New study reveals AGEs in overcooked food can negatively impact brain health

raw meatFor decades, scientists have warned about the dangerous carcinogens associated with grilled foods, but a new study revealed another reason to be wary of overcooking.

The study, completed by the Icahn School of Medicine at Mount Sinai Hospital, showed that a diet high in glycotoxins called advanced glycation end-products (AGEs) – found in high-concentration in well-done meat – is a risk factor in developing age-related dementia.

The study entitled “Oral glycotoxins are a modifiable cause of dementia and the metabolic syndrome in mice and humans” was published in the journal Proceedings of the National Academy of Sciences (PNAS).

Alzheimers News Today and Munchies both reported on this study.


“In the study, mice were who were on a diet high in glycotoxins called Advanced Glycation End products, or AGES, were found to have significantly higher likelihood of developing dementia-like symptoms. They also had greater levels of amyloid beta proteins—the basis of “brain plaque” in Alzheimer’s patients—in their brains.”

Alzheimers News Today

“The research team also assessed AGEs in blood samples from 93 individuals aged over 60 years for a 9-month period. Data on the participants’ cognitive function and eating habits, especially of food products rich in glycotoxins, was analyzed. The insulin sensitivity of each participant was also determined, as it represents a major biomarker for metabolic syndromes, including obesity and diabetes. Similar to the results in mice, participants with higher blood levels of AGEs experienced more cognitive decline and a reduction in insulin sensitivity, suggesting that regular consumption of AGEs in over-cooked food may lead to diabetes and obesity.”

“The team concluded that food-derived AGEs are a modifiable risk factor for both metabolic syndrome disorders and Alzheimer’s disease, and suggest that an AGE-restricted diet may provide an effective therapeutic strategy for both disorders.”


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Copyright 2012 AGE Foundation.