medicated ADHD group compared controls

What about the adolescent with a history of substance abuse, particularly one who has abused stimulants? Surprisingly, a history of substance abuse is a relative, not an absolute, contraindication to stimulant treatment. As noted above, the use of stimulant medication in childhood does not predict increased adult SUD and the development of CD appears to increase the risk of an ADHD child engaging in substance abuse. In the treatment of the substance abusing ADHD+CD teen, the ADHD symptoms themselves may interfere significantly with efforts to obtain abstinence. Impulsiveness makes resisting cravings and the temptation of drugs harder. Inattentiveness increases the likelihood of school or on the job failure. This may subsequently result in sadness and depression, which may increase the craving for alcohol and drugs.

In summary, the relationship between ADHD and SUD is complex. Evidence suggests that the increased risk of SUD for ADHD children is primarily linked to the development of comorbid CD and MD. However, if ADHD symptoms persist into late adolescence and adulthood, ADHD individuals do appear to be at increased risk for SUD compared to non-ADHD cohorts. Finally, it seems clear that the treatment of ADHD with stimulant medication is, not only the treatment of choice, but that it also seems to significantly reduce the risk of SUD.