Intermittent fasting(IF) has been shown to have multiple effects on the hippocampus, a critical brain structure for learning and memory. IF can promote increased neuron production, called neurogenesis, and increases the production of signaling molecules that promote neural health and function - such as brain derived neurotrophic factor (BDNF), glutamate, insulin, and GLP-1. While the precise role of increased neuron production is not well-established, there is accumulating evidence linking the creation of new neurons to cognition and mood.1
Figure 1. IF results in increased activity in neurons involved in communication between the entorhinal cortices and the hippocampus, and increased neurogenesis (creation and integration of new neurons from stem cell replication) in the hippocampus. In addition, molecular pathways that promote neural health are upregualted by IF, including brain derived neurotrophic factor (BDNF), glutamate, insulin, and GLP-1 signaling.
However, a 2003 study in mice found that IF demonstrated improved neuroprotection from stress, as well as a greater reduction of serum glucose. Suggesting that longer fasting periods can have a greater effect on cognitive functioning, over general caloric restriction.4
In terms of modulating mood, a 2014 study demonstrated that measures of depression-like behavior in mice, could be ameliorated by IF. And furthermore, co-administration of an anti-depressant pharmaceutical, imipramine, with IF further improved the behavioral response. Molecularly, IF and imipramine also enhanced molecular pathways associated with learning and memory. These data suggest that the powerful molecular effects of IF can have measurable outcomes on mood and cognition.
A study involving 50 elderly adults showed that caloric restriction over a period of 3 months was associated with improved memory, as measured by the verbal learning test (a memory test involving recall of words). This positive change in memory was also associated with a decrease in C reactive protein (CRP) levels, which are a marker for inflammation.5
Figure 2. Restriction of calories results in improved memory capacity compared to supplementation with a unsaturated fatty acid diet (UFA - a diet suggested to improve memory) and control (no change in diet).
Studies in animals have shown improvements in memory in response to intermittent fasting as well. A study in rats showed that short-term, intermediate-term and long-term memory improves with intermittent fasting. Furthermore, the combination of intermittent fasting with exercise was more helpful in improving memory compared to just fasting or exercise alone.6
Figure 3. In rats, exercise combined with intermediate fasting at every other day (EXE/EODF) was more helpful for improving short, intermediate and long-term memory compared to a sedentary lifestyle (SED), or either intervention alone (EXE, EODF).
Bruce-Keller, A. J., Umberger, G., McFall, R., & Mattson, M. P. (1999). Food restriction reduces brain damage and improves behavioral outcome following excitotoxic and metabolic insults. Ann Neurol, 45(1), 8-15.
Qiu, G., Spangler, E. L., Wan, R., Miller, M., Mattson, M. P., So, K. F., . . . Ingram, D. K. (2012). Neuroprotection provided by dietary restriction in rats is further enhanced by reducing glucocortocoids. Neurobiol Aging, 33(10), 2398-2410. doi:10.1016/j.neurobiolaging.2011.11.025
Anson, R. M., Guo, Z., de Cabo, R., Iyun, T., Rios, M., Hagepanos, A., . . . Mattson, M. P. (2003). Intermittent fasting dissociates beneficial effects of dietary restriction on glucose metabolism and neuronal resistance to injury from calorie intake. Proc Natl Acad Sci U S A, 100(10), 6216-6220. doi:10.1073/pnas.1035720100
Khabour, O. F., Alzoubi, K. H., Alomari, M. A., & Alzubi, M. A. (2010). Changes in spatial memory and BDNF expression to concurrent dietary restriction and voluntary exercise. Hippocampus, 20(5), 637-645.
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