Chronic Inflammatory Response Syndrome (CIRS) and Metabolism

Abstract

According to the visionary work of James Ryan, PhD, 80% of CIRS patients have “molecular hypometabolism (MHM),” which occurs by the suppression of mRNA subunits, mRNA nuclear-encoded mitochondrial genes (including ATP synthases), electron transport chain genes and translocases. Dr. Ryan’s work deftly connects biotoxin illness, environment and common medical conditions. Dr. Ryan used a novel approach to describe cellular dysfunction with the shared mechanism of aerobic glycolysis. MHM results in T-reg deficiencies, pulmonary hypertension, insulin resistance and neuronal injury. Cases of IRS2-positive and MHM-positive individuals showed pulmonary hypertension, grey matter atrophy and widened anion gap, which improved with the Shoemaker Protocol and vasoactive intestinal peptide (VIP) usage. VIP is instrumental in reversing MHM and the accompanying changes in metabolism, as evidenced in proteomic and transcriptomic studies. MHM results in voltage-dependent anion channel (VDAC) closure. Azole antifungal use amplifies grey matter atrophy due to damage to microtubules via tubulin A4A upregulation.

Key Biomarkers

Symptom Clusters