Friday Hope: A Low-Carb/High-Fat Diet May Reverse Spike-Induced Autoimmunity

Looking at results from last year, a low-carb/high-fat diet may support tolerogenic reprogramming.

High carbohydrate (HC) feeding aggravated CNS autoimmunity while high fat (HF) was protective.
A. Study timeline. Mice were fed on high protein (HP), high carbohydrate (HC) and high fat (HF) diets for 6-7 weeks before experimental autoimmune encephalomyelitis (EAE) induction and were kept on the same diet throughout the EAE clinical course. B. EAE clinical course for HP (red), HC (blue) and HF (light yellow) groups (n=10/group). C. Histological analysis of neuroinflammation and demyelination of the spinal cord from HP, HC and HF mice isolated on D28 of EAE paraffin-sectioned and stained with H&E and Luxol fast blue (LFB). Scale bars = 20 μm. D. Heatmap comparisons for the gene expression of Ifng, Tnfa, Nlrp3, Ccl2, and Cd68 in the spinal cord of HP, HC and HF mice isolated on D28 of EAE analyzed by qPCR. E. Representative flow cytometric plots of CNS-infiltrating T cells of HP, HC and HF mice on D28 of EAE. F. Proportions of infiltrating immune cells and activated microglia (MHChi Mic) within the CNS of HP, HC and HF mice on D28 of EAE determined by flow cytometry. G. Representative flow cytometric plots of splenic Th1 (IFNγ-producing CD4+ T cells) and Th17 (IL-17-producing CD4+ T cells) cells of HP, HC and HF mice on D28 of EAE. H. Proportions of pro-inflammatory cytokine-producing T cells in the spleens of HP, HC and HF mice were determined by cytometry. I. Total number of Treg in draining lymph nodes (dLNs) of HP, HC and HF mice on D7 of EAE determined by flow cytometry. J. IL-10 production in immune cells from dLNs of HP, HC and HF mice quantified by flow cytometry. (K-L) Representative flow cytometric plots (K) and scattering dot plots (L) of dLN Th1 and Th17 cells. M-O. Proliferation of dLN Th1 (M), Th17 (N), and IFNγ-producing CD8+ T cells (O) of HP, HC and HF mice, with (filled dots) and without (hollow dots) stimulation, quantified by Ki67 staining. P-R. IFNγ production in dLN CD4+ (P), CD8+ (Q) and γδT cells (R) of HP, HC and HF mice upon MOG antigen stimulation. S. Proliferation of dLN Treg of HP, HC and HF mice, with (filled dots) and without (hollow dots) stimulation, quantified by Ki67 staining. N=6-10, Data are represented as mean ± S.E.M., with * p<0.05, ** p<0.01, *** p<0.001, **** p<0.0001, by one-way ANOVA for most analyses, two-way ANOVA for the clinical curve analysis, and paired t-test for the proliferation assay analysis. (See also Figure S2-6)

One of the many devastating effects of the Spike Protein is its ability to induce autoantibodies. For those who may not know, autoantibodies are a way the body’s immune system can attack the self.

This induction of autoantibodies can be either from infection:

Clustering of all obtained trajectories revealed three distinct categories of new-onset autoantibodies shown in Fig. 2a: stable (n = 225), transient (n = 177), and delayed (n = 103) new-onset autoantibodies. Four additional clusters of relatively unchanging trajectories were detected and not classified as new-onset (Supplementary Fig. 2). The new-onset autoantibody landscape of individuals and antigens with at least one detected new-onset autoantibody (n individuals = 204, n antigens = 187) is displayed in Supplementary Fig. 3. These autoantigens represent extracellular (n = 57) and intracellular (n = 119) proteins corresponding to 176 genes as classified in the Human Protein Atlas.

Prevalent and persistent new-onset autoantibodies in mild to severe COVID-19
https://www.nature.com/articles/s41467-024-53356-5

Or vaccination:

Line-blot technology was performed using the following kit: EUROLINE ANA profile 3 plus DFS70 (IgG). Our research suggests that mRNA based anti-SARSCoV-2 vaccines can induce the production of de novo ANA (antinuclear antibodies, ANA) in 22/77(28,57%) of subjects and that the percentage of positivity seems to be directly correlated to the number of vaccine expositions: 6/77 (7,79%) after 2 doses; 16/77 (20,78%) after 3 doses. Since it is known that hyperstimulation of the immune system could lead to autoimmunity, these preliminary results seem to further sustain the idea that the hyperstimulation of the immune system might lead to an autoinflammatory mechanism and eventually to autoimmune disorders. However, the link between SARS-CoV-2 vaccination and the development of autoimmune diseases needs to be further investigated.

The onset of de novo autoantibodies in healthcare workers after mRNA based anti-SARS-CoV-2 vaccines: a single centre prospective follow-up study
https://www.tandfonline.com/doi/full/10.1080/08916934.2023.2229072

Therefore, it is necessary to treat and hopefully reverse the development of these Spike Protein-induced autoantibodies. Fortunately, Nature has provided us with a regimen that may cause our immune systems to correct themselves by a process that is called tolerogenic reprogramming. When you develop autoantibodies, your B Cells are “programmed” wrong. If they lose tolerance to the self, they can create autoantibodies. Of course, they are not supposed to make antibodies that attack yourself, they are supposed to make antibodies that only attack non-self. Once they enter this state of producing autoantibodies, if possible, they need to be “reprogrammed” to tolerate the self and go back to only producing antibodies that only attack non-self.

Following a diet that is low in carbohydrates and high in fat (Ketogenic) has been shown to accomplish precisely this – tolerogenic reprogramming. Let’s look at a study from Australia published last summer.

Here, this study comprehensively interrogated the associations between diet and nutrient environment and MS for the first time. We showed that globally, increased carbohydrate supply correlated with higher MS disease burden. A preclinical MS mouse model EAE confirmed a causative effect of diet on EAE severity with a high carbohydrate diet aggravating EAE by promoting Th1 and Th17 responses and CNS neuroinflammation. Contrarily, an isocaloric diet low in carbohydrate but high in fat protected against EAE by supporting tolerogenic reprogramming.

High fat low carbohydrate diet is linked to protection against CNS autoimmunity
https://www.biorxiv.org/content/10.1101/2024.07.23.604865v1.full

This may be extremely beneficial for those who are Spike-injured and/or who have Long COVID. Also, if tolerogenic reprogramming is successful, then the diet need not be permanent. In any case, a low-carb diet is a significant therapeutic in treating conditions that produce autoantibodies.

For example, another study from last year found that a low-carb diet ameliorated autoantibodies in Hashimoto’s thyroiditis.

Methods

Forty patients with Hashimoto’s thyroiditis were recruited for this study and randomly divided into two groups: one with a normal diet and the other with a low-carbohydrate diet. Antibodies against thyroid peroxidase (TPOAb) and thyroglobulin (TgAb) were measured for all participants. Additionally, thyroid water content was semi-quantitatively measured using Dixon-T2WI. The same tests and measurements were repeated for all participants after 6 months.

Results

After 6 months of a low-carbohydrate diet, patients with Hashimoto’s thyroiditis showed a significant reduction in thyroid water content (94.84 ± 1.57% vs 93.07 ± 2.05%, P < 0.05). Concurrently, a decrease was observed in levels of TPOAb and TgAb (TPOAb: 211.30 (92.63–614.62) vs 89.45 (15.9–215.67); TgAb: 17.05 (1.47–81.64) vs 4.1 (0.51–19.42), P < 0.05). In contrast, there were no significant differences in thyroid water content or TPOAb and TgAb levels for patients with Hashimoto’s thyroiditis following a normal diet after 6 months (P < 0.05).

MRI quantitative assessment of the effects of low-carbohydrate therapy on Hashimoto’s thyroiditis
https://ec.bioscientifica.com/view/journals/ec/13/5/EC-23-0477.xml

And in overweight patients with autoimmune thyroiditis:

We have evaluated the amount of either thyroid hormones, or antithyroid, or anti-microsomal, or anti-peroxidase antibodies (Abs) in patients with high amounts of Abs. In a diet devoid of carbohydrates (bread, pasta, fruit, and rice), free from goitrogenic food, and based on body mass index, the distribution of body mass and intracellular and extracellular water conducted for 3 weeks gives the following results: patients treated as above showed a significant reduction of antithyroid (−40%, P<0.013), anti-microsomal (−57%, P<0.003), and anti-peroxidase (−44%, P<0,029) Abs.

Effects of low-carbohydrate diet therapy in overweight subjects with autoimmune thyroiditis: possible synergism with ChREBP
https://pmc.ncbi.nlm.nih.gov/articles/PMC5028075/

Granted, the above studies reference autoimmune thyroiditis and the mouse model of MS. However, I believe the Ketogenic diet should be trialed for those afflicted with Spike Protein Injury/ Long COVID. Given the suffering that the Spike Protein causes, we need answers. Safe answers that can be implemented immediately.

Please do not start a Ketogenic, or low-carb/high-fat diet, without consulting your Primary Care Provider. These diets can be dangerous for some. This is a work of medical research, and not medical advice. Of course, please feel free to share this article with your Primary Care Provider for them to evaluate its merits with regards to your particular situation.

Thank you. Thank you, as always, for your readership, dialogue and support. I will keep discovering and sharing what I learn with you. It is an honor to have your readership. Please have a blessed and hopeful Passover/Palm Sunday weekend.