Keto diet may protect against cognitive decline
A keto diet is high in fat, low in carbohydrates, and has an adequate amount of protein.
This kind of diet is meant to trigger ketosis, which is a metabolic process through which the body breaks down fat and protein and transforms them into energy, leading to weight loss.
Besides triggering weight loss, a keto diet may also bring other health benefits, as studies have recently suggested. For instance, one such study argued that keto diets could help reduce the side effects of certain cancer therapies.
Now, researchers from the Sanders-Brown Center on Aging at the University of Kentucky in Lexington, KY, are assessing evidence suggesting that keto diets may also help stave off cognitive decline.
The scientists conducted two studies, both in mice. The findings indicate that keto-type diets can protect neurovascular function, as well as metabolic function, in general, which may help the animals maintain healthy cognitive function.
Keto diet clears out beta-amyloid
The first study, whose results appear in the journal Scientific Reports, looked at the effects of a keto diet on neurovascular function, which includes sensory and motor functions, as well as circulation.
The team worked with two groups of nine mice each, all of which were aged 12-14 weeks. The animals received either a ketogenic diet or a regular diet for 16 weeks.
After this period, the scientists found that the mice that had followed the keto regimen had not only improved blood flow to the brain, but also better bacterial balance in the gut, as well as lower blood glucose (sugar), and lower body weight.
Moreover, and most importantly, the keto diet also seemed to boost the clearance of beta-amyloid protein in the brain — the “building blocks” that, in Alzheimer’s, stick together, forming toxic plaques which interfere with neuronal signaling.
“Neurovascular integrity, including cerebral blood flow and blood-brain barrier function, plays a major role in cognitive ability,” notes study author Ai-Ling Lin.
“Recent science has suggested that neurovascular integrity might be regulated by the bacteria in the gut,” she adds, “so we set out to see whether the ketogenic diet enhanced brain vascular function and reduced neurodegeneration risk in young healthy mice.”
‘Using diet to mitigate risk’ of dementia
“While diet modifications, the ketogenic diet, in particular, has demonstrated effectiveness in treating certain diseases, we chose to test healthy young mice, using diet as a potential preventative measure,” she further explains.
“We were delighted to see that we might indeed be able to use diet to mitigate risk for Alzheimer’s disease.”
Although it is unclear exactly which mechanisms are set in motion by the keto diet in this context, Lin speculates that the protective effects for the brain may be due the fact that this regimen essentially inhibits a nutrient sensor known as mechanistic target of rapamycin (mTOR).
Previous research has suggested that mTOR signaling has an important impact on aging processes and an individual’s lifespan.
Lin further notes that it is also possible to target mTOR through caloric restriction — a dietary regimen which, as the name suggests, restricts the intake of calories — or by administering the enzyme rapamycin.
‘Tremendous implications for clinical trials’
In the second study — whose findings they published in the journal Frontiers in Aging Neuroscience — the researchers scanned the brains of mice who received one of three interventions: a dose of rapamycin, exposure to the keto diet, or simple caloric restriction.
In this case, the researchers worked with both young and aging animals to understand the effects of these interventions on cognitive functioning.
“Our earlier work already demonstrated the positive effect rapamycin and caloric restriction had on neurovascular function,” notes Lin, adding that: “We speculated that neuroimaging might allow us to see those changes in the living brain.”
The researchers’ data indicated that caloric restriction could improve neurovascular and metabolic functioning in aging mice, thus protecting their brain health.
Lin notes that in this mouse model neurovascular and metabolic function appears to work better than in younger mice whose diets were not restricted.
“Ai-Ling’s lab was the first to use neuroimaging to see these changes in a living brain, and the potential link to changes in the gut microbiome,” notes Linda Van Eldik, Director of the Sanders-Brown Center on Aging.
“Her work has tremendous implications for future clinical trials of neurological disorders in aging populations,” says Van Eldik.
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