Native Americans who often ate processed meat in a can, generically known as "spam" and a common food on reservations, one subsidized by the government -- had a two-fold increased risk of developing type 2 diabetes over those who ate little or none, according to a U.S. study.
Native Americans are at especially high risk of developing diabetes, with nearly half having the condition by age 55.
Researchers writing in the American Journal of Clinical Nutrition surveyed 2,000 Native Americans from Arizona, Oklahoma and North and South Dakota to look into potential reasons for the high rate.
"A lot of communities in this study are in very rural areas with limited access to grocery stores... and they want to eat foods that have a long shelf life," said Amanda Fretts, the lead author and a researcher at the University of Washington School of Medicine.
None of the survey participants, whose average age was 35, had diabetes at the start of the study when they answered questions about diet and other health and lifestyle factors.
After five years, a follow-up survey found that 243 people had developed diabetes.
Among the 500 people in the original study group who ate the most canned processed meat, 85 developed diabetes. In contrast, among the 500 people who ate the least amount of "spam," just 44 developed the disease.
Though Spam is a brand-name pork product, the lower-case term is also used to describe any kind of processed, canned meat, Fretts said. Canned meat is available freely to many Native Americans on reservations as part of the U.S. Department of Agriculture's food assistance program.
Fretts and her colleagues found that unprocessed meat did not have the same relationship with diabetes, with people equally likely to develop diabetes regardless of how much hamburger or cuts of pork or beef they ate.
"I think what this study indicates is processed meats should be a priority for reduction (in the diet), especially among American Indians where they can go to food assistance programs and they can get discounted spam," said Dariush Mozaffarian, a professor at the Harvard School of Public Health who was not involved in the study.
Mozaffarian and his colleagues two years ago conducted an analysis that found that processed meats were tied to a 19 per cent higher diabetes risk, while unprocessed meats were neutral.
"I think the biggest difference between processed and unprocessed meats is sodium," he said, though he added that there is no clear explanation for the link of processed meats and diabetes.
Fretts and her colleagues noted that the people who ate the most processed meats tended also to be heavier, with larger waistlines, raising the possibility that processed meats contribute to obesity, which raises the risk of diabetes.
In an emailed statement to Reuters Health, The American Meat Institute, which represents companies that process meat, said that "processed meats are a safe and nutritious part of a balanced diet."
Fretts said the study could not prove that eating processed meats was to blame for the increased risk of diabetes.
"I think there needs to be more follow-up," she said.
An ingredient in plastics and food-can linings coaxes cells from the pancreas to inappropriately secrete the hormone insulin, a finding that bolsters earlier links between type 2 diabetes and low-dose exposure to the chemical.
Bisphenol-A, or BPA, can mimic the effects of estrogen, a hormone that is involved in regulating insulin production in the body. Although controversy persists over BPA’s potency as an estrogen mimic, the new study, published online February 8 in PLoS ONE, finds that the pollutant is every bit as potent as the body’s natural estrogen in terms of triggering insulin release.
“I don’t think that anyone can say now that low-dose effects don’t occur,” says endocrinologist Ana Soto of the Tufts University School of Medicine in Boston, who was not involved in the new work. “It shows that changes happen in human cells — and at concentrations comparable to current levels of human exposure.”
The new work shows that BPA stimulates insulin release through a hormone-activating protein called estrogen receptor beta, or ER-beta, says Angel Nadal of Miguel Hernández University in Elche, Spain, who led the new study. Tiny concentrations of either estrogen or BPA boost the release of insulin. When his group tested mice engineered to produce no ER-beta, the effect went away, demonstrating that the protein is integral to BPA’s perturbation of insulin secretion.
For people with diabetes, oversecretion of insulin might be viewed as a positive development, he says. But in healthy individuals, it could eventually desensitize tissues to the hormone, creating insulin resistance — a hallmark of type 2 diabetes.
“If this happens in people with a genetic predisposition to diabetes, it will accelerate the induction of that disease,” Nadal says. His team has shown that exposure to BPA elevates an animal’s risk of developing insulin resistance. And people with type 2 diabetes — the type caused by the body’s diminished sensitivity to insulin — tend to have elevated concentrations of BPA in urine, a 2008 study showed.
“I don’t think BPA alone will cause type 2 diabetes,” says Franck Mauvais-Jarvis of Northwestern University’s Feinberg School of Medicine in Chicago. Dozens of environmental chemicals can mimic hormones, he says, “and I suspect it’s a cocktail of these nasties that predisposes individuals to developing metabolic disease, whether its type 2 diabetes or obesity.”
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