Intermittent Fasting - Implications for Neurogenesis and the Treatment of Neurological and Neurodegenerative Disorders
/By Roomana Patel
May, 2016
The practice of intermittent fasting (IF), or cycling between periods of ingesting and abstaining from food, has long been revered in religious and spiritual communities as a demonstration of self-restraint, discipline, empathy, and as a method of mental and bodily detoxification.
Scientists have only recently begun testing and validating the significance of IF, discovering a host of compelling findings resulting from the practice. Some of these findings include the onset of ketogenesis, substantial shifts in metabolic pathways and some cellular processes, retardation of age-related neurodegenerative diseases such as Alzheimer’s Disease and Huntington’s Disease, and the increase of hippocampal neurogenesis (Bruel-Jungerman E, et al., 2007; Longo V. & Mattson M., 2013; Manzanero S., et al., 2014). The implementation of IF, therefore, has the potential to serve as a potent, noninvasive and inexpensive strategy within prevention and treatment modalities for several neurological, metabolic, and mood disorders.
Neurons in the hippocampus play an essential role in cognitive processes such as learning and memory, and they are susceptible to dysfunction and deterioration in cases of stroke, traumatic brain injury, epilepsy and age-related neurodegenerative disorders like Alzheimer’s Disease (Longo V. & Mattson M., 2013). As humans and animals age, there is also a general decline in the production of hippocampal neurons, increasing the existing neurons’ vulnerability to these traumas and degeneration. IF induces a mild stress response in brain cells, increasing activity in hippocampal neurons, and producing brain-derived neurotropic factor (BDNF). BDNF, a key protein in brain plasticity, stimulates the growth and upkeep of synapses and dendrites, and increases neurogenesis (Longo V. & Mattson M., 2013; Martin B., et al., 2006). These findings imply that IF can be a viable tool to help replace injured, diseased, and non-proliferating hippocampal neurons, reducing the impact of trauma, and aiding in the deceleration of some neurodegenerative disorders.
Recent studies have also shown that the proliferation of hippocampal neurons can decrease symptoms of major depression (Castrén E. & Rantamäki T., 2009). Researchers utilize structural high resolution Magnetic Resonance Imaging (MRI) on patients exhibiting traits of major depression, deducing that decreased hippocampal volume directly correlates with executive dysfunction. Accordingly, most treatment modalities for depressed patients include prescribing some form of antidepressant, psychotropic medication that balances neurotransmitters by reducing the toxic effects of stress and increasing hippocampal neurogenesis (Bremner, J. D., et al., 2000). Working in a similar manner, IF could be employed as a supplementary tool for patients with major depression to modify brain neurochemistry and increase hippocampal neurogenesis.
The practice of IF has already garnered quite a bit of attention for its promising implications on the future of neurogenesis and in the treatment of neurodegenerative and psychological disorders. By altering the neurochemistry of the brain and the activity of the neuronal network, IF enhances brain function, acts as an important mechanism in treatment modalities for afflicted patients, and can be integrated into an overall plan for preventative medicine.
References
1. Longo, V., & Mattson, M. (2014). Fasting: Molecular Mechanisms and Clinical Applications. Cell Metabolism, 19(2), 181-192. doi:10.1016/j.cmet.2013.12.008
2. Martin, B., Mattson, M. P., & Maudsley, S. (2006). Caloric restriction and intermittent fasting: Two potential diets for successful brain aging. Ageing Research Reviews, 5(3), 332-353. doi:10.1016/j.arr.2006.04.002
3. Martin, B., Mattson, M. P., & Maudsley, S. (2006). Caloric restriction and intermittent fasting: Two potential diets for successful brain aging. Ageing Research Reviews, 5(3), 332-353. doi:10.1016/j.arr.2006.04.002
4. Lee, M. M., Reif, A., & Schmitt, A. G. (2012). Major Depression: A Role for Hippocampal Neurogenesis? Behavioral Neurobiology of Depression and Its Treatment Current Topics in Behavioral Neurosciences, 153-179. doi:10.1007/7854_2012_226
5. Castrén, E., & Rantamäki, T. (2010). The role of BDNF and its receptors in depression and antidepressant drug action: Reactivation of developmental plasticity. Devel Neurobio Developmental Neurobiology, 70(5), 289-297. doi:10.1002/dneu.20758
6. Bremner, J. D., Narayan, M., Anderson, E. R., Staib, L. H., Miller, H. L., & Charney, D. S. (2000). Hippocampal Volume Reduction in Major Depression. American Journal of Psychiatry AJP, 157(1), 115-118. doi:10.1176/ajp.157.1.115
