Rethinking Attention Deficit Hyperactivity Disorder Diagnosis in Adults

Published on July 31, 2016

Recent research suggests a radical new conceptualization of ADHD: Do you have subclinical ADHD and are you receiving appropriate treatment?


ADHD (attention-deficit/hyperactivity disorder) is a condition characterized by problems with attention and/or hyperactivity and impulsivity. ADHD has been conceptualized as a neurodevelopmental disorder by the American Psychiatric Association (APA) in its latest version of the “Diagnostic and Statistical Manual of Mental Disorders”, 5th Edition (DSM-V).  The term neurodevelopmental implies that at some specific time during development something abnormal happened to the nervous system which consequently resulted in the onset of ADHD symptoms.

However, establishing when ADHD symptoms arise is an extremely arduous task because it requires quantitatively assessing for age of onset of ADHD in a large number of individuals across years and even decades of time. Consequently when the APA provided the criteria for diagnosing ADHD, little research had been carried out determining when specifically ADHD first appeared in the life span of the individual. 

There was only the general clinical opinion that ADHD seemed to arise during early childhood. On the basis of this limited and qualitative evidence, APA  required that in order for someone to receive the diagnosis of ADHD, there must be evidence that “Some hyperactive-impulsive or inattentive symptoms that caused impairment were present before age 7 years.”(DSM-IV). More recently the age of onset requirement was altered to “Several inattentive or hyperactive-impulsive symptoms were present prior to age 12 years.” (DSM-V).  

The Discovery

However, in the last couple of years, three recent research studies have challenged, if not refuted, the DSM-V age of onset requirements by finding evidence for much later ages of onset (Moffitt et al., 2015; Agnew-Blais et al., 2016; Caye et al., 2016).  Specifically, the Moffitt study tracked 1037 individuals from birth to age 38; the Agnew-Blais study tracked 2040 twins from early childhood until age 18; and the Caye study investigated 5200 individuals from early childhood until age 18 or 19.  Evidence of adult onset of ADHD, that is the occurrence of ADHD symptoms after the DSM cut-off date of 12 years of age, was found in all three studies. Rates were 2.7% in the Moffitt study; 5.5% in the Agnew-Blais study; and 12.2 % in the Caye study.

As Castellanos (2015) wrote in an editorial about the Moffitt study “The inescapable conclusion is that a substantial number of individuals, in a representative community sample, exhibit impairing symptoms that are consistent with ADHD in all aspects except childhood onset.” And more recently, Faraone and Biederman (2016) say in an editorial on all three studies “For researchers, these new data are a “call to arms” to study adult-onset ADHD, …  The current age-at-onset criterion for ADHD, although based on the best data available, may not be correct. We hope that future research will determine whether and how it should be modified.”

A paradigm shift in the conceptualization of ADHD

These two separate editorial comments by leaders in ADHD research indicate that the seemingly innocuous finding of adult onset ADHD is causing a paradigm shift in the conceptualization of ADHD.  The stimulus for this shift lies in the fact that there is a ready explanation for adult onset ADHD but this explanation involves introducing two factors that up to now have not been considered in the diagnostic process. These two well-known factors are: first, that genetics plays a fundamental role in ADHD, and secondly, that ADHD is not an all-or-none phenomenon but exists on a continuum.

Let us briefly consider these two factors separately. First, there is very good evidence that ADHD is strongly linked to genetic influences (Faraone and Mick, 2010; Brikell, Kuja-Halkola, and Larsson, 2015). This influence is called heritability and refers to the amount of variation in ADHD symptoms due to variations in the genes involved. Surprisingly the heritability for ADHD is the highest observed for any psychiatric disorder and this heritability has been shown to remain constant over the lifespan (Faraone and Mick, 2010). 

Also, it is well known in biology that the phenotype (the adult with all its unique characteristics) is the end result of three developmental forces (Greven et al., 2016):

  1. genes (G)
  2. environment (E)
  3. interaction between these two factors (GxE). 

The phenotype then depends on the relative strength of these three factors. 

As mentioned above, in the case of ADHD, heritability is relatively very strong causing 76% of the variation in the phenotype (Faraone and Mick, 2010). Even so, the ADHD phenotype then depends on the relative strength of the three factors, G, E, and GxE.  So it is possible that if an individual has the gene set for ADHD but is brought up in a very benign environment, the genes are not fully activated and the person does not develop full-blown ADHD.

However, it is likely that he or she might have some sub-clinical (subthreshold) behaviours characteristic of ADHD. However, if this person with subclinical ADHD is exposed to sufficient stressors in adulthood, they this could lead to the development of adult onset ADHD.  Hence interaction effects (GxE) between genetics and environmental conditions can explain variations in age of onset of ADHD.

Evidence for the second factor, that ADHD exists on a continuum, already exists (Greven et al., 2016) and is currently being actively investigated. What the continuum hypothesis means is that ADHD severity can vary continuously from very mild to very severe. One likely explanation for the continuous nature of ADHD symptom variation is that it results from the fact that both genetics and environmental factors influence ADHD.

In other words, it is quite reasonable to posit that the 3 terms, G, E, and GxE, vary in a random way in from individual to individual in a population leading to the well-known statistical normal distribution for the resultant symptoms of ADHD. This new model of ADHD recognizes the role of genetics (G), environment (E), and the possibility of that environmental forces can influence gene activation (GxE).  This new conceptualization can readily, theoretically at least, explain the continuum model of ADHD, the variable age of onset of ADHD diagnosis, and the exacerbations and remissions of ADHD symptoms across the life span which are sometimes observed. 

"Everything you know is wrong"

The Firesign Theatre, 1974 (Quoted by Castellanos, 2015).

Practical significance of the new model of ADHD

There are two important practical conclusions from this new conceptualization of ADHD. Firstly, there is a significant number of adults with ADHD symptoms who have been excluded from receiving professional help because they lacked childhood symptoms. In an interview, Luis Augusto Rohde, one of the principal investigators in the Caye study, said “The main take-home message is that adult patients experiencing significant and lasting symptoms of inattention, hyperactivity or impulsivity that cause impairment should seek evaluation, even if they began recently by their perception, or if family members deny their existence in childhood”. Or as Faraone puts it “If you treat adults, recognize that adult onset of ADHD exists. Patients should not be denied services because DSM-5 requires an earlier onset.” 

The second implication of the new model of ADHD, is that there is a significant number of children who have subclinical ADHD symptoms and who consequently do not receive a formal diagnosis of ADHD but who quite likely could develop clinically significant symptoms in adulthood. Moreover the new way of thinking about ADHD suggests that interventions in childhood subthreshold ADHD likely would prevent, or at least reduce, the severity of symptoms in adulthood. Or in the words of Faraone and Biederman (2016)  “If we are correct, then we will improve public health by developing methods to detect subthreshold child ADHD before it emerges as adolescent- or adult-onset ADHD.” (Faraone and Biederman, 2016).

The full recognition of the hitherto rarely mentioned the role of genetics and the continuum perspective in ADHD has profound implications for how people with ADHD symptoms can be helped by mental health professionals. If fully accepted, the new perspective leads to the conclusion that subclinical cases should not be neglected as they tend to be now by mental health professionals. And this applies to both children and adults. 

It can be argued that intervening in subclinical cases of ADHD should replace the current practice of only providing services to those whose symptoms are suprathreshold using the current cut-off criteria of the DSM-V. This new model of ADHD will lead to improved treatment and outcomes for persons with ADHD, particularly for the many who slip through the current strict diagnostic criteria.  In the end, it will mean that subthreshold individuals will start receiving the treatment they need to lead happier and more productive lives.



Agnew-Blais, J. C., Polanczyk, G. V., Danese, A., Wertz, J., Moffitt, T. E., & Arseneault, L. (2016). Evaluation of the Persistence, Remission, and Emergence of Attention-Deficit/Hyperactivity Disorder in Young Adulthood. JAMA psychiatry.

Brikell I, Kuja-Halkola R, Larsson H. (2015). Heritability of Attention-Deficit Hyperactivity Disorder in Adults. Am J Med Genet Part B 168B:406–413.

Castellanos, F. X. (2015). Is Adult-Onset ADHD a Distinct Entity? American Journal of Psychiatry, 172(10), 929-931.

Caye, A., Rocha, T. B. M., Anselmi, L., Murray, J., Menezes, A. M., Barros, F. C., ... & Swanson, J. M. (2016). Attention-Deficit/Hyperactivity Disorder Trajectories From Childhood to Young Adulthood: Evidence From a Birth Cohort Supporting a Late-onset Syndrome. JAMA psychiatry.

Faraone, S. V., & Biederman, J. (2016). Can Attention-Deficit/Hyperactivity Disorder Onset Occur in Adulthood?. JAMA psychiatry.

Faraone, S. V., & Mick, E. (2010). Molecular genetics of attention deficit hyperactivity disorder. Psychiatric Clinics of North America, 33(1), 159-180.

Greven, C. U., Merwood, A., Meer, J. M., Haworth, C., Rommelse, N., & Buitelaar, J. K. (2015). The opposite end of the attention deficit hyperactivity disorder continuum: genetic and environmental aetiologies of extremely low ADHD traits. Journal of Child Psychology and Psychiatry.

Moffitt, T. E., Houts, R., Asherson, P., Belsky, D. W., Corcoran, D. L., Hammerle, M., . . . Caspi, A. (2015). Is adult ADHD a childhood-onset neurodevelopmental disorder? Evidence from a four-decade longitudinal cohort study. The American Journal of Psychiatry, 172(10), 967-977.

Copyright © 2016,  Brian S. Scott

Category(s):Adult ADHD, Attention Deficit Hyperactivity Disorder (ADHD), Child Development

Written by:

Brian Scott

Dr. Scott is a clinical psychologist based in Singapore with three decades of counseling and psychotherapy experience in helping adults with many kinds of psychological difficulties. These include anxiety, depression, addictions (cybersex, love), and Adult Attention Deficit Hyperactivity Disorder (Adult ADHD).

Brian Scott belongs to Scott Psychological Centre in Singapore

Mental Health News