SWAlexander
Senior Member
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This 1-hour lecture is a well spend time for everyone still searching for answers.
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I watch the video. It's very good.
May be a possible key in so many of our cases. Sad that doctors are not being trained to recognize it.![]()
Wow. Thanks for sharing. In a crash but will def watch it. I'm very interested in the proliferation of MC and their role in ME.Did you hear him saying, that by one patient he needed 4 years to find out what works for her?
Wow. Thanks for sharing. In a crash but will def watch it. I'm very interested in the proliferation of MC and their role in ME.
I think it's important to acknowledge that you can have MCAD without the common symptoms. And in fact it could be kind of “asymptomatic” causing inflammation that contributes to our disease. It's a very interesting topic.
For me personally I think it's pathogens but you're right: we need GOOD research on this as we are “overloaded” with bad papers that could never be reproduced.but we need to find what did it
For me personally I think it's pathogens but you're right: we need GOOD research on this as we are “overloaded” with bad papers that could never be reproduced.
I think we have a problem here with scientific journals nowadays and the quality of papers that provide poor evidence but are accepted for publication bc of low standards in peer review etc. I can only hope that serious researchers investigate the reason for MC proliferation ME. I know that VanElzakker has it on his list.
Would like to add that this supposedly also causes autonomy dysfunction (POTS/”renin-aldosterone paradox”): https://www.healthrising.org/blog/2...onic-fatigue-syndrome-pots-renin-aldosterone/when it enters the ACE-2 receptor by elevating Ang II levels, it produces mitochondrial dysfunction and accumulations of the superoxide radical and other oxygen and nitrogen species.
Would like to add that this supposedly also causes autonomy dysfunction (POTS/”renin-aldosterone paradox”): https://www.healthrising.org/blog/2...onic-fatigue-syndrome-pots-renin-aldosterone/
Badykinin is very interesting in this context.
This example for instance fits me perfectly.
"Given that the immune cells generate oxidative stress to kill pathogens, it’s no surprise that oxidative stress would be increased in acute COVID infections. SARS-CoV-2, though, comes with a special twist: when it enters the ACE-2 receptor by elevating Ang II levels, it produces mitochondrial dysfunction and accumulations of the superoxide radical and other oxygen and nitrogen species.
With over a dozen studies finding a redox imbalance in ME/CFS, high levels of oxidative/nitrosative stress may be the most consistent finding in all of ME/CFS. Interestingly, levels of oxidative/nitrosative stress rise to particularly high peaks after exercise in ME/CFS. Metabolomic studies indirectly suggest the presence of high levels of oxidative stress.
A variety of studies have also found high levels of pro-oxidants – chemicals that either directly produce oxidative stress or impair antioxidant levels – in both ME/CFS and COVID. They include ferritin, free iron, homocysteine, neutrophil extracellular traps, altered levels of nitric oxide and hydrogen sulfide (in COVID), and altered tryptophan metabolism." https://www.healthrising.org/blog/2021/08/21/free-radicals-chronic-fatigue-syndrome-long-covid-pasc/