A diet high in saturated fat can quickly rob the brain of a key chemical that helps protect against Alzheimer’s disease, according to new research.
In a small study published online on June 17 in the journal JAMA Neurology, researchers found that dietary saturated fat cut the body’s levels of the chemical apolipoprotein E, also called ApoE, which helps “chaperone” amyloid beta proteins out of the brain.
“People who received a high-saturated-fat, high-sugar diet showed a change in their ApoE, such that the ApoE would be less able to help clear the amyloid,” said research team member Suzanne Craft, a professor of medicine at Wake Forest School of Medicine.
Amyloid beta proteins left loose in the brain are more likely to form plaques that interfere with neuron function, the kind of plaques found in the brains of people with Alzheimer’s disease.
Diet also directly affected the amount of loose amyloid beta found in cerebrospinal fluid, Craft said. Those on a high-saturated-fat diet had higher levels of amyloid beta in their spinal fluid, while people on a low-saturated-fat diet actually saw a decline in such levels, she said.
“An amyloid that is not cleared – or attached to ApoE to get cleared – has a greater likelihood of becoming this toxic form,” Craft said.
The clinical trial, led by Dr. Angela Hanson of the Veterans Affairs Puget Sound Health Care System in Seattle, involved 20 seniors with normal cognition and 27 with mild thinking impairment, a precursor to Alzheimer’s disease.
The patients, all in their late 60s, were randomly assigned to diets that contained the same amount of calories but were either high or low in saturated fat. The high-saturated-fat diets had 45 percent of total energy coming from fat, and more than a quarter of the total fat came from saturated fats. The low- saturated-fat diets had 25 percent of energy coming from fat, with saturated fat contributing less than 7 percent to total fat.
After just a month, the diets caused changes in the amounts of amyloid beta and ApoE in the study participants’ cerebrospinal fluid, researchers said. “Diet can really change levels of these toxic proteins and of these mediators that help clear these amyloids,” Craft said. “Diets that are very high in bad cholesterol seem to interfere with ApoE’s ability to clear amyloid.”
One gerontology expert, who wrote an editorial accompanying the study in the journal, didn’t think the link was quite that clear.
Although the study shows that diet can affect brain chemistry, it does not definitely tie diet to a person’s risk for Alzheimer’s disease, said Dr. Deborah Blacker, director of the Gerontology Research Unit at Massachusetts General Hospital in Boston.
“Is it plausible to say this could affect the risk of having Alzheimer’s pathology in your brain? It’s not showing that,” said Blacker, who also is with the Harvard School of Public Health. “It’s showing that some of the chemicals related to Alzheimer’s pathology can shift in response to dietary factors.”
The study does, however, offer important insight into the value of good nutrition, she said.
“The important lesson from the study is that dietary intervention can change brain amyloid chemistry in largely consistent and apparently meaningful ways, in a short period of time,” Blacker wrote in the editorial. “Does this change clinical practice for those advising patients who want to avoid
dementia? Probably not, but it adds another small piece to the growing evidence that taking good care of your heart is probably good for your brain too.”
People focus on diet in terms of weight and heart health, but they overlook that nutrition can be key to cognitive function as well, Craft said.
“Diet is a very underappreciated factor in terms of brain function,” she said. “It’s quite well accepted for your heart and your cholesterol and your blood, but diet is critical for a healthy brain aging. Many of the things the brain needs to function properly – fatty acids, certain amino acids – come only from food.”
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