Chronic Fatigue Study Unlocks LDN Beneficial Mechanisms

Updated: Feb 1

The most credible up-to-date information about Low Dose Naltrexone (LDN) for Physicians, Researchers

Australian and Japanese researchers decided to explore the mechanism by which these patients were experiencing benefits from LDN.


Chronic Fatigue Syndrome (CFS) - also called Myalgic Encephalomyelitis (ME) - is a debilitating multi-system disorder. Among the often-severe symptoms of CFS are extreme tiredness, sleep problems, muscle/joint pain, headaches, sore throat/glands, cognitive difficulties, dizziness, and heart palpitations. Its cause is currently unknown and there are few identified treatments.


The study by the Griffith University and Aichi-Gaku University researchers compared 9 patients with CFS who took 3.0-4.5mg of LDN for at least 4 weeks to 9 healthy participants not taking LDN. The CFS patients reported improved thinking/concentrating, less cognitive overload, and fewer immune disturbances (less sore throats, enlarged/tender lymph nodes, colds/flu) after taking LDN.


In unlocking the mechanism by which LDN helps, the study found that, among the patients with CFS/ME who took LDN, their previously dysfunctional cell activities were restored. Specifically, they found that LDN restored TRPM3-like dysfunction, an impairment that is known to be associated with CFS but previously had no effective treatment.


MEDICAL INFORMATIO

Potential Therapeutic Benefit of Low Dose Naltrexone in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Role of Transient Receptor Potential Melastatin 3 Ion Channels in Pathophysiology and Treatment


Publication Type : Journal Article


Research Type:Title

Potential Therapeutic Benefit of Low Dose Naltrexone in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Role of Transient Receptor Potential Melastatin 3 Ion Channels in Pathophysiology and Treatment


Publication Type Journal Article


Research Type Human


Reported as Case Report/Series/Restrospective Study


Date July 13, 2021


Authors H. Cabanas, K. Muraki, N. Eaton-Fitch, D.R. Staines, S. Marshall-Gradisnik


Institution Griffith University, Aichi-Gakuin University


Link

https://pubmed.ncbi.nlm.nih.gov/34326841/


Abstract

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a debilitating multi-systemic chronic condition of unknown aetiology classified as an immune dysfunction syndrome and neurological disorder. The discovery of the widely expressed Transient Receptor Potential Melastatin 3 (TRPM3) as a nociceptor channel substantially targeted by certain opioid receptors, and its implication in calcium (Ca2+)-dependent Natural Killer (NK) cell immune functions has raised the possibility that TRPM3 may be pharmacologically targeted to treat characteristic symptoms of ME/CFS. Naltrexone hydrochloride (NTX) acts as an antagonist to the mu (μ)-opioid receptor thus negating its inhibitory function on TRPM3. Based on the benefits reported by patients on their symptoms, low dose NTX (LDN, 3.0-5.0 mg/day) treatment seems to offer some potential benefit suggesting that its effect may be targeted towards the pathomechanism of ME/CFS. As there is no literature confirming the efficacy of LDN for ME/CFS patients in vitro, this study investigates the potential therapeutic effect of LDN in ME/CFS patients. TRPM3 ion channel activity was measured after modulation with Pregnenolone sulfate (PregS) and ononetin in NK cells on 9 ME/CFS patients taking LDN and 9 age- and sex-matched healthy controls using whole-cell patch-clamp technique. We report that ME/CFS patients taking LDN have restored TRPM3-like ionic currents in NK cells. Small ionic currents with a typical TRPM3-like outward rectification were measured after application of PregS, a TRPM3-agonist, in NK cells from patients taking LDN. Additionally, PregS-evoked ionic currents through TRPM3 were significantly modulated by ononetin, a TRPM3-antagonist, in NK cells from ME/CFS patients taking LDN. These data support the hypothesis that LDN may have potential as a treatment for ME/CFS by characterising the underlying regulatory mechanisms of LDN treatment involving TRPM3 and opioid receptors in NK cells. Finally, this study may serve for the repurpose of marketed drugs, as well as support the approval of prospective randomized clinical studies on the role and dose of NTX in treating ME/CFS patients.





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