Exercise May Combat Memory Declines Linked to High-Fat Foods

July 10, 2013

Rats and mice fed a high-fat diet show declines in memory and thinking skills. But exercise may combat the detrimental effects of fatty foods on the brain, two new studies show. While it’s a long way from rats to people, the research raises intriguing questions about whether the Western diet, high in saturated fats, can contribute to declines in memory, and what we can do to minimize any damage.

In one of the studies, researchers at the University of Minnesota studied rats that had been trained to respond to a musical tone, moving from one part of their pen to another to avoid an electric shock. The test is regarded as a good measure of rodents’ ability to remember and the functioning of the hippocampus, the same part of the brain that is critical to memory in people.

Some of the animals were fed a high-fat diet that mimicked the kind of diet typical of many Americans, containing 40 percent fat. Others got a regular diet with lower fat content. Both groups ate the same number of daily calories.

After 16 weeks, the rats fed the fatty diet did much worse on the memory tests than they had at the start of the study. The rodents eating the leaner chow, on the other hand, continued to score just as well.

But if the rats that were eating the high-fat diet were given access to a running wheel and rodent-sized treadmill, their memories started to improve. Compared to sedentary rats that did not have access to exercise equipment, the active animals continued to score higher on memory tests over the following weeks. By week seven, they scored as well as they had at the start of the study, despite consuming the fat-rich diet. It was as if exercise counteracted the brain-diminishing effects of the fatty foods.

The findings may have implications for people with Alzheimer’s disease, as another study conducted at Kyoto University in Japan suggests. Those scientists looked at mice that had been bred to develop a disease that resembles Alzheimer’s in people. Earlier research had shown that a high-fat diet hastened memory loss and the progression to dementia, while low-fat foods and exercise slowed cognitive decline.

In the latest experiment, the researchers sought to determine whether diet or activity level was most important for preserving brain function. For 10 weeks, they fed the mice a high-fat diet, similar to the Minnesota study.

Over the following 10 weeks, some of the mice were switched to a low-fat diet. Some of the mice in each group were also given access to a running wheel, while others remained sedentary.

At the end of the study, the scientists found that those who exercised scored higher on memory tests, regardless of diet. They also had fewer brain plaques, a hallmark of Alzheimer’s disease, than the sedentary mice.

The findings underscore the likelihood that high-fat foods may have detrimental effects on the brain, at least in rodents. The researchers speculate that fatty acids, the form of fats that circulates in the bloodstream, may enter the brain, triggering the formation of Alzheimer’s plaques.

Much more research needs to be done to determine how diet affects the human brain, especially in people who may be at increased risk for Alzheimer’s disease. But the findings highlight the benefits of exercise on the brain.

Other studies have shown that even moderate exercise, like a daily walk, may have benefits for the brain and reduce Alzheimer’s risk. If you’re eating a high-fat diet, as so many people do, that walk may be even more important.

By ALZinfo.org, The Alzheimer’s Information Site. Reviewed by William J. Netzer, Ph.D., Fisher Center for Alzheimer’s Research Foundation at The Rockefeller University.

Source: Mavanji V, Little MR, Noble EE, et al: “Exercise Reduces Cognitive Decline Induced by Dietary Fat.” Society for Neuroscience Annual Meeting poster presentation.

Masato Maesako, Kengo Uemura, Masakazu Kubota, et al. “Exercise is more effective than diet control in preventing high fat diet-induced [beta]-amyloid deposition and memory deficit in amyloid precursor protein transgenic mice.” The Journal of Biological Chemistry, 287, 23024-23033, June 29, 2012.


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