Etiological Factors (page 3)
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.)
Structural (Neuroanatomical) Factors
Considerable evidence exists of differences in the structure or size of the brain as possible determinants of ADHD. Brain structure differences could be inherited or externally altered through brain damage. Researchers have speculated about which areas of the brain may be especially vulnerable to insult. Pennington (1991) suggested that areas of the brain that have evolved most recently in the history of the human species would be more likely to be affected by genetic and environmental variation. These are (a) the prefrontal cortex, which is involved in planning, response inhibition, selective attention or visual search, maintenance of attention, self-monitoring, recognition memory, and even creativity, and (b) the left-hemisphere language functions, which are involved in phonological processing (Pennington, 1991; Pennington & Ozonoff, 1996). The left-hemisphere dysfunctions have been found in association with language-learning disabilities and dyslexia (Shaywitz & Shaywitz, 1991).
Developmental models focus on the unfolding of a child’s biological nature over time. From a developmental perspective, we could expect children to eventually grow out of this disorder. Developmental changes take place in activity and attention. However, the major symptoms of ADHD persisted into adulthood in 33% of an adult ADHD study sample (see Pennington, 1991) and in 67% of children with a childhood diagnosis (Barkley, 1997a, 1997b; Barkley, Fischer, Edelbrock, & Smallish, 1990). In addition, physiological data (event-related potentials) do not support maturational differences between students with and without ADHD (Callaway, Halliday, & Naylor, 1983).
Even so, there appears to be behavioral evidence suggesting that children with ADHD are developmentally immature. For example, the behavioral and emotional responses of students with ADHD are similar to responses of younger children (e.g., Moon, Zentall, Grskovic, Hall, & Stormont, 2001). In addition, deficiencies in basic skills have been documented for these children that improve over time (e.g., fine motor skills, math accuracy [Zentall, 1990; Zentall, Moon, Hall, & Grskovic, 2001]).
Some ecological/developmental models emphasize the fit between the child’s skills and the requirements of the context (e.g., of family, school, culture). Behavioral differences are attributed to the child’s inability to regulate behavior in line with new developmental or cultural tasks. Preschool and young elementary students must learn to conform to behavioral expectations, and older elementary students learn to conform to academic (attentional) demands of increasingly difficult tasks, whereas students in high school are practicing more complex social skills (requiring response inhibition) in preparation for the vocational and relational tasks of young adulthood. Perhaps for this reason, gross motor hyperactivity characterizes preschool- and elementary-age students, which becomes restlessness and inattentiveness during later elementary and middle school years and social disorders in high school.
Evidence of differences exists also in the neurochemistry of individuals with ADHD. It is generally accepted that the neurotransmitters dopamine and norepinephrine are involved in ADHD (for a review, see Riccio et al., 1993). What has been suggested is that dopamine may be deficient in the prefrontal synapses, or connection points between cells (Goldman-Rakic, 1992; Pliszka, McCracken, & Maas, 1996). The role of neurotransmitters is further supported by evidence that psychostimulants (e.g., Ritalin) increase the availability of the neurotransmitter dopamine at the synapses.
Whereas much of the previously mentioned research involves a post hoc examination of biogenetics, a deterministic understanding can be made of nutrition. That is, it is possible to randomly assign individuals to placebo versus real (additive) diets. Findings from this research indicate that a subgroup of children with hyperactivity, perhaps as few as 3% to 5%, may be sensitive to food dyes or sugar; typically, these are preschoolers (for a review, see Barkley, 1997a; Whalen, 1989). Eliminating artificial food colors has been demonstrated to decrease parent (not teacher) ratings of behavioral difficulties. (For a meta-analysis review, see Schab & Trinh, 2004.) One study of food additives and sugar found a slight decrease in activity with no performance effects, while another study found an association between sugar intake and aggressiveness/restlessness in children with hyperactivity, with the opposite pattern observed for controls (for a review, see Leibowitz, 1991).
Although the evidence to date does not support placing children on restrictive diets, some evidence (Stevens et al., 1995) suggests gains from supplementing diets with essential fatty acids for those children with ADHD who had deficiencies (i.e., improvements over placebo on sustained attention, parent ratings of conduct, and teacher ratings of inattention). About 40% of children with ADHD in contrast to about 10% of comparison children had deficiencies in essential fatty acids. When children with reading disability and ADHD (not assessed for their level of deficiencies) were supplemented with a combination of omega-3 and -6 fatty acids, reductions in a wider range of ADHD symptoms were found (psychosomatic problems, cognitive problems, anxiety, attention problems, hyperactivity, and a global index measuring a broad range of behavior problems) over placebo conditions (Richardson & Puri, 2002).
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