Calorie restriction and stroke

In the western world the average calorie intake has steadily risen as have associated diseases. Calorie restriction (CR) is defined as a decrease in energy intake without lowering nutritional value. This simple intervention has shown, in a wide range of laboratory animals, to extend lifespan and decrease the incidence of several age-related diseases [1]. In humans, CR can reduce markers of oxidative stress and inflammation [2,3], and can lower cardiovascular disease risk [4]. Dietary energy restriction also benefits neurons, as suggested by data showing that CR protects neurons against dysfunction and degeneration in animal models of epileptic seizure, stroke and neurodegenerative diseases [5,6].The risk of ischemic stroke, the second major cause of morbidity and mortality worldwide, can be reduced through diet and lifestyle modification [7]. The mechanisms responsible for neuronal death caused by stroke are believed to involve metabolic compromise, over activation of glutamate receptors, cellular calcium overload, oxidative stress and inflammation [8]. Studies using in vivo and in vitro stroke models have identified several proteins and signalling pathways that can protect neurons against ischemic injury, including: neurotrophic factors, such as brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF); protein chaperones, including heat shock protein 70 (Hsp70) and glucose regulated protein 78 (GRP78); antioxidant enzymes, such as heme oxygenase-1 (HO-1) and the regulator of mitochondrial biogenesis PGC-1α. Several studies suggest CR may promote neuronal survival and plasticity in ischemic stroke, by inducing neuroprotective factors and suppressing inflammatory pathways. The present article reviews findings supporting the neuroprotective effects of CR and discusses the mechanisms activated by CR in ischemic stroke.Experiments performed seven decades ago showed that CR increases the lifespan of rodents [9,10], and this has been