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.