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7 months ago

978-1572305441

autism

Sally, Ann, and Danny

Sally, Ann, and Danny 121 and has no play skills because of profound learning disability, the child may display behaviors also seen in higher-functioning children with autism. In these cases, the autistic features are a result of the severe cognitive disability, not necessarily a result of autism. Why some children with tuberous sclerosis develop autism and others do not is a mystery. In general, the more severe the cognitive disability, whatever the cause, the greater the likelihood that signs of autism will also be present, though this is not always the case. Of the other ninety percent of cases of ASD without an accompanying neurological disorder we know even less, but certainly more than we used to. We know the disorder is inherited in some fashion; autism and ASD are genetic disorders, though what is inherited, and how, is still very much an open question. About three to five percent of the siblings of children with autism also have autism. Although this is a very low rate, it’s much more common than in the general population (roughly two per thousand), suggesting that autism runs in families. But the best evidence for the genetic cause of autism comes from comparisons of twins, at least one of whom has autism. Several studies have compared the rates of autism in the co-twins of identical and fraternal twins. Twins share the same intrauterine environment but differ essentially in the number of genes they have in common. Identical twins share one hundred percent of their genes, whereas fraternal twins share, on average, fifty percent of their genes. The results of these twin studies are conclusive; the identical co-twins of autistic children have autism much more frequently than fraternal co-twins. This can be explained only by the action of genes that confer susceptibility to autism and ASD. The chance that non-twin siblings will have autism is three to five percent, much lower than the incidence in identical twins. This must be because multiple genes are involved in the etiology or some environmental factor interacts with genetic susceptibility. This does not mean that environmental factors are irrelevant; in fact there is good evidence that thalidomide and maternal anticonvulsants taken during pregnancy may cause autism. Other environmental risk factors may exist (but have not yet been discovered in spite of years of research), and if they do, they may exert their influence in the context of genetic vulnerability. But the genetics of the disorder are complex. There are at least four findings that cannot be explained by our current understanding. First, not all identical co-twins are affected—usually about sixty percent (a finding similar to many other developmental and neurological disor-

122 A MIND APART ders). If there were a simple genetic explanation, one might expect all identical co-twins also to be affected with autism. Second, the low rate of siblings who themselves are affected with autism/ASD and the sex ratio of more boys than girls make it unlikely that the disorder is caused by a single gene acting in isolation, like the gene for other disorders, such as cystic fibrosis and Huntington’s disease. Multiple genes must be involved, but how they interact is completely unknown. Third, it’s difficult to understand why the prevalence of the disorder is not decreasing. After all, the vast majority of people with autism do not have children; they do not pass their genes on to their offspring. If the disorder is genetic, it should be less common now than it was generations ago; the genes should be becoming less prevalent. In fact we know that people with autism were described at least three hundred years ago by Itard, who wrote about the wild boy of Aveyron. If anything, the number of children receiving the diagnosis has increased over the last ten years or so, but whether the disorder itself is more common, we simply do not know. It’s true that there has been a dramatic increase in the number of children receiving an ASD diagnosis in the last fifteen years or so. A lot of concern has been raised that the increase coincides with the widespread introduction of the MMR vaccine, and this has been one of the findings that has fueled the controversy about the vaccine. The most important point to remember is that there is no evidence that the disorder is actually increasing in the community; it’s the number of children being recognized in the community that is increasing. There are no community surveys that have been done twice in the same area using the same measurement tools that could tell us definitively whether the increase is real, or an artifact of better recognition. In fact, we have reasons to believe that changes in recognition could account for a large part of the increase: 1. The diagnostic criteria for autism have been broadened to include a larger number of children. 2. The diagnosis can now be applied to more children at both ends of the spectrum (that is, those who are high functioning and those who are low functioning). 3. The diagnosis is now applied more often to children with other disorders such as Down syndrome and tuberous sclerosis. 4. We are now able to make the diagnosis more easily in very young children and adults.

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