The popularization of the term “adult ADHD” belies the conclusions of the medical research reviewed below. If this research had been as well publicized, we may not be having the present conversation. Here, I swim against the tsunami of “ADHD” hegemony. Valid diagnoses get lost when the concepts of diagnostic hierarchy and diagnostic validators are not used: most frequently mood disorders (mixed depression or mania, mood temperaments of cyclothymia or hyperthymia, or mild manic symptoms) which are frequently mistaken as “ADHD.” As you will see below the DSM’s method of defining comorbidity is diagnostically confusing and unnecessary, and it detracts from a proper diagnosis and treatment. 

To review from 5.0, ‘attention deficit’, i.e., inattention, is shown in studies to be a temporary delay in cortical maturation which usually normalizes in early adolescence. Attention is a normal cognitive trait that can be represented on a bell-shaped curve. Low attention itself is not a disease nor is high attention. Similar to height, weight, blood pressure, or blood sugar, it is only the extremes that are problematic and may be called diseases, i.e., dwarfism and gigantism, hypertension or diabetes.  A moderate amount of inattention is normal for most people. 

Extremes of high attention are characteristic of OCD and psychosis, i.e., some people can’t restrain their attention and are overly focused on details, sounds, or visual phenomenon. 

Some causes of inattention in adults are normal traits or are caused by depression, mild mania, mixed states, mood temperaments of hyperthymia, and cyclothymia, anxiety conditions, and the normal personality trait of anxiousness, dementias/delirium, psychotic states, and substance abuse.

These diagnostic considerations should be subjected to a Diagnostic Hierarchy elaborated in 5.0 (Part I) i.e., a poly symptomatic diagnosis has more explanatory value than a lower tier diagnosis and should be treated first. This would be a medical model as what is followed in other medical specialties. Adult ADD should be a diagnosis of exclusion. Genetic and epidemiologic studies of adult ADD over the past 20 years do not use this ‘rule out’ approach in the findings, and therefore conclusions are essentially contaminated by other conditions mentioned above. Unfortunately, “adult ADD” has been unduly popularized in our society. 

Differential Diagnosis of Inattention

(Advanced Diagnosis Course 2021 – psychiatryletter.net)

•   Inattention as a normal trait on a bell-shaped curve
•   Caused by another disease or metabolic condition
•   Mood Illness: Depression, (hypo)Mania or mixed states or Mood temperaments between episodes.
•   Anxiety 
•   Psychosis 
•   Dementia/cognitive
• Substance abuse 
• “ADD” as a diagnosis:  only after all of the above has been ruled out first
• Most Epidemiological/Genetic studies do not take a ‘rule out’  approach and use the non-medical model DSM type of “comorbidity” (counting symptoms) not used in other specialties. 

The Rise of “adult ADD”

Prior to the 2003 approval of Strattera (also known as atomoxetine, a non-stimulant intended to address a supposed need in the adult population), the general consensus of researchers was that ADD did not persist into adulthood in the vast majority of patients. 

According to nine prospective studies conducted prior to 2003, for a total of 718 patients followed for 13-25 years from childhood into adulthood from a mean age of 10-25 years old, the prevalence of ADD fell by 90%. 

“Post Strattera research, mostly by pharmaceutical companies marketing stimulants, reported higher rates of persistence into early adulthood, but even then, the full ADD syndrome is reported to be present in only about 40% of children followed to age 18-20. The claim was that some ADD symptoms persisted into 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 showing that the majority of children with ADD have syndromal remission by age 18: they no longer meet ADD criteria.” (from Clinical Psychopharmacology 2019).

Strattera was first studied as an antidepressant, but the pharmaceutical company changed their intent to request approval as an “ADHD” med to capitalize on the anticipated market for adults in 2003. 

Virtually none of the post-2003 studies rule out hyperthymic or cyclothymic mood temperaments or hypomanic, mixed or (hypo) manic symptoms nor do they address the normal distribution of attention/inattention as a normative trait on a bell-shaped curve in the general population all of which can be mistaken as “ADHD.” 

The normative rate for low attention in the adult population is 3-4% which is also claimed to be the same rate of adult prevalence for “ADHD.” (see Adults with attention-deficit hyperactivity disorder – diagnosis or normality? Shah, Premal; Morton, MichaelBritish Journal of Psychiatry. 203(5):317-319, November 2013)

“In sum…we would argue caution in the diagnosis and treatment of adult ADHD, always giving preference to initially diagnosing and treating mood disorders until euthymia is achieved before making the ADHD diagnosis or seeking to treat it with stimulants. Most experts would agree (given the abuse potential of stimulants) that prescribing such agents for cognitive symptoms of distractibility without first trying to treat concurrent mood or anxiety conditions is not scientifically or clinically well informed. ” (bold added – Manic Depressive Illness – Bipolar Disorders and Recurrent Depression, Frederic K. Goodwin and Kay Jamison 2007, p. 107)

CDC data indicate there is a variation in ADD diagnosis of up to 10% between regions in the US with the Southeastern states having as high as a 15.9% diagnosis rate and Western states as low as a 5.6% rate. Most researchers promote ADD as a genetic disease but do not provide an explanation for this state-by-state disparity in the rates. CDC data also indicates that heart disease has a greater incidence in the Southeast region of the U.S. and cardiologists focus on the higher rates of poverty and poor diet but psychiatric researchers do not consider these socioeconomic factors in their studies. 

http://www.cdc.gov/ncbddd/adhd/data.html

In any clinical assessment, the diagnostic validator of family history plays a major role in diagnosis. The family history includes, parents, grandparents, great-grandparents, siblings, second-degree relatives, and children.  This evaluation is essential and should not be skipped, especially as related to a hypothetical patient requesting to be evaluated for adult ADD.  For example, if a patient 21-years or older wants to be evaluated for ADD and relates that a parent or other first-degree relative has been diagnosed with a bipolar disorder, the ADD evaluation should stop, since the heritability for Bipolar Illness is 85% (like eye color or height).  Then, an evaluation of a mood disorder, mixed, mild manic, cyclothymic or hyperthymic should take place.  It is up to practitioners to then explain to the patient that the two conditions are not comorbid. Even experts who follow the unscientific DSM definition of comorbidity based on counting symptoms for a threshold diagnosis, recommended that the mood disorder be treated first and as fully as possible before addressing supposed adult ADHD. 

The differential diagnostic considerations then becomes:

(Clinical Psychopharmacology 2019)

• A history of mild manic or full manic episodes.
• A history of mixed mood episodes of mild mania and depression which can be assessed by the validated KMDRS (Koukopoulos Mixed Depression Rating Scale).
• A hyperthymic or cyclothymic mood temperament which can be assessed by the TEMPS-A questionnaire.

• Inattention as a normative trait on a bell-shaped curve. 

• In adults, increased activity and inattention is likely a mood disorder until proven otherwise. 

It is common for patients to report, “I took Adderall (or any other prescription stimulant) and it helped my concentration/attention/ productivity.” This is a flawed diagnostic criterion, as a stimulant medication will have a similar effect on any human being, and thus cannot be used as a “diagnostic” test or justification for its use. Similarly, any human will feel more relaxed with a benzodiazepine (i.e., Xanax) but that does not prove he has an anxiety disorder.  In other words, that a stimulant increases someone’s focus is not evidence of ADD. Stimulants can  increase focus in a normal person. The effects of a medication on a person should not replace the more important diagnostic validators of age of onset, course, and family history.

There is a disconnect between the research reviewed above and what gets into doctors’ residency programs, CME (ongoing training), and board exams. The DSM definition of “ADHD” is one of the sacred cows of psychiatry and to question this prevailing notion is considered heretical by many in the profession. It would take a sociologist or medical historian to delve into all the reasons why this diagnosis has become so popularized in the general public. I do not have the time or energy to do that, and I don’t want to speculate here.  

The research presented in 5.0 and 5.1, hiding in plain sight, calls into question many of the basic assumptions of “ADHD” presumed to be true by doctors and the public. Patients suffer the consequence of not getting the proper treatment, i.e., mood stabilizers or dopamine blockers, when mood disorders, first in the diagnostic hierarchy (see 5.0), are not addressed.  Stimulants frequently make mood disorders worse. (see Clinical Psychopharmacology 2019).  ADD, lower in the diagnostic hierarchy below mood disorders, psychotic conditions, and anxiety disorders (OCD, PTSD) should not be considered comorbid in a medical model, and as a consequence, they should not be treated simultaneously.

The DSM’s threshold method for comorbidity is not used in general medicine. According to the DSM definition, counting symptoms to a numerical threshold allows for multiple diagnoses. It’s the equivalent of defining cough, chest congestion, sputum production, chest discomfort, and fatigue as separate diagnoses when only one diagnosis is necessary: pneumonia.  When the pneumonia is treated with the correct antibiotic, all the other symptoms go away.

The classic comorbidity medical model was defined in a 1970 publication by the famous epidemiologist Alvan R. Feinstein, MD.  In Feinstein’s formulation, the implication was that a completely different and independent disease occurred at the same time as another disease. These two diseases co-occurred, more often than not, randomly. Feinstein AR. J Chronic Dis 1970;23:455-68. 

Examples are: Lupus and asthma or type II diabetes and bipolar illness. 

I would advocate the DSM return to the classically defined medical comorbidity as described above.