One of the reasons I am glad that most of my clinical work is in the acute wards is that I don’t have to deal with the current spate of referrals of adults who report ADHD and want treatment for this. I was taught by a very conservative old cuss of a child psychiatrist that if you did not have child ADHD you can’t have adult ADHD. I thus think it is rare.
What I think I’ve missed is that ADHD does not mean what the original authors meant it to mean. It is now a checklist. And that checklist is met by a different bunch of people, many of whom did not have ADHD as a kid.
What I have done here is quote the results from abstracts, with the main diagram, from two studies in the same issue of JAMA psychiatry. I have then looked at the editorial, which tries to make what are clearly two populations one.
Of 2232 participants in the E-Risk Study, 2040 were included in the present analysis. In total, 247 individuals met diagnostic criteria for childhood ADHD; of these, 54 (21.9%) also met diagnostic criteria for the disorder at age 18 years. Persistence was associated with more symptoms (odds ratio [OR], 1.11 [95% CI, 1.04-1.19]) and lower IQ (OR, 0.98 [95% CI, 0.95-1.00]). At age 18 years, individuals with persistent ADHD had more functional impairment (school/work: OR, 3.30 [95% CI, 2.18-5.00], home/with friends: OR, 6.26 [95% CI, 3.07-12.76]), generalized anxiety disorder (OR, 5.19 [95% CI, 2.01-13.38]), conduct disorder (OR, 2.03 [95% CI, 1.03-3.99]), and marijuana dependence (OR, 2.88 [95% CI, 1.07-7.71]) compared with those whose ADHD remitted. Among 166 individuals with adult ADHD, 112 (67.5%) did not meet criteria for ADHD at any assessment in childhood. Results from logistic regressions indicated that individuals with late-onset ADHD showed fewer externalizing problems (OR, 0.93 [95% CI, 0.91-0.96]) and higher IQ (OR, 1.04 [95% CI, 1.02-1.07]) in childhood compared with the persistent group. However, at age 18 years, those with late-onset ADHD demonstrated comparable ADHD symptoms and impairment as well as similarly elevated rates of mental health disorders.
At 11 years of age, childhood ADHD (C-ADHD) was present in 393 individuals (8.9%). At 18 to 19 years of age, 492 individuals (12.2%) fulfilled all DSM-5 criteria for young adult ADHD (YA-ADHD), except age at onset. After comorbidities were excluded, the prevalence of YA-ADHD without comorbidities decreased to 256 individuals (6.3%). Children with C-ADHD had a male preponderance not observed among children without ADHD (251 [63.9%] vs 1930 [47.9%] male, P?< ?.001), whereas the YA-ADHD group had a female preponderance (192 [39.0%] vs 1786 [50.4%] male, P?
Another reason for disagreement is noted in the Brazilian study: the “false-positive paradox.” This maxim states that, even when false-positive rates are low, many, or even most, diagnoses in a population study can be false. For example, if the prevalence of ADHD is 5% and the false-positive rate is 5%, then half the diagnoses in a population study will be false. The false-positive rate is sensitive to the method of diagnosis. The child diagnoses in the studies from Brazil, the United Kingdom, and New Zealand used reports from parents and/or teachers, but the adult diagnoses were based on self-report. Self-reports of ADHD in adults are less reliable than informant reports, which is why the heritability of adult ADHD is low using self-reports but high using informant reports. In fact, the UK study found a very low heritability for adult ADHD (35%), which could be a sign of substantial measurement error and false-positive diagnoses. Of further concern, another longitudinal study6 found that current symptoms of ADHD were underreported by adults who had had ADHD in childhood and overreported by adults who did not have ADHD in childhood. Because these concerns suggest that the UK, Brazilian, and New Zealand studies may have underestimated the persistence of ADHD and overestimated the prevalence of adult-onset ADHD, it would be a mistake for practitioners to assume that most adults referred to them with ADHD symptoms will not have a history of ADHD in youth.
Now, most of the research on ADHD is done on kids. What I’m seeing in the adult literature is that CBT is as effective as medication, and in one trial adding stimulants to CBT made no difference.
Many of the people I do see with “ADHD” have co occuring substance abuse. I am quite cautious about prescribing to such. However, some of my colleagues are more free. My worry is that we may be medicating a population that has something else, and that what works with a severely disabled group of children (for medication should only be used at the severe end) may not work with this new, different, adult population. Because the probably have something else.
The real problem is they smashed ADD and Hyperactivity together and then decided that was how you should treat all of them. It’s muddled the data even worse, grouping what seems to be physiologically different issues together. (Granted, when I was researching it a few years back, after cutting through all of the verbiage, a number of studies suggested that the cause was “home stress” in about 1/2 the cases.)
I’m glad to see, though, that there are some effective treatments that aren’t drug-based.