April 7, 2021
There is a growing interest (and controversy) in 'adult-onset ADHD. No current diagnostic system allows for the diagnosis of ADHD in adulthood, yet clinicians sometimes face adults who meet all criteria for ADHD, except for age at onset. Although many of these clinically referred adult-onset cases may reflect poor recall, several recent longitudinal population studies have claimed to detect cases of adult-onset ADHD that showed no signs of ADHD as a youth (Agnew-Blais, Polanczyk et al. 2016, Caye, Rocha, et al. 2016). They conclude, not only that ADHD can onset in adulthood, but that childhood-onset and adult-onset ADHD may be distinct syndromes(Moffitt, Houts, et al. 2015)
In each study, the prevalence of adult-onset ADHD was much larger than the prevalence of childhood-onset adult ADHD). These estimates should be viewed with caution. The adults in two of the studies were 18-19 years old. That is too small a slice of adulthood to draw firm conclusions. As discussed elsewhere (Faraone and Biederman 2016), the claims for adult-onset ADHD are all based on population as opposed to clinical studies.
Population studies are plagued by the "false positive paradox", which states that, even when false positive rates are low, many or even most diagnoses in a population study can be false.
Another problem is that the false positive rate is sensitive to the method of diagnosis. The child diagnoses in the studies claiming the existence of adult-onset ADHDused 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 raises concerns about measurement error. Another longitudinal study found that current symptoms of ADHD were under-reported by adults who had had ADHD in childhood and over-reported by adults who did not have ADHD in childhood(Sibley, Pelham, et al. 2012). These issues strongly suggest that the studies claiming the existence of adult-onset ADHD underestimated the prevalence of persistent ADHD and overestimated the prevalence of adult-onset ADHD. Thus, we cannot yet accept the conclusion that most adults referred to clinicians with ADHD symptoms will not have a history of ADHD in youth.
The new papers conclude that child and adult ADHD are "distinct syndromes", "that adult ADHD is more complex than a straightforward continuation of the childhood disorder" and that adult ADHD is "not a neurodevelopmental disorder". These conclusions are provocative, suggesting a paradigm shift in how we view adulthood and childhood ADHD. Yet they seem premature. In these studies, people were categorized as adult-onset ADHD if full-threshold add had not been diagnosed in childhood. Yet, in all of these population studies, there was substantial evidence that the adult-onset cases were not neurotypical in adulthood (Faraone and Biederman 2016). Notably, in a study of referred cases, one-third of late adolescent and adult-onset cases had childhood histories of ODD, CD, and school failure(Chandra, Biederman, et al. 2016). Thus, many of the "adult onsets" of ADHD appear to have had neurodevelopmental roots.
Looking through a more parsimonious lens, Faraone and Biederman(2016)proposed that the putative cases of adult-onset ADHD reflect the existence of subthreshold childhood ADHD that emerges with full threshold diagnostic criteria in adulthood. Other work shows that subthreshold ADHD in childhood predicts onsets of full-threshold ADHD in adolescence(Lecendreux, Konofal, et al. 2015). Why is onset delayed in subthreshold cases? One possibility is that intellectual and social supports help subthreshold ADHD youth compensate in early life, with decompensation occurring when supports are removed in adulthood or the challenges of life increase. A related possibility is that the subthreshold cases are at the lower end of a dimensional liability spectrum that indexes risk for onset of ADHD symptoms and impairments. This is consistent with the idea that ADHD is an extreme form of a dimensional trait, which is supported by twin and molecular genetic studies(Larsson, Anckarsater, et al. 2012, Lee, Ripke, et al. 2013). These data suggest that disorders emerge when risk factors accumulate over time to exceed a threshold. Those with lower levels of risk at birth will take longer to accumulate sufficient risk factors and longer to onset.
In conclusion, it is premature to accept the idea that there exists an adult-onset form of ADHD that does not have its roots in neurodevelopment and is not expressed in childhood. It is, however, the right time to carefully study apparent cases of adult-onset ADHD to test the idea that they are late manifestations of a subthreshold childhood condition.
Agnew-Blais, J. C., G.V. Polanczyk, A. Danese, J. Wertz, T. E. Moffitt and L. Arseneault (2016)."Persistence, Remission and Emergence of ADHD in Young Adulthood:Resultsfrom a Longitudinal, Prospective Population-Based Cohort." JAMA.Caye, A., T. B.-M. Rocha, L. Luciana Anselmi, J. Murray, A. M.B. Menezes, F. C. Barros, H. Gonçalves, F. Wehrmeister, C. M. Jensen, H.-C.Steinhausen, J. M. Swanson, C. Kieling and L. A. Rohde (2016). "ADHD doesnot always begin in childhood: E 1 vidence from a large birth cohort." JAMA.
Chandra, S., J. Biederman and S. V. Faraone (2016)."Assessing the Validity of the Ageat Onset Criterion for Diagnosing ADHD in DSM-5." J Atten Disord.
Faraone, S. V. and J. Biederman (2016). "CanAttention-Deficit/Hyperactivity Disorder Onset Occur in Adulthood?" JAMAPsychiatry.
Larsson, H., H. Anckarsater, M. Rastam, Z. Chang and P.Lichtenstein (2012). "Childhood attention-deficit hyperactivity disorderas an extreme of a continuous trait: a quantitative genetic study of 8,500 twinpairs." J Child Psychol Psychiatry53(1): 73-80.
Lecendreux, M., E. Konofal, S. Cortese and S. V. Faraone(2015). "A 4-year follow-up of attention-deficit/hyperactivity disorder ina population sample." J Clin Psychiatry76(6): 712-719.
Lee, S. H., S. Ripke, B. M. Neale, S. V. Faraone, S. M.Purcell, R. H. Perlis, B. J. Mowry, A. Thapar, M. E. Goddard, J. S. Witte, D.Absher, I. Agartz, H. Akil, F. Amin, O. A. Andreassen, A. Anjorin, R. Anney, V.Anttila, D. E. Arking, P. Asherson, M. H. Azevedo, L. Backlund, J. A. Badner,A. J. Bailey, T. Banaschewski, J. D. Barchas, M. R. Barnes, T. B. Barrett, N.Bass, A. Battaglia, M. Bauer, M. Bayes, F. Bellivier, S. E. Bergen, W.Berrettini, C. Betancur, T. Bettecken, J. Biederman, E. B. Binder, D. W. Black,D. H. Blackwood, C. S. Bloss, M. Boehnke, D. I. Boomsma, G. Breen, R. Breuer,R. Bruggeman, P. Cormican, N. G. Buccola, J. K. Buitelaar, W. E. Bunney, J. D.Buxbaum, W. F. Byerley, E. M. Byrne, S. Caesar, W. Cahn, R. M. Cantor, M.Casas, A. Chakravarti, K. Chambert, K. Choudhury, S. Cichon, C. R. Cloninger,D. A. Collier, E. H. Cook, H. Coon, B. Cormand, A. Corvin, W. H. Coryell, D. W.Craig, I. W. Craig, J. Crosbie, M. L. Cuccaro, D. Curtis, D. Czamara, S. Datta,G. Dawson, R. Day, E. J. De Geus, F. Degenhardt, S. Djurovic, G. J. Donohoe, A.E. Doyle, J. Duan, F. Dudbridge, E. Duketis, R. P. Ebstein, H. J. Edenberg, J.Elia, S. Ennis, B. Etain, A. Fanous, A. E. Farmer, I. N. Ferrier, M.Flickinger, E. Fombonne, T. Foroud, J. Frank, B. Franke, C. Fraser, R.Freedman, N. B. Freimer, C. M. Freitag, M. Friedl, L. Frisen, L. Gallagher, P.V. Gejman, L. Georgieva, E. S. Gershon, D. H. Geschwind, I. Giegling, M. Gill,S. D. Gordon, K. Gordon-Smith, E. K. Green, T. A. Greenwood, D. E. Grice, M.Gross, D. Grozeva, W. Guan, H. Gurling, L. De Haan, J. L. Haines, H. Hakonarson,J. Hallmayer, S. P. Hamilton, M. L. Hamshere, T. F. Hansen, A. M. Hartmann, M.Hautzinger, A. C. Heath, A. K. Henders, S. Herms, I. B. Hickie, M. Hipolito, S.Hoefels, P. A. Holmans, F. Holsboer, W. J. Hoogendijk, J. J. Hottenga, C. M.Hultman, V. Hus, A. Ingason, M. Ising, S. Jamain, E. G. Jones, I. Jones, L.Jones, J. Y. Tzeng, A. K. Kahler, R. S. Kahn, R. Kandaswamy, M. C. Keller, J.L. Kennedy, E. Kenny, L. Kent, Y. Kim, G. K. Kirov, S. M. Klauck, L. Klei, J.A. Knowles, M. A. Kohli, D. L. Koller, B. Konte, A. Korszun, L. Krabbendam, R.Krasucki, J. Kuntsi, P. Kwan, M. Landen, N. Langstrom, M. Lathrop, J. Lawrence,W. B. Lawson, M. Leboyer, D. H. Ledbetter, P. H. Lee, T. Lencz, K. P. Lesch, D.F. Levinson, C. M. Lewis, J. Li, P. Lichtenstein, J. A. Lieberman, D. Y. Lin,D. H. Linszen, C. Liu, F. W. Lohoff, S. K. Loo, C. Lord, J. K. Lowe, S. Lucae,D. J. MacIntyre, P. A. Madden, E. Maestrini, P. K. Magnusson, P. B. Mahon, W.Maier, A. K. Malhotra, S. M. Mane, C. L. Martin, N. G. Martin, M. Mattheisen,K. Matthews, M. Mattingsdal, S. A. McCarroll, K. A. McGhee, J. J. McGough, P.J. McGrath, P. McGuffin, M. G. McInnis, A. McIntosh, R. McKinney, A. W. McLean,F. J. McMahon, W. M. McMahon, A. McQuillin, H. Medeiros, S. E. Medland, S.Meier, I. Melle, F. Meng, J. Meyer, C. M. Middeldorp, L. Middleton, V.Milanova, A. Miranda, A. P. Monaco, G. W. Montgomery, J. L. Moran, D.Moreno-De-Luca, G. Morken, D. W. Morris, E. M. Morrow, V. Moskvina, P. Muglia,T. W. Muhleisen, W. J. Muir, B. Muller-Myhsok, M. Murtha, R. M. Myers, I.Myin-Germeys, M. C. Neale, S. F. Nelson, C. M. Nievergelt, I. Nikolov, V.Nimgaonkar, W. A. Nolen, M. M. Nothen, J. I. Nurnberger, E. A. Nwulia, D. R.Nyholt, C. O'Dushlaine, R. D. Oades, A. Olincy, G. Oliveira, L. Olsen, R. A.Ophoff, U. Osby, M. J. Owen, A. Palotie, J. R. Parr, A. D. Paterson, C. N.Pato, M. T. Pato, B. W. Penninx, M. L. Pergadia, M. A. Pericak-Vance, B. S.Pickard, J. Pimm, J. Piven, D. Posthuma, J. B. Potash, F. Poustka, P. Propping,V. Puri, D. J. Quested, E. M. Quinn, J. A. Ramos-Quiroga, H. B. Rasmussen, S.Raychaudhuri, K. Rehnstrom, A. Reif, M. Ribases, J. P. Rice, M. Rietschel, K.Roeder, H. Roeyers, L. Rossin, A. Rothenberger, G. Rouleau, D. Ruderfer, D.Rujescu, A. R. Sanders, S. J. Sanders, S. L. Santangelo, J. A. Sergeant, R.Schachar, M. Schalling, A. F. Schatzberg, W. A. Scheftner, G. D. Schellenberg,S. W. Scherer, N. J. Schork, T. G. Schulze, J. Schumacher, M. Schwarz, E.Scolnick, L. J. Scott, J. Shi, P. D. Shilling, S. I. Shyn, J. M. Silverman, S.L. Slager, S. L. Smalley, J. H. Smit, E. N. Smith, E. J. Sonuga-Barke, D. StClair, M. State, M. Steffens, H. C. Steinhausen, J. S. Strauss, J. Strohmaier,T. S. Stroup, J. S. Sutcliffe, P. Szatmari, S. Szelinger, S. Thirumalai, R. C.Thompson, A. A. Todorov, F. Tozzi, J. Treutlein, M. Uhr, E. J. van den Oord, G.Van Grootheest, J. Van Os, A. M. Vicente, V. J. Vieland, J. B. Vincent, P. M.Visscher, C. A. Walsh, T. H. Wassink, S. J. Watson, M. M. Weissman, T. Werge,T. F. Wienker, E. M. Wijsman, G. Willemsen, N. Williams, A. J. Willsey, S. H.Witt, W. Xu, A. H. Young, T. W. Yu, S. Zammit, P. P. Zandi, P. Zhang, F. G.Zitman, S. Zollner, B. Devlin, J. R. Kelsoe, P. Sklar, M. J. Daly, M. C.O'Donovan, N. Craddock, P. F. Sullivan, J. W. Smoller, K. S. Kendler and N. R.Wray (2013). "Genetic relationship between five psychiatric disordersestimated from genome-wide SNPs." Nat Genet45(9): 984-994.
Moffitt, T. E., R. Houts, P. Asherson, D. W. Belsky, D. L.Corcoran, M. Hammerle, H. Harrington, S. Hogan, M. H. Meier, G. V. Polanczyk,R. Poulton, S. Ramrakha, K. Sugden, B. Williams, L. A. Rohde and A. Caspi(2015). "Is Adult ADHD a Childhood-Onset Neurodevelopmental Disorder?Evidence From a Four-Decade Longitudinal Cohort Study." Am J Psychiatry:appiajp201514101266.
Sibley, M. H., W. E. Pelham, B.S. Molina, E. M. Gnagy, J. G. Waxmonsky, D. A. Waschbusch, K. J. Derefinko, B.T. Wymbs, A. C. Garefino, D. E. Babinski and A. B. Kuriyan (2012). "Whendiagnosing ADHD in young adults emphasize informant reports, DSM items, and impairment."J Consult Clin Psychol80(6):1052-1061.
Background:
Stimulants, such as methylphenidate and amphetamines, are currently considered effective medications for treating ADHD. However, approximately one-third of patients do not have an adequate response to these treatments. Additionally, long-term adherence is relatively low, with only about half of the patients still using methylphenidate after six years.
Recently, there has been increasing attention to the concept of microdosing with psychedelic drugs such as psilocybin and LSD. A microdose typically ranges from one-tenth to one-twentieth of a recreational dose and does not produce noticeable perceptual effects or interfere with daily activities.
The Study:
A European research team recently published the findings of the first double-blind, placebo-controlled randomized clinical trial examining the safety and efficacy of repeated low doses of LSD in adults diagnosed with ADHD.
The six-week trial took place at University Hospital in Basel, Switzerland, and Maastricht University, Netherlands. Participants, aged 18 to 65, had clinical diagnoses of ADHD with moderate to severe symptoms.
The team excluded persons with a past or present diagnosis of psychotic disorders, substance use disorders, or other psychiatric or somatic disorders likely to require hospitalization or treatments.
Participants were randomly assigned in a 1:1 ratio to receive either LSD or placebo. Neither study staff nor participants were aware of the assignments until the conclusion of the trial.
During the six-week trial, participants received twice-weekly doses on-site, amounting to a total of 12 doses. Following the first and final doses, participants were asked to determine whether they had been administered LSD or a placebo in order to assess blinding. Four weeks after the conclusion of the microdosing period, participants returned for an evaluation of the treatment's safety and efficacy.
Twenty-seven of the 53 participants were randomized to receive the LSD microdosing treatment in a liquid solution, and 26 to receive placebo. Placebo consisted of the same drinking solution, minus the microdose of LSD.
The average age was 37, and 42% of participants were female. Forty-six of the 53 participants completed the study.
Out of 29 participants, 21 from the LSD group and eight from the placebo group correctly guessed their allocation, totaling 63% overall.
As assessed through the Adult ADHD Investigator Symptom Rating Scale, ADHD symptoms improved by 7.1 points in the LSD group and 8.9 points in the placebo group, with no significant difference between them.
Regarding safety, the LSD group experienced nearly double the adverse events compared to the placebo group. None of the events in either group were classified as serious. The five most frequent adverse events were headache, nausea, fatigue, insomnia, and visual alterations, occurring around three times more frequently in the LSD group than in the placebo group.
The team concluded, “although repeated low-dose LSD administration was safe in an outpatient setting, it failed to demonstrate efficacy compared with placebo in improving ADHD symptoms among adults.”
Conclusion: Microdosing with LSD did not offer significant advantages over placebo in treating ADHD symptoms, despite being physically safe and well tolerated in the trial setting. This suggests that further research is needed to explore alternative treatments for ADHD.
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Attention Deficit Hyperactivity Disorder (ADHD) is a common condition affecting children and adolescents worldwide, characterized by symptoms such as hyperactivity, impulsivity, and inattention. While traditional treatments like medication and behavioral therapy are often used, some individuals are turning to complementary and alternative therapies (CAM) for help. One such option gaining attention is acupuncture. But does it really work for ADHD?
A recent comprehensive study aimed to evaluate the effectiveness of acupuncture in treating ADHD symptoms. Here’s a breakdown of the findings, with a focus on the age groups included in the research and what these findings could mean for ADHD treatment options.
The study in question conducted a systematic review and meta-analysis (SR/MA) of acupuncture trials for ADHD, comparing its effects to traditional treatments such as pharmacotherapy and behavioral therapy. The researchers focused on acupuncture’s impact on core ADHD symptoms like hyperactivity, impulsivity, inattention, and conduct problems, while also exploring how acupuncture might help with other issues, such as learning difficulties and psychosomatic symptoms.
One key feature of this study was the inclusion of a broad age range of participants, specifically children and adolescents. These two groups are the most commonly diagnosed with ADHD, and their responses to treatments can vary significantly. Understanding how acupuncture works for these age groups is critical for evaluating its effectiveness as an ADHD treatment.
Here’s what the study found across the different age groups:
Despite these promising results, the study also highlighted several limitations:
In short, and as is so often the way of evidence-based medicine, we still can’t say with absolute certainty one way or the other. These studies may show promise in improving hyperactivity, impulsivity, inattention, and conduct problems– in both children and adolescents. However, the evidence is not yet strong enough to recommend it as a primary treatment. While it may serve as a helpful complement to standard therapies, especially for those struggling with medication side effects or access to behavioral therapy, more research is needed to establish its effectiveness.
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This New York Times article, “5 Takeaways from New Research about ADHD”, earns a poor grade for accuracy. Let’s break down their (often misleading and frequently inaccurate) claims about ADHD.
The Claim: A.D.H.D. is hard to define/ No ADHD Biomarkers exist
The Reality: The claim that ADHD is hard to define “because scientists haven’t found a single biological marker” is misleading at best. While it is true that no biomarker exists, decades of rigorous research using structured clinical interviews and standardized rating scales show that ADHD is reliably diagnosed. Decades of validation research consistently show that ADHD is indeed a biologically-based disorder. One does not need a biomarker to draw that conclusion and recent research about ADHD has not changed that conclusion.
Additionally, research has in fact confirmed that genetics do play a role in the development of ADHD and several genes associated with ADHD have been identified.
The Claim: The efficacy of medication wanes over time
The Reality: The article’s statement that medications like Adderall or Ritalin only provide short-term benefits that fade over time is wrong. It relies almost entirely on one study—the Multimodal Treatment Study of ADHD (MTA). In the MTA study, the relative advantage of medication over behavioral treatments diminished after 36 months. This was largely because many patients who had not initially been given medication stopped taking it and many who had only been treated with behavior therapy suddenly began taking medication. The MTA shows that patients frequently switched treatments. It does not overturn other data documenting that these medications are highly effective. Moreover, many longitudinal studies clearly demonstrate sustained benefits of ADHD medications in reducing core symptoms, psychiatric comorbidity, substance abuse, and serious negative outcomes, including accidents, and school dropout rates. A study of nearly 150,000 people with ADHD in Sweden concluded “Among individuals diagnosed with ADHD, medication initiation was associated with significantly lower all-cause mortality, particularly for death due to unnatural causes”. The NY Times’ claim that medications lose their beneficial effects over time ignores compelling evidence to the contrary.
The Claim: Medications don’t help children with ADHD learn
The Reality: ADHD medications are proven to reliably improve attention, increase time spent on tasks, and reduce disruptive behavior, all critical factors directly linked to better academic performance.The article’s assertion that ADHD medications improve only classroom behavior and do not actually help students learn also oversimplifies and misunderstands the research evidence. While medication alone might not boost IQ or cognitive ability in a direct sense, extensive research confirms significant objective improvements in academic productivity and educational success—contrary to the claim made in the article that the medication’s effect is merely emotional or perceptual, rather than genuinely educational.
For example, a study of students with ADHD who were using medication intermittingly concluded “Individuals with ADHD had higher scores on the higher education entrance tests during periods they were taking ADHD medication vs non-medicated periods. These findings suggest that ADHD medications may help ameliorate educationally relevant outcomes in individuals with ADHD.”
The Claim: Changing a child’s environment can change his or her symptoms.
The Reality: The Times article asserts that ADHD symptoms are influenced by environmental fluctuations and thus might not have their roots in neurobiology. We have known for many years that the symptoms of ADHD fluctuate with environmental demands. The interpretation of this given by the NY Times is misleading because it confuses symptom variability with underlying causes. Many disorders with well-established biological origins are sensitive to environmental factors, yet their biology remains undisputed.
For example, hypertension is unquestionably a biologically based condition involving genetic and physiological factors. However, it is also well-known that environmental stressors, dietary
habits, and lifestyle factors can significantly worsen or improve hypertension. Similarly, asthma is biologically rooted in inflammation and airway hyper-reactivity, but environmental triggers such as allergens, pollution, or even emotional stress clearly impact symptom severity. Just as these environmental influences on hypertension or asthma do not negate their biological basis, the responsiveness of ADHD symptoms to environmental fluctuations (e.g., improvements in classroom structure, supportive home life) does not imply that ADHD lacks neurobiological roots. Rather, it underscores that ADHD, like many medical conditions, emerges from the interplay between underlying biological vulnerabilities and environmental influences.
Claim: There is no clear dividing line between those who have A.D.H.D. and those who don’t.
The Reality: This is absolutely and resoundingly false. The article’s suggestion that ADHD diagnosis is arbitrary because ADHD symptoms exist on a continuum rather than as a clear-cut, binary condition is misleading. Although it is true that ADHD symptoms—like inattention, hyperactivity, and impulsivity—do vary continuously across the population, the existence of this continuum does not make the diagnosis arbitrary or invalidate the disorder’s biological basis. Many well-established medical conditions show the same pattern. For instance, hypertension (high blood pressure) and hypercholesterolemia (high cholesterol) both involve measures that are continuously distributed. Blood pressure and cholesterol levels exist along a continuum, yet clear diagnostic thresholds have been carefully established through decades of clinical research. Their continuous distribution does not lead clinicians to question whether these conditions have biological origins or whether diagnosing an individual with hypertension or hypercholesterolemia is arbitrary. Rather, it underscores that clinical decisions and diagnostic thresholds are established using evidence about what levels lead to meaningful impairment or increased risk of negative health outcomes. Similarly, the diagnosis of ADHD has been meticulously defined and refined over many decades using extensive empirical research, structured clinical interviews, and validated rating scales. The diagnostic criteria developed by experts carefully delineate the point at which symptoms become severe enough to cause significant impairment in an individual’s daily functioning. Far from being arbitrary, these thresholds reflect robust scientific evidence that individuals meeting these criteria face increased risks for the serious impairments in life including accidents, suicide and premature death.
The existence of milder forms of ADHD does not undermine the validity of the diagnosis; rather, it emphasizes the clinical reality that people experience varying degrees of symptom severity.
Moreover, acknowledging variability in severity has always been a core principle in medicine. Clinicians routinely adjust treatments to meet individual patient needs. Not everyone diagnosed with hypertension receives identical medication regimens, nor does everyone with elevated cholesterol get prescribed the same intervention. Similarly, people with ADHD receive personalized treatment plans tailored to the severity of their symptoms, their specific impairments, and their individual circumstances. This personalization is not evidence of arbitrariness; it is precisely how evidence-based medicine is practiced. In sum, the continuous nature of ADHD symptoms is fully compatible with a biologically-based diagnosis that has substantial evidence for validity, and acknowledging symptom variability does not render diagnosis arbitrary or diminish its clinical importance.
In sum, readers seeking a balanced, evidence-based understanding of ADHD deserve clearer, more careful reporting. By overstating diagnostic uncertainty, selectively interpreting research about medication efficacy, and inaccurately portraying the educational benefits of medication, this article presents an overly simplistic, misleading picture of ADHD.
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