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Research in Focus: The potential protective effects of ketogenic diets in brain disorders

Wednesday, 24 June 2020

The ketogenic diet is a recognised therapy for epilepsy in children with poorly controlled seizures, as well as, more recently, in adults. It is a strict diet high in fats and low in carbohydrates, which makes the body burn fat for energy instead of glucose (a process called ketosis).

This has led researchers to investigate the potential benefits of nutritional ketosis in other conditions, with possible improvements being reported in mild cognitive impairment, early Alzheimer’s disease, Parkinson's disease, schizophrenia, bipolar disorder, and autistic spectrum disorder. These share abnormalities in the metabolism of glucose, suggesting that a ketogenic diet may be useful.

It is important to understand how ketosis brings about these improvements before it can be considered as a potential treatment for brain disorders. Researchers at the IMPACT Institute, a collaboration between Barwon Health and Deakin University, conducted a review of worldwide research to provide a potential answer to this question.

This study suggests that ketosis may reduce the damage to the brain caused by brain disorders by changing the way some brain cells, known as astrocytes, react to the damage. Astrocytes are star shaped cells that have a supporting role in making sure the brain remains healthy and functions normally. When damaged by disease or injury, astrocytes try to defend the brain by growing bigger and multiplying via a process called astrogliosis.

Ironically, the effects of astrogliosis often play a major role in the development and acceleration of brain disorders, and is it through changing this pathway that nutritional ketosis is thought to have its protective effect.

Title: Nutritional ketosis as an intervention to relieve astrogliosis: Possible therapeutic applications in the treatment of neurodegenerative and neuroprogressive disorders 

Authors: Gerwyn Morris, Michael Maes, Michael Berk, André F. Carvalho and Basant K. Puri

Citation: European Psychiatry, 63(1), e8, 1–21

Department: IMPACT