Recent research in humans shows that intermittent fasting results in greater diversity of the gut microbiota. Furthermore, intermittent fasting resulted in weight loss, reduced inflammation and enhanced immune response. In particular, intermittent fasting decreased sugar and increased dietary fibre.
Unfortunately, human studies on the potential benefits of intermittent fasting for dementia have yet to be undertaken. However, tantalising work on the effects of intermittent fasting in mice strongly suggests likely benefits for dementia. Remarkably, that research suggests thatintermittent fasting may protect against the development of Alzheimer’s disease. At least, this holds true in a mouse model of Alzheimer’s disease. Here’s why…
We know that Alzheimer’s disease is associated with abnormally high levels of a protein called beta-amyloid (Aβ) in the brain. For reasons that are poorly understood, Aβ accumulates in the brains of patients with Alzheimer’s disease, whereas in healthy individuals Aβ is cleared from the brain. Aβ is directly implicated in the neuropathology associated with Alzheimer’s disease.
Clearance of Aβ from the brain is influenced by multiple factors, including membrane proteins called aquaporins that are involved in the transfer of water and small solutes across cell membranes. In the brain, aquaporins play a role in the production and homeostasis of cerebral spinal fluid (CSF), and in fluid balance in general. CSF is produced in the choroid plexus epithelium by the secretion of water and salts and it is known that the functioning of the choroid plexus deteriorates Alzheimer’s disease.
There are 10 isoforms of the aquaporins. One of them, AQP4, is expressed by astrocytes and plays a crucial role in modulating water flow in and out of the brain. The polarity of AQP4 is influenced by the ratio of two subtypes of AQP4, M1 and M23. The M1:M23 ratio is influenced by histone deacetylase 3 (HD3), which is known to be significantly increased in Alzheimer’s disease. Fasting increases the levels of an HD3 inhibitor, β-hydroxybutyrate, resulting in down-regulation of the M1:M23 ratio of AQP4.
When these ideas were put to the test in mice with a murine form of Alzheimer’s disease, it was found that AQP4 polarity was restored, and the deposition of Aβ in the brain was prevented. Furthermore, cognitive functioning improved in the fasting mice. Thus, intermittent fasting has the effect of resetting AQP4 polarity in the brain, resulting in improved clearance of toxic substances from the brain, such as Aβ, and improving cognition.
Perhaps you should consider hitting the reset button in your brain?
