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ADHD is broadly defined and pervasive, and it is likely that the symptoms attributed to ADHD have a variety of different causes. The initial triggers could include genetic vulnerabilities, viral or bacterial infections, brain injury, or nutritional deficits. A 1990 study at the U.S. National Institute of Mental Health correlated ADHD with a series of metabolic abnormalities in the brain, providing further evidence that ADHD is a neurological disorder. While heredity is often indicated, some believe that problems in prenatal development, birth complications, or later neurological damage may contribute to ADHD, although no satisfactory proof exists for this. There has been a surge in alternative approaches to ADHD, but these have been vigorously disputed.
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It has been demonstrated that children who have at least one parent diagnosed with ADHD are more likely to be diagnosed with ADHD. Scientific evidence suggests most strongly that, in many cases, the disorder is genetically transmitted, and is caused by an imbalance or deficiency in certain chemicals that regulate the efficiency with which the brain controls behavior. Current research is examining which genes may be involved. A team at the University of California suggest that genes contributing to (ADHD) overlap an area of chromosome 16p13 where the genes for autism are. The two conditions appear related, with both (ADHD) and autism, frequently involving inattentiveness and/or hyperactivity.
This investigative path also suggests an associated hypothesis that environmental factors, handed down from generation to generation, may trigger the symptoms associated with ADHD. There also exists a possibility that a family with one diagnosed member may have a heightened awareness of the disorder, along with a willingness to seek formal diagnosis, which would make detection and diagnosis more likely, thus skewing the data on heritability. |
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There is increasing evidence that variants in the gene for the dopamine transporter are related to the development of ADHD (Roman et al., 2004, American Journal of Pharmacogenomics 4:83-92). This evidence is consonant with the theory of inefficacy of dopamine in people with ADD/ADHD; according to other recent studies, people with ADHD usually have relatively high dopamine transporter levels, which clears dopamine from between neurons before the full effect is gained from dopamine. Stimulant medications used to treat ADHD are all capable of either inhibiting the action of dopamine transporter (as methylphenidate does) or promoting the release of dopamine itself (as the amphetamine-class medications do). Therefore, it is theorized that stimulant medication allows the brain to enhance the effect of dopamine by blocking dopamine transporters or increasing the release of dopamine. Currently this is the most widely accepted model of ADD/ADHD etiology in the scientific and medical community. |
The finding of another possible cause stemmed from the observation that children of women who smoked during pregnancy are more likely to be diagnosed with ADHD. Given that nicotine is known to cause hypoxia (too little oxygen) in the uterus, and that hypoxia causes brain damage, smoking during pregnancy could be an important contributing factor leading to ADHD. It may even help explain in part the increase in ADHD diagnoses, as the number of women smokers has increased. However, there are not nearly enough women smoking during pregnancy to account for all the ADHD diagnoses, and the mothers of many of those diagnosed with ADHD did not smoke during or before pregnancy. It is also possible that cause and effect could be confounded in this study, since many mothers who smoke during pregnancy may be ADHD suffers themselves; therefore the cause may simply be the shared genetic material of mother and child, rather than the mother's smoking.
Brain development in the uterus and during the first year of life, possibly related to drug use during pregnancy or environmental toxins may also be possible causes, but again, little proof seems to exist as yet, and it can again be pointed out that the parents of many if not most individuals with ADHD did not consume drugs during regency.
It has also been suggested that ADHD may be the result of a poor diet and other external factors, rather than from any physiological source. Studies of changes in diets of children provide some anecdotal and scientific evidence for this, but current majority opinion seems to be that the available evidence is insufficient to either prove or disprove this. However, it has been noticed that some children with ADHD seem to be addicted to milk. It has been proposed by Norwegian and British scientists that this is due to the casomorphins, peptides formed by incomplete digestion of the whey protein.
It has, however, been established conclusively that a small percentage of children are sensitive to dyes and other food additives, sugar, caffeine, etc.
Children with ADHD have lower levels of key fatty acids. In fact, one study found that the lower the levels, the worse the symptoms. The possibility that fatty acid deficiency is a trigger for ADHD is especially plausible as nutrition scientists have recently demonstrated that the American diet is extremely deficient in omega-3 fatty acids. At the same time, ADHD diagnoses are rapidly increasing. More support for this idea comes from findings that breast-fed children have much lower levels of ADHD, and that until quite recently, infant formula contained NO omega-3 fatty acids.
A recent randomized double-blind experiment compared a fatty acid supplement with placebo in children with developmental coordination disorder (which exhibits a high degree of overlap with ADHD diagnoses). Fatty acid supplements improved spelling, reading, and behavior after three months. While not directly showing a causal link between ADHD and fatty acids, increased levels of fatty acids has a beneficial effect on related behavior.
However, creating a deficiency of omega-3 fatty acids in pregnant rats produces pups that are hyperactive and that have altered brain levels of dopamine in the same brain regions as seen in humans and other rat models of hyperactivity. |
