Mice with the mouse model of Alzheimer's disease show improvements intheir condition when treated with a high-fat, low-carbohydrate diet. Areport published today in the peer-reviewed, open access journalNutrition and Metabolism, showed that a brain protein, amyloid-beta,which is an indicator of Alzheimer's disease, is reduced in mice on theso-called ketogenic diet.
The report, by Samuel Henderson, from Accera, Inc, Colorado andcolleagues from Belgium runs counter to previous studies suggesting anegative effect of fat on Alzheimer's disease.
"This work supports the premise that key aspects ofAlzheimer's disease can be altered by changes in metabolism. It alsohighlights the interaction of dietary components and how suchcomponents influence the metabolic state", write the authors.
The authors believe that insulin and the related hormone,insulin-related growth factor-1 (IGF-1), are the key players. "Insulinis often considered a storage hormone, since it promotes deposition offat but insulin may also work to encourage amyloid-beta production."
Richard Feinman, editor of the journal, explains the relationbetween nutrients: "You might say that fat is the bomb, and insulin(from carbohydrate) is the fuse. Most studies of the deleteriouseffects of fat have been done in the presence of high carbohydrate. Ifcarbs are high, dietary fat is not oxidized and is instead stored asbody fat." When carbohydrates are very low and fat is high, compoundscalled ketone bodies are generated (ketosis) and these compounds mayplay a role in the observed reduction in amyloid-beta. In associationwith a group from University of Washington led by Dr. Suzanne Craft,Henderson has previously shown cognitive improvement in patients withmild AD who were given a diet that raises ketone bodies.
In an accompanying editorial, Feinman says, "Although it istoo early to tell how the results will fit into the treatment of AD,the implication for diet in general is also important." The primacy ofinsulin as a control element is the basis of popular weight-loss dietsbased on carbohydrate restriction. Such regimens allow dieters toregulate fat and calorie intake by appetite alone as long ascarbohydrate intake remains minimal. Feinman points out, "Henderson'seffort is one of several recent studies that point the way tounderstanding metabolism beyond the issues surrounding simple fatreduction."
A ketogenic diet reduces amyloid beta 40 and 42 in amouse model of Alzheimer's disease
Ingrid Van der Auwera, Stefaan Wera, Fred Van Leuven, and Samuel T.Henderson
Nutrition & Metabolism, in press
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