Joseph Biederman AIA rX8AEq
This blog addresses the relationship between executive function deficits in general and working memory (WM) deficits in particular and attention-deficit/hyperactivity disorder (ADHD). 

Although some neuropsychological models of ADHD have proposed that ADHD arises from deficits in executive functions, accumulating clinical evidence show that it afflicts some but not all individuals with ADHD and suggests that ADHD and executive function deficits represent separate clinical conditions.

Because executive functions refer to a wide and diverse group of high order mental functions, one approach to evaluate this important issue is to focus on one prominent facet of executive functions, mainly working memory. Working memory (WM) refers to a key brain system that provides temporary storage and manipulation of information essential for adequate cognitive functioning.  It focuses attention, inhibits irrelevant stimuli, recognizes priority patterns and hierarchies and selects the goals that are best suited to solving a problem.

Since these cognitive processes are critical for learning, their impairment can lead to deficits in functioning including social and educational dysfunction, low educational achievement and can have a serious impact on educational success. 

To address this issue we examined referred youth with and without ADHD, and with and without WM deficits in functional, social and academic outcomes. We used Resting State FMRI imaging to examine whether the neural circuits subserving WM deficits overlap with those of ADHD.  We investigated this issue in preclinical studies where we examined spatial WM and dopamine receptor activity in rodents.  Our preclinical findings demonstrate that the magnitude of improvement in WM produced by the D4 receptor agonist is significantly greater than that produced by methylphenidate.

CBT treats Executive Dysfunction Free ADHD CME WyUaeE
In human studies, we examined whether the most standard treatment for ADHD has a different effect on measures of WM and ADHD. This body of research provides evidence for a clinical, pharmacological and neurobiological dissociation between ADHD and WM deficits.  Our human treatment study with methylphenidate provided evidence for very different effects for ADHD and WM deficits Our clinical studies show that significantly more youth with ADHD had WM deficits than controls (31.9% vs. 13.7%) and their presence is significantly and specifically associated with academic failure.

In our imaging study, we found that brain activations to a WM test were different in subjects with ADHD with associated WM deficits compared to controls and ADHD subjects without WM deficits.

This body of work indicates that WM deficits afflict a minority of subjects with ADHD and when present they significantly and selectively increase the risk for academic dysfunction in subjects with ADHD, they have separate neural underpinning, and respond differently to treatments for ADHD.

Screening for WM deficits may help identify individuals with ADHD at high risk for academic dysfunction.



P. LEE, N. PINEDA, T. BRUNE, K. PATEL, A. GANNON, T. J. SPENCER, J. BIEDERMAN, P. G. BHIDE, J. ZHU. Hyperactivity and working memory deficits induced by prenatal nicotine exposure are associated with dopamine D1 and D4 receptor dysfunction. Society for Neuroscience Annual Meeting, Washington, DC, November, 2014

Fried R, Chan J, Feinberg L, Pope A, Woodworth KY, Faraone SV, et al. Clinical correlates of working memory deficits in youth with and without ADHD: A controlled study. Journal of clinical and experimental neuropsychology. 2016;38(5):487-96.

Mattfeld AT, Whitfield-Gabrieli S, Biederman J, Spencer T, Brown A, Fried R, et al. Dissociation of working memory impairments and attention-deficit/hyperactivity disorder in the brain. NeuroImage Clinical. 2016;10:274-82.

Biederman J, Chan J, Spencer TJ, Woodworth KY, Kenworthy T, Fried R, Bhide P, Faraone SV. Evidence of a pharmacological dissociation between the robust effects of methylphenidate on ADHD symptoms and weaker effects on working memory. Journal of Brain Sciences. 2015; 1(2): 43-53.




Anthony_L_Rostain_MD_MA_-_ADHD_in_AdultsA Research Review

Psychiatry Research 2016 236:136-141.  DOI: 10.1016/j.psychres.2015.12.017  “Supplementary guanfacine hydrochloride as a treatment of attention deficit hyperactivity disorder in adults: A double blind, placebo-controlled study.” Butterfield ME, Saal J, Young B, Young JI.

Guanfacine hydrochloride is a selective alpha-2A partial agonist that is FDA approved for the treatment of ADHD in children and adolescents (see recent reviews by Faraone et al, 2013; Hirota et al, 2014 and Ruggiero et al 2014).  It can be given alone or in combination with psychostimulant medication as its mechanism of action is complementary to these agents.   Despite growing scientific evidence of its effectiveness for this age group, very little is known about the potential benefits of guanfacine for the treatment of ADHD in adults.

In view of concerns about the importance of finding suitable non-stimulant ADHD medications for this population, the authors carried out a randomized placebo controlled trial of extended release guanfacine (GXR) as supplemental treatment for subjects with a suboptimal response to stimulant-only medication treatment. 

Subjects were recruited from local advertisements and from the clinic practice of the authors in suburban Detroit.  Entry criteria included a current diagnosis of ADHD, current treatment with a stimulant medication, and suboptimal response to this medication as evidenced by a score of > 28 on the Attention Deficit Hyperactivity Disorder Rating Scale (ADHD-RS) or of > 4 on the Clinical Global Impression – Severity (CGI-S) Scale.  Exclusion criteria included having another severe Axis I psychiatric disorder, along with subjects with a history of autism, chemical dependence or psychosis.  Subjects with hypertension or any medical condition that might be exacerbated by the study medication.  A total of 26 subjects in the age range of 19 – 62 years were recruited for the study, of which roughly 50% were women, and 85% were Caucasian.  Subjects were randomly assigned to receive either placebo or incremental doses of GXR ranging from 1 to 6 mg daily on a weekly basis over a 10-week study period. 

The primary outcome measures were the ADHD Rating Scale and the Clinical Global Impression – Severity.  Secondary outcome measures included the Arizona Sexual Experience Questionnaire, the Fatigue Symptom Inventory, the Pittsburgh Sleep Quality Index, the Hamilton Anxiety Inventory and the Hamilton Depression Rating Scale.  Baseline and weekly measures of cardiovascular status were collected throughout the study. 

Contrary to the study authors’ expectations, although subjects in both the placebo and the treatment arms of the study showed significant improvements in both primary and secondary outcome measures, the two groups did not differ from one another.  For instance, the mean ADHD-RS score of the placebo group decreased by 10.92 (from 35.23 to 24.31) and that of the GXR treated group decreased by 11.85 (from 35.92 to 24.08).  The CGI-S score in the placebo group decreased by 1.00 and that of the GXR group by 0.85.  There were no differences between the two groups on measures of tolerability, hemodynamics, sleep, anxiety or depression.  Moreover, no treatment x time x group effects were noted. 

The authors comment that several explanations can account for these findings including a strong placebo effect, a generalized study effect (i.e. participating in a clinical trial itself may be beneficial in and of itself), a “regression to the mean” effect for the placebo group, and a potential bias induced by participating in a clinical trial.   Of note, there were no between group differences seen in fatigue, sleep problems, sexual functioning or in hemodynamic measures – a finding that supports the tolerability and safety of GXR in adult patients. 

While this is a “negative study,” it is helpful in clarifying that GXR can be used safely in combination with stimulant medications, that it does not worsen other psychiatric symptoms (e.g. anxiety, depression) and that it may be a helpful adjunctive treatment for adults with ADHD whose stimulant medication is not sufficiently helpful in reducing their symptoms.  Further research with a larger sample size and with measures taken to minimize the placebo effect are certainly warranted.  In the meantime, clinicians who are considering using GXR can be reassured that it is well tolerated in this population.


Faraone SV, McBurnett K, Sallee FR, Steeber J, López FA (2013). Guanfacine extended release: a novel treatment for attention-deficit/hyperactivity disorder in children and adolescents. Clinical Therapeutics Nov;35(11):1778-93. doi: 10.1016/j.clinthera.2013.09.005

Hirota T, Schwartz S, Correll CU (2014). Alpha-2 Agonists for Attention-Deficit/Hyperactivity Disorder in youth: A Systematic Review and Meta-Analysis of Monotherapy and Add-On Trials to Stimulant Therapy. J. Amer.. Acad. Child Adolesc. Psychiatry 53(2):153–173.

Ruggiero S, Clavenna A, Reale L, Capuano A, Rossi F, Bonati M (2014). Guanfacine for attention deficit and hyperactivity disorder in pediatrics: A systematic review and meta-analysis.  European Neuropsychopharmacology 24: 1578-1590.

David_Goodman_MD_ADHD_in_AdultsAttention Deficit Hyperactivity Disorder is the most common childhood psychiatric disorder and the second most prevalent adult psychiatric disorder second to Major Depression. Yet, until recently, ADHD in adults over age 50 was not identified. As we have come to understand, ADHD symptoms with impairments persist into adulthood for 60% of ADHD children.

For those adults with ADHD, how many will have symptoms that persist for the rest of their lives? How do these symptoms and impairments present? How do we discern ADHD symptoms from other factors contributing to cognitive change with age? How do we obtain clinical history in those patients who can’t remember childhood or adolescent symptoms? Would objective tests differentiate diagnoses? What treatments work well for this age group? What medical considerations are necessary for prescribing ADHD treatments to those with medical illness and multiple medications? What safety parameters need to be considered in this age group when prescribing ADHD medications? What are the drug-drug interactions that may be clinically relevant?

For clinicians and researchers, these questions represent opportunities to expand our fund of knowledge to better serve the needs of ADHD patients in all age categories.

The population of persons older than 65 years of age in the U.S. will grow from 43.1 million to 88.5 million between 2012 and 2050. A recent review of the literature on ADHD in older adults reports a prevalence rate of 2.8% in the Netherlands, 3.5% in Sweden, and 3.5% in Germany. A meta-analysis of ADHD prevalence in studies utilizing different age ranges spanning 18-78 years suggests that prevalence may decline with age. However, given that these studies used DSM-IV criteria with a symptom age threshold of 7 and the absence of a validated ADHD symptom profile for older adults, these cited prevalences may underestimate the ADHD population.

Reliance on childhood ADHD diagnosis to substantiate ADHD in older adults is often not useful because in the National Comorbidity Survey Replication in the U.S., 75% of ADHD adults ages 18-44 had not been diagnosed as children and no ADHD adults ages 60-77 were diagnosed as children. Remember that these people grew up in the 1950s and 1960s when ADHD was rarely identified and then only in the most hyperactive/impulsive and disruptive males.

I believe that ADHD in older adults will become the next clinical frontier. While there is some research beginning to accumulate to support identifying and treating this population, the relative absence of trained ADHD clinicians for this population means many unidentified older adults will be diagnosed inaccurately with age related cognitive disorders. To exemplify this likelihood, a U.S. study canvassing memory clinics demonstrated that only 1 in 5 clinics currently screen for ADHD. Therefore, older adults with ADHD are not identified and offered effective ADHD medication and treatment. The result may be ineffective treatment, unnecessary increased medical costs, and the decline in quality of life.

For those of you reading this blog, I would encourage you to consider ADHD in older adults whose cognitive complaints have been long-standing, whose negative consequences and impairments echo an ADHD life course, and in whom a first degree relative has ADHD.

A Brief Interview with Dr. David Goodman

Joseph Biederman MD ADHD in Adults

Is ADHD Always a Childhood Onset Disorder?

by Joseph Biederman, MD – August 4, 2016

Recent population based studies raise the intriguing question as to whether adult ADHD is always preceded by childhood onset of symptoms or can develop anew in adult life. From Brazil, one group argues that child and adult ADHD are “distinct syndromes”; from the United Kingdom (UK), another group states that adult ADHD is “more complex than a straightforward continuation of the childhood disorder” and from New Zealand (NZ), a third group claimed that adult ADHD is “not a neurodevelopmental disorder”.

In each study, adult onset ADHD refers to cases in which full-threshold ADHD had not been diagnosed by the investigators at prior assessments. In the NZ study, compared with controls, the adult onset ADHD group had more teacher-rated symptoms of ADHD, more conduct disorder (CD) in childhood and were more likely to have had a combined parent/teacher report of ADHD symptom onset prior to age 12. (DSMV recognizes onset of ADHD until the age of 12.) Likewise, the adult onsets in the UK study had high rates of ADHD symptoms, CD and oppositional defiant disorder (ODD) in childhood. Thus, many “adult onsets” of ADHD cases appear to have neurodevelopmental roots.

DSM V Guide to ADHD Diagnosis downloadBecause population studies use non-referred samples, those being diagnosed may not be self-aware of their symptoms, which increases the risk of false negatives. In population studies the ability of the subject to report on his or her own symptoms is critical since it requires insight and self awareness. It has been well documented that youth with ADHD are very poor reporters of their own symptoms. Such difficulties can certainly extend to adult years. Consistent with this idea, 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.4 Thus, the UK, Brazilian and NZ studies may have underestimated the persistence of ADHD and overestimated the prevalence of adult onsets. In contrast, self awareness is not an issue for subjects referring themselves to clinical care since, by definition, it is their self awareness that brings them to the clinic.

These reports do very little to help clarify whether these “adults” do not recall childhood symptoms, are unable to report on them, or are unable to distinguish onset of symptoms form onset of symptoms-associated impairments that may account for the different ages of onset. In these cases, the onset of symptoms and impairment could be separated by many years, particularly among those with strong intellectual abilities and those living in supportive, well-structured childhood environments. Such intellectual and social scaffolding would help ADHD youth to compensate in early life, only to decompensate into a full ADHD syndrome when the scaffolding is removed.

Such an interpretation would suggest that the etiology of ADHD leads to a wide variability in age at onset of initial symptoms, symptoms exceeding diagnostic threshold and impairment arising from those symptoms. Such variability is accepted for many other medical disorders. It is also consistent with the idea that ADHD is the extreme and impairing tail of a continuum. This view of posits that ADHD symptoms and ADHD impairment emerge due to the accumulation of environmental and genetic risk factors. Those with lower levels of risk at birth will take longer to accumulate sufficient risk factors and longer to onset with symptoms and impairment. Yet, because these effects are multifactorial, there is no clean separation of etiologic factors in people above and below a certain age.

In this context it is important to remember that the age of onset of ADHD of 12 years proposed in DSM-V, while an improvement from the previous age of onset of 7 years, is still completely arbitrary, creating the immediate dilemma on how to diagnose patients who have an onset of symptoms after 12 years of age. Such a scenario may suggest that ADHD may be a disorder with a continuum of ages of onset, with some subjects starting their symptoms earlier while others later.

These concerns do not argue against the existence of adult onset ADHD or the idea that it is a clinically relevant syndrome. In fact, as a group, the adult onset cases showed significant functional impairments. Moreover, some of the studies ruled out the idea that adult onset ADHD is a misdiagnosis of another disorder. Further support for the validity of adult onset ADHD comes from a study of referred adults who retrospectively reported childhood symptoms 5. Based on clinical features and familial transmission, that study concluded that onsets of ADHD in late adolescence and early adulthood were valid.5


ADHD Consensus Statement download




1. Faraone S, Biederman J, Mick E. The Age Dependent Decline Of Attention-Deficit/Hyperactivity Disorder: A Meta-Analysis Of Follow-Up Studies. Psychological Medicine. 2006;36(2):159-165.
2. Moffitt TE, Houts R, Asherson P, et al. Is Adult ADHD a Childhood-Onset Neurodevelopmental Disorder? Evidence From a Four-Decade Longitudinal Cohort Study. Am J Psychiatry. 2015:appiajp201514101266.
3. Fayyad J, De Graaf R, Kessler R, et al. Cross-national prevalence and correlates of adult attention-deficit hyperactivity disorder. Br J Psychiatry. 2007;190:402-409.
4. Sibley MH, Pelham WE, Molina BS, et al. When diagnosing ADHD in young adults emphasize informant reports, DSM items, and impairment. J Consult Clin Psychol. 2012;80(6):1052-1061.
5. Chandra S, Biederman J, Faraone S. Assessing the Validity of the Age at Onset Criterion for Diagnosing ADHD in DSM-5. Journal of attention disorders. In Press.
6. Lecendreux M, Konofal E, Cortese S, Faraone SV. A 4-year follow-up of attention-deficit/hyperactivity disorder in a population sample. J Clin Psychiatry. 2015;76(6):712-719.
7. Asherson P, Trzaskowski M. Attention-deficit/hyperactivity disorder is the extreme and impairing tail of a continuum. J Am Acad Child Adolesc Psychiatry. 2015;54(4):249-250.

Adult Onset ADHD: Does it Exist?
Is it Distinct from Youth Onset ADHD?

by Stephen V. Faraone, PhD – August 4, 2016

Stephen V Faraone, PhD, ADHD in AdultsThere is a growing interest (and controversy) about ‘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 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 b 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 ADHD 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 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.

ASRS Professional Screener DownloadThe 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 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 ADHD 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 the 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:Results from 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 does not 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 Age at Onset Criterion for Diagnosing ADHD in DSM-5.” J Atten Disord.
Faraone, S. V. and J. Biederman (2016). “Can Attention-Deficit/Hyperactivity Disorder Onset Occur in Adulthood?” JAMA Psychiatry.
Larsson, H., H. Anckarsater, M. Rastam, Z. Chang and P. Lichtenstein (2012). “Childhood attention-deficit hyperactivity disorder as an extreme of a continuous trait: a quantitative genetic study of 8,500 twin pairs.” J Child Psychol Psychiatry 53(1): 73-80.

Lecendreux, M., E. Konofal, S. Cortese and S. V. Faraone (2015). “A 4-year follow-up of attention-deficit/hyperactivity disorder in a population sample.” J Clin Psychiatry 76(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. St Clair, 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 disorders estimated from genome-wide SNPs.” Nat Genet 45(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). “When diagnosing ADHD in young adults emphasize informant reports, DSM items, and impairment.” J Consult Clin Psychol 80(6): 1052-1061.

Jonathan Marx AIA 15 YadkbH
This ADHD in Adults program is very exciting to us for a number of reasons.

First, it’s a groundbreaking campaign where we can educate all kinds of health professionals about the realities of ADHD, the treatment protocols we know that work, and the medications and other kinds of modalities that help make ADHD patients successful.

We’ve got the participation of the best clinicians and researchers in the country, who are taking part in educating healthcare professionals about this adult ADHD disorder. They’ll be bringing us the latest information and updates.

We’re also using the latest technologies that help you as practitioners learn about adult ADHD. You’ll benefit from videos, from group updates, from emails, and you’ll really be able to take this information into your practice so that you can best change your practice behaviors and help your ADHD patients.

We’re looking to build a leadership-base of physicians, nurses, nurse practitioners, physician assistants, who want to take out this new research and information about ADHD and bring it to their patients for the benefit not only of the patients, but the millions of people who are around them.

We have fertile ground now in the treatment of ADHD. We have the research that proves it exists, we have the medications and treatment modalities that are successful. All we need now is to get the information out there so that everyone can benefit.

Join us in our information and educational program at We will be helping over ten million adults and, as I mentioned before, everyone who supports them. Thank you.

David Giwerc ADHD in Adults 2KdZ7t
ADHD Coaching an Integral Component of Effective Comprehensive Treatment for Adults with ADHD

Research clearly indicates psychopharmacology’s prominent role as an ADHD intervention.

Even if the primary care physician is comfortable with treating an ADHD adult, the typical office visit does not allow sufficient time to address every issue that confronts the newly diagnosed adult ADHD patient. The patient may leave with an appropriate ADHD medication regimen, but many other critical problems related to the diagnosis may remain unaddressed.

Medications can significantly improve focus while reducing other symptoms of ADHD. However, ADHD medications alone cannot teach the patient how to compensate for life skills that were never learned due to the years of executive function impairment.

ADHD coaching builds a bridge between biology and behavior and narrows the gap between ability and performance. Patients and physicians are beginning to realize the importance of including an ADHD coach as part of the treatment team. Just as an athletic coach motivates an athlete, ADHD coaches are very adept at motivating their clients who have ADHD, while partnering with them to develop and practice newly learned personal, social, and professional skills. For some patients, these skills may not have been developed due to lack of ADHD education, proper diagnosis, and treatment.

CBT_treats_Executive_Dysfunction_Free_ADHD_CME_CJkZtu.png.jpgThe stigma surrounding ADHD as nothing more than an “unruly child syndrome,” coupled with the popularity of incorrectly self-diagnosing an ADHD impairment, means too many patients are conditioned not to speak up and not to seek support, especially in the workplace. Adult ADHD coaching clients have often stated that an ADHD coach was the first person to not only understand the frustration of their invisible challenges, but also to sincerely believe all of their ADHD stories.

Physicians can rarely provide the level of attention and encouragement an adult patient needs within the restrictions of the typical office visit. The coach, therefore, can reinforce their patients’ natural talents and successes. The PAAC* or ICF**-certified ADHD coach can create an environment that encourages open communication (necessary for behavioral changes to occur) and forms a foundation of unconditional acceptance. Coupled with science-based instruction about ADHD, the coach focuses on identifying the patient’s natural talents and successes and develops a plan to convert that into daily strengths.

ADHD coaches help the client develop coping strategies, a valuable adjunct to medication management. They are highly specialized professionals, well-versed in ADHD-specific coaching competencies. The coach provides psycho-educational support, improves self-awareness of how symptoms of ADHD, and helps translate that into improved short and long-term performance.

While coaching cannot replace stimulant medications or therapy as a treatment, a coach can provide customized strategies and education that work alongside medication. The ADHD coach may suggest lifestyle changes such as proper sleep, nutrition, physical activity, and breathing exercises. In addition, ADHD coaching is accessible, with most coaching being conducted via phone/Skype, eliminating the need for geographical proximity or disruption to the work day.

*PAAC: Professional Association of ADHD Coaches, (PAAC)

**ICF: International Coach Federation

Cardiovascular Safety of ADHD Medications - ADHD in Adults


Lidia Zylowska, The Mindfulness Prescription for Adult ADHD (Boston, Trumpeter, 2012)

Thomas E. Brown, A New Understanding of ADHD in Children and Adults, Executive Function Impairments (New York, Rutledge, 2013)

David Giwerc, Permission to Proceed: The Keys to Creating a Life of Passion, Purpose and Possibility (Albany New York, ADD Coach Academy Press, 2011)

John Ratey, Spark Revolutionary New Science of Exercise & the Brain (New York, Little, Brown & Co. 2008)

Clin Psychiatry. 2015; 76(3):279-283.
“Cultural Background and Barriers to Mental Health Care for African American Adults”
Rostain, A.L., Ramsay, J.R., Waite, R.

This article delineates key patient and provider cultural biases that interfere with access to care for African American Adults with ADHD. It provides an important framework for understanding how these biases come about and what clinicians can do to address them. A brief review of the relationship between psychiatry and African Americans points out that beginning with slavery and continuing through the Tuskegee experiment, there is a legacy of racism in American medicine that influences the way patients view health care providers (and vice versa).

For instance, drapetomania was a clinical diagnosis given to slaves who demonstrated resistance to the institution by running away, refusing to follow rules, destroying property and fighting the plantation slave owners. In this fashion, psychiatry played an important role in supporting racism and racist beliefs. Similar analogies can be made to the ways that psychiatry classified homosexuality as a mental illness.


The point of this historical review is to underscore the longstanding mistrust that exists within the African American community toward medicine in general and psychiatry in particular. Add to this, the stigma associated with mental illness and substance abuse, it becomes easier to understand why many African American adults fail to seek treatment for disorders like ADHD.

The article goes on to discuss barriers to obtaining mental health treatment including patient factors (e.g. low income, lack of health insurance, fear and other negative attitudes) and health care system factors (e.g. limited access to culturally and technically competent providers and provider biases). Without question, higher rates of poverty and of lack of insurance among the minority population leads to markedly reduced access to care. The article points out that whereas rates of adequate mental health treatment among whites is 33%, the figure drops to 12% for African Americans. Moreover. white 
children are twice as likely to receive ADHD medication as African American children. Cultural biases among providers may lead them to be insufficiently attuned to the presence of ADHD in adult patients, ascribing the symptoms of ADHD, such as inattention, restlessness and disorganization either to personal failing (e.g. lack of self-discipline) or to environmental factors (e.g. low SES, lack of education) rather than to the influence of ADHD.

The paper concludes with practical recommendations for clinicians to address these barriers including providing accurate science based information, listening and being sensitive to stigmatizing experiences that African American patients may have encountered, and recognizing the deleterious effects of conscious and unconscious biases among well-meaning providers.



Stephen_Faraone_PhD_ADHD_in_AdultsEditor’s Note:  It is important to read the FULL Blog post.

Suicide is one of the most feared outcomes of any psychiatric condition.  Although its association with depression is well known, a small but growing research literature shows that ADHD is also a risk factor for suicidality.  

Suicide is difficult to study. Because it is relatively rare, large samples of patients are needed to make definitive statements.  Studies of suicide and ADHD must also consider the possibility that medications might elevate that risk. 

For example, the FDA placed a black box warning on atomoxetine because that ADHD medication had been shown to increase suicidal risk in youth.   A recent study of 37,936 patients with ADHD now provides much insight into these issues (Chen, Q., Sjolander, A., Runeson, B., D’Onofrio, B. M., Lichtenstein, P. & Larsson, H. (2014). Drug treatment for attention-deficit/hyperactivity disorder and suicidal behaviour: register based study. BMJ 348, g3769.).    In Sweden, such large studies are possible because researchers have computerized medical registers that describe the disorders and treatments of all people in Sweden.  Among 37,936 patients with ADHD, 7019 suicide attempts or completed suicides occurred during 150,721 person years of follow-up.  This indicates that, in any given year, the risk for a suicidal event is about 5%. 


Ask the ADHD Experts  Prescribing ADHD Medications

For ADHD patients, the risk for a suicide event is about 30% greater than for non-ADHD patients.  Among the ADHD patients who attempted or completed suicide,the risk was increased for those who had also been diagnosed with a mood disorder, conduct disorder, substance abuse or borderline personality.  This is not surprising; the most serious and complicated cases of ADHD are those that have the greatest risk for suicidal events.  

The effects of medication were less clear.   The risk for suicide events was greater for ADHD patients who had been treated with non-stimulant medication compared with those who had not been treated with non-stimulant medication.  A similar comparison showed no effect of stimulant medications. 

This first analysis suffers from the fact that the probability of receiving medication increases with the severity of the disorder.  To address this problem, the researchers limited the analyses to ADHD patients who had had some medication treatment and then compared suicidal risk between periods of medication treatment and periods of no medication treatment.  This analysis found no increased risk for suicide from non-stimulant medications and, more importantly, found that for patients treated with stimulants, the risk for suicide was lower when they were taking stimulant medications.  This protective effect of stimulant medication provides further evidence of the long-term effects of stimulant medications which have also been shown to lower the risks for traffic accidents, criminality, smoking and other substance use disorders.

Lenard_A_Adler_MD_ADHD_in_AdultsBreda,V;, Rovaris, DL; Schneider Vitola, E.; et al.  Does collateral retrospective information about childhood attention- deficit/hyperactivity disorder symptoms assist in the diagnosis of attention- deficit/hyperactivity disorder in adults? Findings from a large clinical sample.  Australian & New Zealand Journal of Psychiatry, 1–9, DOI: 10.1177/0004867415609421.

Collateral information is commonly used in making the diagnosis of ADHD in a child or adolescent. The role of collateral retrospectives in making the diagnosis in adults presenting for evaluation for ADHD has been less well investigated. 

ADHD Diagnosis Collateral Retrospectives
This is an investigation of the relative importance of childhood collateral information in making a diagnosis of ADHD in an adult presenting for evaluation.  449 adults with ADHD and 143 controls were evaluated for the diagnosis of ADHD and co-morbidities with a modification of the K-SADS, ADHD symptoms with the SNAP-IV, and current/childhood impairment with the Barkley Current and Childhood Symptom scales.  Collateral childhood ADHD symptoms/impairments were also evaluated with the Barkley Childhood Symptom Scale, completed by a first or second degree relative. 

Click: Managing   ADHD MedicationsA diagnosis of ADHD via patient or collateral report required full childhood symptom onset prior to the age of 12.  A subset of adults with ADHD were also treated with methylphenidate immediate release (0.13-1.23 mg/kg/day); treatment response was measured via changes in SNAP-IV from baseline to endpoint. 

The data analyses were performed on three cohorts: 1) adults with ADHD where there was agreement as to childhood symptoms from the subject and informant (n=277), 2) adults with ADHD where there was disagreement between subjects and informants (n=172) and 3) controls.  ADHD patients (all) vs. controls did not significantly differ in terms of age, gender, years of education or income, but did have significantly more school failure problems with discipline and problems with the law.   The levels of impairment for the ADHD cohort were quite similar (collateral agreement + vs. -), except that the group with collateral and patient childhood agreement had higher levels of school suspensions and problems with discipline.  It is not that surprising that the collaterals and subjects had better agreement in these areas as school suspensions and discipline problems are more likely to be remembered by both subjects and collaterals. 

The ADHD cohorts (collateral agreement + vs. -) had similar levels of co-morbidity and treatment response to methylphenidate.  The combined ADHD cohorts had higher rates of tobacco use, bipolar disorder, current ODD, conduct disorder and non-alcohol SUD than controls.  A salient finding of this investigation is that 40% of subjects with adult ADHD had collateral informants who were unable to extensively corroborate their symptoms. 

Limitations of this study include the self-report nature of the SNAP-IV and the fact that this scale has not been validated for adults.  Also, of note, the subjects with adult ADHD had full childhood onset of the disorder retrospectively, which is a more stringent criteria than was utilized in DSM-IV.  It is not clear how utilizing more strict childhood criteria will influence the generalizability of these findings to clinically evaluated subjects using DSM-IV or DSM-5 guidelines. Download DSM-V Guidelines  for ADHD Diagnosis

Clinicians remain the final and optimal arbiter in establishing a diagnosis of adult ADHD; it remains up to clinicians to integrate information from all sources in establishing this diagnosis, be it from the subject, current significant others, collateral informants about childhood or clinician observations during the interview.