The pathophysiology of ADHD is unclear and there are a number of competing theories. ADHD as a biological difference Frequently observed differences in the brain between ADHD and non-ADHD patients have been discovered, but it is uncertain if or how these differences give rise to the symptoms of ADHD. ADHD is highly heritable: twin studies suggest that genetics explain 70 to 80 percent in the variation of ADHD. However, interest in the potential role of gene-environment interactions in ADHD is also increasing; maternal alcohol or tobacco use during pregnancy may be one contributor. It has also been argued that ADHD is a heterogeneous disorder with multiple genetic and environmental factors converging on similar neurological changes. Authors of a review of ADHD etiology in 2004 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." However, many further studies have occurred since, and the same is true for many other heritable human traits (e.g., schizophrenia). Social construct theory Concerns have been raised over the threshold at which symptoms are pathologized, and how strongly social constructs surrounding the symptoms and diagnosis of ADHD may differ between cultures. The social construction theory of ADHD argues that<unk><unk><unk>  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. 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. A popular proponent of this theory, Thomas Szasz, has argued that ADHD was "invented and not discovered." 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' but that western society creates stress on families which in turn suggests environmental causes for children expressing the symptoms of ADHD. 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<unk> ion, 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. 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. 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<unk> s of the individual child. 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. 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 in certain brain regions. They believe many neuroimaging studies are oversimplified in both popular and scientific discourse and given undue weight despite<unk> ncies in experimental methodology. 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. 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<unk> ive biological, neurological, or genetic etiology for 'mental illness'." His critics argue that ADHD is a heterogeneous disorder 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." Criticism Timimi's view has been seriously criticized by Russell Barkley and numerous experts in Clinical 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. Significant differences in the prevalence of ADHD across different countries have been reported, however.
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