Jan. 17, 2003 -- A genetic difference might help explain why some babies are more prone to sudden infant death syndrome (SIDS) than others. Researchers have identified a genetic link between SIDS and a gene that regulates a substance in the brain associated with consciousness and mood.
A new study provides further evidence of a connection between the mysterious syndrome and the gene 5-HTT, which regulates serotonin uptake in the brain. The results appear in the Jan. 17 online edition of the American Journal of Medical Genetics.
Previous research had suggested such an association based on SIDS cases in Japan, and in this study American researchers found more information to support that link.
Researcher Debra E. Weese-Mayer, MD, professor of pediatrics at Rush-Presbyterian-St. Luke's Medical Center in Chicago, and colleagues, collected DNA samples from 87 U.S. SIDS cases, some white and some African-American and compared them with a second set of DNA samples from a group without a family history of SIDS. The researchers alsocompared the SIDS DNA with 334 random DNA samples to determine the frequency of this genetic difference in the general population.
SIDS affects more than 2,500 babies each year in the U.S., but African-Americans are much more likely to die from SIDS than others.
The study found an association between SIDS risk and the presence of a specific genetic rearrangement within the 5-HTT gene. There were differences in this specific arrangement of genes between blacks and whites, and between genders.
Researchers say those results suggest that there is a strong relationship between the 5-HTT gene and SIDS.
"There was a significant difference in genotype distribution and an increased frequency of SIDS cases versus ethnicity/gender matched controls with no family history of SIDS," write the researchers.
Researchers say if more studies confirm these results in larger samples, scientists may be able to develop tests to screen for genetic risk factors for SIDS and identify babies at risk.
SOURCE: American Journal of Medical Genetics, Jan. 17, 2003.