Eating more calories and fats may contribute to an increased risk of Alzheimer’s disease (AD) in some people, according to an article in the August issue of The Archives of Neurology.
According to background information given, significantly reduced calorie diets have been associated with longer life spans in mice and rats. Researchers believe that the relationship is a result of the production of fewer free radicals, destructive molecules formed during the breakdown of food and oxygen in cells. Free radicals damage cells and may increase the damage done by beta amyloids, the glue-like particles found in the brains of people with AD.
Jose A. Luchsinger, M.D., of Columbia University, New York, NY, and colleagues studied the association between caloric intake and AD in 980 elderly individuals without AD at the start of their study. The researchers followed these patients for an average of 4 years and recorded how many calories they ate, and tested for the presence of the apolipoprotein E (APOE) epsilon 4 allele, a gene that has been associated with AD.
During the study, 242 patients developed AD, and 28 percent tested positive for the APOE epsilon 4 gene. The average daily caloric intake of the women studied (67 percent of the study population) was 1,267 kcals. Men consumed an average of 1,316 kcals per day. Average daily fat consumption in both groups was 38 grams.
The researchers divided the study group into four groups depending on how many calories were consumed daily. The group that consumed the most calories had a 50 percent greater chance of developing AD.
The researchers also looked at the effect of the APOE epsilon 4 gene. Of the participants, 263 tested positive for the APOE epsilon 4 gene, and among them, those who consumed the most calories had a 2.3 times greater chance of developing AD compared to those who ate the fewest calories.
The authors write that "Calorie restriction may also decrease [nerve cell] death and increase expression of neurotrophic [nerve-protecting] factors in the brain. Reduced calorie intake can increase the brain's capacity for plasticity and repair in neurodegenerative disorders, including AD."
The researchers conclude: "Our analyses of 242 cases of incident AD… revealed that the risk of AD is associated with higher total calorie intake and fat intake in individuals [with] the APOE epsilon 4 [gene]. In individuals without the APOE epsilon 4 [gene], calorie and fat intake were not associated with risk of AD."