Secondary Issues Observed in MS

Multiple sclerosis is marked by quite a few irregularities, including:

  • Metabolic dysfunction
  • Mitochondrial dysfunction
  • Hypoxia
  • Oxidative stress
  • Sphingolipid rheostat imbalance (ceramides vs. sphingosine-1-phosphate)
  • Glutamate endotoxicity
  • Hypercitrullination (arginine/citrulline imbalance)
  • Elevated lactate levels

While some of these factors seem to contribute to the pathology of the disease (e.g., glutamate via glutamate excitotoxicty and inflammation via oxidative stress), the significance of the others (e.g., lactate, ceramides, citrulline) is less clear.

More likely than not, these issues are consequential to causes that are more upstream.

Here I demonstrate how a macrophage can contribute to all of the aforementioned irregularities when its TLR4 receptors are continually stimulated by things such as "bad" (Gram-negative) gut bacteria, wheat proteins (gliadin, amylase-trypsin inhibitors [ATIs]), and saturated fats.

TLR4 overstimulation: A macrophage model

Food For Thought

Inoculations (e.g., for inducing autoimmunity in lab experiments) and vaccines are usually administered with an adjuvant in order to elicit a heightened immune response to an antigen in order to temporarily reduce immune tolerance and encourage antibody production.

TLR4 ligands such as LPS are often used for this purpose. Logically, if TLR4 is constantly being activated by dysbiosis-mediated conditions (excess LPS) and by dietary factors (e.g., wheat proteins, saturated fats), it makes the immune system more likely to produce antibodies for food antigens (such as wheat proteins and milk proteins), which may then cross-react with neuronal tissue.

Obligatory disclaimer: This content is meant to be informational. As everyone's body is different, what works for others may not work for you. I am not a doctor and you're probably not either. You should consult with your doctor before trying anything. Don't sue me.
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