Intermittent Fasting and its effect on the Brain

Intermittent Fasting is the act of abstaining from calorie consumption for extended periods of time. Usually this spans between 16-24 hours. This article will explore the neuroprotective benefits of Intermittent Fasting.
A study conducted in 1984 restricting the calorie intake of rodents through alternate day IF, resulted in the mice having an enhanced ability to navigate through complex mazes.[1] Since then, there have been numerous studies linking Intermittent Fasting to improved cognitive function in mice and other animals.[2][3][4] A more recent study highlighted the fact that a diet high in fats and sugars actually reduced the mental capacity in mice.[5] Although, these are animal studies, it is clear that there is a correlation between intermittent fasting and increased brain function. It begs the question, why?

“Intermittent Fasting” causes Hormesis. Hormesis is a biological event in which a low dose of a toxic chemical causes a positive effect, resonant with the colloquial phrase ‘what doesn’t kill you makes you stronger’

“Recent findings have elucidated the cellular signaling pathways and molecular mechanisms that mediate hormetic responses which typically involve enzymes such as kinases and deacetylases, and transcription factors such as Nrf-2 and NF-kappaB. As a result, cells increase their production of cytoprotective and restorative proteins including growth factors, phase 2 and antioxidant enzymes, and protein chaperones.”[6]
A publication revealed that IF induced sirtuin 1 protein expression in deficient mice resulting in improved brain function:
“After eight weeks of intermittent fasting, sirtuin 1 protein expression was recovered in SAMP8. This recovery was accompanied by a reduction in the two acetylated targets
 Our findings provide new insights into the participation of sirtuin 1 in ageing and point to a potential novel application of this enzyme to prevent frailty due to ageing processes in the brain.”[7]
A recent review of the therapeutic effect of fasting found:
“Several interrelated cellular mechanisms contribute to the beneficial effects of IF on the nervous system including reduced accumulation of oxidatively damaged molecules, improved cellular bioenergetics, enhanced neurotrophic factor signaling, and reduced inflammation
.intermittent fasting may also promote restoration of damaged nerve cell circuits by stimulating synapse formation and the production of new neurons from neural stem cells (neurogenesis)”[8]

This study reveals that not only does IF have neuroprotective factors but it may in fact help recover lost brain cells and improve brain function.

  • Goodrick CL. Effects of lifelong restricted feeding on complex maze performance in rats. Age.1984;7:1–2.
  • Singh R, Lakhanpal D, Kumar S, Sharma S, Kataria H, Kaur M, Kaur G, Age (Dordr). Late-onset intermittent fasting dietary restriction as a potential intervention to retard age-associated brain function impairments in male rats.2012 Aug; 34(4):917-33.
  • FontĂĄn-Lozano A, SĂĄez-Cassanelli JL, Inda MC, de los Santos-Arteaga M, Sierra-DomĂ­nguez SA, LĂłpez-Lluch G, Delgado-GarcĂ­a JM, CarriĂłn AM. Caloric restriction increases learning consolidation and facilitates synaptic plasticity through mechanisms dependent on NR2B subunits of the NMDA receptor.J Neurosci. 2007 Sep 19; 27(38):10185-95.
  • Lee J, Seroogy KB, Mattson MP. Dietary restriction enhances neurotrophin expression and neurogenesis in the hippocampus of adult mice.J Neurochem. 2002 Feb; 80(3):539-47.
  • Molteni R, Barnard RJ, Ying Z, Roberts CK, GĂłmez-Pinilla F. A high-fat, refined sugar diet reduces hippocampal brain-derived neurotrophic factor, neuronal plasticity, and learning. Neuroscience.2002;110:803–814.
  • Mattson MP. Hormesis defined. Ageing Res. Rev. 2008;7:1–8
  • Tajes M1, Gutierrez-Cuesta J, Folch J, Ortuño-Sahagun D, Verdaguer E, JimĂ©nez A, Junyent F, Lau A, Camins A, PallĂ s M. Neuroprotective role of intermittent fasting in senescence-accelerated mice P8 (SAMP8). Rejuvenation Res. 2015 Apr;18(2):162-72. doi: 10.1089/rej.2014.1624.