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LETTER TO THE EDITOR |
UND Life Sciences
13800 Fairhill Road, no. 321
Shaker Heights, OH 44120
E-mail: undurti{at}hotmail.com
Dear Sir:
The conclusion of the recent systemic review of the published studies that breastfeeding in infancy is associated with a reduced risk of type 2 diabetes, with marginally lower insulin concentrations in later life, and with lower blood glucose and serum insulin concentrations in infancy (1) is interesting.
Human milk contains tumor necrosis factor 
(TNF-), interleukin (IL)-1, IL-6, transforming growth factor ß1 and ß2 (TGF-ß1 and TGF-ß2), chemokine growth-related oncogene protein , monocyte chemoattractant protein-1, IL-8, IL-1 receptor antagonist, soluble forms of the receptors for TNF-, the antiinflammatory cytokine IL-10, and RANTES (regulated upon activation, normal T cell expressed, and secreted) (2–5). Lysozyme present in human milk suppresses chemotaxis and respiratory burst activity in human polymorphonuclear leukocytes (6). The presence of an ascorbate-like material, uric acid, -tocopherol, and ß-carotene in human milk ensures that phagocyte-produced oxidant molecules cannot persist, and this contributes to the antiinflammatory effects of milk. Thus, human milk exerts antiinflammatory effects and still exerts significant protective action against infections in breastfed infants. In addition, human breast milk is a good source of polyunsaturated fatty acids (PUFAs), especially of 
-linolenic acid (GLA), arachidonic acid (AA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA) (7).
Breastfed infants have a significantly higher percentage of DHA and other PUFAs in muscle phospholipids than do nonbreastfed infants. Higher PUFA concentrations in the skeletal muscle membrane are associated with lower fasting plasma glucose concentrations (8), whereas low concentrations of DHA and other PUFAs can result in insulin resistance. We showed that prior oral administration of pure GLA, AA, EPA, and DHA (which are present in human breast milk) prevents alloxan-induced diabetes mellitus by protecting pancreatic ß cells from the apoptotic actions of alloxan (9, 10) supports the conclusions made by Owen et al (1).
Early nutrition is an important environmental signal that can induce lifetime effects on metabolism, growth, and neurodevelopment and on major disease processes, such as diabetes mellitus (11). It is likely that breastfeeding ensures adequate nutrition and PUFAs that are essential for brain growth and development (7, 12). Recent studies indicate a significant role for brain insulin receptors in the control of insulin secretion and carbohydrate metabolism (12). It is likely that breastfeeding ensures an adequate supply of PUFAs, which, in turn, will lead not only to the growth and development of brain but also to adequate numbers of insulin receptors in the brain to maintain normal glucose metabolism (13). In view of this evidence, it will be interesting to study whether perinatal supplementation of PUFAs could prevent or postpone the development of diabetes mellitus in high-risk subjects (14, 15).
ACKNOWLEDGMENTS
The author had no conflict of interest.
REFERENCES
. Pediatr Res 1997;41:80a(abstr).
-3 fatty acids. Nutrition 2003;19:213–28.[Medline]-6 fatty acids. Nutrition 2003;19:93–114.[Medline]
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