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Dr. Lawrence B. Afrin, MD, Immunology and Allergy: Mast Cell 101

SWAlexander

Senior Member
Messages
1,897
This 1-hour lecture is a well spend time for everyone still searching for answers.

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Martin aka paused||M.E.

Senior Member
Messages
2,291
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.
 

SWAlexander

Senior Member
Messages
1,897
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.

So sorry you are down.
I´m watching and recollecting to find out what could (have) trigger proliferation. It could be one or many triggers at the same time, but we need to find what did it.
Hang in there.
 

Martin aka paused||M.E.

Senior Member
Messages
2,291
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.
 

SWAlexander

Senior Member
Messages
1,897
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.

It was for me Herpes in the beginning. Later came a Corynebacterium species and many more.
I know there is a lot of "5 cent Magazine wisdom" out there. We need to select, cross-reference, check for errors and reject the one without peer reviews. Gain knowledge is the keyword, so we can apply what works for us.
 
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SWAlexander

Senior Member
Messages
1,897
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/
 

Martin aka paused||M.E.

Senior Member
Messages
2,291

SWAlexander

Senior Member
Messages
1,897

SWAlexander

Senior Member
Messages
1,897
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/

Here we go again, „aldosterone hormone“. Extensive catecholamine’s the most neglected section in all tests and least understood and too often dismissed in relation to energy level. This includes include adrenaline, noradrenaline.
Anytime my cortisol is low (below 5), aldosterone is low. How do I know this? I can´t taste salt or I grave salt but I can’t taste when it is too salty or not enough salt. Low sodium levels lead in my case to muscle cramps or weakness nausea, and dizziness and feel like life sneeking out of my body.