A molecular trigger that may explain how dietary restriction and high-caloric diet produce protective effects against aging and disease has been identified by researchers at Mount Sinai School of Medicine.
Lead researcher Dr Charles Mobbs, Professor of Neuroscience and of Geriatrics and Palliative Medicine at Mount Sinai School of Medicine, has found that within certain parameters, a lower-calorie diet slows the development of some age-related conditions such as Alzheimer's disease, as well as the aging process.
How the diet is restricted - whether fats, proteins or carbohydrates are cut - does not appear to matter.
"It may not be about counting calories or cutting out specific nutrients but how a reduction in dietary intake impacts the glucose metabolism, which contributes to oxidative stress," Mobbs said.
Meanwhile, a high calorie diet may accelerate age-related disease by promoting oxidative stress.
The researchers found that dietary restriction induces a transcription factor called CREB-binding protein (CBP), which controls the activity of genes that regulate cellular function.
By developing drugs that mimic the protective effects of CBP - those usually caused by dietary restriction - scientists may be able to extend lifespan and reduce vulnerability to age-related illnesses.
The team found an optimal dietary restriction, estimated to be equivalent to a 30 percent caloric reduction in mammals, increased lifespan over 50 percent while slowing the development of an age-related pathology similar to Alzheimer's disease.
They further looked at what happens to CBP in a high-calorie diet that has led to diabetes, a disease in which glucose metabolism is impaired.
The team examined mice and found that diabetes reduces activation of CBP. Mobbs concluded that a high-calorie diet that leads to diabetes would have the opposite effect of dietary restriction and would accelerate aging.
The study is published in the journal Public Library of Science Biology.