Scientists have had a long-held belief that the keto diet could help regulate an overly active immune system and benefit individuals suffering from conditions like multiple sclerosis (MS). Recent findings have provided evidence to support this idea.
Scientists have had a long-held belief that the keto diet could help regulate an overly active immune system and benefit individuals suffering from conditions like multiple sclerosis (MS).
New research has given them a reason for optimism.
Researchers from UC San Francisco have found that the ketogenic diet influences the gut and its bacteria to generate two substances that reduce symptoms of MS in a mouse model.
If these findings apply to humans, it could signal a new treatment strategy for MS and other autoimmune diseases through dietary supplements.
The keto diet restricts foods rich in carbohydrates, such as bread, pasta, fruits, and sugars, while permitting unlimited fat intake.
In the absence of carbohydrates for energy, the body begins to metabolize fat, resulting in the creation of ketone bodies. These compounds not only provide cellular energy but also have an impact on the immune system.
In their experiments with a mouse model of MS, the research team observed that mice producing higher levels of a specific ketone body known as β-hydroxybutyrate (βHB) experienced milder disease symptoms.
This increased βHB prompted the gut bacterium Lactobacillus murinus to create a metabolite called indole lactic acid (ILA), which inhibits the activation of T helper 17 immune cells linked to MS and other autoimmune diseases.
Peter Turnbaugh, PhD, from the Benioff Center for Microbiome Medicine, expressed enthusiasm about the potential for dietary changes to protect mice from inflammatory diseases.
Earlier, Turnbaugh demonstrated that βHB released by the gut could counteract immune system activation. This discovery motivated a former postdoctoral researcher in his lab, Margaret Alexander, PhD, to investigate whether βHB could alleviate MS symptoms in mice.
The findings of their latest research, published on Nov. 4 in Cell Reports, indicated that mice genetically modified to lack βHB production in their intestines exhibited more intense inflammation.
However, when these mice had their diets supplemented with βHB, they showed improvement.
To further understand the impact of βHB on gut bacteria, the team examined bacteria from the intestines of three groups of mice with varying diets: those following the keto diet, a high-fat diet, or a high-fat diet supplemented with βHB.
They then analyzed the metabolic outputs of the unique microbial communities in each group using an immune assay and determined that the beneficial effects were attributed to the Lactobacillus strain, particularly L. murinus.
Additional techniques like genome sequencing and mass spectrometry confirmed the presence of indole lactic acid produced by L. murinus, which is known to influence the immune response.
Eventually, the researchers treated the mice with MS using either ILA or L. murinus, leading to symptom improvement.
Turnbaugh cautioned that this supplementation approach requires further investigation in humans with autoimmune conditions.
“The key question now is how much of this will apply to real patients,” he noted. “However, these results offer hope for finding a more manageable alternative to help these individuals rather than requiring strict adherence to a challenging diet.”
Funding: This research was supported by the NIH (grants P30 DK063720, R01DK114034, R01HL122593, R01AR074500, R01AT011117, F32AI14745601, K99AI159227, R00AI159227-03, K08HL165106, K08AR073930, R01AG067333, R01DK091538, R01AG069781) and the Damon Runyon Cancer Research Foundation (DRR4216). Turnbaugh is also a Chan Zuckerberg Biohub-San Francisco Investigator.
