This info on microglia is fascinating and very valuable as is the inflammation aspect.
I have recommended NAC as well as more standard vitamin and nutritional supplements for elderly SARS-CoV-2 positive patients suffering from mental confusion/fog and in multiple cases, have received positive confirmation of it reducing symptoms.
This was in patients receiving ivermectin, HCQ, and not, as well as patients receiving follow up treatment for bacterial lung infection.
Elderly people need a whole host of supplements to achieve peak function, and recover whatever they lost through life/following stupid doctor recommendations. The minimum would be whey protein and creatine, old folk usually have trouble digesting and metabolizing animal protein.
Elderly would benefit from my "brain stack", because a lot of people who tried, all ages got benefit, but the older you are the more benefit you get. Most old people have horrible mitochondrial function, too much oxidative stress, etc, their bodies are just overwhelmed by everything.
Following this most old people recover fast and get better faster.
What is confusing the amyloid proponents is 1. The exact or even a hypothesized mechanism 2. Not realizing that systemic inflammation through alteration of the extracellular matrix results in pathological processes in and of itself. I have an idea the ultimate answer to this disease will have a silver lining and that it will be extensible to other chronic diseases of aging.
You are correct about ROS. Excessive ROS can by itself lead to mitochondrial dysfunction. The pathways you are talking about are consistent with this.
I got a 7 day ban from Twitter right after talking about the paper I am working on. If you have any ideas where to submit this I would appreciate it. I am retired and not affiliated with any university. I think this will be some obstacle. I have recently applied for membership as a contributor at the Am J Resp and CC Med.
My first observations in 2021 were already from a ferroptosis/mitochondrial perspective, so I just keep trying to refine the pathways.
Everything this disease causes is often treatable, the earlier the better, but that is the problem isn’t it, the ones at the most need to address everything we have uncovered, don’t, they insist in harming themselves.
I will warn people you got a 7 days suspension from Twitter. I don’t have any ideas but I will ask someone I know it does. Daoyu just published in somewhere, I forgot the name, I even shared his paper, and you can independently publish there too. Submitting to other places often involved hefty sums.
All a huge scam IMO the publishing business. Eager to read your work.
Thanks, I appreciate it. It may be a useful idea to have the work reviewed by people who have published.
I appreciate your work. You aren't bouncing around having "discovered" what this disease is from week to week and everything you are talking about is consistent with the other things you talk about. I need to review what you are recently finding as there is still some void in where I am looking. I believe there are common threads as you have described. I was reviewing your mouse model article graphic this morning. Where I am looking for is a common tie for as many of these pathways as possible realizing that we still don't fully understand sterile inflammation as it relates to the chronic degenerative early aging diseases. I believe what the spike does is perpetuate a negative feedback loop as you have also elucidated to. In looking at the processes I am looking at historical levels of certain trace nutrients which the RDA for is low because we only understand parts of how these nutrients are used in metabolic pathways and we further underestimate these are recycled in normal pathways therefore even borderline deficiencies can lead to dramatic manifestation. It's simple and complicated at the same time. Being careful how this will be positioned in the presentation.
I found the site and his paper, it is Zenodo -> https://zenodo.org/record/4486195#.Ys16u9XQ9sX You might want to look into publishing there too. I don't know how these things work though, so I might be completely off. I did tweeted about your suspension too.
I don't know many people who have published though, I... kinda blocked most of them lmao.
Thank you, I try to be honest and stay consistent within what I know. Wait until I finish the Kynurenine ones because it will make much more sense when I post everything and connect the dots.
That has been my aim for over a year, what is the common tie for many of these pathways, but neither me nor the person who helped me research the PAID hypothesis can find one, neither Doorless who is also a good fellow and honest person. There is too many parts of too many diseases. It is beyond me what 20 different viruses, bacterias and molecular clamps from retroviruses have in common.
" In looking at the processes I am looking at historical levels of certain trace nutrients which the RDA for is low because we only understand parts of how these nutrients are used in metabolic pathways and we further underestimate these are recycled in normal pathways therefore even borderline deficiencies can lead to dramatic manifestation. It's simple and complicated at the same time."
That is pretty much were I am at. Couldn't but it better myself. Since I am not an academic I take a free approach to everything, but I agree you should be careful because your aim is to be published. Hopefully you will get there. Praying hands emoji here.
Thanks, I see the post. I appreciate it. I made a Truth account using my laptop but I have nobody there to see anything yet. I also made a account at osf.io. It looks good so far as a place to publish to. I can publish a preprint and people can read and comment. Thats really what I want most is for this boondoggle to end. It won't be long now. Positioning the content is my biggest concern. Torn between one mammoth paper and several pieces that lead to the same place. I think I found a common thread. I haven't tied it to everything yet. Then again there's a lot We don't understand and if I am right we could never understand it unless we know up front the nutrients involved and start asking questions... this pathway works this way... but what IF a couple trace nutrients levels were double as just an example in the extracellular matrix... how would or could these reactions shift? In looking at this I see something hidden in plain sight. I will link the osf paper here when I get a small piece or the one giant piece done. Like you I still see systemic inflammation as doing the damage. Those getting off on amyloidosis for example are missing something. This spike accelerates these degenerative processes through a feedback loop. We know ROS causes atherosclerosis for example. Those stringy rubbery deposits aren't sticking to arterial walls so well... then again we are comparing this to atherosclerosis over a lifetime as compared to over 6 months. How would we know what rapidly accelerated atherosclerosis would or should look like? We have never seen anything like this. It's the same processes I believe for all the degenerative diseases of aging. They are all manifesting in an accelerated way and we aren't seeing it for what it is because as atherosclerosis for one example deposits over many years the body has time to lay calcium over it as it forms. Here because it happens so fast there isn't time or resources for it to manifestas we expect.
Dimitry Medvedev: ‼️“These are not predictions. This is what has already happened . This can be treated differently, but we can assume that the “horsemen of the Apocalypse” are already on their way and all hope is only in the Lord God, in the Most High,” Dmitry Medvedev😀
Russian Telegram channel, with right click translate. (excellent channel by the way, no BS)
Do your comments about disease pathogenesis vs acceleration also apply to the concerns other writers are expressing regarding the spike potentially causing amyloidosis and fibrosis? Thanks...
Can the spike protein and the viral infection cause amyloidosis on their own ? Yes under very specific circumstances, and with very specific scenarios. Fibrosis the same, it won't cause in every single person infected, too much things have to happen for that.
The amyloidosis happens within certain mechanisms, and mitochondrial function is one of the most important aspects of it all. Maybe I will finish my amyloid post to put whatever bullshit he is spousing to rest.
Although I can understand less than a third of all of this, it seems you are saying you have to watch the mitochondrial functions. Mine is Kaput, but not from Covid. In addition to NAC and liposomal (was it glycine - see can you tell?) what else is needed to get these mitochondrials working again (in addition to fasting). Sorry, I am so tired today I can't keep a thought in my head. Tryptophan? and what vitamin is nicomaside??sp?
This info on microglia is fascinating and very valuable as is the inflammation aspect.
I have recommended NAC as well as more standard vitamin and nutritional supplements for elderly SARS-CoV-2 positive patients suffering from mental confusion/fog and in multiple cases, have received positive confirmation of it reducing symptoms.
This was in patients receiving ivermectin, HCQ, and not, as well as patients receiving follow up treatment for bacterial lung infection.
Elderly people need a whole host of supplements to achieve peak function, and recover whatever they lost through life/following stupid doctor recommendations. The minimum would be whey protein and creatine, old folk usually have trouble digesting and metabolizing animal protein.
Elderly would benefit from my "brain stack", because a lot of people who tried, all ages got benefit, but the older you are the more benefit you get. Most old people have horrible mitochondrial function, too much oxidative stress, etc, their bodies are just overwhelmed by everything.
Following this most old people recover fast and get better faster.
What is confusing the amyloid proponents is 1. The exact or even a hypothesized mechanism 2. Not realizing that systemic inflammation through alteration of the extracellular matrix results in pathological processes in and of itself. I have an idea the ultimate answer to this disease will have a silver lining and that it will be extensible to other chronic diseases of aging.
You are correct about ROS. Excessive ROS can by itself lead to mitochondrial dysfunction. The pathways you are talking about are consistent with this.
I got a 7 day ban from Twitter right after talking about the paper I am working on. If you have any ideas where to submit this I would appreciate it. I am retired and not affiliated with any university. I think this will be some obstacle. I have recently applied for membership as a contributor at the Am J Resp and CC Med.
My first observations in 2021 were already from a ferroptosis/mitochondrial perspective, so I just keep trying to refine the pathways.
Everything this disease causes is often treatable, the earlier the better, but that is the problem isn’t it, the ones at the most need to address everything we have uncovered, don’t, they insist in harming themselves.
I will warn people you got a 7 days suspension from Twitter. I don’t have any ideas but I will ask someone I know it does. Daoyu just published in somewhere, I forgot the name, I even shared his paper, and you can independently publish there too. Submitting to other places often involved hefty sums.
All a huge scam IMO the publishing business. Eager to read your work.
Thanks, I appreciate it. It may be a useful idea to have the work reviewed by people who have published.
I appreciate your work. You aren't bouncing around having "discovered" what this disease is from week to week and everything you are talking about is consistent with the other things you talk about. I need to review what you are recently finding as there is still some void in where I am looking. I believe there are common threads as you have described. I was reviewing your mouse model article graphic this morning. Where I am looking for is a common tie for as many of these pathways as possible realizing that we still don't fully understand sterile inflammation as it relates to the chronic degenerative early aging diseases. I believe what the spike does is perpetuate a negative feedback loop as you have also elucidated to. In looking at the processes I am looking at historical levels of certain trace nutrients which the RDA for is low because we only understand parts of how these nutrients are used in metabolic pathways and we further underestimate these are recycled in normal pathways therefore even borderline deficiencies can lead to dramatic manifestation. It's simple and complicated at the same time. Being careful how this will be positioned in the presentation.
I found the site and his paper, it is Zenodo -> https://zenodo.org/record/4486195#.Ys16u9XQ9sX You might want to look into publishing there too. I don't know how these things work though, so I might be completely off. I did tweeted about your suspension too.
I don't know many people who have published though, I... kinda blocked most of them lmao.
Thank you, I try to be honest and stay consistent within what I know. Wait until I finish the Kynurenine ones because it will make much more sense when I post everything and connect the dots.
That has been my aim for over a year, what is the common tie for many of these pathways, but neither me nor the person who helped me research the PAID hypothesis can find one, neither Doorless who is also a good fellow and honest person. There is too many parts of too many diseases. It is beyond me what 20 different viruses, bacterias and molecular clamps from retroviruses have in common.
" In looking at the processes I am looking at historical levels of certain trace nutrients which the RDA for is low because we only understand parts of how these nutrients are used in metabolic pathways and we further underestimate these are recycled in normal pathways therefore even borderline deficiencies can lead to dramatic manifestation. It's simple and complicated at the same time."
That is pretty much were I am at. Couldn't but it better myself. Since I am not an academic I take a free approach to everything, but I agree you should be careful because your aim is to be published. Hopefully you will get there. Praying hands emoji here.
Thanks, I see the post. I appreciate it. I made a Truth account using my laptop but I have nobody there to see anything yet. I also made a account at osf.io. It looks good so far as a place to publish to. I can publish a preprint and people can read and comment. Thats really what I want most is for this boondoggle to end. It won't be long now. Positioning the content is my biggest concern. Torn between one mammoth paper and several pieces that lead to the same place. I think I found a common thread. I haven't tied it to everything yet. Then again there's a lot We don't understand and if I am right we could never understand it unless we know up front the nutrients involved and start asking questions... this pathway works this way... but what IF a couple trace nutrients levels were double as just an example in the extracellular matrix... how would or could these reactions shift? In looking at this I see something hidden in plain sight. I will link the osf paper here when I get a small piece or the one giant piece done. Like you I still see systemic inflammation as doing the damage. Those getting off on amyloidosis for example are missing something. This spike accelerates these degenerative processes through a feedback loop. We know ROS causes atherosclerosis for example. Those stringy rubbery deposits aren't sticking to arterial walls so well... then again we are comparing this to atherosclerosis over a lifetime as compared to over 6 months. How would we know what rapidly accelerated atherosclerosis would or should look like? We have never seen anything like this. It's the same processes I believe for all the degenerative diseases of aging. They are all manifesting in an accelerated way and we aren't seeing it for what it is because as atherosclerosis for one example deposits over many years the body has time to lay calcium over it as it forms. Here because it happens so fast there isn't time or resources for it to manifestas we expect.
I'm sure you can use this somewhere.
Dimitry Medvedev: ‼️“These are not predictions. This is what has already happened . This can be treated differently, but we can assume that the “horsemen of the Apocalypse” are already on their way and all hope is only in the Lord God, in the Most High,” Dmitry Medvedev😀
Russian Telegram channel, with right click translate. (excellent channel by the way, no BS)
t.me/s/RVvoenkor
t.me/RVvoenkor/14657
Do your comments about disease pathogenesis vs acceleration also apply to the concerns other writers are expressing regarding the spike potentially causing amyloidosis and fibrosis? Thanks...
You mean the moronic ideas Walter espouses ? Here is me months ago calling him on his asinine bullshit -> https://twitter.com/ThingsHiddenn/status/1437564042479034368
Can the spike protein and the viral infection cause amyloidosis on their own ? Yes under very specific circumstances, and with very specific scenarios. Fibrosis the same, it won't cause in every single person infected, too much things have to happen for that.
The amyloidosis happens within certain mechanisms, and mitochondrial function is one of the most important aspects of it all. Maybe I will finish my amyloid post to put whatever bullshit he is spousing to rest.
Although I can understand less than a third of all of this, it seems you are saying you have to watch the mitochondrial functions. Mine is Kaput, but not from Covid. In addition to NAC and liposomal (was it glycine - see can you tell?) what else is needed to get these mitochondrials working again (in addition to fasting). Sorry, I am so tired today I can't keep a thought in my head. Tryptophan? and what vitamin is nicomaside??sp?
Depending on age, underlying condition and symptoms the supplements vary, but mostly if you use my "brain stack" it will help you.
NAC, liposomal glutathione, and if you want faster results Nicotinamide Mononucleotide, a specific metabolite of Vitamin B3.
Tryptophan might be helpful too.
Thank you John Paul. Sorry to be so fuzzy at day's end.
No problem !!!
Also, it would be helpful as I do not know if I had covid back in March of 2020. It hurt to breathe and I thought I had flu....But I'm still standing.
That sounds like Covid followed by a short case of pneumonia, pretty common back in March when Alpha was dominant. Lots of people had that.