Energy balance
Dietary restriction (DR), including caloric restriction and intermittent fasting, extends lifespan and protects against neurodegenerative diseases (Alzheimer's, Parkinson's, stroke) by inducing a cellular stress response that upregulates neurotrophic factors (BDNF) and protein chaperones (HSP-70).
Adopting dietary restriction through caloric reduction or intermittent fasting can trigger biological mechanisms that protect the brain against aging and neurodegenerative diseases. This is achieved by increasing the production of protective proteins like BDNF and heat-shock proteins. While animal studies show robust protection, human application should focus on sustainable patterns of reduced intake or fasting windows, acknowledging that individual responses may vary.
The beneficial effects of DR, particularly those of intermittent fasting, appear to be the result of a cellular stress response that stimulates the production of proteins that enhance neuronal plasticity and resistance to oxidative and metabolic insults; they include neurotrophic factors such as brain-derived neurotrophic factor (BDNF), protein chaperones such as heat-shock proteins, and mitochondrial uncoupling proteins.
Why this rating
Strong evidence from multiple animal models (mice, rats) and some human epidemiological data, though direct human clinical trials for neuroprotection are not the primary focus of this review.
Source
Meal size and frequency affect neuronal plasticity and vulnerability to disease: cellular and molecular mechanisms
Mark P. Mattson et al. · Journal of Neurochemistry · 2003
DOI 10.1046/j.1471-4159.2003.01586.x
More from this paper
- Dietary restriction stimulates neurogenesis (the generation of new neurons) in the adult hippocampus, primarily by enhancing the survival of newly generated cells via BDNF, rather than increasing the proliferation rate of stem cells.Good
- Dietary restriction does not protect against all neurodegenerative conditions; specifically, it fails to protect and may accelerate disease progression in models of ALS caused by Cu/Zn-SOD mutations.Moderate
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