ADHD Affects the Efficacy of Treatment for Eating Disorders in Adult Women

Stephen V. Faraone, PhDSwedish researchers examined outcomes for adult women who sought treatment at the Stockholm Centre for Eating Disorders over a period of two years and nine months. Out of 1,517 women who came to the clinic 1,143 remained eligible for the study, after excluding women whose symptoms did not fulfill the DSM-IV criteria for eating disorders or had incomplete records.

Of these, seven hundred patients could not be reached or declined to participate, leaving 443 for follow-up. To guard against the possibility that the follow-up group might not be representative of the overall treatment group, researchers compared age, body mass index, and scores on tests for depression, anxiety, compulsivity, inattention, and hyperactivity. The only statistically significant differences were small ones. The median age of the group lost to follow-up was one year younger, they were less likely to be living alone, and on average scored a single point higher on the depression test. Otherwise they were broadly similar.

The one-year follow-up on the study group found a substantial difference in rate of recovery from eating disorders between those wEating disorders and ADHDith and without comorbid ADHD. Almost three out of four patients (72%) who scored lower (between 0-17) on the World Health Organization adult ADHD self-report scale had recovered from their eating disorder. Among those scoring 18 and higher, on the other hand, it was less than half (47%). This difference was extraordinarily unlikely (one chance in one thousand) to be due to chance (p=.001).

Another way of expressing this is through odds ratios. Those scoring 18 and up on the ADHD self-report scale were about two and a half times less likely to recover from their eating disorders following treatment. More specifically, they were about three times less likely to recover from loss of control and binging, and almost three and a half times less likely to recover from purging.

To improve outcomes, the researchers suggest “identifying concomitant ADHD symptoms and customizing treatment interventions based on this.” They specifically propose controlled clinical trials to explore the effect of combining stimulant medications with standard treatment for eating disorders.

REFERENCES
Nils Erik Svedlund, Claes Norring, Ylva Ginsberg, Yvonne von Hausswolff‐Juhlin, “Are treatment results for eating disorders affected by ADHD symptoms? A one‐year follow‐up of adult females,” European Eating Disorders Review (2018).

Stephen V. Faraone, PhDAn international group of twelve experts recently published a consensus report examining the state of the evidence and offering recommendations to guide screening, diagnosis, and treatment of individuals with ADHD-SUD comorbidity.1

In a clear sign that we are still in the early stages of understanding this relationship, five of the thirteen recommendations received the lowest recommendation grade (D), eight received the next-lowest (C), and none received the highest (A and B).

The lower grades reflected the absence of the highest level of evidence, obtained from meta-analyses or systematic reviews of relevant randomized controlled trials (RCTs).

Nevertheless, with these limitations in mind, the experts agreed on the following points:

ADHD Diagnosis

  • The strongest recommendation, the only one based on a 2+ level of evidence (well-conducted case control or cohort studies with a low risk of confounding or bias and a moderate probability that the relationship is causal) is that the “Short Version of the Adult ADHD Self-Report Scale (ASRS-SV) screener is currently the most widely used and investigated screening tool in individuals with ADHD and comorbid SUD, with good sensitivity and specificity across studies.”
  • Two other recommendations were graded C: The diagnostic process should include current and past substance abuse and seek to involve partners and relatives in evaluating symptoms and functional impairments.
  • Four recommendations got the lowest grade, D. The experts suggested starting the diagnostic process as soon as possible and focusing on drug- and alcohol-free periods in the patient’s life during history taking. They also recommended that physicians and clinical psychologists should only make diagnoses if they have extensive training in diagnosing ADHD, as well as experience with adults with ADHD and with addiction care, and that they should consider treating adults with sufficiently severe ADHD symptoms.

ADHD Treatment

  • In general, evidence was stronger in this area, and only one of the six recommendations was graded D. The other five recommendations were graded C, with the highest level of evidence being 2 (cohort or case and control studies with undetermined risk of bias), although in three cases it was level 3 (non-analytical studies, such as case reports and case series).
  • The grade D recommendation was to always consider a combination of psychotherapy and pharmacotherapy.
  • The grade C recommendations included considering adequate medical treatment of both ADHD and SUD; integrating ADHD treatment with SUD treatment as soon as possible; considering psychotherapy targeting both; use of long-acting methylphenidate, extended-release amphetamines, and atomoxetine because of their low potential for abuse; and careful clinical management to avoid abuse and diversion of prescribed stimulants.

Note: Andrew Reding is a co-author on this post.

REFERENCES
1Cleo L. Crunelle at al., “International Consensus Statement on Screening, Diagnosis and Treatment of Substance Use Disorder Patients with Comorbid Attention Deficit/Hyperactivity Disorder,” European Addiction Research, published online March 6, 2018, DOI: 10.1159/000487767.

   
Joseph_Biederman_AIA_rX8AEqAmy_Yule_w_credentials_nHHCtD
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.

 

REFERENCE

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.

http://medicalwritingtraining.com/Over the past few decades, a consensus has emerged among psychopathologists that some patients exhibit a well-defined syndrome referred to as sluggish cognitive tempo or SCT. There are no diagnostic criteria for SCT because it has not yet been accepted as a separate disorder by the American Psychiatric Association. People with SCT are slow-moving, indolent and mentally muddled. They often appear to be lost in thoughts, daydreaming, drowsy or listless. In reviewing these symptoms and the literature, Barkley suggested that SCT be referred to as Concentration Deficit Disorder (CDD). This term is less pejorative but is not yet commonly used. Becker and colleagues recently evaluated the internal and external validity of SCT via a meta-analysis of 73 studies. Internal validity addresses the consistency of SCT symptoms as measure of an underlying construct. Based on factor analytic studies using more than 19,000 participants, the authors concluded that the items purported to measure SCT are sufficiently correlated with one another to justify the idea that they measure the same underlying construct. Further support for internal validity was found in studies reporting high test-retest and interrater reliability. As regards ADHD, the authors found that SCT correlated significantly with both inattentive (r = 0.72) and hyperactive-impulsive (r = 0.46) symptoms in adults. The greater correlation with inattentive symptoms makes sense given the nature of SCT symptoms. So these data confirm two key points about SCT: 1) it is definitely associated with ADHD symptoms and 2) it is a meaningful construct in its own right. Very little is known about the implications of SCT for the treatment of ADHD. In a naturalistic study of 88 children and adolescents with ADHD, Ludwig and colleagues examined the effect of SCT on the response of ADHD symptoms to methylphenidate. They found no significant differences in treatment response between subjects with and without SCT. McBurnett and colleagues tested the effects of atomoxetine on SCT in children with ADHD and dyslexia (ADHD+D) or dyslexia only. Atomoxetine treatment led to significant reductions in both ADHD symptoms and SCT outcomes. Because controlling for changes in ADHD symptoms did not predict changes in SCT outcomes, the authors concluded that change in SCT in response to atomoxetine is mostly independent of change in ADHD. Although these data are preliminary and in need of replication, they do provide some guidance for clinicians dealing with ADHD patients who also have SCT.
 

REFERENCE
Becker, S. P., Leopold, D. R., Burns, G. L., Jarrett, M. A., Langberg, J. M., Marshall, S. A., McBurnett, K., Waschbusch, D. A. & Willcutt, E. G. (2016). The Internal, External, and Diagnostic Validity of Sluggish Cognitive Tempo: A Meta-Analysis and Critical Review. J Am Acad Child Adolesc Psychiatry 55, 163-78.

Ludwig, H. T., Matte, B., Katz, B. & Rohde, L. A. (2009). Do sluggish cognitive tempo symptoms predict response to methylphenidate in patients with attention-deficit/hyperactivity disorder-inattentive type? J Child Adolesc Psychopharmacol 19, 461-5.

McBurnett, K., Clemow, D., Williams, D., Villodas, M., Wietecha, L. & Barkley, R. (2016). Atomoxetine-Related Change in Sluggish Cognitive Tempo Is Partially Independent of Change in Attention-Deficit/Hyperactivity Disorder Inattentive Symptoms. J Child Adolesc Psychopharmacol.

Barkley, R. A. (2014). Sluggish cognitive tempo (concentration deficit disorder?): current status, future directions, and a plea to change the name. J Abnorm Child Psychol 42, 117-25.

Stephen_Faraone_PhD_AIA_2016_XM7MQd.png.jpgAdults with ADHD are more likely to have accidents, to drive unsafely, to have unsafe sex and to abuse substances. These ‘real world’ impairments suggest that people with ADHD may be predisposed to making risky decisions. Many studies have attempted to address this but is only recently that their results have been aggregated into a systematic review and meta-analysis. This paper by Dekkers and colleagues reports of 37 laboratory studies of risky decision making that studied a total of 1175 ADHD patients and 1222 controls. In these laboratory tasks, research participants are given a task to complete which require that they make choices which have varying degrees of risk and reward. Using the results of such experiments, researchers can score the degree to which participants make risky decisions. When Dekkers and colleagues analyzed the 37 studies together, they found substantial evidence that ADHD people are more likely to make risky decisions than people without ADHD. The tendency to make risky decisions was greatest for those who, in addition to having ADHD, also had conduct or oppositional disorders, which both have features that indicate antisocial behavior and aggressiveness. We cannot tell from these studies why ADHD patients make risky decisions. One explanation is that it is simply the impulsivity of ADHD people that leads to rash, unwise decisions. Another theory postulates that risky decisions reflect deficits in one’s sensitivity to rewards and punishments. If we are very motivated by reward and not aware of or affected by the possibility of punishment, then risky decisions will be common. The studies analyzed in the meta-analysis were not designed to demonstrate a link between risky decision making in the lab and the real world risky decisions that lead to accidents and other outcomes. It is reasonable to hypothesize such a link, which is why clinicians should consider risky decision making when planning treatments. If you suspect deficits in this area, it will not change your approach to pharmacologic treatment but, given the potential adverse consequences of risky decisions, you should consider referring such patients to cognitive behavior therapy for adult ADHD as this talk therapy may be able to teach ADHD adults how to cope with their decision making deficits.
 

REFERENCE
Dekkers, T. J., Popma, A., Agelink van Rentergem, J. A., Bexkens, A. & Huizenga, H. M. (2016). Risky decision making in Attention-Deficit/Hyperactivity Disorder: A meta-regression analysis. Clin Psychol Rev 45, 1-16.

http://medicalwritingtraining.com/One of the many great contributions of Dr. Russell Barkley was his conceptualization of ADHD as a disorder of self-regulation. ADHD people have difficulties regulating their behavior, which lead to the classic diagnostic criteria of hyperactivity and impulsivity and they have problem regulating cognitive processes which leads to the well-known inattentive diagnostic criteria for the disorder. In a 2010 paper, Dr. Barkley argued persuasively that deficient emotional self-regulation should also be considered a core component of ADHD alongside deficient behavioral and cognitive self-regulation. Although the DSM 5 did not add any emotional symptoms to the revised criteria for ADHD a new paper by Graziano and Garcia supports Dr. Barkley’s position. They conducted a meta-analysis of 77 studies of emotional dysregulation that comprised a total of 32,044 participants. They defined emotional dysregulation as the failure to modify emotional states in a manner that promotes adaptive behavior and leads to the success of goal directed activities. They identified three types of emotional dysregulation: emotion recognition and understanding (ERU), emotional reactivity/negativity/lability (ERNL) and empathy/callous-unemotional traits (ECUT). ERU refers to the ability to perceive, process and infer one’s own emotions and the emotions of others. ERNL refers to the intensity and valence of the emotional response. Reactivity refers to the rapidity of the emotional response (e.g., is a person quick tempered rather than reflective); negativity refers to the valence of the emotion. Is it extreme or appropriate to the situation; and lability refers to how quickly emotional states shift or cycle over time. The ECUT dimension has two poles. At one extreme is the empathic person whose reactions are guided by a clear understanding of the emotional states of others. At the other pole is the psychopath who shows little or no emotion to stimuli that evoke strong emotional reactions in the average person. When the data from the 77 studies was sorted into these three categories, the authors found that ADHD people had impairments in all three domains. The magnitude of impairment was a bit greater for ERNL than it was for ECUT and ERU, but not dramatically so. The association between ADHD and these domains of emotional dysregulation increased with increasing age. It is for this reason that some ADHD experts think that emotional dysregulation should be included in the diagnostic criteria for adult ADHD. Because behavioral hyperactivity diminishes with age, these criteria are less sensitive for adult ADHD than they are for child ADHD. Substituting emotional dysregulation items for hyperactivity items could, potentially, improve diagnoses of adult ADHD. Future work will address this issue. In the meanwhile, those who screen and diagnose adult ADHD should be aware that symptoms of emotional dysregulation might be the most prominent for some adults with the disorder.

 
REFERENCE
Barkley, R. A. (2010). Deficient Emotional Self-Regulation: A Core Component of Attention-Deficit/Hyperactivity Disorder. Journal of ADHD and Related Disorders 1, 5-37.

Graziano, P. A. & Garcia, A. (2016). Attention-deficit hyperactivity disorder and children’s emotion dysregulation: A meta-analysis. Clin Psychol Rev 46, 106-23.

Joseph_Biederman_AIA_rX8AEq.png.jpgThis blog addresses the relationship between executive function deficits in general and working memory (WM) deficits in particular and attention-deficit/hyperactivity disorder (ADHD). Although some neuropsychological models of ADHD have proposed that ADHD arises from deficits in executive functions, accumulating clinical evidence show that it afflict some but not all individuals with ADHD and suggests that ADHD and executive function deficits represent separate clinical condition. Because executive functions refer to a wide and diverse group of high order mental functions, one approach to evaluate this important issue is to focus on one prominent facet of executive functions, mainly working memory. Working memory (WM) refers to a key brain system that provides temporary storage and manipulation of information essential for adequate cognitive functioning. It focuses attention, inhibits irrelevant stimuli, recognizes priority patterns and hierarchies and selects the goals that are best suited to solving a problem. Since these cognitive processes are critical for learning, their impairment can lead to deficits in functioning including social and educational dysfunction, low educational achievement and can have a serious impact on educational success. To address this issue we examined referred youth with and without ADHD with and with without WM deficits in functional, social and academic outcomes. We used Resting State FMRI imaging to examine whether the neural circuits subserving WM deficits overlap with those of ADHD. We investigated this issue in preclinical studies where we examined spatial WM and dopamine receptor activity in rodents. In human studies, we examined whether the most standard treatment for ADHD has a different effect on measures of WM and ADHD. This body of research provides evidence for a clinical, pharmacological and neurobiological dissociation between ADHD and WM deficits. Our preclinical findings demonstrate that the magnitude of improvement in WM produced by the D4 receptor agonist is significantly greater than that produced by methylphenidate. Our human treatment study with methylphenidate provide evidence for very different effects for ADHD and WM deficits Our clinical studies show that significantly more youth with ADHD had WM deficits than controls (31.9% vs. 13.7%) and their presence is significantly and specifically associated with academic failure. In our imaging study, we found that brain activations to a WM test were different in subjects with ADHD with associated WM deficits compared to controls and ADHD subjects without WM deficits. This body of work indicates that WM deficits afflict a minority of subjects with ADHD and when present they significantly and selectively increase the risk for academic dysfunction in subjects with ADHD, they have separate neural underpinning, and respond differently to treatments for ADHD. Screening for WM deficits may help identify individuals with ADHD at high risk for academic dysfunction.
 

References
K. P. LEE, N. PINEDA, T. BRUNE, K. PATEL, A. GANNON, T. J. SPENCER, J. BIEDEMAN, P. G. BHIDE, J. ZHU. Hyperactivity and working memory deficits induced by prenatal nicotine exposure are associated with dopamine D1 and D4 receptor dysfunction. Society for Neuroscience Annual Meeting, Washington, DC, November, 2014.
Fried R, Chan J, Feinberg L, Pope A, Woodworth KY, Faraone SV, et al. Clinical correlates of working memory deficits in youth with and without ADHD: A controlled study. Journal of clinical and experimental neuropsychology. 2016;38(5):487-96.

Mattfeld AT, Whitfield-Gabrieli S, Biederman J, Spencer T, Brown A, Fried R, et al. Dissociation of working memory impairments and attention-deficit/hyperactivity disorder in the brain. NeuroImage Clinical. 2016;10:274-82.
Biederman J, Chan J, Spencer TJ, Woodworth KY, Kenworthy T, Fried R, Bhide P, Faraone SV. Evidence of a pharmacological dissociation between the robust effects of methylphenidate on ADHD symptoms and weaker effects on working memory. Journal of Brain Sciences. 2015; 1(2): 43-53.

http://medicalwritingtraining.com/Although some people view the impulsivity and inattentiveness of ADHD adults as a normal trait, these symptoms have adverse consequences, which is why doctors consider ADHD to be a disorder. The list of adverse consequences is long and now we can add another: broken bones. A recent study by Komurcu and colleagues examined 40 patients who were seen by doctors because of broken bones and 40 people who had not broken a bone. After measuring ADHD symptoms in these patients, the study found that the patients with broken bones were more impulsive and inattentive than those without broken bones. These data suggest that, compared with others, adults with ADHD symptoms put themselves in situations that lead to broken bones. What could those situations be? Well, we know for starters that ADHD adults are more likely to have traffic accidents. They are also more likely to get into fights due to their impulsivity. As a general observation, it makes sense that people who are inattentive are more likely to have accidents that lead to injuries. When we don’t pay attention, we can put ourselves in dangerous situations. Who should care about these results? ADHD patients need to know about this so that they understand the potential consequences of their disorder. They are exposed to so much media attention to the dangers of drug treatment that it can be easy to forget that non-treatment also has consequences. Cognitive behavior therapy is also useful for helping patients learn how to avoid situations that might lead to accidents and broken bones. This study also has an important message for administrators and how they make decisions about subsidizing or reimbursing treatment for ADHD. They need to know that treating ADHD can prevent outcomes that are costly to the healthcare system, such as broken bones. For example, in a study of children and adolescents, Leibson and colleagues showed that healthcare costs for ADHD patients were twice the cost for other youth, partly due to more hospitalizations and more emergency room visits. Do these data mean that every ADHD patient is doomed to a life of injury and hospital visits? Certainly not. But they do mean that patients and their loved ones need to be cautious and need to seek treatments that can limit the possibility of accidents and injury.
 

REFERENCES
Komurcu, E., Bilgic, A. & Herguner, S. (2014). Relationship between extremity fractures and attention-deficit/hyperactivity disorder symptomatology in adults. Int J Psychiatry Med 47, 55-63.
Leibson, C. L., S. K. Katusic, et al. (2001). “Use and Costs of Medical Care for Children and Adolescents With and Without Attention-Deficit/Hyperactivity Disorder.” Journal of the American Medical Association 285(1): 60-66.

http://medicalwritingtraining.com/Suicide is one of the most feared outcomes of any psychiatric condition. Although its association with depression is well known, a small but growing research literature shows that ADHD is also a risk factor for suicidality.

Suicide is difficult to study. Because it is relatively rare, large samples of patients are needed to make definitive statements. Studies of suicide and ADHD must also consider the possibility that medications might elevate that risk.

For example, the FDA placed a black box warning on atomoxetine because that ADHD medication had been shown to increase suicidal risk in youth. A recent study of 37,936 patients with ADHD now provides much insight into these issues (Chen, Q., Sjolander, A., Runeson, B., D’Onofrio, B. M., Lichtenstein, P. & Larsson, H. (2014). Drug treatment for attention-deficit/hyperactivity disorder and suicidal behaviour: register based study. BMJ 348, g3769.). In Sweden, such large studies are possible because researchers have computerized medical registers that describe the disorders and treatments of all people in Sweden. Among 37,936 patients with ADHD, 7019 suicide attempts or completed suicides occurred during 150,721 person years of follow-up. This indicates that, in any given year, the risk for a suicidal event is about 5%.

For ADHD patients, the risk for a suicide event is about 30% greater than for non-ADHD patients. Among the ADHD patients who attempted or completed suicide, the risk was increased for those who had also been diagnosed with a mood disorder, conduct disorder, substance abuse or borderline personality. This is not surprising; the most serious and complicated cases of ADHD are those that have the greatest risk for suicidal events.

The effects of medication were less clear. The risk for suicide events was greater for ADHD patients who had been treated with non-stimulant medication compared with those who had not been treated with non-stimulant medication. A similar comparison showed no effect of stimulant medications.

This first analysis suffers from the fact that the probability of receiving medication increases with the severity of the disorder. To address this problem, the researchers limited the analyses to ADHD patients who had had some medication treatment and then compared suicidal risk between periods of medication treatment and periods of no medication treatment. This analysis found no increased risk for suicide from non-stimulant medications and, more importantly, found that for patients treated with stimulants, the risk for suicide was lower when they were taking stimulant medications. This protective effect of stimulant medication provides further evidence of the long-term effects of stimulant medications which have also been shown to lower the risks for traffic accidents, criminality, smoking and other substance use disorders.

Stephen_Faraone_PhD_ADHD_in_AdultsEditor’s Note:  It is important to read the FULL Blog post.

Suicide is one of the most feared outcomes of any psychiatric condition.  Although its association with depression is well known, a small but growing research literature shows that ADHD is also a risk factor for suicidality.  

Suicide is difficult to study. Because it is relatively rare, large samples of patients are needed to make definitive statements.  Studies of suicide and ADHD must also consider the possibility that medications might elevate that risk. 

For example, the FDA placed a black box warning on atomoxetine because that ADHD medication had been shown to increase suicidal risk in youth.   A recent study of 37,936 patients with ADHD now provides much insight into these issues (Chen, Q., Sjolander, A., Runeson, B., D’Onofrio, B. M., Lichtenstein, P. & Larsson, H. (2014). Drug treatment for attention-deficit/hyperactivity disorder and suicidal behaviour: register based study. BMJ 348, g3769.).    In Sweden, such large studies are possible because researchers have computerized medical registers that describe the disorders and treatments of all people in Sweden.  Among 37,936 patients with ADHD, 7019 suicide attempts or completed suicides occurred during 150,721 person years of follow-up.  This indicates that, in any given year, the risk for a suicidal event is about 5%. 

 

Ask the ADHD Experts  Prescribing ADHD Medications

For ADHD patients, the risk for a suicide event is about 30% greater than for non-ADHD patients.  Among the ADHD patients who attempted or completed suicide,the risk was increased for those who had also been diagnosed with a mood disorder, conduct disorder, substance abuse or borderline personality.  This is not surprising; the most serious and complicated cases of ADHD are those that have the greatest risk for suicidal events.  

The effects of medication were less clear.   The risk for suicide events was greater for ADHD patients who had been treated with non-stimulant medication compared with those who had not been treated with non-stimulant medication.  A similar comparison showed no effect of stimulant medications. 

This first analysis suffers from the fact that the probability of receiving medication increases with the severity of the disorder.  To address this problem, the researchers limited the analyses to ADHD patients who had had some medication treatment and then compared suicidal risk between periods of medication treatment and periods of no medication treatment.  This analysis found no increased risk for suicide from non-stimulant medications and, more importantly, found that for patients treated with stimulants, the risk for suicide was lower when they were taking stimulant medications.  This protective effect of stimulant medication provides further evidence of the long-term effects of stimulant medications which have also been shown to lower the risks for traffic accidents, criminality, smoking and other substance use disorders.