A Poor Diet Impairs Memory, But Exercise May Help
Julia C. Basso, PhD
Obesity is a worldwide epidemic.
Since 1980, obesity rates have nearly doubled, with 35% of adults over the age of 20 classified as overweight and 11% classified as obese. It is theorized that the increase in obesity is due to the modern lifestyle, which is characterized by highly available, energy dense foods and the lack of a need for physical activity.
Day after day, many of us go straight from our home, to the car, to the office and back again – without getting more than a few steps of exercise.
With obesity comes many other problems, such as cardiovascular disease and diabetes. In addition, obesity is related to cognitive impairment and specifically learning and memory functions that are dependent on a part of the brain called the hippocampus. The hippocampus enables us to remember information for long periods of time. That is, it regulates our long-term memories. In addition, the hippocampus enables us to navigate around our environment.
How do we know how to get from our house to our local grocery market? The hippocampus!
Physical Activity Helps
Unlike obesity, exercise helps our hippocampus. Physical activity improves our ability to remember information and improve dementia-related symptoms in patients with neurodegenerative disorders such as Alzheimer’s disease. In addition, long-term exercise has been shown to both increase the size of the hippocampus and prevent age-related atrophy of the hippocampus.
The hippocampus is unique in that it is one of only two regions in the adult brain that produces new neurons – a process called neurogenesis. Animal studies have revealed that high fat diets and physical activity have opposite effects on neurogenesis; the former inhibits it whereas the latter promotes it.
Because of these differences, scientists at the University of Medicine in Germany recently asked whether exercise could prevent or perhaps even reverse the cognitive impairment associated with exposure to a high fat diet and whether hippocampal neurogenesis played a part in this process.
The first set of experiments utilized exercise in a preventative manner. The scientists exposed adolescent mice to either a high-fat diet or a control diet for 12 weeks, that is, into adulthood. Throughout the entirety of the 12 weeks, half of the mice exercised (were given free access to running wheels) whereas the other half remained sedentary (were not given running wheels).
The second set of experiments utilized exercise in a therapeutic manner. For these studies, adult mice were given either high-fat or control diets for 12 weeks. After this time period, they were exposed to either an exercise or sedentary experience for 14 days.
In adolescent mice, 12 weeks of a high fat diet (this is like spending your entire adolescence into your adulthood eating fatty foods) resulted in impaired memory performance. In addition, this memory deficit was accompanied by fewer new cells in the hippocampus.
Exercising during this time period, however, prevented the memory impairment caused by the fatty diet and increased the number of new neurons in the hippocampus.
In adult mice, the high fat diet did not cause memory impairment and the short-term exercise regimen did not cause any further improvements in memory.
This research demonstrated that the adolescent brain may be particularly susceptible to high fat foods. Considering that so many fatty foods are available to teenagers, it also revealed the extreme importance of adding physical activity into the lives of our children. It just may help prevent any cognitive impairments that come with a poor diet. Future research will be needed to examine the interaction of high fat diets and exercise in adults.
Related Article: Exercise-Induced Increases In Brain Size
Klein, C., Jonas, W., Iggena, D., Empl, L., Rivalan, M., Wiedmer, P., … & Steiner, B. (2016). Exercise prevents high-fat diet-induced impairment of flexible memory expression in the water maze and modulates adult hippocampal neurogenesis in mice. Neurobiology of learning and memory, 131, 26-35.
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