The Power Crisis Behind Long Covid & ME/CFS | Latest Mitochondrial Research Explained скачать в хорошем качестве

The Power Crisis Behind Long Covid & ME/CFS | Latest Mitochondrial Research Explained

This video is part of the recent series of interviews I posted with Professor Klaus Wirth. It describes how mitochondria work and why their dysfunction might be the key to understanding Long COVID and ME/CFS - based on Professors Scheibenbogen’s and Wirth’s most recent paper. Important note regarding sodium/calcium intake for those who have expressed concerns - see below explanation from Prof Wirth himself: "There is (demonstrated) intramuscular sodium rise as a harmful mechanism in skeletal muscle. High intracelluar sodium finally causes calcium overload and mitochondrial damage via reversing the transport mode of the sodium-calcium-exchanger NCX from exporting calcium to importing calcium. On the other hand patients are recommended to take up sufficient sodium to combat hypovolemia and orthostatic intolerance that causes perfusion disturbances and a high level of stress (to desensitize ß2-adrenergic receptors that are so important for activating the Na+/K+ATPase). There is no contradiction. Intracellular (intramuscular sodium) is regulated by ion channels and transporters. Intramuscular sodium in ME/CFS is raised by excitation (sodium channel opening during excitation) and ion transporters (such as NHE1). One cannot lower (harmful elevated) intracellular sodium by restricting sodium intake which would worsen the orthostatic intolerance and the subsequent pathophysiology. Raising sodium intake in the situation of hypovolemia does not raise sodium concentrations in the blood but leads to an expansion of the volume (with no or very little change in the sodium concentration). Patients should take in the recommended amounts of salt – not low and not excessive." Channel Membership (new! 99p!)    / @rundmc1   CHAPTERS: 0:00 Introduction 0:21 What Are Mitochondria 1:38 Connection to LC & ME/CFS 2:44 Sodium-Calcium Problem 3:54 Vicious Cycle 5:13 Why LC becomes ME/CFS 6:03 Treatment Implications 6:35 Conclusion LINKS: Part 1 of the Interview with Prof. Klaus Wirth:    • The Latest Research on Mitochondrial Dysfu...   Part 2 of the Interview with Prof Klaus Wirth:    • Treating the Root Cause of Fatigue & PEM i...   Key Pathophysiological Role of Skeletal Muscle Disturbance in Post COVID and Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): Accumulated Evidence (Scheibenbogen / Wirth) - 27 Dec 2024 https://onlinelibrary.wiley.com/doi/1... An attempt to explain the neurological symptoms of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (Wirth / Scheibenbogen, Paul) - 22 Nov 2021 https://pubmed.ncbi.nlm.nih.gov/34809... A Unifying Hypothesis of the Pathophysiology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): Recognitions from the finding of autoantibodies against ß2-adrenergic receptors (Wirth / Scheibenbogen) Jun 2020