Social construct theory of ADHD

The social construction theory of ADHD argues that attention deficit hyperactivity disorder is not necessarily an actual pathology, but that an ADHD diagnosis is a socially constructed explanation to describe behaviors that simply do not meet prescribed social norms.[1]

Some proponents of the social construct theory of ADHD seem to regard the disorder as genuine, though over-diagnosed in some cultures. These proponents cite as evidence that the DSM IV, favored in the United States for defining and diagnosing mental illness, arrives at levels of ADHD three to four times higher than criteria in the ICD 10, the diagnostic guide favored by the World Health Organization.[2] A popular proponent of this theory, Thomas Szasz, has argued that ADHD was "invented and not discovered."[3][4]

ADHD as a social construct

Psychiatrists Peter Breggin and Sami Timimi oppose pathologizing the symptoms of ADHD. Sami Timimi, who is an NHS child and adolescent psychiatrist, argues that ADHD is not an objective 'disorder'[5] but that western society creates stress on families which in turn suggests environmental causes for children expressing the symptoms of ADHD.[6] They also believe that parents who feel they have failed in their parenting responsibilities can use the ADHD label to absolve guilt and self-blame.

A common argument against the medical model of ADHD asserts that while the traits that define ADHD exist and may be measurable, they lie within the spectrum of normal healthy human behaviour and are not dysfunctional. However, by definition, in order to diagnose with a mental disorder, symptoms must be interpreted as causing a person distress or be especially maladaptive. In the United States, the Diagnostic and Statistical Manual (DSM-IV) requires that "some impairment from the symptoms is present in two or more settings" and that "there must be clear evidence of significant impairment in social, school, or work functioning" for a diagnosis of ADHD to be made.[7]

In this view, in societies where passivity and order are highly valued, those on the active end of the active-passive spectrum may be seen as 'problems'. Medically defining their behaviour (by giving labels such as ADHD and ADD) serves the purpose of removing blame from those 'causing the problem'. Controversy over the social constructionist view comes from a number of studies that cite significant psychological and social differences between those diagnosed with the disorder, and those who are not. However, the specific reasons for these differences are not certain, and this does not suggest anything other than a difference in behavior. Studies have also shown neurological differences, but whether this signifies an effect rather than a cause is unknown. Such differences could also be attributed the drugs commonly prescribed to people with this disorder. Studies have also been able to differentiate ADHD from other psychiatric disorders in its symptoms, associated features, life course, and comorbidity.[5][8][9][10]

Gerald Coles, an educational psychologist and formerly an associate professor of clinical psychiatry at Robert Wood Johnson Medical School and the University of Rochester who has written extensively on literacy and learning disabilities, asserts that there are partisan agendas behind the educational policy-makers and that the scientific research that they use to support their arguments regarding the teaching of literacy are flawed. These include the idea that there are neurological explanations for learning disabilities. Gerald Coles argues that school failure must be viewed and treated in the context of both the learning environment and the child's individual abilities, behavior, family life, and social relationships. He then presents a new model of learning problems, in which family and school environments are the major determinants of academic success. In this "interactive" paradigm, the attitudes and methods of education are more important than inherent strengths or deficits of the individual child.[11]

Questioning the pathophysiological and genetic basis of ADHD

Some social constructionist theories of ADHD reject the dominant medical opinion that ADHD has a distinct pathophysiology and genetic components. The 'symptoms' of ADHD also happen to be morally questionable attributes, this is why the symptoms are described as 'inappropriate'. Many social constructionists trenchantly question deterministic views of behaviour, such as those views sometimes put forth within behavioural/abnormal psychology and the biological sciences.

Currently, the pathophysiology of ADHD is unclear; although research has found evidence of differences in the brain between ADHD and non-ADHD patients.[12][13][14][15][16][17] Critics, such as Jonathan Leo and David Cohen who reject the characterization of ADHD as a disorder, contend that the controls for stimulant medication usage were inadequate in some lobar volumetric studies which makes it impossible to determine whether ADHD itself or psychotropic medication used to treat ADHD is responsible for decreased thickness observed[18] in certain brain regions.[19][20] They believe many neuroimaging studies are oversimplified in both popular and scientific discourse and given undue weight despite deficiencies in experimental methodology.[19]

From a biological/genetic point of view, ADHD is said to be highly heritable and twin studies suggest genetics are a factor in about 75% of ADHD cases,.[21] However, the genetic connection is questionable. Dr. Joseph Glenmullen states, "no claim of a gene for a psychiatric condition has stood the test of time, in spite of popular misinformation. Although many theories exist, there is no definitive biological, neurological, or genetic etiology for 'mental illness'."[22] His critics argue that ADHD is a heterogeneous disorder[21] caused by a complex interaction of genetic and environmental factors and thus cannot be modeled accurately using the single gene theory. Authors of a review of ADHD etiology have noted: "Although several genome-wide searches have identified chromosomal regions that are predicted to contain genes that contribute to ADHD susceptibility, to date no single gene with a major contribution to ADHD has been identified."[23]

Sudbury model of democratic education schools' alternative

Describing current instructional methods as homogenization and lockstep standardization, alternative approaches are proposed, such as the Sudbury schools' democratic education approach in which children, by enjoying personal freedom thus encouraged to exercise personal responsibility for their actions, learn at their own pace rather than following a chronologically-based curriculum.[24][25][26][27][28]

Criticism

Timimi's view has been seriously criticized by Russell Barkley and numerous experts in Child and Family Psychology Review (2005). In any case, it has been shown that Chinese and Indonesian clinicians give significantly higher scores for hyperactive-disruptive behaviors than did their Japanese and American colleagues when evaluating the same group of children.[29] Significant differences in the prevalence of ADHD across different countries have been reported, however.[30]

See also

• Hunter vs. farmer hypothesis
• Neurodiversity
• Low arousal theory - Alternate theory of ADHD
• Attention-deficit hyperactivity disorder controversies

References

1. Parens E, Johnston J (2009). "Facts, values, and Attention-Deficit Hyperactivity Disorder (ADHD): an update on the controversies". Child Adolesc Psychiatry Ment Health. 3 (1): 1. doi:10.1186/1753-2000-3-1. PMC 2637252. PMID 19152690.
2. Singh I (December 2008). "Beyond polemics: science and ethics of ADHD". Nature Reviews Neuroscience. 9 (12): 957–64. doi:10.1038/nrn2514. PMID 19020513.
3. Chriss, James J. (2007). Social control: an introduction. Cambridge, UK: Polity. p. 230. ISBN 978-0-7456-3858-4.
4. Szasz, Thomas Stephen (2001). Pharmacracy: medicine and politics in America. New York: Praeger. p. 212. ISBN 0-275-97196-1.
5. Timimi, Sami; Taylor, Eric (January 2004). "In Debate: ADHD is best understood as a cultural construct". British Journal of Psychiatry. 184 (1): 8–9. doi:10.1192/bjp.184.1.8. PMID 14702221.
6. Timimi, S. & Begum, M. (2006). Critical Voices in Child and Adolescent Mental Health. London: Free Association Books.
7. "Archived copy". Archived from the original on 2009-08-25. Retrieved 2009-08-09.CS1 maint: archived copy as title (link)
8. Taylor E.; Chadwick O.; Heptinstall E.; et al. (1996). "Hyperactivity and conduct problems as risk factors for adolescent development". Journal of the American Academy of Child and Adolescent Psychiatry. 35 (9): 1213–1226. doi:10.1097/00004583-199609000-00019. PMID 8824065.
9. Taylor, E., Sandberg, S., Thorley, G., et al. (1991) The Epidemiology of Childhood Hyperactivity. Maudsley Monograph No. 33. Oxford: Oxford University Press.
10. Meltzer, H., Gatward, R., Goodman, R., et al. (2000) Mental Health of Children and Adolescents in Great Britain. London: Stationery Office.
11. Coles, Gerald (15 January 1989). The Learning Mystique: A Critical Look at "Learning Disabilities". Ballantine Books. ISBN 978-0449903513.
12. Brain Matures a Few Years Late in ADHD, But Follows Normal Pattern Archived 2009-05-23 at the Wayback Machine NIMH Press Release, November 12, 2007
13. Lou HC, Andresen J, Steinberg B, McLaughlin T, Friberg L (Jan 1998). "The striatum in a putative cerebral network activated by verbal awareness in normals and in ADHD children". Eur J Neurol. 5 (1): 67–74. doi:10.1046/j.1468-1331.1998.510067.x. PMID 10210814.
14. Gene Predicts Better Outcome as Cortex Normalizes in Teens with ADHD Archived 2009-05-23 at the Wayback Machine NIMH Press Release, August 6, 2007
15. Dougherty DD, Bonab AA, Spencer TJ, Rauch SL, Madras BK, Fischman AJ (1999). "Dopamine transporter density in patients with attention deficit hyperactivity disorder". Lancet. 354 (9196): 2132––33. doi:10.1016/S0140-6736(99)04030-1. PMID 10609822.
16. Dresel SH, Kung MP, Plössl K, Meegalla SK, Kung HF (1998). "Pharmacological effects of dopaminergic drugs on in vivo binding of [99mTc]TRODAT-1 to the central dopamine transporters in rats". European Journal of Nuclear Medicine. 25 (1): 31–9. doi:10.1007/s002590050191. PMID 9396872.
17. Coccaro EF, Hirsch SL, Stein MA (2007). "Plasma homovanillic acid correlates inversely with history of learning problems in healthy volunteer and personality disordered subjects". Psychiatry Research. 149 (1–3): 297–302. doi:10.1016/j.psychres.2006.05.009. PMID 17113158.
18. Shaw, Philip; Lerch, Jason; Greenstein, Deanna; Sharp, Wendy; Clasen, Liv; Evans, Alan; Giedd, Jay; Castellanos, F. Xavier; Rapoport, Judith (2006). "Longitudinal Mapping of Cortical Thickness and Clinical Outcome in Children and Adolescents With Attention-Deficit/Hyperactivity Disorder". Arch Gen Psychiatry. 63 (5): 540–549. doi:10.1001/archpsyc.63.5.540. PMID 16651511.
19. David Cohen; Jonathan Leo (2004). "An Update on ADHD Neuroimaging Research" (PDF). The Journal of Mind and Behavior. The Institute of Mind and Behavior, Inc. 25 (2): 161–166. ISSN 0271-0137.
20. David Cohen; Jonathan Leo (2003). "Broken brains or flawed studies? A critical review of ADHD neuroimaging studies". The Journal of Mind and Behavior. 24: 29–56.
21. Barkley, Russel A. "Attention-Deficit/Hyperactivity Disorder: Nature, Course, Outcomes, and Comorbidity". Retrieved 2006-06-26.
22. Glenmullin, Joseph (2000). Prozac Backlash. New York: Simon & Schuster, 192-198
23. M. T. Acosta; M. Arcos-Burgos; M. Muenke (2004). "Attention deficit/hyperactivity disorder (ADHD): Complex phenotype, simple genotype?". Genetics in Medicine. 6 (1): 1–15. doi:10.1097/01.GIM.0000110413.07490.0B. PMID 14726804.
24. Greenberg, D. (1992), Education in America, A View from Sudbury Valley, "Special Education" -- A noble Cause Sacrificed to Standardization.
25. Greenberg, D. (1992), Education in America, A View from Sudbury Valley, "Special Education" -- A Noble Cause Run Amok.
26. Greenberg, D. (1987), Free at Last, The Sudbury Valley School, Chapter 1, And 'Rithmetic.
27. Greenberg, D. (1987), Free at Last, The Sudbury Valley School, Chapter 5, The Other 'R's'.
28. Greenberg, D. (1987), Free at Last, The Sudbury Valley School, Chapter 19, Learning.
29. E. M. Mann; Y. Ikeda; C. W. Mueller; A. Takahashi; K. T. Tao; E. Humris; B. L. Li; D. Chin (1992). "Cross-cultural differences in rating hyperactive-disruptive behaviors in children". American Journal of Psychiatry. 149 (11): 1539–1542. doi:10.1176/ajp.149.11.1539. PMID 1415822.
30. Dwivedi, KN; Banhatti, RG (February 2005). "Attention deficit/hyperactivity disorder and ethnicity". Archives of Disease in Childhood. 90 (Suppl 1): i10–i12. doi:10.1136/adc.2004.058180. PMC 1765276. PMID 15665149.

Further reading

• Joseph, Jay (December 2000). "Not in Their Genes: A Critical View of the Genetics of Attention-Deficit Hyperactivity Disorder". Developmental Review. 20 (4): 539–567. doi:10.1006/drev.2000.0511.
• Wedge, Marilyn (8 March 2012). "Why French Kids Don't Have ADHD". Suffer the Children. Psychology Today.