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

There 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.

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 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.

 

REFERENCES
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.

Adult Onset ADHD

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

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 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.
 

REFERENCES
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.

Risk of Suicide in ADHD

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%.

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.

ADHD and Suicide

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%. 

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.

ADHD Medication and Parenting

Raising children is not easy. I should know. As a clinical psychologist, I’ve helped parents learn the skills they need to be better parents. And my experience raising three children confirmed my clinical experience. Parenting is a tough job under the best of circumstances but it is even harder if the parent has ADHD. For example, an effective parent establishes rules and enforces them systematically. This requires attention to detail, self-control and good organizational skills. Given these requirements, it is easy to see how ADHD symptoms interfere with parenting. These observations have led some of my colleagues to test the theory that treating ADHD adults with medication would improve their parenting skills. I know about two studies that tested this idea. In 2008, Dr. Chronis-Toscano and colleagues published a study using a sustained release form of methylphenidate for mothers with ADHD. As expected, the medication decreased their symptoms of inattention and hyperactivity/impulsivity. The medication also reduced the mothers use of inconsistent discipline and corporal punishment and improved their monitoring and supervision of their children. In a 2014 study, Waxmonsky and colleagues observed ADHD adults and their children in a laboratory setting once when the adults were off medication and once when they were on medication. They used the same sustained release form of amphetamine for all the patients. As expected, the medications reduced ADHD symptoms in the parents. This laboratory study is especially informative because the researchers made objective ratings of parent-child interactions rather than relying on the parent’s report of those interactions. Twenty parents completed the study. The medication led to less negative talk and commands and more praise by parents. It also reduced negative and inappropriate behaviors in their children. Both studies suggest that treating ADHD adults with medication will improve their parenting skills. That is good news. But they also found that not all parenting behaviors improved. That makes sense. Parenting is a skill that must be learned. Because ADHD interferes with learning, parents with the disorder need time to learn these skills. Medication can eliminate some of the worst behaviors but doctors should also provide the adjunct behavioral or cognitive behavioral therapies that could help ADHD parents learn parenting skills and achieve their full potential as parents.
 

REFERENCES
Chronis-Tuscano, A., K. E. Seymour, et al. (2008). “Efficacy of osmotic-release oral system (OROS) methylphenidate for mothers with attention-deficit/hyperactivity disorder (ADHD): preliminary report of effects on ADHD symptoms and parenting.” J Clin Psychiatry 69(12): 1938-1947.
Waxmonsky, J. G., D. A. Waschbusch, et al. (2014). “Does pharmacological treatment of ADHD in adults enhance parenting performance? Results of a double-blind randomized trial.” CNS Drugs 28(7): 665-677.

ADHD and Broken Bones

Adult ADHD is a Risk Factor for Broken Bones

 

Although some people view the impulsivity and inattentiveness of ADHD adults as a normal trait, these symptoms have adverse consequences, which is why doctors consider ADHD to be a disorder. The list of adverse consequences is long and now we can add another: broken bones.   A recent study by Komurcu and colleagues examined 40 patients who were seen by doctors because of broken bones and 40 people who had not broken a bone.  After measuring ADHD symptoms in these patients, the study found that the patients with broken bones were more impulsive and inattentive than those without broken bones.

 

These data suggest that, compared with others, adults with ADHD symptoms put themselves in situations that lead to broken bones.  What could those situations be?  Well, we know for starters that ADHD adults are more likely to have traffic accidents.   They are also more likely to get into fights due to their impulsivity.   As a general observation, it makes sense that people who are inattentive are more likely to have accidents that lead to injuries.  When we don’t pay attention, we can put ourselves in dangerous situations. 

 

Who should care about these results?  ADHD adult patients need to know about this so that they understand the potential consequences of their disorder.  They are exposed to so much media attention to the dangers of drug treatment that it can be easy to forget that non-treatment also has consequences.  Cognitive behavior therapy is CBT_treats_Executive_Dysfunction_Free_ADHD_CME_CJkZtualso useful for helping patients learn how to avoid situations that might lead to accidents and broken bones.

 

This study also has an important message for insurance administrators and how they make decisions about subsidizing or reimbursing treatment for ADHD.  They need to know that treating ADHD can prevent outcomes that are costly to the healthcare system, such as broken bones.   For example, in a study of children and adolescents, Leibson and colleagues showed that healthcare costs for ADHD patients were twice the cost for other youth, partly due to more hospitalizations and more emergency room visits. 

 

Do these data mean that every ADHD patient is doomed to a life of injury and hospital visits?   Certainly not.  But they do mean that patients and their loved ones need to be cautious and need to seek treatments that can limit the possibility of accidents and injury.

 

REFERENCES

 

Komurcu, E., Bilgic, A. & Herguner, S. (2014). Relationship between extremity fractures and attention-deficit/hyperactivity disorder symptomatology in adults. Int J Psychiatry Med 47, 55-63.

 

Leibson, C. L., S. K. Katusic, et al. (2001). “Use and Costs of Medical Care for Children and Adolescents With and Without Attention-Deficit/Hyperactivity Disorder.” Journal of the American Medical Association 285(1): 60-66.

ADHD and Insomnia

ADHD itself is associated with sleep difficulties, independent of ADHD medications. Thus, it is very important that sleep quality is assessed prior to treatment so that the changes due to treatment can be correctly inferred.


(Editor’s Note: See our Ask the ADHD Experts session on ADHD and Sleep.)


In clinical trials of stimulant ADHD medications, insomnia is typically noted a side effect of the medications. But most of these studies have used subjective patient or parent reports of sleep quality. A new meta analysis, reviews 9 studies of a total of 246 patients enrolled in randomized controlled trials of a stimulant medication.


Ask_the_ADHD_Experts_-_Prescribing_MedicationsTo be included, studies must have had an objective measure of sleep quality, either polysomnography or actigraphy. The analysis showed that stimulant medications led to a) a longer time to get to sleep; b) worse sleep efficiency and c) a shorter duration of sleep. Some of these sleep measures worsened with an increasing number of doses and a shorter time on medication.


Given the adverse effects that lack of sleep can have on cognition and behavior, these data provide further impetus for clinicians, parents and patients to monitor the effects of stimulant ADHD medication on sleep and to take appropriate action (e.g., dose reduction, change of medication) as warranted.


REFERENCES


J Am Acad Child Adolesc Psychiatry. 2009 Sep;48(9):894-908. doi: 10.1097/CHI.0b013e3181ac09c9.

Sleep in children with attention-deficit/hyperactivity disorder: meta-analysis of subjective and objective studies.

Cortese S1, Faraone SV, Konofal E, Lecendreux M.


Pediatrics. 2015 Dec;136(6):1144-53. doi: 10.1542/peds.2015-1708.

Stimulant Medications and Sleep for Youth With ADHD: A Meta-analysis.

Kidwell KM1, Van Dyk TR2, Lundahl A2, Nelson TD2.

Sleep and ADHD Medications

ADHD itself is associated with sleep difficulties, independent of ADHD medications. Thus, it is very important that sleep quality is assessed prior to treatment so that the changes due to treatment can be correctly inferred.

In clinical trials of stimulant medications for ADHD, insomnia is typically noted a side effect of the medications. But most of these studies have used subjective patient or parent reports of sleep quality. A new meta analysis, reviews 9 studies of a total of 246 patients enrolled in randomized controlled trials of a stimulant medication. To be included, studies must have had an objective measure of sleep quality, either polysomnography or actigraphy. The analysis showed that stimulant medications led to a) a longer time to get to sleep; b) worse sleep efficiency and c) a shorter duration of sleep. Some of these sleep measures worsened with an increasing number of doses and a shorter time on medication.
Given the adverse effects that lack of sleep can have on cognition and behavior, these data provide further impetus for clinicians, parents and patients to monitor the effects of stimulant ADHD medication on sleep and to take appropriate action (e.g., dose reduction, change of medication) as warranted.
 

REFERENCES
http://www.ncbi.nlm.nih.gov/pubmed/?term=PMID%3A+26598454
http://www.ncbi.nlm.nih.gov/pubmed/?term=cortese%5Bau%5D+sleep%5Bti%5D+meta%5Bti%5D

Psychotherapy for ADHD

Professor Larry Seidman is world renowned for his neuropsychology and neuroimaging research. In addition to all of his creative science, he has found the time to create what he calls “Neuropsychologically Informed Strategic Psychotherapy (NISP) in Teenagers and Adults with ADHD.” Let’s start with what NISP is not. NISP is not cognitive behavior therapy (CBT). CBT emphasizes teaching patients to identify thinking patterns that lead to problem behaviors. NISP describes how the interpersonal interaction we call psychotherapy can help patients increase self-regulation and self-control. NISP treatments vary in duration from brief psycho-educational interventions of one to five sessions to much longer term therapies of indefinite duration. The duration of therapy is tailored to the needs and goals of the individual. The methods of NISP can be adaptively applied into well-known therapy modalities such as CBT and family therapy. By creating a solid therapeutic alliance, NISP improves adherence to medications and addresses ADHD’s psychiatric comorbidities and functional disabilities. NISP is “neuropsychologically informed” because it follows a comprehensive neuropsychological assessment of strengths and weaknesses. This leaves the therapist with an understanding of the patient’s personal experience of ADHD, the meaning of the disorder, how it affects self-esteem, and how cognitive deficits limit the ability to self-regulate and adapt to changing circumstances. Attending to the patient’s strengths is a key feature of Prof. Seidman’s method. ADHD is a disorder and it usually has serious consequences. But ADHD people also have strong points in their character and their neuropsychological skills. These sometimes get lost in assessments of ADHD but, as Dr. Seidman indicates, by addressing strengths, patient outcomes can be improved. A NISP assessment also seeks to learn about the psychological themes that underlie each patient’s story. He gives the all too common example of the patients who view themselves as failed children who have not tried hard enough to succeed. A frank discussion of neuropsychological test results can be the first step to helping patients reconceptualize their past and move on to an adaptive path of self-understanding and self-regulation.

 

Prof. Seidman’s approach seems sensible and promising. As he recognizes, it has not yet, however, been subject to the rigorous tests of evidenced-based medicine (my blog on EBM: http://tinyurl.com/ne4t7op). So I would not recommend using it as a replacement for an evidenced-based treatment. That said, if you are a psychotherapist who treats ADHD people, read Prof. Seidman’s paper. It will give you useful insights that will help your patients.

 

 

REFERENCES

Seidman, L. J. (2014). Neuropsychologically Informed Strategic Psychotherapy in Teenagers and Adults with ADHD. Child Adolesc Psychiatr Clin N Am 23, 843-852. (In: Faraone, S. V. & Antshel, K. M. (2014). ADHD: Non-Pharmacologic Interventions. Child Adolesc Psychiatr Clin N Am 23, xiii-xiv.)

ADHD: Facts or Fiction

Many ADHD myths have been manufactured over the years.  Facts that are clear and compelling to most scientists and doctors have been distorted or discarded from popular media discussions of the disorder.   Sometimes, the popular media seems motivated by the maxim “Never let the facts get in the way of a good story.”  That’s fine for storytellers, but it is not acceptable for serious and useful discussions about ADHD.

ADHD Myths are easy to find.  These myths have confused patients and parents and undermined the ability  of professionals to appropriately treat the disorder.   When patients or parents get the idea that the diagnosis of ADHD is a subjective invention of doctors, or that ADHD medications cause drug abuse, that makes it less likely they will seek treatment and will increase their chances of having adverse outcomes.


Fortunately, as John Adams famously said of the Boston Massacre, “Facts are stubborn things.”  And science is a stubborn enterprise; it does not tolerate shoddy research or opinions not supported by fact.   ADHD scientists have addressed many of the myths about the disorder in the International Consensus Statement on ADHD, a published summary of scientific facts about ADHD endorsed by a of 75 international ADHD scientists in 2002.  The statement describes evidence for the validity of ADHD, the existence of genetic and neurobiologic causes for the disorder and the range and severity of impairments caused by the disorder.


Download The Consensus Statement


The Statement makes several key points:


The U.S. Surgeon General, the American Medical Association, the American Psychiatric Association, the American Academy of Child and Adolescent Psychiatry, the American Psychological Association, and the American Academy of Pediatrics recognize ADHD as a valid disorder.

ADHD involves a serious deficiency in a set of psychological abilities and that these deficiencies pose serious harm to most individuals possessing the disorder.

Many studies show that the psychological deficits in people with ADHD are associated with abnormalities in several specific brain regions.

The genetic contribution to ADHD is routinely found to be among the highest for any psychiatric disorders.

ADHD is not a benign disorder. For those it afflicts, it can cause devastating problems.

Hundreds of studies have shown the effectiveness of ADHD medications and multiple therapies.

The facts about ADHD will prevail if you take the time to learn about them.   This can be difficult when faced with a media blitz of information and misinformation about the disorder.  In future blogs, I’ll separate the ADHD facts from the fiction by addressing several popular myths about ADHD.


Editor’s note:  Our Ask the ADHD Experts sessions are designed specifically for experts to present updates and the latest unbiased research information on ADHD and related disorders.  Ask your questions.  Get them answered.  Subscribe and learn.