Why Small Babies Face Heart Trouble Later

Study finds clue to their increased risk of cardiovascular disease as adults

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MONDAY, Aug. 18, 2003 (HealthDayNews) -- An abnormal parental gene transfer may explain why small babies have a greater risk of heart disease as adults, says a Canadian study in the Journal of Medical Genetics.

This preliminary research included about 500 babies born after 24 weeks of pregnancy. Their weight was below what would be expected for their developmental stage and gender. All the babies were born at one center between 1998 and 2000.

Researchers extracted genetic material taken from blood samples collected from the babies and their mothers, and from mouth swabs taken from the fathers. Those genetic samples were tested for the presence of the APOE gene in 440 mother and baby pairs and 194 fathers.

The APOE gene encodes for the protein component of the fat and protein complexes found in blood plasma. The gene comes in three varieties -- e2, e3 and e4 alleles. APOE is involved in brain development, numerous immune processes, and control of cell growth.

Previous studies with animals have shown that a deficiency in APOE expression increases susceptibility to narrowing and hardening of the arteries. When the APOE gene is overexpressed, it exerts anti-inflammatory effects and protects against "furring up" of the arteries.

In this study, researchers found that parental transmission of the e2 variant of APOE was greatly reduced in small babies, e3 was passed on marginally more than would be expected, and e4 was passed on normally.

The results suggest that e2 is the critical variant of the APOE gene and seems to protect against low birth weight, the authors write. Since it is transmitted less frequently to small babies, and given that small babies are more prone to cardiovascular disease, the e2 allele could be the key cause of why small babies have an increased risk of heart disease as adults.

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SOURCE: BMJ Specialist Journals, news release, Aug. 18, 2003


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