Formula-feeding linked to metabolic stress and increased risk of later disease
- Date:
- June 5, 2013
- Source:
- American Chemical Society
- Summary:
- New evidence from research suggests that infants fed formula, rather than breast milk, experience metabolic stress that could play a part in the long-recognized link between formula-feeding and an increased risk of obesity, type 2 diabetes and other conditions in adult life.
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New evidence from research suggests that infants fed formula, rather than breast milk, experience metabolic stress that could play a part in the long-recognized link between formula-feeding and an increased risk of obesity, type 2 diabetes and other conditions in adult life.
The study appears in ACS' Journal of Proteome Research.
Carolyn Slupsky and colleagues explain that past research showed a link between formula-feeding and a higher risk for chronic diseases later in life. Gaps exist, however, in the scientific understanding of the basis for that link. The scientists turned to rhesus monkeys, stand-ins for human infants in such research, that were formula-fed or breast-fed for data to fill those gaps.
Their analysis of the monkeys' urine, blood and stool samples identified key differences between formula-fed and breast-fed individuals. It also produced hints that reducing the protein content of infant formula might be beneficial in reducing the metabolic stress in formula-fed infants. "Our findings support the contention that infant feeding practice profoundly influences metabolism in developing infants and may be the link between early feeding and the development of metabolic disease later in life," the study states.
Story Source:
Materials provided by American Chemical Society. Note: Content may be edited for style and length.
Journal Reference:
- Aifric O’Sullivan, Xuan He, Elizabeth M. S. McNiven, Neill W. Haggarty, Bo Lönnerdal, Carolyn M. Slupsky. Early Diet Impacts Infant Rhesus Gut Microbiome, Immunity, and Metabolism. Journal of Proteome Research, 2013; 130523132331005 DOI: 10.1021/pr4001702
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