increase in BMI, there was a change in methylation by 0.0009 for both genes and that for every unit increase in WC, there was a change in methylation by 0.0004. According to another story, MSI2 methylation can be a predictor of BMI, accounting 24% of variance. Lastly, in a study conducted in 2018, the gene SOCS3, a cytokine signaling suppressor, was found to be upregulated in obesity and was shown to induce leptin and insulin resistance. The paper states "increased SOCS3 expression in obese individuals is associated with several metabolic disorders, including reduced energy expenditure, increased food intake and adiposity, and insulin and leptin resistance. In addition, recent studies found that SOCS3 expression regulates energy and glucose homeostasis in several metabolic conditions, such as pregnancy, caloric restriction, and refeeding". To conclude, it cannot be said that physical exercise itself is causing epigenetic changes to reverse obesity. However, it’s been made clear that physical exercise is implicated in certain factors (BMI, metabolic rate, waist circumference) that are the parameters for diagnosing obesity. These parameters themselves are shown to be correlated with epigenetic changes, whether causative or as a symptom. Effects on neurodegenerative diseases An increasing amount of evidence shows that physical exercise is also involved in the potential treatment and prevention of neurodegenerative diseases. A key assessment thus far is that physical exercise is a key factor for increasing hippocampal adult neurogenesis. Physical exercise has also shown to reduce the excessive neuroinflammation generally regarded as the root cause of many neurodegenerative disorders. Epilepsy Studies have found that physical exercise is a viable, non-pharmaceutical approach to resisting and even undoing the harmful processes that cause sudden abnormal changes in brain cell activity resulting in seizures that characterize epilepsy. One area of focus looks to the effect on brain-derived neurotrophic factor (BDNF) levels following a seizure event. Proper regulation of BDNF levels is necessary to maintain the BDNF-TrkB signaling pathway responsible for healthy synaptic plasticity. It has been observed that seizure events are consistently followed by a significant increase then drastic drop in BDNF levels which results in reduced cognition and further increases the probability of seizure events in the future. However, animal models have shown that epileptic patients undergoing physical exercise, especially if it's routine, develop more consistent BDNF levels similar to those unafflicted by the disorder. This return to normal-like BDNF fluctuations not only promotes generally healthier brain functioning but also