Etiology Possible Causes And Modifiers

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Some of the presumed causes of ADHD are no longer discussed, and the remaining chapters of the book will bring the readers up to date on important new developments. Conclusions from myriad studies suggest the following:

1. Lead and related issues are rarely a cause (197).

2. Food additives (salicylates, food dyes, and preservatives), have a trivial effect at best (82,198,199).

3. Sugars desserts, and candy bars appear to have little or no effect in exaggerating ADHD symptoms (177,200,201).

4. Alcohol can be a cause but certainly but explains only a minority of cases (202,203).

5. Parental conflict, common in families with ADHD children does not cause ADHD but can certainly exaggerate the severity of symptoms (204-213).

6. Genetic factors appear to be more important than all others as a cause of both ADHD and LD.

8.1. Genetic Research

Of the many studies in this area, among the best are those by John DeFries, Bruce Pennington, and colleagues at the University of Colorado and those of Jim Stevenson and associates in England. Gillis et al. (214) used a sophisticated regression model developed by DeFries and Fulker (215,216) to estimate the heritability of ADHD. Subjects were 37 pairs of monozygotic (MZ) and 37 pairs of dizygotic (DZ) twins. At least one member of each pair of twins had a reading disability and at least one member of each pair, not necessarily the one with a reading disability, satisfied criteria for ADD as diagnosed by the parent form of the DICA-P developed by Herjanic and Reich (169). Proband-wise concordance rates for ADHD were 79% for MZ and 32% for DZ twins. Age was not a significant predictor of DICA-P scores; i.e., the heritability (h2) of ADD as diagnosed by the DICA did not vary with age. The h2 coefficient was very high (0.98); i.e., nearly all the variance in DICA-P scores was attributed to heredity (coefficient varies from 0 to 1). It was concluded that HYP symptoms as expressed by the DICA are highly heritable.

Stevenson et al. (217) reported results from two twin samples, one from London (n = 190 pairs) and one from Colorado (n = 260 pairs). The proportion of ADHD probands that also had a spelling disability was 24% and the proportion of spelling probands that were ADHD was 30%. It was estimated that about 75% of the co-occurrence of these two conditions was a result of shared genetic influences. The differences between these two estimates were not statistically significant, which lends credence to the supposition of a subgroup of children in which both spelling and ADHD are influenced by a common gene or genes. The almost equal two-way percentages in this study are contradictory to the general impression that while ADHD can "cause" LD, the reverse is less likely (218).

There are a number of other studies pointing to the importance of heredity. Familial risk for ADD/ADHD and antisocial behaviors is higher among the relatives of children who have a conjoint diagnosis of both ADD/ADHD and CD than among the relatives of children who are only ADD/ADHD (219-225). Faraone et al. (222) found that the family members of probands with ADHD and ODD had a higher risk for ADHD and CD than the family members of probands with ADHD alone. However, the risk was lower for "familial spread" than in a group who were comorbid for both ADD/ADHD and CD. Biederman et al. (226) report significant prevalence of mood, anxiety, and antisocial disorders in the first-degree relatives of ADHD children. Elsewhere, Biederman et al. (227) report an association between anxiety disorders and ADD/ADHD, with the risk of anxiety disorders among the relatives of ADD/ADHD children higher than that for the relatives of normal children (220,227).

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