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Researchers found that following a ketogenic diet for 6 months can reprogram immune cell metabolism and promote anti-inflammatory phenotypes in patients with MS.
A new study demonstrated that a modified Atkins diet (MAD) for 6 months can reprogram immune cell metabolism and promote anti-inflammatory phenotypes in patients with MS. These findings are among the first to support the immunomodulatory potential of ketogenic diets in patients with MS.
A better insight into the relation between nutrition and the immune system is of great interest to patients with immune diseases and healthcare professionals. They may create the opportunity of lifestyle changes to alter the course of diseases like MS. Ketogenic diets have been shown to produce anti-inflammatory effects in animal models of MS. However, the effects of ketogenic diets in patients with MS are still unknown. Michael Kornberg, MD, Johns Hopkins University, Maryland and colleagues previously published a phase 2 study of the ketogenic MAD diet in patients with MS1. MAD is less restrictive and easier to sustain than many other ketogenic diets.
Dr. Kornberg and co-workers analyzed peripheral blood mononuclear cells (PBMCs) and plasma of 39 participants who had completed said phase 2 study, at baseline and after 6 months of MAD (samples were analyzed as matched pairs)2. Using multi-omic profiling, the aim was to broadly characterize the immunologic and immunometabolic effects of a 6-month MAD. PBMCs were analyzed using single-cell RNA sequencing, flow cytometry, and ex vivo stimulation assays.
According to Dr. Kornberg, 6 months of MAD substantially changed the composition and transcriptional profiles of peripheral immune subsets associated with both innate and adaptive immunity. One of these changes was a reduction in inflammatory markers in myeloid cells. MAD also altered lymphocyte composition and activation, inducing a shift from memory to naive CD8 cells, increased and more suppressive regulatory T (Treg) cells, and decreased B-cell activation. Furthermore, MAD induced immune metabolic reprogramming from glycolysis to fatty acid oxidation across immune subsets, which was corroborated by plasma metabolomics.
Medical writing support was provided by Michiel Tent.
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