Cocaine dependence is in part genetic, and it shares genetic risk factors with other psychiatric conditions and personality traits.

Cocaine is one of the most used illicit drugs worldwide and its abuse produces serious health problems. In Europe, around 5.2% of adults (from 15 to 64 years old) have tried cocaine, but only 20% will develop addiction. Why? Genetics is part of the answer. Cocaine dependence is a complex psychiatric disorder that results from the interaction of both environmental and genetic risk factors. Twin and adoption studies indicate that genetic alterations contribute substantially to cocaine dependence susceptibility, which has an estimated genetic load (heritability) as high as 65-79%. Although many studies with focus on candidate genes have been performed, only a few risk variants for cocaine dependence have been identified and replicated so far.


In this study we performed a meta-analysis of genome-wide association studies (GWAS) of cocaine dependence using more than 6,000 European ancestry individuals. This approach allowed us to inspect a huge number of genetic variants distributed all along the genome that are common in the general population. We identified a gene (HIST1H2BD) associated with cocaine dependence that is located in a region on chromosome 6 enriched in genes that encode histones, proteins that combine with DNA, protecting it and contributing to the activation (or inhibition) of genes. Some of these genes have previously been associated with schizophrenia.

Several studies have shown that substance use disorders (SUD), and especially cocaine dependence, co-occur in patients with other psychiatric disorders and personality traits. Such comorbidity is associated with increased severity for all disorders, although it is unclear whether this relationship is causal or the result of shared genetic and/or environmental risk factors. We calculated the shared genetics (genetic correlation) between cocaine dependence and six comorbid conditions. For the first time we found significant genetic correlation with attention deficit/hyperactivity disorder (ADHD), schizophrenia, major depression and risk- taking behavior. We also used another approach (polygenic risk score analysis, PRS) to prove that all tested comorbid conditions are associated with cocaine dependence status, suggesting that cocaine dependence is more likely in individuals that carry genetic risk factors for the tested conditions than in those that do not.

To our knowledge, this is the largest reported GWAS meta-analysis in European-ancestry individuals with cocaine dependence. We identified suggestive risk factors for the disorder in several genomic regions and found evidence for shared genetic risk factors between cocaine dependence and several co-occurring psychiatric traits. However, the size of the sample is still limited and further studies are needed to confirm our results.

Read more at:

Judit Cabana-Domínguez and Bru Cormand

Judit Cabana Domínguez is a Postdoctoral researcher at the Genetics, Microbiology and Statistics Department at the University of Barcelona.

Bru Cormand is Full Professor of Genetics at the Genetics, Microbiology and Statistics Department at the University of Barcelona.

Light therapy and its influence on ADHD: An interview


Nina (27 years, Dutch) participated in the PROUD-study and followed our light therapy. In this interview she describes the influences light therapy had on her ADHD symptoms.

What is it like to live with ADHD?

Please describe your main symptoms.

The symptom I experience as the most troublesome is making new friends. It is harder for me to make new friends, knowing I have fewer emotional and cognitive skills than peers. I am more sensitive to persons and situations and I experience them as more severe.

Besides, it is harder for me to see things in perspective and my perspectives change a lot over short periods of time. This makes it harder to look further in the future when making decisions. I also have less patience and it is harder for me to concentrate on a task. 

How does ADHD influence your life?

As I explained in the question before it can be tough to make friends. Concerning work, my ADHD has positive and negative effects. The negative effects are my lack of concentration, sometimes a job has to be done at a certain moment when I have no concentration, which can be a real struggle. The positive side is that I am creative and my spatial development is good. These are qualities that come handy at my job. Also my intelligence helps me. Because I am smart I can work fast at the moments my concentration is good, in order to compensate for the moments where my concentration is lost.

Do you think ADHD has any positive influences in your life?

It sure has, but these influences often last for a short period of time. I can be really enthusiastic and I am good at identifying people. This quality makes me a really good friend. Also my creativity is a positive effect of ADHD.

How have you been treated (medication/ psychotherapy)? What are the effects?

For a year and a half I have lived internally in a group especially for adolescents with ADHD and/or autism. Here I followed a training to improve my social abilities, how to engage in relationships with others and to be more independent.

From my 16th I take medication. I have switched a lot and tried different kinds of medication. Much of them did not work well for me, I even tried anti-depressants which made me feel sad. I am currently taking Stratera (short acting) and this works well for me. I don’t take it regularly but only at moments where I think I need it.

Study and intervention

How did you learn about the study?

I am regularly searching the internet to learn more about ADHD. This time I was searching information about comorbidity and neurodiversity and this is how I found your website, by chance.

What motivated you to participate?

It is a good thing that more research is done and I find it important to contribute. The more research is being conducted, the better others with ADHD can be helped. It is of great importance of me to be able to be a part in this. As long as we do not contribute to this kind of research, nothing will chance.

What were your expectations about the study before you started?

To be honest I did not have any expectations because I did not want to be affected by them.

What intervention did you participate in? When?

I participated in the bright light therapy from the 18th of October (2018) until the 10th of January (2019).

What did you like about the intervention? What did you dislike about the intervention?

At the beginning it was kind of hard, I found it really hard to be sitting still half an hour in the morning. Normally I rush through the mornings and do not really sit still at all. My solution was to put the lamp at my nightstand and sit in bed for half an hour in the morning, waking up next to the lamp. You can adjust the brightness of the lamp so I started with dimmed light and increased brightness step by step. Important is to sit upright because otherwise there is a chance of falling back to sleep!

In the beginning I had not realized what an impact this therapy has on your daily life, you really need the motivation to sit through, every day. After some time I got adapted to a new rhythm which made it easier to follow the light therapy for 6 times week. Only on Saturdays I skipped the sessions because of the weekend.

Was the intervention helpful?

It definitely has positive influences. The biggest change I have experienced is the adaptation to a more natural day/night rhythm. I was hoping a side effect would be falling asleep faster but unfortunately this was not the case for me.

The first days I experienced some negative side effects, which are explained in the bright light manual. Maybe it would be better if I had not read the manual because I was so focused on the experience of these side effects. What I felt was a really grumpy mood in the mornings. Luckily it only lasted for a few days.

Are you planning on continuing the intervention?

No, I have no plans of buying a lamp myself. Looking back at the intervention I think I would benefit more by participating in the aerobic exercise intervention, because sitting still for half an hour without a clear purpose is tough. Of course I did adapt to a better and more natural day/night rhythm because of the bright light therapy, but I think this could also be accomplished by going to bed at the same time every day.

Was it difficult/easy to use the App?

Definitely not difficult. The researches informed me about the sensor and how it might be inconvenient in the beginning but I only had to get used to it during the nights. The app was really clear and straight-forward, easy to use. I did forget the phone a few times, making me drive back home, but if you wear pants with pockets this should not be a problem.

Would you recommend other people with ADHD to participate in the study? Why?

I would definitely recommend it to people who are interested in this study and are motivated to participate. You really have to do it because you want it, not only because you want to help others.

Any suggestions/ways that the researchers could improve the experience for people in this study?

In my experience the study is set up well. Sometimes something went wrong (system was not installed right so they had to send me a new set, this set came without a wristband, red.) but the researchers handled it well and professionally. The researchers were cooperative and I liked participating in this study.

Lisa Bos, MSC works at Karakter Child and Youth Psychiatry and Radboud UMC (Nijmegen, the Netherlands) where she works as a researcher for the TRACE project and the PROUD-study. Both studies focus on additional treatments for ADHD and a healthy lifestyle which are also her main interests. She finds importance in studying socially relevant topics and improving the quality of care for ADHD patients.

ADHD and autism – similar or different disorders?

Have you ever thought that ADHD and autism could perhaps be the same disorder? – Or have you thought that they are way too different, two different planets in the psychiatric universe? Researchers do not agree on this. We know that both ADHD and autism are neurodevelopmental conditions with onset in childhood and that they share some common genetic factors, however, they appear with quite different phenotypical characteristics. We also know that people with ADHD or autism have an increased risk of getting other psychiatric disorders, so-called comorbidities, and smaller studies have shown that individuals with ADHD or autism get different psychiatric disorders, and at a different degree.

How can we utilize this knowledge about different psychiatric comorbidities between ADHD and autism? How can we get closer to an answer to this question; are ADHD and autism similar or different conditions? By using large datasets; unique population-based registries in Norway, we wanted to compare the pattern of psychiatric comorbidities in adults diagnosed with ADHD, autism or both disorders. In addition, we wanted to compare the pattern of genetic correlations between ADHD and autism for the same psychiatric traits, and for this, we exploited summary statistics from relevant genome-wide association studies.

In the registries, we identified 39,000 adults with ADHD, 7,500 adults with autism and 1,500 with both ADHD and autism. We compared these three groups with the remaining population of 1.6 million Norwegian adult inhabitants without either ADHD or autism. The psychiatric disorders we studied were anxiety, bipolar, depression, personality disorder, schizophrenia spectrum (schizophrenia) and substance use disorders (SUD).

Interestingly, we found different patterns of psychiatric comorbidities between ADHD and autism, overall and when stratified by sex (Fig.1). These patterns were also reflected in the genetic correlations, however, only two of the six traits showed a significant difference between ADHD and autism (Fig.2).

Figure 1 - Solberg et al. 2019
Figure 1. Prevalence ratios of psychiatric disorders in adults with ADHD, autism or both ADHD and autism, relative to the remaining population, by sex. As can be seen in the figure, schizophrenia is more frequent in autism or ADHD+autism than ADHD alone, while the reverse is true for substance use disorder. There are also significant differences in prevalence between men and women. Figure from Solberg et al. 2019, CC-BY-NC-ND.

Figure 2. Left: The pattern of prevalence ratios of psychiatric comorbidity in adults with ADHD or autism observed in this study (ADHD; n=38,636, autism; n=7,528). Right: genetic correlations (rg) calculated from genome wide association studies. Psychiatric conditions are highly prevalent in both ADHD and ASD, with schizophrenia being most prevalent in ASD and antisocial personality disorders in ADHD. Genetic correlations are also high with both disorders, with especially high correlations between ADHD and alcohol dependence, smoking behavior and anti-social behavoiur. Major depressive disorder has high genetic correlations with both ADHD and autism. Figure from Solberg et al. 2019, CC-BY-NC-ND.

The most marked differences were found for schizophrenia and SUD. Schizophrenia was more common in adults with autism, and SUD more common in adults with ADHD. Associations with anxiety, bipolar and personality disorders were strongest in adults with both ADHD and autism, indicating that this group of adults suffers from more severe impairments than those with ADHD or autism only. The sex differences in risk of psychiatric comorbidities were also different among adults with ADHD and ASD.

In conclusion, our study provides robust and representative estimates of differences in psychiatric comorbidities between adults diagnosed with ADHD, autism or both ADHD and autism. With the results from analyses of genetic correlations, this finding contributes to our understanding of these disorders as being distinct neurodevelopmental disorders with partly shared common genetic factors.

Clinicians should be aware of the overall high level of comorbidity in adults with ADHD, autism or both ADHD and autism, and the distinct patterns of psychiatric comorbidities to detect these conditions and offer early treatment. It is also important to take into account the observed sex differences. The distinct comorbidity patterns may further provide information to etiologic research on biological mechanisms underlying the pathophysiology of these neurodevelopmental disorders.

This study was done at Stiftelsen Kristian Gerhard Jebsen Centre for Neuropsychiatric disorders, University of Bergen, Norway, and published OnlineOpen in Biological Psychiatry, April 2019, with the title:

“Patterns of psychiatric comorbidity and genetic correlations provide new insights into differences between attention-deficit/hyperactivity disorder and autism spectrum disorder”.

Figure 1 and 2 are re-printed by permission

Berit Skretting Solberg is a PhD-candidate at the Department of Biomedicine/Department of Global Health and Primary Care, University of Bergen, Norway. She is also a child- and adolescent psychiatrist/adult psychiatrist. She is affiliated with the CoCa-project, studying psychiatric comorbidities in adults with ADHD or autism, using unique population-based registries in Norway.


Epigenetic signature for attention-deficit/hyperactivity disorder

Attention-deficit/hyperactivity disorder (ADHD) is considered a complex disorder caused by underlying genetic and environmental risk factors. To make it even more complex, environmental factors can influence the expression of genes. This is called epigenetics.

Given the large proportion of the heritability of ADHD still to be explained, there is a growing interest in the epigenetic mechanisms that modulate gene expression. microRNAs (miRNA) are small parts in the human genome that do not code for genes, but instead regulate the expression of other genes by promoting the degradation or suppressing the translation of those target genes. miRNA therefore provide a means to integrate effects of genetic and environmental risk factors.

The human genome encodes more than 2500 different miRNAs, the majority of which are expressed in the brain. miRNAs are known to be involved in the development of the central nervous system and in many neurological processes including synaptic plasticity and synaptogenesis. Given the limited accessibility of the human brain for studying epigenetic modifications, miRNA profiling in peripheral blood cells is often used as a non-invasive proxy to study transcriptional and epigenetic biosignatures, and to identify potential clinical biomarkers for psychiatric disorders.

We recently investigated the role of microRNAs in ADHD at a molecular level, by conducting the first genome-wide integrative study of microRNA and gene expression profiles in blood of individuals with ADHD and healthy controls. We identified three miRNAs (miR-26b-5p, miR-185-5p and miR-191-5p) that have different expression levels in people with ADHD, compared to those without ADHD. When we investigated downstream miRNA-mediated mechanisms underlying the disorder this provided evidence that aberrant expression profile of these three miRNA may underlie changes in the expression of genes related with myo-inositol signaling. This mediates the biological response of a large number of hormones and neurotransmitters on target cells. We also found that these miRNAs specifically targeted genes involved in neurological disease and psychological disorders.

These findings show that epigenetic modifications through microRNAs play a role in ADHD, and provide novel insights into how these miRNA-mediated mechanisms contribute to the disorder. In the future, these miRNAs may be used as peripheral biomarkers that can be easily detected from blood, as is shown in the figure.

What´s next?

The mechanism through which miRNAs modify gene expression is complex and dynamic. Therefore, future studies are required to provide deeper insights into the epigenetic mechanisms underlying ADHD, and to identify specific molecular networks that may be crucial in the development of the disorder.

Further reading

Cristina Sánchez-Mora et al. Epigenetic signature for attention-deficit/hyperactivity disorder: identification of miR-26b-5p, miR-185-5p, and miR-191-5p as potential biomarkers in peripheral blood mononuclear cells, Neuropsychopharmacology, volume 44, pages 890–897 (2019).

About the author

Cristina Sánchez-Mora is postdoctoral researcher at the Psychiatry, Mental Health and Addictions group at Vall d’Hebron Institut de Recerca (VHIR). Her research is part of the CoCA consortium that investigates comorbid conditions of ADHD

ADHD and cannabis use

It is not uncommon for individuals to suffer from two or more psychiatric disorders at the same time. The appearance of these disorders frequently follows a specific order, and one disorder may predispose to others, all of which in combination contribute to the worsening of the quality of life of the individuals who suffer them. This is usually associated with more severe symptoms and worse prognosis. In addition, making a diagnosis and applying personalized treatments becomes more challenging in this context. By investigating the genetic overlap between disorders, we gain better understanding of why the disorders frequently co-occur.

In mental health, substance use disorders often appear when there is another mental condition. This is the case for attention-deficit/hyperactivity disorder (ADHD) and substance use disorder, where individuals with ADHD are more likely to use drugs during their lifetime than individuals who do not have ADHD. In particular, cannabis is the most commonly used substance among individuals with ADHD, which can also lead to the use of other drugs and to the worsening of their symptoms. ADHD is one of the most common neurodevelopmental disorders, affecting around 5% of children and 2.5% of adults, and is characterized by attention deficit, hyperactivity and impulsivity. Both ADHD and cannabis use are conditions determined partly by environmental factors but where genetic factors also play an important role.

We recently investigated the genetic overlap between ADHD and cannabis use, and found that the increased probability of using cannabis in individuals with ADHD, can be, in part, due to a common genetic background between the two conditions. We identified four genetic regions involved in increasing the risk of both ADHD and cannabis use, which could point to potential druggable targets and help to develop new treatments. In addition, we confirmed a causal link between ADHD and cannabis use, and estimated that individuals with ADHD are almost 8 times more likely to consume cannabis than those who do not have ADHD. This evidence goes in line with a temporal relationship, where the ADHD appears in childhood and the use of cannabis during adolescent or adulthood. This suggests that having ADHD increases the risk of using cannabis, and not vice versa.

This research has only been possible thanks to large international collaborations by the Psychiatric Genomics Consortium (PGC), iPSYCH, and the International Cannabis Consortium (ICC), where the genomes of around 85 000 individuals were analysed.

Overall, these results support the idea that psychiatric disorders are not independent, but have a common genetic background, and share biological pathways, which put some individuals at higher risk than others. This will help to overcome the stigma of addiction and mental disorders. In addition, the potential of using genetic information to identify individuals at higher risk will have a strong impact on prevention, early detection and treatment.

Further reading

María Soler Artigas et al. Attention-deficit/hyperactivity disorder and lifetime cannabis use: genetic overlap and causality, Molecular Psychiatry (2019) –

About the author

María Soler Artigas is postdoctoral researcher at the Psychiatry, Mental Health and Addictions group at Vall d’Hebron Institut de Recerca (VHIR), also part of the Biomedical Research Networking Center in Mental Health (CIBERSAM). Her research is part of the CoCA consortium that investigates comorbid conditions of ADHD.

Are you genetically determined to act aggressively?

From road rage and bar fights to terror attacks and global confrontations, humans tend to be an aggressive species. On the average, members of the same species cause only 0.3 percent of deaths among mammals [1]. Astoundingly, in Homo sapiens the rate is around 2% (1 in 50), nearly 7 times higher! There are two crucial aspects that favor this kind of behavior: dwelling in social groups and being ferociously territorial. The chances are that struggle for various resources like suitable habitat, mates and food played a key role in shaping aggression in humans, favoring genetic variants that promote aggression and therefore increase changes of survival. Indeed, anthropologists who lived with exceptionally violent hunter-gatherers found that men who committed acts of homicide had more children, as they were more likely to survive and have more offspring [2]. This lethal legacy may be the reason we are here today.

You probably know some people that could be characterized as “having a short fuse”. Perhaps you have even pondered why they seem to have such a hard time to keep their temper in check? Indeed – while scientists have known for decades that aggression is hereditary, there is another crucial component to those angry flare-ups: self-control. In humans, the impulses to react violently stem from the ancient structures located deep within the brain. The part capable of controlling those impulses is evolutionally much younger and located just behind the forehead – the frontal lobes. Unfortunately, this “top-down” conscious control of aggressive impulses is slower to act compared to the circuits of eruptive violence deep in the brain.

People who are genetically predisposed toward aggression actually usually behave more violently than the average only when provoked. People not genetically susceptible to violent outbursts seem to be better able to remain calm and “brush it off”. The ones who are predisposed in fact try hard to control their anger, but have inefficient functioning in brain regions that control emotions – in the frontal lobes [2]. Several studies have found that men genetically susceptible to act aggressively are especially likely to engage in violence and other antisocial behavior if they were exposed to childhood abuse [3]. Again, we see that although genes may carry certain predispositions, there are essential environmental aspects that determine the final outcome.

Early physical aggression needs to be dealt with care. Long-term studies of physical aggression clearly indicate that most children, adolescent and even adults eventually learn to use alternatives to physical aggression [4]. Still, the importance of proper guidance and favorable environment cannot be understated. As mentioned before, Homo sapiens have been found to cause 2 percent of deaths among their fellows. However, this has fluctuated substantially throughout the history and in different cultures. During the medieval period, human-on-human violence was responsible for stunning 12 percent of recorded deaths. For the last century, people have been relatively peaceable compared to the Middle Ages, violence being the cause of death in just 1.33 percent of fatalities worldwide. In the least violent parts of the world today, the homicide rates are as low as 0.01 percent [1].

Our brains have evolved to monitor for danger and spark aggression in response to any perceived hazard as a defense mechanism. Aggression is part of the normal behavioral repertoire of most, if not all, species; however, when expressed in humans in the wrong context, aggression leads to social maladjustment and crime [5]. By identifying genes and brain mechanisms that predispose people to the risk of being violent – even if the risk is small – we may eventually be able to tailor prevention programs to those who need them most.


[1] Gómez, J. M., Verdú, M., González-Megías, A., Méndez, M. (2016). The phylogenetic roots of human lethal violence. Nature 538(7624), 233–237.

[2] Denson, T. F., Dobson-Stone, C., Ronay, R., von Hippel, W., Schira, M. M. (2014). A functional polymorphism of the MAOA gene is associated with neural responses to induced anger control. J Cogn Neurosci 26(7), 1418–1427.

[3] Cicchetti, D., Rogosch, F. A., Thibodeau, E. L. (2014). The effects of child maltreatment on early signs of antisocial behavior: Genetic moderation by Tryptophan Hydroxylase, Serotonin Transporter, and Monoamine Oxidase-A-Genes. Dev Psychopathol 24(3), 907–928.

[4] Lacourse, E., Boivin, M., Brendgen, M., Petitclerc, A., Girard, A., Vitaro, F., Paquin, S., Ouellet-Morin, I., Dionne, G., Tremblay, R. E. (2014). A longitudinal twin study of physical aggression during early childhood: Evidence for a developmentally dynamic genome. Psychol Med 44(12):2617–2627.

[5] Asherson, P., Cormand, B. (2016). The genetics of aggression: Where are we now? Am J Med Genet B Neuropsychiatr Genet 171(5), 559–561.

About the author:

Mariliis Vaht, PhD

Research Fellow of Neuropsychopharmacology at Institute of Psychology, University of Tartu, Estonia. Area of research: genetic and environmental factors in longitudinal health study designs.

German study first to show direct medical costs of ADHD and its comorbid conditions across the lifespan

Having ADHD is expensive. A study of German insurance data has shown that the medical costs of a person with ADHD are 1500 euro higher per year, compared to a person without ADHD. But that’s not all; individuals with ADHD are far more likely to suffer from additional conditions such as mood and anxiety problems, substance abuse or obesity. Treatment of these conditions can cost up to an additional 2800 euro per year. As ADHD – especially in adults – is still poorly recognised and diagnosed, these numbers may not reflect the complete picture of ADHD medical costs. Improving diagnosis and adult mental healthcare may prevent mental health problems later in life and actually reduce costs, argue Berit Libutzki and her co-authors.

ADHD (Attention Deficit / Hyperactivity Disorder) is a developmental condition. Symptoms arise before the age of 12 and are characterised by age-inappropriate and impairing behaviour in terms of problems with attention, impulsivity and hyperactivity. World-wide prevalence of children with ADHD is estimated around 5%, while in adults this is around 2.5%. This means that in about half of the children problems do not subside with age. For these people, ADHD is a lifelong condition that often impairs health, career and social life.

To estimate the economical costs of ADHD, Berit Libutzki and her colleagues from HGC Healthcare Consultants GmbH analysed the (anonymised) health insurance data of almost four million Germans. They compared the medical costs of people with an ADHD diagnosis to those of a well-matched group without ADHD.

medical costs per person_figure

The results showed that the medical costs of a person with ADHD are on average 1508 euro higher than those of a person without ADHD. These costs are mainly due to treatments in hospitals and by psychiatrists. ADHD medication itself (such as Methylphenidate) are in third place, contributing to only 11% of the additional costs. Other interesting findings from the study are that medical costs are a bit higher in women compared to men, and that costs are much higher in individuals over 30 years old compared to younger age groups. After the age of 18, the costs of for example ADHD medication drop, while psychiatrist costs and costs for other (non-ADHD) medications increase notably. Also sick payment is high in adult ADHD patients, leading to a significant increase in costs. One of the explanations for these cost increases could be a gap in care after leaving the regular care of a paediatrician at age 18, and the development of disorders that arise in addition to ADHD.

medical costs increase_figure

ADHD plus additional (mental) health problems

It has been shown before that having ADHD puts you at a much higher risk of developing additional (comorbid) disorders. Mood disorders – such as depression – and anxiety are most frequent; in the German data two-thirds of ADHD individuals over 30 had such an additional diagnosis (compared to only a fifth of adults without ADHD). Substance abuse and obesity are more common in people with ADHD as well. These comorbidities should not be underestimated as they add strongly to the burden of disease. The study shows that substance abuse and morbid obesity are even the most costly, especially in adulthood. In total, the surplus costs associated with these conditions are 1420-2715 euro higher for ADHD individuals, compared to individuals who suffer from mood or anxiety disorder, substance abuse, or obesity alone.

comorbid disorders_figure

Scientists think that certain genetic factors that play a role in ADHD also make a person more vulnerable for these comorbid health conditions. Libutzki and her team are part of the European research consortium Comorbid Conditions of ADHD (CoCA) that investigates the shared biological mechanisms of ADHD and these additional disorders. “Through this research we hope to find leads to prevent these disorders from developing, and improve mental health care.”, says the leader of the CoCA consortium Prof. Dr. Andreas Reif of the University Hospital Frankfurt.

“It is intriguing to speculate that these comorbidities, which were shown to be the important cost drivers in adulthood, could be prevented if mental healthcare were provided more constantly over the lifespan” write the authors. “The prevention of the development of comorbidities with age should be the focus of mental health care. Early treatment starting in childhood and continued treatment of adolescents into adulthood seem therefore advisable.”

Improving diagnosis and adult mental health care

There is one caveat in the study by Libutzki, that is also acknowledged by the authors: many people, especially adults, are not diagnosed with ADHD, even though they experience the symptoms. “Our knowledge gap is especially large in adulthood”, says Dr. Catharina Hartman from the University Medical Centre Groningen, The Netherlands. “The prevalence of adult ADHD in the health insurance data was very low (0.2 %). Given that the population prevalence for adult ADHD is 2,5 %, this indicates that many adults with ADHD are currently not diagnosed or treated. They may nonetheless make high direct costs since their ADHD may not be recognised, or they make indirect costs through unemployment or criminality.” This would indicate that the costs reported by the study are underestimated. On the other hand, adults often find out about their ADHD only after consulting a psychiatrist for other mental health problems. This would indicate that estimated costs and prevalence of comorbid disorders with ADHD in adulthood are overestimated, compared to when you were to include also all undiagnosed people with ADHD, and diagnosed persons who do not make costs (i.e. milder cases of ADHD).

The study thus provides a partial view on the costs of ADHD during the lifespan. That said, it is among the first to show in detail the lifespan medical costs of ADHD and comorbid disorders in Germany. These findings are likely to be representative of other western-European countries. Policy makers in these countries are strongly advised to investigate ways to improve the transition from child to adult mental healthcare and increase awareness about adult ADHD. This will not only improve the quality of life of many adults but may also save money.

Further reading

Libutzki, Ludwig, May, Jacobsen, Reif and Hartman (2019). Direct medical costs of ADHD and its comorbid conditions on basis of claims data analysis.  European Psychiatry, 58: 38-44.

The findings from this study are also summarised in an infographic: