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Originally published August 25 2012

Toxic byproduct of heat-processed food may contribute to weight gain and diabetes, scientists find

by Ethan A. Huff, staff writer

(NaturalNews) Eating foods cooked with dry heat could be making you fat, inflamed, diabetic, and cancer-prone. These are the suggested findings of a new study published in the journal Proceedings of the National Academy of Sciences, which outlines how exposure to methylglyoxal (MG), a chemical byproduct of certain heat-processed foods, is linked to abdominal weight gain, early insulin resistance, and type-2 diabetes, among other conditions.

Dr. Helen Vlassara, M.D., Professor and Director of the Division of Experimental Diabetes and Aging at the Mount Sinai School of Medicine in New York set out to learn how MG, an advanced glycation endproduct (AGE) that is present in both dry heat-cooked and processed foods, might be affecting health. To do this, she fed a group of mice a diet high in MG over the course of four generations, and compared the animals' overall health to a control group of mice fed an MG-free diet. Both groups consumed the same overall amount of calories and fat.

What Dr. Vlassara and her team observed at the conclusion of the study is that the MG mice grew much fatter than the MG-free mice, and also developed early insulin resistance, while the MG-free mice remained generally healthy. Specifically, MG was found to impair or damage certain protective mechanisms in the mice's bodies that help control inflammation, metabolize glucose and insulin, and ultimately protect against disease.

The MG mice also had a marked deficiency in silent mating type information regulation 2 homolog (SIRT1), a survival factor enzyme that protects cells from free radical damage, and from dying early as a result of oxidation. Often referred to as the "skinny gene," SIRT1 inhibits unhealthy fat storage and increases fat metabolism, reducing the risk of heart attack and stroke, diabetes, arthritis, osteoporosis, and various other conditions.

In the MG-fed mice that lacked SIRT1, fat cells gradually began to accumulate and produce cytokines, which are highly inflammatory molecules that impair glucose metabolism and inhibit fat turnover. Meanwhile, MG-free mice had normal SIRT1 levels, and none of them developed diabetes, an astounding result that has huge implications for humans trying to avoid weight gain and diabetes.

"This was a prolonged but rewarding study showing that a specific AGE compound abundant in foods, within only a few generations in mouse terms, contributes to the increase in weight gain, insulin resistance, and diabetes, reproducing the pattern seen increasingly in humans over the last decades," said Dr. Vlassara about her findings.

"The study demonstrates how the prolonged ingestion of seemingly innocuous substances common in human food, such as MG, can reduce defenses and compromise native resistance to metabolic and other diseases."

Cutting out MG rather than high-fat, high-carb foods found to effectively combat diabetes

Interestingly, both groups of mice in the study ate the same overall amounts of carbohydrates, proteins, and fats, illustrating that obesity is not so much an issue of calorie consumption as it is the type of calories consumed. After all, MG-free mice who ate the same amount of overall calories as their MG-eating counterparts fared much better health-wise, proving that a healthy diet is so much more than just a math equation that computes caloric intake.

MG is typically found in coffee, beer, liquor, soft drinks, toasted breads, crackers, cakes, and soy sauce, all of which are produced using certain heating and processing methods that create MG as a toxic byproduct. MG is also produced when meats are cooked over an open flame, for instance, or when sugars are heated or browned using high temperatures.

Besides causing diabetes and weight gain, MG is also a known genotoxin, which means it harms both genes and chromosomes. MG also damages proteins and lipids, and has been linked to causing permanent genetic changes and cancer.

Sources for this article include:

http://www.eurekalert.org/pub_releases/2012-08/tmsh-stb082012.php

http://forum.lef.org/default.aspx?f=35&m=64393

http://www.medicaldaily.com






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