I think I just wrote that I wouldnot write anything about diets, but I have been challenged You said “I know diet is seen as quackery on this blog. However it seams to be actually showing evidence of neuroprotection more than any of the drugs trialed so far”. I would argue not at all, ProfG may have talked about them, indeed he has just sent me a book on diets as has DoctorLove.
However, I have stayed clear because I know nothing about them, don’t and haven’t paid attention to the data and am not making any suggestions. Mice get pellets. I have other things I want to think about, I am not hollistic I am narrow-minded and focussed.
We all know a balanced lifesytle has health benefits, but it may nessesarily not be the same as saying this is better than a drug, which is clearly doing something. However Andrea from the group may do a post on this. I prefer to stick to the hard-core science. I am not going to be making life-style recommendations….ever.
But as the guantlet was thrown down, I thought I would have a look and a paper on ketogenic diet and neurofilaments. First one I looked at was in Neurology2019. I wont give the reference so there is no link to my comments but it says ketogenic diet “(n = 17), we found a significant decrease in the sNfL level from 8.5 at baseline (no dietary intervention) to 7.1 pg/mL (mean difference -1.307; 95% CI -2.256 to -0.357; p < 0.05) at the end of the study after 6 months. So there you have it significant benefit. So then I asked what does a potent MS drug do. The first report out of Google it said “Exposure to ocrelizumab resulted in a lowering of NfL levels to comparable to 118 healthy donors which established NfL ranges of 5.5—9.8 pg/mL for blood serum and 4.3–7.9 pg/mL for blood plasma”.
So go back to paper on diet it could mean that on the diet the people went from a normal Nfl level to a normal NFl level.. This is harder to get excited about. The paper also say”We found a significant association between sNfL and age (r = 0.347, p < 0.05)”, etc. I dont consider r=0.3 to be a biologically meaningful association in terms of prediction, such that I could know what my Nfl level would be if I were a certain age.
But a paper has just been reported on Intermitant fasting. This sparked my attention as intermittant fasting has been reported to promote a repairing environment in animals that can be chemically-mimicked. But before you can say “metformin”, we have a study looking at caloric restriction. It seems that caloric restriction can influence T cell numbers (see below). However, one has to say this (5%) is not in the same league as the reduction seen with potent disease modifying treatments (95% with alemtuzumab). Whether or not this influenced repair is not the subject matter of the paper. What did it do to B cells, which would raise my personal interest more? I dont know that either.:-)
Intermittent calorie restriction alters T cell subsets and metabolic markers in people with multiple sclerosis Kathryn C. Fitzgerald, Pavan Bhargava, Matthew D. Smith, Diane Vizthum, Bobbie Henry-Barron, Michael D. Kornberg, Sandra D. Cassard, Dimitrios Kapogiannis, Patrick Sullivan, David J. Baer, Peter A. Calabresi, Ellen M. Mowry. medRxiv 2022.01.11.22269094; doi: https://doi.org/10.1101/2022.01.11.22269094
Background: Intermittent fasting or calorie restriction (CR) diets provide anti-inflammatory and neuroprotective advantages in models of multiple sclerosis (MS); data in humans are sparse.
Methods: We conducted a randomized-controlled feeding study of different CR diets in 36 people with MS over 8 weeks. Patients were randomized to receive either: a daily CR diet (22% reduction in calories, 7 days/week), an intermittent CR diet (75% reduction, 2 days/week; 100%, 5 days/week), or a weight-stable diet (100%, 7 days/week). Untargeted metabolomics was performed on plasma samples at weeks 0, 4 and 8 at Metabolon Inc (Durham, NC). Flow cytometry of cryopreserved peripheral blood mononuclear cells at weeks 0 and 8 were used to identify CD4+ and CD8+ T cell subsets including effector memory, central memory, and naïve cells.
Results: 31 (86%) completed the trial. Over time, individuals randomized to intermittent CR had significant reductions in CD4+Central Memory [CM] -4.87%; 95%CI: -8.59%, -1.15%; p=0.01), CD4+Effector Memory [EM] (-3.82%; 95%CI: -7.44, -0.21; p=0.04), and CD8+EM (-6.96%; 95%CI: -11.96, -1.97; p=0.006) with proportional increases in naïve subsets (CD4+Naïve: 5.81%; 95%CI: -0.01, 11.63%; p=0.05; CD8+Naïve: 10.11%; 95%CI: 3.30, 16.92%; p=0.006). No changes were observed for daily CR or weight-stable diets. Larger within-person changes in lysophospholipid and lysoplasmalogen metabolites in intermittent CR were associated with larger reductions in memory T cell subsets and larger increases in naïve T cell subsets.
Conclusions: In people with MS, an intermittent CR diet was associated with reduction in memory T cell subsets. The observed changes may be mediated by changes in specific classes of lipid metabolites. Trial Registration: This study is registered on Clinicaltrials.gov with identifier NCT02647502.
Disclaimer: These are opinions of the author and do not represent any institutional view