Department of Psychiatry and Behavioral Sciences, Stanford University School of
Medicine, Palo Alto, CA, 94304, USA. joachimh@stanford.edu
Autism is considered by many to be the most strongly genetically influenced
multifactorial childhood psychiatric disorder. In the absence of any known gene
or genes, the main support for this is derived from family and twin studies. Two
recent studies (Greenberg et al. 2001; Betancur et al. 2002) suggested that the
twinning process itself is an important risk factor in the development of
autism. If true, this would have major consequences for the interpretation of
twin studies. Both studies compared the number of affected twin pairs among
affected sib pairs to expected values in two separate samples of multiplex
families and reported a substantial and significant excess of twin pairs. Using
data from our epidemiological study in Western Australia, we investigated the
possibility of an increased rate of autism in twins. All children born between
1980 and 1995 with autism, Asperger syndrome, or pervasive developmental
disorder not otherwise specified (PDD-NOS) were ascertained. Of the 465 children
with a diagnosis, 14 were twin births (rate 30.0/1,000) compared to 9,640
children of multiple births out of a total of 386,637 births in Western
Australia between 1980 and 1995 (twin rate weighted to number of children with
autism or PDD per year 26.3/1,000). These data clearly do not support twinning
as a substantial risk factor in the etiology of autism. We demonstrate that the
high proportion of twins found in affected-sib-pair studies can be adequately
explained by the high ratio of concordance rates in monozygotic (MZ) twins
versus siblings and the distribution of family size in the population studied.
Our results are in agreement with those of two similar studies by Croen et al.
(2002) in California and Hultman et al. (2002) in Sweden.
PMID: 12228841 [PubMed - as supplied by publisher]
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