Social construct theory of ADHD

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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 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[edit]

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 / espec. maladaptive. In America, 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.[8][9][10][11]

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.[12]

Questioning the pathophysiological and genetic basis of ADHD[edit]

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.[13][14][15][16][17][18] 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[19] in certain brain regions.[20][21] They believe many neuroimaging studies are oversimplified in both popular and scientific discourse and given undue weight despite deficiencies in experimental methodology.[20]

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,.[22] 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'."[23] His critics argue that ADHD is a heterogeneous disorder[22] 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."[24]

Alternatives to medication[edit]

Social critics question if environmental changes should be the main line of treatment for those with a diagnosis of ADHD, instead of the medical model which predominantly uses medication and to a lesser extent, behavior modification. Critics believe schools and the health system force children to conform to a narrow, predefined standard of child development.[citation needed] These critics believe that these institutions are propagating the dangerous viewpoint that children with ADHD are maladaptive and disabled simply because they do not conform to a socially constructed norm.[who?] Some people including retired neurologist and CCHR medical expert Fred Baughman have suggested that this viewpoint is ultimately being pushed by the pharmaceutical industry in order to sell Anti-ADHD drugs.[25] Moreover, the argument against ADHD asserts that changing the child through medication regimes may cheat them of certain unique and positive personal characteristics that in turn may limit our collective future.

Sudbury model of democratic education schools' alternative[edit]

Some critics of the concept of learning disabilities and of special education take the position that every child has a different learning style and pace and that each child is unique, not only capable of learning but also capable of succeeding. These critics assert that applying the medical model of problem-solving to individual children who are pupils in the school system, and labeling these children as disabled, systematically prevents the improvement of the current educational system.

Describing current instructional methods as homogenization and lockstep standardization, alternative approaches are proposed, such as the Sudbury model of democratic education schools, an alternative 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.[26][27][28][29][30] Proponents of unschooling have also claimed that children raised in this method do not suffer from learning disabilities.

Criticism[edit]

Critics of the social constructionist view contend that it presents no hard evidence in support of its own position. Proponents of this view disagree that criteria for falsifiability are lacking. One way, for example, is to show that there exists an objective characteristic possessed by virtually all diagnosed individuals which does not exist in any non-diagnosed individual. However, because diagnosis of psychiatric disorders is based on opinion, this would be difficult to prove. Also, whether this would demonstrate any actual abnormality as opposed to the labeling of certain behaviors is unknown. Current candidates for falsifiability include PET scans, genes, neuroanatomical differences, and life outcomes. However, none of these have been shown to be precise predictors of a diagnosis or lack thereof. Also, as previously stated, neurological differences do not indicate a cause, nor do genes indicate a direct impact.[citation needed] Such criteria are generally fulfilled by well-understood medical diseases.[citation needed]

Critics of this view also assert that it is not consistent with known findings. For instance, they claim that ADHD is as frequent in Japan and China as in the US[citation needed], yet in such societies (which supposedly favor child obedience and passivity) one would expect higher rates of ADHD if this theory were correct.[clarification needed] However, this is also disputed on the grounds that more aggressively obedient societies may suppress 'symptoms' of rebellion or 'ADHD'. The style in which individuals of these nationalities interact in their home countries, which is typically much more reserved and serious than in the United States, seems to suggest this[citation needed]. However, there is no solid proof of this assertion. Additionally, rates of medical diagnoses in China cannot be a reliable indicator of ADHD prevalence, especially for such non-life-threatening disorders as ADHD, due to the large peasant population in that country who cannot easily seek the services of a trained child psychologist. 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.[31] Significant differences in the prevalence of ADHD across different countries have been reported, however.[32] Timimi himself cites a range of prevalence that goes from 0.5% to 26% as support for his theory.[citation needed]

See also[edit]

Further reading[edit]

References[edit]

  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 0-7456-3858-9. 
  4. ^ Szasz, Thomas Stephen (2001). Pharmacracy: medicine and politics in America. New York: Praeger. p. 212. ISBN 0-275-97196-1. 
  5. ^ http://bjp.rcpsych.org/cgi/content/full/184/1/8 (Timimi, 2002
  6. ^ Timimi, S. & Begum, M. (2006). Critical Voices in Child and Adolescent Mental Health. London: Free Association Books.
  7. ^ http://www.psychiatryonline.com/content.aspx?aID=7721
  8. ^ Sami Timimi and Eric Taylor (2004) In Debate: ADHD is best understood as a cultural construct. The British Journal of Psychiatry 184: 8-9.
  9. ^ 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. 
  10. ^ Taylor, E., Sandberg, S., Thorley, G., et al. (1991) The Epidemiology of Childhood Hyperactivity. Maudsley Monograph No. 33. Oxford: Oxford University Press.
  11. ^ Meltzer, H., Gatward, R., Goodman, R., et al. (2000) Mental Health of Children and Adolescents in Great Britain. London: Stationery Office.
  12. ^ Gerald Coles (1987). The Learning Mystique: A Critical Look at "Learning Disabilities". Accessed November 25, 2008.
  13. ^ Brain Matures a Few Years Late in ADHD, But Follows Normal Pattern NIMH Press Release, November 12, 2007
  14. ^ 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. 
  15. ^ Gene Predicts Better Outcome as Cortex Normalizes in Teens with ADHD NIMH Press Release, August 6, 2007
  16. ^ 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. 
  17. ^ 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. 
  18. ^ 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. 
  19. ^ Philip Shaw, MD; Jason Lerch, PhD; Deanna Greenstein, PhD; Wendy Sharp, MSW; Liv Clasen, PhD; Alan Evans, PhD; Jay Giedd, MD; F. Xavier Castellanos, MD; Judith Rapoport, MD (2006). "Longitudinal Mapping of Cortical Thickness and Clinical Outcome in Children and Adolescents With Attention-Deficit/Hyperactivity Disorder". Arch Gen Psychiatry 5 (63): 540–549. doi:10.1001/archpsyc.63.5.540. PMID 16651511. 
  20. ^ a b 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. 
  21. ^ 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. 
  22. ^ a b Barkley, Russel A. "Attention-Deficit/Hyperactivity Disorder: Nature, Course, Outcomes, and Comorbidity". Retrieved 2006-06-26. 
  23. ^ Glenmullin, Joseph (2000). Prozac Backlash. New York: Simon & Schuster, 192-198
  24. ^ 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. 
  25. ^ adhdfraud.org
  26. ^ Greenberg, D. (1992), Education in America, A View from Sudbury Valley, "Special Education" -- A noble Cause Sacrificed to Standardization.
  27. ^ Greenberg, D. (1992), Education in America, A View from Sudbury Valley, "Special Education" -- A Noble Cause Run Amok.
  28. ^ Greenberg, D. (1987), Free at Last, The Sudbury Valley School, Chapter 1, And 'Rithmetic.
  29. ^ Greenberg, D. (1987), Free at Last, The Sudbury Valley School, Chapter 5, The Other 'R's'.
  30. ^ Greenberg, D. (1987), Free at Last, The Sudbury Valley School, Chapter 19, Learning.
  31. ^ 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. PMID 1415822. 
  32. ^ http://adc.bmjjournals.com/cgi/content/full/90/suppl_1/i10 (Dwivedi, 2005)