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| ==Causes== | | ==Causes== |
| According to a majority of medical research in the United States, as well as other countries, ADHD is today generally regarded as a chronic disorder for which there are some effective treatments, but no true cure.<ref>[http://www.ninds.nih.gov/disorders/adhd/adhd.htm NINDS Attention Deficit-Hyperactivity Disorder Information Page.] National Institute of Neurological Disorders and Stroke (NINDS/NIH) February 9, 2007. Retrieved on 2007-08-13.</ref> Evidence suggests that hyperactivity has a strong heritable component, and in all probability ADHD is a heterogeneous disorder, meaning that several causes could create very similar symptomology.<ref>{{cite web|url=http://www.continuingedcourses.net/active/courses/course003.php|title=Attention-Deficit/Hyperactivity Disorder: Nature, Course, Outcomes, and Comorbidity|last=Barkley|first=Russel A.|accessdate=2006-06-26}}</ref> Candidate genes include [[dopamine transporter]] (DAT), [[dopamine receptor]] D4 (DRD4), [[dopamine beta-hydroxylase]] (DBH), [[monoamine oxidase]] A (MAOA), [[catecholamine]]-methyl transferase (COMT), serotonin transporter promoter (SLC6A4), 5-hydroxytryptamine 2A receptor (5-HT2A), and 5-hydroxytryptamine 1B receptor (5-HT1B). Researchers believe that a large majority of ADHD arises from a combination of various genes, many of which affect [[dopamine]] transporters.<ref name="dopamine">Roman T, Rohde LA, Hutz MH. (2004). "Polymorphisms of the dopamine transporter gene: influence on response to methylphenidate in attention deficit-hyperactivity disorder." ''American Journal of Pharmacogenomics'' 4(2):83–92 PMID 15059031 </ref> Suspect genes include the 10-repeat allele of the DAT1 gene,<ref name="gene">Swanson JM, Flodman P, Kennedy J, et al. "Dopamine Genes and ADHD." ''Neurosci Biobehav Rev.'' 2000 Jan;24(1):21–5. PMID 10654656</ref> the 7-repeat allele of the DRD4 gene,<ref name="gene"/> and the dopamine beta hydroxylase gene (DBH TaqI).<ref>Smith KM, Daly M, Fischer M, et al. "Association of the dopamine beta hydroxylase gene with attention deficit hyperactivity disorder: genetic analysis of the Milwaukee longitudinal study." ''Am J Med Genet B Neuropsychiatr Genet.'' 2003 May 15;119(1):77–85. PMID 12707943</ref>
| | ADHD likely stems from an interaction between genetic factors and external factors, including trauma or exposure to toxins. The genetic component of the disease has been demonstrated by the increased likelihood that a person for whom ADHD runs in his/her family is more likely to have ADHD than a person with no family history of the disorder. Studies have also shown that there is a familial transmission of the disorder which does not occur through adoptive relationships. Twin studies indicate that the disorder is highly heritable and that genetics contribute about three quarters of the total ADHD population, leaving the contribution of non-genetic factors at around 25%. <ref name="#18">OurMed. (2010). "Attention-deficit hyperactivity disorder."</ref> |
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| Genome wide surveys have shown linkage between ADHD and loci on chromosomes 7, 11, 12, 15, 16, and 17.<ref>{{cite journal | author=M. T. Acosta, M. Arcos-Burgos, M. Muenke | title=Attention deficit/hyperactivity disorder (ADHD): Complex phenotype, simple genotype? | journal=Genetics in Medicine | year=2004 | volume=6 | issue=1 | pages= 1–15}}</ref> If anything, the broad selection of targets indicates the likelihood that ADHD does not follow the traditional model of a "genetic disease" and is better viewed as a complex interaction among genetic and environmental factors. As the authors of a review of the question 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."<ref>{{cite journal | author=M. T. Acosta, M. Arcos-Burgos, M. Muenke | title=Attention deficit/hyperactivity disorder (ADHD): Complex phenotype, simple genotype? | journal=Genetics in Medicine | year=2004 | volume=6 | issue=1 | pages= 1–15}}</ref>
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| Studies show that there is a familial transmission of the disorder which does not occur through adoptive relationships.<ref name="BarkleyContEd">Barkley, Russell A. [http://www.continuingedcourses.net/active/courses/course003.php Attention-Deficit/Hyperactivity Disorder: Nature, Course, Outcomes, and Comorbidity.] ContinuinedEdCourse.Net. Retrieved on [[2007-08-12]].</ref> [[Twin study|Twin studies]] indicate that the disorder is highly heritable and that genetics contribute about three quarters of the total ADHD population.<ref name="BarkleyContEd"/> While the majority of ADHD is believed to be genetic in nature,<ref name="BarkleyContEd"/> roughly one-fifth of all ADHD cases are thought to be acquired after conception due to [[Traumatic brain injury|brain injury]] caused by either toxins or physical trauma prenatally or postnatally.<ref name="BarkleyContEd"/> | |
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| ==References== | | ==References== |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Charmaine Patel, M.D. [2]
Overview
There are no established causes of ADHD. Studies suggest that ADHD results from a complex interaction between genetic and environmental factors.
Causes
ADHD likely stems from an interaction between genetic factors and external factors, including trauma or exposure to toxins. The genetic component of the disease has been demonstrated by the increased likelihood that a person for whom ADHD runs in his/her family is more likely to have ADHD than a person with no family history of the disorder. Studies have also shown that there is a familial transmission of the disorder which does not occur through adoptive relationships. Twin studies indicate that the disorder is highly heritable and that genetics contribute about three quarters of the total ADHD population, leaving the contribution of non-genetic factors at around 25%. [1]
References
- ↑ OurMed. (2010). "Attention-deficit hyperactivity disorder."
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