Last month’s special article focused on childhood ADD. We come now to adult ADD.
It is worth noting that the concept hardly existed before Eli Lilly marketed the drug Strattera (atomoxetine) for it about a decade ago. Before then, the general consensus of researchers was that ADD did not persist into adulthood in the vast majority of persons. 9 prospective studies were conducted before Strattera came to the US market in 2003; in a total of 718 persons followed for 13-25 years from childhood into adulthood, from a mean of age 10 to age 25, the prevalence of ADD fell by 90%. In other words, only 10% of children with ADD continued to have it in their mid 20s. This observation contrasts with the common opinion these days that the majority of children with ADD will continue to have it as adults. Post-strattera research, often funded by pharmaceutical companies marketing adult ADD, report higher rates of persistence into adulthood, but even then, the full ADD syndrome is reported to be present in only about 40% of children followed to age 18-20. In other words, the majority still lose the diagnosis by early adulthood. Now the claim is made that despite syndromic remission, ADD symptoms still persist and cause functional impairment. But, even if so, it is worth noting that all studies show that the majority of children with ADD have syndromal remission by about age 18: they no longer meet ADD criteria.
Again, the question of treatment comes up. In general, in these studies, some children are treated and some are not, and the studies do not assess outcomes based on treatment in any systematic fashion, nor are they randomized. Thus they cannot answer this question, but since a good number of the study subjects are untreated, it cannot be assumed that the results are the effect of treatment. Natural history still remains an important possible interpretation of the results.
The most cited recent data represent the National Comorbidity Survey (NCS) epidemiological study in the US, which found that about 3% of adults are diagnosable with ADD, which means that they meet criteria as adults in a current cross-sectional assessment as part of the NCS study, and that they retrospectively met those criteria as children.
The classic article of the month in this issue examines an analysis from that study in detail. The key aspect discussed there is the finding that 45% of those who met adult ADD criteria also met bipolar disorder criteria and 39% of those who met adult ADD criteria also met major depressive disorder (MDD) criteria. In other words, 84% of those who can be diagnosed with current adult ADD are also diagnosable with current bipolar disorder or MDD. Here is the question: What causes what? Are they just unlucky, and every time they have one disease they have two diseases? Or does the ADD cause depression, as many ADD experts assume? Does ADD also cause recurrent manic episodes? This would seem biologically implausible.
At least in the case of bipolar illness, the proponents of the adult ADD diagnosis haven’t explained why almost half those patients also have manic episodes. They haven’t explained why we should believe they have two diseases, when one disease could explain all the symptoms, since a cardinal feature of mania is distractibility. Why should pneumonia always happen with “fever disorder”?
One of the most interesting studies that can add to this literature was a recent publication that represents the longest prospective outcome of ADD: a 33 year outcome study following children diagnosed with ADD at age 8, and compared with matched controls who did not have ADD. They were all followed to age 41. Here is an interesting observation: ADD was diagnosable in the control group in 5% as adults. These were children who were NOT assessed to have ADD as children, but simply chosen at random from matched controls, and then they met the criteria 30 years later. How is this possible? This is not adult ADD, because the diagnosis is supposed to reflect persistence of childhood ADD, but this group did not have childhood ADD, and yet it is almost twice as large as the prevalence claimed in the NCS study for adults who had persistence of childhood ADD.
Here is one potential explanation: the 5% who did not have ADD in childhood but met adult criteria are simply adults who have statistically abnormal attention spans. They don't have a disease, and they don't have a developmental delay of the maturing brain; they are just at an extreme of the normal curve for the cognitive trait for attention. Recall that most psychological and biological traits are distributed on a normal curve in the general population, as shown in the figure. Most of us are at or near the 50th percentile. At 2 standard deviations from the middle of the curve, on each end, there is about 2% of the population. This is not disease, and it is not “disorder”. Some people are short, some are tall; some are skinny, some are not; some are shy, some are extroverted; some are hyper focused in attention, some are distractible. 4-5% in fact.
Fig 1. Sufficiently large samples of parameters with well-defined expected values and variance, including at psychometrics, tend to the Gaussian distribution, also known as bell curve. Central limit theorem. Horizontal axis, standard deviation.
So what is “adult ADD”? Could it just be the extreme of the psychological trait of attention, which is not a bad thing.
If we think about attention as a cognitive trait with a normal curve, you might ask the question: Are we humans supposed to be highly attentive? Nature seems to have evolved in such a way that many of the “symptoms” which we treat are in fact quite normal when present to a mild to moderate degree. It’s normal to be somewhat anxious. It’s normal at times to be sad. It’s normal even to be somewhat illogical in our thought processes. These are all proven to be common traits in the normal population. All are distributed as in an inverted U-shaped curve. What about attention? Is it normal to be a little inattentive?
Of course it is. What would life be like if you focused on every little thing that crossed your mind? You would have this idea, then that, then another; you would focus on one, then the other, then the next. It is normal to filter sensations and thoughts, and focus on some but not others. Inattention is normal. When we have no filter, and attend too much to all our thoughts and feelings, we are psychotic. That is the nature of the thought disorder of schizophrenia. It is not an accident that amphetamines are used as an animal model of psychosis. Too much attention is psychotic. That’s why we are selected to be normally inattentive. And some people are more inattentive than others. That is expected for any normal psychological trait. It’s not a disease; it’s an extreme of a natural trait.
One might say that even if this is the case, inattention should be treated if it is causing functional impairment. This may be defensible, or perhaps not. We treat the extreme of the normal trait of blood pressure, but not because it causes functional impairment. In fact, it is famous for having no symptoms at all, for being “silent”. We treat high blood pressure because it later causes certain diseases, like coronary artery disease or stroke. What future diseases does inattention cause? None that we know of.
Fig 2. Adults with attention-deficit hyperactivity disorder - diagnosis or normality? Shah, Premal; Morton, Michael. British Journal of Psychiatry. 203(5):317-319, November 2013. Adapted from Shah and Morton.
Still, one might argue for treatment for current functional impairment. But as discussed the last PL issue's Classic Study of the Month (the MTA study), even if this is the case, non-medication treatments are as effective as medication treatments for functional improvement of ADD.
A final comment: In the 33 year prospective study, 78% of subjects with childhood ADD were no longer diagnosable with it as adults. Again, the older literature seems closer to the truth that the majority of children with ADD (about 80% in this study) will not have it as adults. Clinicians need not feel impelled, as is the case these days, to continue amphetamine medications long-term for decades and decades, on the assumption that once the ADD diagnosis is made, then long-term treatment is entailed.
A final important clinical consideration in analyzing apparent adult ADD is the concept of mood temperaments.
This concept is highly under appreciated in contemporary psychiatry. The terms dysthymia and cyclothymia are in DSM, and are thus known, but they are misused or not used at all. Most commonly, dysthymia is used as a “comorbidity” along with MDD or other conditions. In contrast, cyclothymia is not used as a comorbidity, but is thought to be exclusive of the diagnoses of MDD or bipolar illness.
The mood temperament of “hyperthymia”, or mild constant manic symptoms, is not known by most clinicians, mainly because it is not included in DSM. All three terms, described in more detail here, were originally developed about 100 years ago by Kahlbaum and Kraepelin, and later expanded by Ernst Kretschmer, to reflect biological and genetic variants of the diseases of severe depression or manic-depression. They were present as mild forms of those diseases in relatives of persons who had the full disease. In many persons with the full disease states, those mood temperaments also were present in between the clinical episodes of depression or mania. In other words, they are not comorbidities because mood temperaments are not diseases in themselves; they are personality traits in persons, or their relatives, who have mood diseases.
If you are depressed all the time mildly, or manic all the time mildly, or back and forth between mild depression and mild mania all the time, you will not have good concentration. This is because concentration is impaired in both manic and depressive states.
Hence it is commonly the case that adult ADD is mistakenly diagnosed in persons with hyperthymic personality, or cyclothymic personality, or dysthymia. The affective symptoms are chronic, and hence the attentional impairment is constant. But the causal source may be the affective temperament, not a separate disease of adult ADD. The PL experience is that these patients improve in their affective symptoms, including inattention, with low-dose mood stabilizers whereas amphetamines either provide only partial or inconsistent benefit.