What Causes ADHD?
Although we may know the cause of ADHD for a specific child (e.g., an accident), we cannot prove what causes ADHD for the population more generally. That is, for etiologies of genetics or brain damage, it is not possible to (a) damage parts of the brain and directly assess these effects or (b) randomly assign individuals to genetic backgrounds to see which genes result in ADHD. If we were able to do this type of deterministic research, as is done in the hard sciences with animals or plants, we would have greater certainty related to etiologies. However, in the social sciences, we do research that suggests the probability of certain factors. The data reported are often post hoc (after-the-fact) examinations of brain structures or genes that are associated with individuals with ADHD.
Relatives of boys and girls with ADHD have significantly higher rates of ADHD than relatives of students without ADHD (Faraone et al., 1992). Biederman, Faraone, Keenan, Knee, and Tsuang (1991) reported that 28.6% of biological parents of children with hyperactivity also had a history of hyperactivity.
Overall, about 80% of the differences in activity, inattention, and impulsivity between people with and without ADHD can be explained by genetic factors. The high end of this range may be explained by individuals with both ADHD-H and ADHD-I (the combined type), who have a higher probability of inheriting ADHD (as high as .92 to .98 [Willcutt, Pennington, & DeFries, 2000]). In fact, the probability of inheriting activity level is greater than that of inheriting IQ (.55) or of height (.81) (Willerman, 1973).
In addition, at the genetic level, some evidence suggests an association between certain genes and ADHD (DAT1 and DRD4 [Jensen, 2001]). Individuals with ADHD have a longer-than-normal D4 gene, which makes the nerve cell less sensitive to dopamine, a neurotransmitter that conveys signals from one neuron to another. This gene has a well-known association to sensation- or novelty-seeking behavior as well as excitability and impulsiveness (for a review, see LaHoste et al., 1996). Most genetic traits continue because they have provided some advantage to the species (i.e., to survival). Heterogeneity alone has some advantage to the species by allowing more individuals to survive changing environmental conditions (Calabi, 1997).
Even though there is greater genetic correspondence for identical twins to have ADHD (about 80%) than fraternal twins (about 30% same sex [Gillis, Gilger, Pennington, & DeFries, 1992; LaHoste et al., 1996]), about 30% to 50% of identical twins do not both manifest ADHD (Goodman & Stevenson, 1989; Johnston & Mash, 2001; LaHoste et al., 1996). This indicates that “biology shapes our impulses and aptitudes, but it doesn’t act alone. There is always a context and always room for resistance” (Begley, 1995). In other words, external factors remain an important factor in etiology.
Exogenous (external) factors, such as maternal smoking, complications during birth or pregnancy, high levels of lead ingestion, accounted for another 20% to 30% of the causes of ADHD (Pennington, 1991). These prenatal or postnatal insults to the child’s biological system can account for ADHD in about one in five children with ADHD. Specifically, for maternal smoking, 22% of mothers of children with ADHD smoked a pack of cigarettes per day during at least 3 months of pregnancy in contrast to only 8% of mothers of non-ADHD children (Milberger et al., 2002). (It is also possible that these mothers were also ADHD, thus contributing to the association.)
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