It is true that children diagnosed with ADHD have parents with a higher incidence of psychopathology including ADHD (Anastopoulos & Barkley, 1988). Unfortunately, these studies frequently suffer from methodological weaknesses and often do not differentiate between genetic and social transmission of behaviors (Deutsch & Kinsbourne, 1990).
One must note that when discussing concordance rates or heritability, we are merely referring to the degree to which two people show a particular trait. This does not positively implicate a genetic factor; only that it appears to be the trend. In order to identify a genetic factor positively, chromosomal studies are necessary.
The studies that are methodologically stronger do support a genetic contribution to ADHD. For example, behavior genetic studies indicate that there is a higher concordance rate of ADHD with first-degree relatives when compared to adoptive parents. In studies comparing heritability of ADHD among twins, monozygotic (genetically identical) twins show a concordance rate of approximately 65%, whereas dizygotic (non-genetically identical) twins show a concordance rate of approximately 29% (Gilger, Pennington, & DeFries, 1992; Goodman & Stevenson, 1989). Because of this heritability, often parents of children with ADHD will not recognize the problem because they are a "chip off the old block." The statistics suggest that as many as 35% of both the immediate and extended family members and up to 32% of siblings may also be diagnosed with ADHD (Faraone & Biederman, 1994; Faraone, Biederman, & Milberger, 1996). In addition, approximately 33% of fathers who were diagnosed with ADHD have children who are similarly diagnosed (Biederman, Faraone, & Lapey, 1992). Another way of looking at heritability is to examine the severity of the disorder. The research from the twin studies indicates that the more serious the ADHD the greater the genetic contribution to the disorder (Stevenson, 1992).
At one time it was thought that the primary, if not exclusive, cause of ADHD was some form of structural brain damage. Part of this reasoning arose from the effects of an epidemic of encephalitis during World War I. Children stricken with encephalitis displayed a variety of behavioral problems, including the symptoms of hyperactivity and inattention (Kessler, 1980). Moreover, birth trauma and head injury were also believed to contribute to ADHD (Barkley, 1990b). It did not take long for ADHD symptomatology to be attributed to brain damage even in the absence of any evidence. For example, school problems such as poor attention, hyperactivity, and distractibility (Kahn & Cohen, 1934) were attributed to brain stem lesions (Satz & Fletcher, 1980). Given the lack of evidence of brain damage in these children, it was now assumed that "minimal brain dysfunction" was the cause of ADHD but the damage was simply undetectable. By the 1950s, it was pointed out that the term and its implications were circular. The reasoning went like this: Because brain dysfunction can lead to behavioral problems, the presence of these problems indicates brain dysfunction. All this in the absence of any evidence. Given the problems with the circularity of the minimal brain dysfunction explanation, and that fewer than 5% of children with ADHD had a documented history of brain injury, there was greater demand for the explanation to be tied to the evidence.
Over the years, several brain structures have been proposed as responsible for ADHD, and although there is some support for several brain structures being implicated in ADHD, none have received complete support. Brain structures that have been proposed as responsible or participatory in ADHD symptomatology include the corpus callosum, reticular activating system, hypothalamus, limbic system, and the frontal and frontal-limbic areas (Semrud-Clikeman et al., 1994; Zametkin & Rapoport, 1987). It was postulated that the brain damage contributed to the attentional and motor behavior difficulties these children exhibited (Anastopoulos & Barkley, 1988). Difficulties arose in identifying the specific brain structures involved in ADHD (e.g., several brain areas are involved in the attention system). As the research progressed, it became evident, especially in light of the lack of direct data, that children with ADHD did not have structural central nervous system damage (Barkley, 1990b).
An area of the brain that has received considerable attention is the prefrontal cortex. This area is believed to mediate the inhibition of behavior and responses to environmental stimuli (Anastopoulos & Barkley, 1988). Studies of children with ADHD have found that these children have decreased blood flow and glucose utilization in the prefrontal areas. Children with ADHD showed lower electroencephalographic (EEG) activation in the frontal lobes. Moreover, children with ADHD whose parents displayed ADHD symptoms also had a lower metabolism in the frontal areas.
Neurotransmitters are neurochemicals involved in the transmission of nervous system impulses. The level of the neurotransmitter influences the transmission of the nervous system electrochemical impulse. The problem is thought to be a decreased availability of the catecholamines. The catecholamines are the three neurotransmitters dopamine, norepinephrine, and serotonin in the prefrontal cortex (Hechtman, 1991; Taylor, 1994). It is hypothesized that children with ADHD may lack these brain neurochemicals and that these neurochemicals control or inhibit excessive motor behavior and maintain attention. The evidence for the decreased availability of dopamine, norepinephrine, and serotonin is indirect. In other words, the evidence comes from the observed effects of the stimulant drugs, such as Ritalin, Dexedrine, and Cylert, that essentially all children diagnosed with ADHD are prescribed. The use of stimulants seems to make up for this lack of chemical and allows children to better control their impulses (Mercer, 1997). Another way to describe the effects of stimulants is that they may enhance the functioning of executive control processes which overcome the deficits in inhibitory control and short-term memory (Greenhill, 1998). Thus, stimulants allow for the control over children’s behavior by acting as a substitute for the presumed lack of brain neurochemicals (Valenstein, 1998). Other researchers have found that stimulants may either lower the reinforcement threshold in the nervous system or postpone the effects of satiation or habituation, thus allowing greater sensitivity to reinforcement (Haenlein & Caul, 1987; Leith & Barrett, 1976, 1981). In other words, responding increases for activities children engage in by altering the reinforcing properties of the nervous system.
Another approach is to study the level of the neurotransmitter in cerebrospinal fluid or plasma (Zametkin & Rapoport, 1987). As direct as these measures are, no consistent findings between children with and without ADHD have been found
In summary, although the best evidence from these studies indicates that the catecholamines are implicated in ADHD, the findings are not definitive because there is no direct evidence that children with ADHD suffer from a catecholamine deficit.
Although the results from family and co-morbidity studies implicate a hereditary basis, the fact that from generation to generation there is a higher familial incidence of ADHD could be due to environmental factors. Therefore, the genetic hypothesis needs further exploration, particularly in the form of more chromosomal studies. More recent research has attempted to do just that. For example, a relationship between the dopamine transporter gene (DAT) and ADHD has been identified (Cook et al., 1995; Gill, Daly, Heron, Hawi, & Fitzgerald, 1997). These results must be interpreted with caution; there are three reasons for this caution. First, the samples of children studied were quite small and, therefore, may not reflect the population of children with ADHD. A second reason to exercise caution is that these samples include a sub-sample of children with ADHD who had a high level of co-morbidity with other disorders. Thus, it is possible that the findings are not discriminatory for ADHD. What is important about these findings is that the drugs that are prescribed for children with ADHD inhibit the dopamine transporter.
Another approach to determining the genetic basis of ADHD has focused on the gene that codes for the dopamine receptor gene (DRD4). Some of the children with ADHD showed that they had extra replications of trinucleotides (LaHoste et al., 1996). The importance of these findings is that they are correlated with high levels of sensation seeking that involves behaviors that are categorized as impulsive, excitable, and exploratory (Benjamin, Patterson, Greenberg, Murphy, & Hamer, 1996; Ebstein et al., 1996). Taken together, these findings suggest that the child's behavior may be due, in part, to a decreased response to dopamine signals.
In conclusion, although the evidence is accumulating that there is a genetic component to ADHD, it is also true that it is not likely to be a single gene. Rather, researchers in the field agree that the genetic component of ADHD is polygenic. This means that the genetic component of ADHD is the result of the interaction of multiple genes influencing several chromosomes.
In the best case scenario, one would find a direct link between the neurotransmitter and ADHD. Even if this were the case, however, one could still not conclude that there was a cause-and-effect relationship. The reason for this is that although neurotransmitters influence behavior, the opposite may also be true, that is, behavior may influence the level of the neurotransmitter (Whalen, 1989).
Retrospective studies have suggested a number of factors that may adversely affect pre-natal development and, consequently, the expression of ADHD symptoms. There is little evidence that prenatal factors are specific to the development of ADHD. However, these correlational investigations do, periodically, produce interesting results. Exposing the fetus to drugs has also been suggested as causing ADHD. However, these drug effects are also found in other psychopathological conditions. Thus, it is impossible at this time to conclude that drugs cause ADHD. For example, it is known that nicotine from cigarette smoking during pregnancy, cocaine, and crack may adversely affect normal brain development.
The use of alcohol during pregnancy is especially important because of a condition known as Fetal Alcohol Syndrome (FAS). Children diagnosed as exhibiting FAS display the same symptoms as those diagnosed with ADHD: hyperactivity, inattention, and impulsivity. It is also true that mothers of children with ADHD drink more alcohol and smoke more tobacco than do mothers of children without ADHD. Other results indicate that hyperactivity correlated with prenatal alcohol exposure persists into the adolescent years, although at a lower rate than during the childhood years.
Noland et al. (2005) examined the influence of maternal use of cocaine, cigarette, and marijuana use during the child’s prenatal development. The results indicate that there was an increase in commission errors, suggesting that the child had less than optimal selective attention; in other words, the child was more easily distractible. The researchers also reported the more frequent the maternal use of marijuana, the greater the likelihood that the child would show omission errors, that is, the child’s ability to sustain attention on a particular task was negatively impacted. Similar results were reported with children also exposed to cocaine prenatally who were in adoptive or foster care. In comparison to the children not exposed to cocaine prenatally, the cocaine exposed children were rated as having more problems with aggression, externalizing behaviors, and total behavioral problems (Linares et al., 2006). Both studies did not find a relationship between the mother’s own status and the child outcomes. Thus, the results, although correlational, are more suggestive of a direct influence of the drugs on the behavior.
Some researchers have reported a correlation between the length of the labor, hemorrhage, and ADHD. However, the predictive values of these results were rather small. What these results suggest is that prenatal insult may predispose a small fraction of children to ADHD (Chandola, Robling, Peters, Melville-Thomas, & McGuffin, 1992). Children diagnosed with ADHD also show a higher incidence of minor physical abnormalities. These abnormalities appear within the first 3 months post-birth (Anastopoulos & Barkley, 1988). These abnormalities may include a head circumference that is beyond the normal range, low-set ears, and a wide gap between the first and second toes (Whalen, 1989). These minor physical abnormalities are also found in the general population; up to 4% of the general population shows neither known psychological nor physical disorders. Moreover, these minor physical abnormalities are also seen in other psychological disorders such as Down syndrome and autism. Although these relationships suggest a genetic component, especially since first degree relatives of children with ADHD also exhibit a higher proportion of minor physical abnormalities than does the general population, it is difficult to determine the precise relationship between ADHD and minor physical abnormalities.