Much ado about eating: Intermittent fasting and post-stroke neuroprotection

Abstract

A proper diet is important for health and longevity. Controlling the amount of food consumed is immensely beneficial as it promotes multiple cellular and molecular protective mechanisms and simultaneously prevents toxic mechanisms. Intermittent fasting (IF) is a flexible and easy-to-adopt dietary modification that helps to mitigate metabolic disorders like diabetes and hypertension, and thus the devastating age-related diseases like heart attack, stroke and dementia. The benefits of IF seem to be mediated by altered epigenetic and transcriptional programming leading to reduced oxidative stress, inflammation, mitochondrial damage and cell death.

Keywords: Caloric restriction; cell death; cerebral ischemia; inflammation; preconditioning.

Figure 1.

Intermittent fasting (IF) influences the body by multiple mechanisms. IF increases glucose tolerance and controls blood pressure. This leads to better prognosis as diabetes and hypertension are major comorbid conditions for stroke. IF induces several genes that promote plasticity, regeneration and neuroprotection. IF also promotes the pathways that curtail inflammation, oxidative stress and apoptosis leading to neuroprotection after stroke.