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that the environment has a strong influence on the emer- gence of the disorder. This conclusion follows from studies of identical twins, which show that when one twin has ADHD, the probability of the other, genetically identical, twin’s having ADHD is only about 60%. This less than perfect identical twin concordance implicates environmen- tal risk factors. The nature of these risk factors has emerged from studies assessing features of the biological and psycho- social environment that may increase the risk of ADHD.

Biological Adversity

The idea that certain foods could cause ADHD received much attention in the popular press after claims were made that ADHD could be cured by eliminating food additives from the diet. The Feingold diet for ADHD was popular- ized by the media and was accepted by many parents of ill children. Systematic studies, however, showed the diet was not effective and concluded that food additives do not cause ADHD (163). Another popular theory posited that exces- sive sugar intake would lead to ADHD symptoms. Although some positive studies supported this idea, the bulk of sys- tematic, controlled research did not (164).

In contrast to the mostly negative studies of dietary fac- tors, some toxins have been implicated in the origin of at least some cases of ADHD. Several groups have shown that lead contamination leads to distractibility, hyperactivity, restlessness, and lower intellectual functioning (165). How- ever, many children with ADHD do not show lead contami- nation, and many children with high lead exposure do not develop ADHD. Thus, lead exposure cannot account for the bulk of cases of ADHD.

The literature examining the association of ADHD with pregnancy and delivery complications (PDCs) presents con- flicting results; it tends to support the idea that PDCs can predispose children to ADHD (166–168), although some investigators do not (169). The PDCs implicated in ADHD frequently lead to hypoxia and tend to involve chronic expo- sures to the fetus, such as toxemia, rather than acute, trau- matic events, such as delivery complications.

For example, Conners reported that mothers of children with ADHD had high rates of toxemia during pregnancy (166). Hartsough and Lambert described eight PDCs asso- ciated with ADHD: maternal illness, toxemia, eclampsia, older maternal age, parity of child, fetal postmaturity, dura- tion of labor, and fetal distress during labor or birth (170). Nichols and Chen found that hyperactivity was significantly associated with low birth weight (171), and Chandola et al. reported antepartum hemorrhage, maternal age, length of labor, sex, and 1-minute Apgar scores to be significant prenatal and perinatal risk factors for subsequent referral for hyperactivity (172).

Sprich-Buckminster et al. showed that the association between ADHD and PDCs was strongest for children with ADHD who had psychiatric comorbidity (168). PDCs were

Chapter 43: Pathophysiology of ADHD

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also elevated among children with ADHD who had no fam- ily history of ADHD. These investigators concluded that PDCs may be more common among those children with ADHD having a weaker genetic predisposition, but this hypothesis was not confirmed in another study by the same group (167). The latter study found that children with ADHD and a history of PDCs showed more school failure and psychometric evidence of cognitive impairment than other children with ADHD. In addition to confirming the etiologic role of medical complications, this study showed that psychosocial stress during pregnancy predicted subse- quent ADHD and poor cognitive performance in children. Notably, catecholamines are secreted in response to stress, and mouse studies showed that catecholamine administra- tion produces uterine vasoconstriction and fetal hypoxia (173).

One extensively studied risk factor has been maternal smoking during pregnancy. By exposing the fetus to nico- tine, maternal smoking can damage the brain at critical times in the developmental process. The smoking mother is at increased risk of antepartum hemorrhage, low maternal weight, and abruptio placentae (173). Her fetus is at risk of low birth weight (173,174), and because smoking increases carboxyhemoglobin levels in both maternal and fetal blood, it places the fetus at risk of hypoxia (175). Consistent with these effects, maternal smoking during pregnancy predicts behavioral and cognitive impairment in children and ADHD (41,176).

Animal studies in pregnant mice and rats have shown a positive association between chronic exposure to nicotine and hyperactivity in offspring (42). Neonatal nicotine expo- sure prevents the development of low-affinity nicotine re- ceptors (177), and chronic exposure results in tolerance to the drug and an increase in brain nicotinic receptors (178–181). Because nicotinic receptors modulate dopami- nergic activity and dopaminergic dysregulation may be in- volved in the pathophysiology of ADHD, it is theoretically compelling to consider maternal smoking as a risk factor for ADHD.

Little is known about the potential role of in utero expo- sure to viral infections. Because maternal viral infections can affect the fetus and can have an adverse impact on the developing brain, viral infections could be associated with later psychopathology. Because viral infections occur more commonly in winter than in other seasons, season-of-birth data have been used to implicate in utero viral infection for several disorders including schizophrenia (182), autism (183), and dyslexia (184)

Although Mick et al. found no evidence of a strong sea- sonal pattern of birth in children with ADHD (185), they did find statistically significant peaks for September births in children with ADHD who had comorbid learning dis- abilities and in children with ADHD who had no additional psychiatric comorbidity. Thus, it is possible that winter in- fections during the first trimester of pregnancy may account

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