I’d like to share with you a revolutionary new paper, “Multiple Sclerosis is Not a Disease of the Immune System.”
If you attended our December “Metabolic-Immune Axis” workshop, this immuno-metabolic overlap is old hat to you. For those of you that missed the dinner meeting, click here to get a quick synopsis or e-mail me and I’ll get you the notes.
This new paper by Angelique Corthals highlights our current understanding about how modified or oxLDL leads to dysfunctional immune and metabolic signaling, and explains that LDL is as much a transporter of immune-metabolically disruptive, bacteria-derived LPS as it is a lipid transporter.
What can we learn from this new paper about the metabolic origins of multiple sclerosis?
“..the autoimmune framework fails to explain why genetically similar populations exposed to similar pathogens have drastically different incidence of the disease..”
“… oxLDLs, are the core agents of the immune system during the acute- phase response to infection/inflammation….oxLDLs bind to the lipopolysaccharide (LPS) membrane of the infectious agent (bacteria, virus, or parasite), allowing endocytosis by the macrophages via the scavenger receptors.”
- Multiple sclerosis should be thought of as a metabolic disease, NOT a disease of the immune system
- Imbalances in metabolic and lipid homeostasis create a proinflammatory cascade, with sex-specific consequences: atherosclerosis in men and multiple sclerosis in women.
- Dysregulation of lipid metabolism leads to a cascade involving inflammation and impairment of tissue repair
- The pathogenesis of “dysregulated lipid homeostasis” in atherosclerosis and MS are similar
- Statins and PPAR antagonists have shown great promise in the treatment of MS, implying that MS maybe a metabolic disorder.
Stay tuned for my new book discussing this metabolic-immune overlap in more detail….