https://goo.gl/yif8rhBesides its weight loss-related benefits, recent studies have pointed to many other advantages. For instance, Medical News Today recently covered research suggesting that the diet may increase longevity and improve memory in old age.
Other studies have noted the neurological benefits of the diet. The keto diet is used to treat epilepsy, and some have suggested that it may prove helpful in Alzheimer's and Parkinson's disease.
However, the mechanism by which a keto diet may benefit the brain in these illnesses has been a mystery. The new research - which was led by Dr. Raymond Swanson, a professor of neurology at the University of California, San Francisco - suggests that it may do so by reducing brain inflammation.
In the new study, Dr. Swanson and team show the molecular process by which the keto diet reduces brain inflammation. The researchers also identify a key protein that, if blocked, could create the effects of a keto diet.
This means that a drug could be designed to reduce inflammation in patients who cannot follow a keto diet because of other health reasons.
Speaking to MNT about the clinical implications of the study, Dr. Swanson said, "Our findings show that it is [...] possible to get the anti-inflammatory effect of a ketogenic diet without actually being ketogenic."
Dr. Swanson went on to highlight how important it is that the research conducted by he and his team uncovered a causal mechanism rather than simply pointing to an association.
"Most scientists," he told us, "are reluctant to accept cause-effect relationships between events in the absence of a defined mechanism. Here we have provided a biochemical mechanism by which diet affect inflammatory responses."
Dr. Swanson also shared with us some directions for future research. "Our work was very focused on brain trauma," he said, but "next steps will be to expand the list of pro-inflammatory conditions that can be modulated by the CtBP mechanism."
The findings could apply to other conditions that are characterized by inflammation. In diabetes, for example, the excessive glucose produces an inflammatory response, and the new results could be used to control this dynamic.
"[The] ultimate therapeutic goal would be to generate a [drug] that can act on CtBP to mimic the anti-inflammatory effect of [the] ketogenic diet," Dr. Swanson concluded.