Summary: New research suggests that the ketogenic diet may promote the production of beneficial substances in the gut and help with multiple sclerosis ( MS ). In a study, mice on a keto diet produced the ketone body β-hydroxybutyrate ( βHB), which worked with gut bacteria to create immune-modulating metabolites. This contact improved mice’s MS symptoms and reduced inflammation.
If these results translate to humans, the strategy could lead to supplement-based remedies for inflammatory diseases, offering a less stringent alternative than the ketogenic diet. Future studies are required to establish the healing potential of immune conditions.
Major Information
- Keto diet-derived βHB in animals triggered beneficial gut bacteria to develop anti-inflammatory materials.
- Lactobacillus murinus, a gut bacteria, created indole lactic acid ( ILA ), which decreased harmful immune activity linked to MS.
- Studies suggest that supplements may provide a more affordable option for managing MS symptoms.
Origin: UCSF
Scientists have long suspected that the keto diet may help some people with multiple sclerosis and ease an overactive immune system.
Nowadays, they have reason to believe it could be real.
Researchers at UC San Francisco discovered that the colon and its bugs, together, cause two factors that attenuated MS symptoms in mice.
If the investigation is translated into humans, it suggests a novel approach to supplement therapy for MS and other inflammatory conditions.
The ketogenic diet seriously restricts carbohydrate-rich foods like bread, pasta, fruits and sweets, but allows unlimited fat usage.
Without carbs to use as energy, the body breaks down fat rather, producing compounds called ketosis bodies. Kept in check, ketone bodies can modify the immune system and provide energy for tissues to lose.
The researchers used a mouse model of MS to study whether mice with higher levels of a certain ketone system, known as HB, had less severe illness.
The additional βHB also prompted the gut bacterium , Lactobacillus murinus , to produce a metabolite called indole lactic acid ( ILA ). This prevented the T companion 17 immune cells from being activated, which are involved in MS and other inflammatory conditions.
” What was really interesting was finding that we could defend these animals from inflammatory condition just by putting them on a meal that we supplemented with these materials”, said , Peter Turnbaugh, PhD, of the , Benioff Center for Microbiome Medicine.
Earlier, Turnbaugh had shown that when secreted by the colon, βHB negates defense detection. A postdoctoral researcher at the time, Margaret Alexander, PhD, was curious about whether the mixture might help treat MS in rabbits.
In the new study, which appears Nov. 4 in , Cell Reports, the group looked at how the keto body-rich eating affected animals that were unable to make βHB in their gut, and found that their disease was more serious.
The animals improved, however, when the academics ate more HB in their diets.
To find out how βHB affects the gut microbiome, the crew isolated germs from the nerve of three groups of mice that were fed either the keto diet, a high-fat meal, or the βHB supplemented high-fat meal.
Then, they screened the metabolic products of each group’s distinct microbes in an immune assay and determined that the positive effects of the diet were coming from a member of the , Lactobacillus , genus:  , L. murinus.
Two other techniques, genome sequencing and mass spectrometry, confirmed that the L. murinus they found produced indole lactic acid, which is known to affect the immune system.
Finally, the researchers treated the MS mice with either ILA or L. murinus, and their symptoms improved.
Turnbaugh reaffirmed the need to test the supplementation method in patients with autoimmune disorders.
” The big question now is how much of this will translate into actual patients”, he said. However, I believe these results offer hope for the creation of a more agreeable way to support those people than to make them adhere to a difficult restrictive diet.
Authors:  , Additional authors of the study include Margaret Alexander, Vaibhav Upadhyay, Rachel Rock, Lorenzo Ramirez, Kai Trepka, Diego Oreilana, Qi Yan Ang, Caroline Whitty, Jessie Turnbaugh, Darren Dumlao, Renuka Nayak, and John C. Newman of UCSF, Patrycja Puchalska and Peter Crawford of the University of Minnesota, and Yuan Tian and Andrew Patterson Pennsylvania State University.
Funding:  , This work was funded 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 a Chan Zuckerberg Biohub-San Francisco Investigator.
About this news from multiple sclerosis research
Author: Robin Marks
Source: UCSF
Contact: Robin Marks – UCSF
Image: The image is credited to Neuroscience News
Original Research: Open access.
” A diet-dependent host metabolite shapes the gut microbiota to protect from autoimmunity” by Peter Turnbaugh et al. Cell Reports
Abstract
A diet-dependent host metabolite shapes the gut microbiota to protect from autoimmunity
Diet can protect from autoimmune disease, however, whether diet acts via the host and/or microbiome remains unclear. Here, we use a ketogenic diet ( KD ) as a model to dissect these complex interactions.
In a microbiota-dependent manner, a KD rescued the mouse model of multiple sclerosis’ experimental autoimmune encephalomyelitis ( EAE ). Dietary supplementation with a single KD-dependent host metabolite (β-hydroxybutyrate]βHB] ) rescued EAE, whereas transgenic mice unable to produce βHB in the intestine developed more severe disease.
Transplantation of the βHB-shaped gut microbiota was protective.  , Lactobacillus , sequence variants were associated with decreased T helper 17 cell activation , in , vitro.
Finally, we isolated an , L.  , murinus , strain that protected from EAE, which was phenocopied by a , Lactobacillus , metabolite enriched by βHB supplementation, indole lactate.
Thus, diet , alters the immunomodulatory potential of the gut microbiota by shifting host metabolism, emphasizing the utility of taking a more integrative approach to study diet-host-microbiome interactions.
