Reduce or Eliminate
Humans evolved eating mostly plants (Barras, 2016; Dunn, 2012), providing many benefits to the immune system (Jensen et al, 2021), including for better Covid-19 outcomes (Kim et al, 2021; Maguire, 2020). Animal products on the other hand, such as dairy, can lead to autoimmunity where lactose (Chiu et al, 2016), the bovine milk protein casein, and other milk proteins, have been found to target human glycoproteins and destroy myelin (Vojdani, 2014; Chunder et al, 2022). Evidence about the dietary interventions for the autoimmune disease, Multiple Sclerosis, are instructive. Stoiloudis et al (2022) have reviewed the reported adverse effects of saturated fatty acids (SFAs) on the course of MS, emphasizing their proinflammatory character. High intake of SFAs leads to a dysbiosis of gut microbiota. Additionally, the consumption of vegetable oils, which are enriched with trans fatty acids, is associated with gut inflammation and the upregulation of proinflammatory cell. Red meat leads to the formation of nitrous compounds increasing chronic inflammation. Red meat also contains arachidonic acid, which participates in inflammatory pathways by activating Th17 cells. Furthermore, a high consumption of sugar-sweetened beverages and refined cereals leads to the production of insulin, which, in this way, is responsible for the upregulation of synthesis and the production of arachidonic acid. High salt intake can induce the production of Th17 cells and proinflammatory cytokines. Proteins contained in cow-milk may play a role in the mechanisms of pathogenesis of MS. Particularly, butyrophilin can induce EAE by mechanisms of molecular mimicry with myelin oligodendrocyte glycoprotein.
Plant foods are the sole source of dietary fiber, vitamin C, flavonoids, chlorophyll, and good sources of vitamin B1, folic acid, potassium, and magnesium. They are also good sources of omega-3 fatty acids and their precursor molecule, alpha-linolenic acid (ALA), low in saturated fat, and do not contain cholesterol. As an example of the diet of early humans, sodium was solely derived from plants. (MacGregor and de Wardener, 1998), meaning that they ingested minute quantities of sodium. A high salt diet in modern man because of a diet of mostly processed foods and not whole plants causes disturbances in the ecological balance of the gastrointestinal microflora primarily through depletion of lactic acid-producing bacteria in a dose-dependent manner (Hamad et al, 2022). Since moderate increases in salt intake has proven to affect human immune cells, including T cells in vivo (Wilck et al, 2017: Willebrand and Kleinewietfeld, 2018), more specific analysis is needed to establish the role of NaCl in human autoimmune disease (Arroyo Homero et al, 2020), especially at low NaCl concentrations. Further, plant-derived nutrients have been found to be associated with an anti-inflammatory state by acting as ligands of the aryl hydrocarbon receptor (Jorg et al, 2016). AhR acts as a transcription factor in a variety of immune cells, including Th17 and Tregs, and has been associated with susceptibility as well as prevention of autoimmune diseases depending on its ligands. For example, indole-3-carbinol, deriving from crucifers such as broccoli, has been shown to suppress the production of proinflammatory cytokines, whereas the tryptophan-derived AhR ligand FICZ (6-Formylindolo(3,2-b)carbazole) derived from animal products at very high levels specifically increases the Th17 population and, therefore, worsens experimental autoimmune encephalomyelitis (EAE) severity. And chlorophyll ingestion from plants has many benefits beyond its well described anti-cancer properties (Dashwood, 2021), including anti-inflammatory (Subramoniam et al, 2012), and anti-viral properties (Liu et al, 2020). Chlorophyll also plays a role in regenerating CoQ10 (Qu et al, 2013). CoQ10 is an endogenous compound that acts as an antioxidant by scavenging free radicals, protecting our cells from DNA and protein damage (Pala et al, 2018).
Along with reducing or eliminating salt, eliminate glucose, because it disrupts gut barrier function (Zhang et al, 2021), and wheat and milk because the peptide sequences of foods such as milk and wheat are similar to those of human molecules, such as myelin oligodendrocyte glycoprotein (Vojdani, 2015). Sprouted wheat has 47% less gluten (Boukid et al, 2017), and sourdough bread has less gluten (Thiele et al (2004) than standard wheat, but they still contain gluten and can trigger autoimmunity. For myself, I don’t eat dairy, but every time I eat wheat, my symptoms start to exacerbate several hours after the wheat consumption. Wheat, and other gluten containing grains, once ingested, gluten is partially cleaved into gliadin peptides that pass through the intestinal mucosa epithelial barrier due to increased permeability, caused by the inflammatory innate immune response. In the lamina propria (the intermediate connective tissue layer of the intestinal mucosa) occurs an important step in CD pathogenesis, gliadin deamidation by the tissue transglutaminase enzyme, which launches the activation of the adaptive immune system. This adaptive immune response against gliadin involves antigen-presenting cells such as macrophages, dendritic cells, and B cells. The innate immune response to gliadin occurs in the intestinal mucosa epithelial layer and increases the release of cytokines, namely interleukin-15 (IL-15), produced by enterocytes, macrophages, and dendritic cells. This results in intraepithelial leukocyte differentiation into CD8+ cytotoxic T cells that express the marker for natural killer NK-G2D cells causing epithelial cell apoptosis. The accumulation of all these inflammatory mediators leads to intestinal mucosal injury that manifests through flattening of the villi and elongation of the crypts, the histological alterations characteristic of CD. If one chooses to eat cheese, make sure that the cheese doesn’t contain bacteriophage, either purposely added to control bacteria growth (Tabla et al, 2022) or through contamination (Atamer et al, 2013), because ingestion of bacteriophage may cause autoantibody production (Riley, 2004)
Reduce fat consumption because lipid consumption increases autoantibody production and autoimmune disease (Levy et al, 1982; Winer et al, 2011; Pham et al, 2017), and leads to systemic, chronic inflammation (Duan et al, 2018).
Eliminate meat consumption (Jin et al, 2021; Samraj et al, 2014; Bashir et al, 2020). Selenium (McLachlan et al, 2017), and iodine (Burek and Yaylor, 2009) have been found to increase autoantibody production.