SAN FRANCISCO: A new study from UCSF conducted on mice reveals that the diet boosts levels of anti-inflammatory compounds.
Scientists have long theorized that the keto diet could help soothe an overactive immune system, potentially benefiting individuals with conditions such as multiple sclerosis.
Now, they have reason to believe it could be true.
Scientists at UC San Francisco have discovered that the diet makes the gut and its microbes produce two factors that attenuated symptoms of MS in mice.
If the study translates to humans, it points toward a new way of treating MS and other autoimmune disorders with supplements. The keto diet severely restricts carbohydrate-rich foods like bread, pasta, fruit, and sugar, but allows unlimited fat consumption.
Without carbohydrates to use as fuel, the body breaks down fat instead, producing compounds called ketone bodies. Ketone bodies provide energy for cells to burn and can also change the immune system. Working with a mouse model of MS, the researchers found that mice who produced more of a particular ketone body, called β-hydroxybutyrate (βHB), had less severe disease.
The Role of Gut Bacteria in Immune Regulation
The additional βHB also prompted the gut bacterium Lactobacillus murinus to produce a metabolite called indole lactic acid (ILA). This blocked the activation of T helper 17 immune cells, which are involved in MS and other autoimmune disorders.
“What was really exciting was finding that we could protect these mice from inflammatory disease just by putting them on a diet that we supplemented with these compounds,” said Peter Turnbaugh, PhD, of the Benioff Center for Microbiome Medicine.
Earlier, Turnbaugh had shown that when secreted by the gut, βHB counteracts immune activation. This prompted a postdoctoral scholar who was then working in his lab, Margaret Alexander, PhD, to see if the compound could ease the symptoms of MS in mice.
In the new study, which was recently published in Cell Reports, the team looked at how the ketone body-rich diet affected mice that were unable to produce βHB in their intestines, and found that their inflammation was more severe.
