Posted May 6th, 2008 by minortopics | via www.canada.com
Research in Canada seems to prove the long asserted notion that breastfed infants have higher IQs — but only for those with certain genetics.
Scientists have identified a specific gene implicated in the link between breastfeeding and higher IQ in children, suggesting that biology — and not just socio-economics — is involved.
A study published Nov. 5 in the Proceedings of the National Academy of Sciences has found that a variant of a gene involved in metabolizing the fatty acids in breast milk determines whether children get an IQ boost from breastfeeding — on average as much as seven points.
Previous research has shown that breastfed children have higher IQs than those who were bottle-fed. But it wasn’t clear if the advantage was partly the result of other factors such as the mother’s own IQ or socio-economic status, said study author Avshalom Caspi. In Western countries, women from higher socio-economic groups are more likely to breastfeed, he explained.
His study controlled for the mother’s intelligence and social class, as well as for the children’s birth weight and gestational age (other factors known to influence intelligence).
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Posted January 9th, 2008 by minortopics | via content.nejm.org
A report published in the New England Journal of Medicine today indicates that researchers at Massachusetts General Hospital have found a genetic link to autism that may affect approximately 1 percent of people with the disorder, putting scientists one step closer to discovering the cause of this condition that appears in 1 out of every 150 children as well as further damaging the case of those that point to external causes such as thimerosal.
Background Autism spectrum disorder is a heritable developmental disorder in which chromosomal abnormalities are thought to play a role.
Methods As a first component of a genomewide association study of families from the Autism Genetic Resource Exchange (AGRE), we used two novel algorithms to search for recurrent copy-number variations in genotype data from 751 multiplex families with autism. Specific recurrent de novo events were further evaluated in clinical-testing data from Children’s Hospital Boston and in a large population study in Iceland.
Results Among the AGRE families, we observed five instances of a de novo deletion of 593 kb on chromosome 16p11.2. Using comparative genomic hybridization, we observed the identical deletion in 5 of 512 children referred to Children’s Hospital Boston for developmental delay, mental retardation, or suspected autism spectrum disorder, as well as in 3 of 299 persons with autism in an Icelandic population; the deletion was also carried by 2 of 18,834 unscreened Icelandic control subjects. The reciprocal duplication of this region occurred in 7 affected persons in AGRE families and 4 of the 512 children from Children’s Hospital Boston. The duplication also appeared to be a high-penetrance risk factor.
Conclusions We have identified a novel, recurrent microdeletion and a reciprocal microduplication that carry substantial susceptibility to autism and appear to account for approximately 1% of cases. We did not identify other regions with similar aggregations of large de novo mutations.
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