NCNED Co Director Professor Donald Staines said their data supported the hypothesis that LDN has potential as a treatment for ME/CFS by characterising the underlying regulatory mechanisms of LDN treatment. “We now further understand that the pathophysiology of ME/CFS is due to ion channel dysfunction and the interaction of the opioid receptor that causes impaired Ca2+ signalling and Ca2+-mediated cell functions, including immune function,” Professor Marshall-Gradisnik said. NK cells are part of the innate immune system and provide an internationally recognised model for estimating loss of function in calcium signalling systems. “This is the first in vitro study confirming the efficacy and therapeutic benefit of LDN for ME/CFS patients by characterising the underlying regulatory mechanisms of LDN treatment involving a calcium (Ca2+) ion channel called TRPM3 and opioid receptor interaction in NK cells.”Ĭalcium is vital to cellular processes and entry to cells is critically controlled by these calcium channels. “While previous reports have been anecdotal for the benefits of LDN, a drug that targets opioid receptors, no scientific data identifying the cellular mechanism for this potential treatment for ME/CFS patients have been published previously,’’ says NCNED Co-Director Professor Sonya Marshall-Gradisnik. Published in the journal Frontiers in Immunology, the researchers found that patients with ME/CFS taking low-dose Naltrexone (LDN 3.0-5.0mg/day) show significant improvements in cell function in a laboratory study using a model of natural killer (NK) cells from patients. Researchers at Griffith University’s National Centre for Neuroimmunology and Emerging Diseases (NCNED) have announced a world first-discovery in the diagnosis and treatment of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS).