Heat-processed foods may increase risk of Alzheimer's
Compounds commonly found in the so-called “Western diet” known as Advanced Glycation Endproducts (AGEs) may cause brain changes similar to Alzheimer’s disease and pre-diabetes, according to researchers from the Icahn School of Medicine at Mount Sinai in New York.
Researchers on the paper were Caia Wejing, Calogera Simonarod, Jaime Uribarrib, George A. Kuchelc, Li Zhua, Xue Chena, Michal Schnaider-Beerie, Shobha Swamya, Zhengshan Zhaoa, Mark Woodward, Gary E. Strikera, Fabrizio Grosjeana and Helen Vlassaraa.
AGEs, which occur naturally at low levels in the body, have previously been linked to increased body weight and diabetes and are found in high levels mostly in heat-processed animal food products, such as grilled meats.
The study, which was published in the journal Proceedings of the National Academy of Sciences, showed that consumption of such foods by mice raised the body’s level of AGEs, which, among other effects, suppressed levels of SIRT1, a key “host defense” shown to protect against Alzheimer’s disease as well as metabolic syndrome, a pre-diabetic state.
The researchers said that reducing the intake of AGEs could open “new therapeutic avenues” for the treatment of Alzheimer’s disease, as well as diabetes.
“Age-associated dementia or Alzheimer’s disease is currently epidemic in our society and is closely linked to diabetes,” said Helen Vlassara, MD, Professor and Director of the Division of Experimental Diabetes and Aging in the Brookdale Department of Geriatrics at Mount Sinai.
“While more research needs to be done to discover the exact connection of food AGEs to metabolic and neurological disorders, the new findings again emphasise the importance of not just what we eat, but also how we prepare what we eat,” Dr Vlassara said. “By cutting AGEs, we bolster the body’s own natural defense against Alzheimer’s disease as well as diabetes,” she said.
Study method
Dr Vlassara and her team of researchers at Mount Sinai previously identified AGEs as a culprit leading to diabetes and increased body weight, and showed that decreasing the intake of AGEs lowered related health risks and restored the body’s natural defenses.
For this study, Dr Vlassara tracked cognitive health in mice and humans that ingested AGEs at the high levels of a typical Western diet to determine whether AGEs caused neurodegeneration by suppression of a substance called SIRT1, a deacetylase that regulates neuronal, immune and endocrine function. SIRT1 is found suppressed in individuals with neurodegenerative and metabolic diseases such as diabetes or pre-diabetes, as well as those who are aging.
The researchers found that the mice kept on a diet high in AGEs had high levels of AGE in their brains, and suppressed SIRT1 in their blood and brain tissue compared with mice that were fed a diet low in AGEs. Those mice also developed declines in cognitive and motor abilities, and deposits of amyloid-β, a component of the plaques characteristic of Alzheimer’s disease. They also had metabolic syndrome, a combination of medical conditions with increased risk of diabetes and heart disease. The mice fed a low AGE diet remained free of these conditions.
In addition, Dr Vlassara’s team conducted a clinical study of healthy humans over the age of 60 with high blood levels of AGEs. The study showed that, over a nine-month period, those subjects with high blood levels of AGEs developed cognitive decline, signs of insulin resistance and SIRT1 suppression, while those with low blood AGEs remained healthy.
Taken together, the researchers said these results suggest that consumption of foods high in AGEs could suppress production of SIRT1, contributing over time not only to metabolic syndrome, but also to dementia.
The studies were funded through the US National Institutes of Health’s National Institute on Aging and the US National Institute of Diabetes and Digestive and Kidney Diseases.
Experts cautiously welcoming of findings
Other researchers in the area of dementia have welcomed the findings of the study, but emphasised that the research is at an early stage and more work is needed to fully understand the causes of dementia.
“Diabetes has previously been linked to an increased risk of dementia, and this small study provides some new insight into some of the possible molecular processes that may link the two conditions,” said Dr Simon Ridley, Head of Research at Alzheimer’s Research UK. “Although these findings add to some earlier evidence linking a decrease in SIRT1 protein to Alzheimer’s, the most common cause of dementia, it’s important to note that the people in this study did not have dementia,” he said.
“This subject has so far not been well-studied in people, and we don’t yet know whether the amount of AGEs in our diet might affect our risk of dementia,” Dr Ridley said. “The diseases that cause dementia are complex, and our risk of the condition is likely to be affected by a number of genetic and environmental factors that are not yet fully understood,” he said.
Dr Doug Brown Director of Research and Development at the UK’s Alzheimer’s Society said the Mount Sinai research made a “strong case” for further research.
“Diets with low levels of the compounds show promising effects in mice and should be further explored as a way to prevent dementia through changes in diet,” Dr Brown said. “Of course, we must not forget that the majority of research was conducted in mice and the human element of this study is too small to draw any conclusions,” he said.
“Evidence suggests that the best way to reduce your risk of developing dementia is regular exercise, not smoking and following a healthy diet,” Dr Brown said.
