The September 26, 2007 issue of the Journal of the American Medical Association reported the discovery of researchers at the University of Colorado at Denver and Health Sciences Center, Denver that greater intake of omega-3 fatty acids has a positive effect on the prevention of the development of type 1 diabetes in children. Type 1 diabetes is caused by pancreatic islet autoimmunity, which results in destruction of beta cells in the pancreas that produce insulin, causing in an elevation in blood sugar. Cod liver oil given in infancy had previously been found to be associated with a protective effect against the development of childhood diabetes, however, it was not known whether the oilís vitamin D or fatty acid content were responsible for the benefit.
Jill M. Norris, MPH, PhD and colleagues examined the effect of omega fatty acids in 1,770 children determined to be at risk of type 1 diabetes by a genetic marker or by having a first degree relative with the disease. Dietary questionnaires concerning food consumed by the children during the previous year were completed yearly by the childrenís mothers and analyzed for omega-3 and omega-6 fatty acid intake. The children were followed from one year of age to an average of 6.2 years. Islet autoimmunity was determined by testing for insulin, glutamic acid decarboxylase, or insulinoma-associated antigen-2 autoantibodies on two consecutive study visits, and being positive for autoantibodies or having diabetes at the last visit.
At the end of the study, 58 children had developed pancreatic islet autoimmunity. After adjusting for factors such as calorie consumption, the research team found a significantly lower risk of developing islet autoimmunity associated with increased total omega-3 fatty acid intake. When islet autoimmunity was limited to those with two or more autoantibodies, the risk was further lowered. Omega-6 intake was not associated with islet autoimmunity risk.
In a separate study of 244 children whose erythrocyte (red blood cell) membrane fatty acid content was measured, in which 35 participants developed diabetes, higher omega-3 content was also found to be associated with a lower risk of islet autoimmunity.
"Our data suggest that ingestion of omega-3 fatty acids throughout childhood may decrease the risk of islet autoimmunity," the authors write. Commenting on the recent establishment of a clinical trial designed to evaluate the hypothesis that supplementation with the omega-3 fatty acid DHA in utero and infancy will help prevent the development of islet autoimmunity in infants at risk for diabetes, they conclude, "If this trial confirms this hypothesis, dietary supplementation with omega-3 fatty acids could become a mainstay for early intervention to safely prevent the development of type 1 diabetes."
Related Health Concern: Diabetes
Type 1 diabetes, formerly known as insulin-dependent diabetes, is an autoimmune condition that occurs when the body attacks and destroys the cells (called beta cells) that make insulin. Type 1 diabetes accounts for about 5 to 10 percent of cases. Because type 1 diabetics can no longer make insulin, insulin replacement therapy is essential.
Type 2 diabetes, formerly known as non-insulin-dependent diabetes, occurs when the body is no longer able to use insulin effectively and gradually becomes resistant to its effects. It is a slowly progressing disease that goes through identifiable stages. In the early stages of diabetes, both insulin and glucose levels are elevated (conditions called hyperinsulinemia and hyperglycemia, respectively). In the later stages, insulin levels are reduced, and blood glucose levels are very elevated. Although few people are aware of this crucial distinction, therapy for type 2 diabetes should be tailored to the stage of the disease.
In human experiments, omega-3 fatty acids lowered blood pressure and triglyceride levels, thereby relieving many of the complications associated with diabetes. In animals, omega-3 fatty acids cause less weight gain than other fats do; they have also been shown to have a neutral effect on LDL, while raising HDL and lowering triglycerides (Petersen M et al 2002).
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