COVID-19: Facts and Questions

gl69m

Member
Want to recreate this thread from the original LRF from 2020, and I had most of the posts archived on a word file but not all of them, I can get some of them from the Way Back Machine, here is the first few posts:

Post #1 (from firetown)
If you have any facts not yet common knowledge or frequently overlooked, please post it. If you have questions, doubts, uncertainties, this is the thread to clear them up. Please limit responses to what is factual and what matters.

I will start:

FACT:

A large amount of people worldwide are dying due to being unable to receive medical care necessary to keep them alive.

QUESTION:

What percentage of those deaths are being attributed to COVID-19?
Shame he never followed up on this really good question in this thread.

Post #2 (from Truthissweet)
FACT:
Pompeo 3/20 press conference and Governor Cuomo press conference about 2 weeks ago. Pompeo says live exercise and Cuomo says preparedness drill.

QUESTION:
Why is media not questioning this (we know why).
Excellent facts there!

Post #3 (from firetown)
FACT:

The presumed outbreak began around the time of Chinese New Year when Chinese tourists travel the most. In Thailand for example: 1 Million Chinese visitors came for their New Year's celebration, 20,000 of them from Wuhan.

QUESTION:

Why did the total number of cases not exceed 100 until 2 months later?

Post #4 (from gl69m)
From firetown (post#1)



Quote:

If you have any facts not yet common knowledge or frequently overlooked, please post it. If you have questions, doubts, uncertainties, this is the thread to clear them up. Please limit responses to what is factual and what matters.

I will start:

FACT:

A large amount of people worldwide are dying due to being unable to receive medical care necessary to keep them alive.

QUESTION:

What percentage of those deaths are being attributed to COVID-19?
__________________
"FACT:

A large amount of people worldwide are dying due to being unable to receive medical care necessary to keep them alive."

This may well be a fact, but if we present this as "fact" to sheople without backing "evidence" to prove it is a fact, they will dismiss it as a "fact". Can you please put up at least three links to support each "fact" that may not be entirely obvious on the surface that they are "facts"? My request, not a demand.


From Truthissweet (post #2)



Quote:

FACT:
Pompeo 3/20 press conference and Governor Cuomo press conference about 2 weeks ago. Pompeo says live exercise and Cuomo says preparedness drill.

QUESTION:
Why is media not questioning this (we know why).
Nice start from you Rob, thanks, right to the point. I'd say on the surface, sheople can not argue with this, but a follow up on sources would be necessary if they (sheople) query and were too lazy to look it up for themselves. But I myself would like to see a link/video we can show people of Cuomo's statements on camera about NYC being in a "preparedness drill". I have seen the video posted on Facebook by our mutual friend Jerry Lafreniere, but I haven't looked up a link for it yet.


From Firetown (post #3),



Quote:

FACT:

The presumed outbreak began around the time of Chinese New Year when Chinese tourists travel the most. In Thailand for example: 1 Million Chinese visitors came for their New Year's celebration, 20,000 of them from Wuhan.

QUESTION:

Why did the total number of cases not exceed 100 until 2 months later?
This seems to be more likely to be "fact" on the surface, better than the first post. But why are you not following up with your own question to find proof of that as to what's going on, particularly before you go onto another "fact"? Take this is as constructive criticism, the thread will be a lot better off and better supported with "evidence" and much more informative if you do that, thanks.

Post #5 (from Viking911)
QUESTION:

What percentage of those deaths are being attributed to COVID-19?

Only God know the answer to that question, as no clear instruction exist to pinpoint the course of death of Covid-19.
Covid-19 has been promoted by all means on death certificates, even
a person has not been tested positive for the specific Virus.


https://www.cdc.gov/nchs/data/nvss/c...-19-deaths.pdf

thum_113435eaf2b1c0b45e.jpg


Better to read the notice here:
https://twitter.com/HenryMakow/statu...rymakow.com%2F
Not sure if the Henry Makow link works or not.

Here is the CDC COVID-19 Alert No. 2 from March 24th 2020 (from the NVSS[National Vital Statistics System])
COVID-19 Alert No. 2 March 24, 2020
New ICD code introduced for COVID-19 deaths This email is to alert you that a newly-introduced ICD code has been implemented to accurately capture mortality data
for Coronavirus Disease 2019 (COVID-19) on death certificates.

Please read carefully and forward this email to the state statistical staff in your office who are involved in the
preparation of mortality data, as well as others who may receive questions when the data are released. What is the new code? The new ICD code for Coronavirus Disease 2019 (COVID-19) is U07.1, and below is how it will appear in formal tabular
list format.
U07.1 COVID-19
Excludes: Coronavirus infection, unspecified site (B34.2)
Severe acute respiratory syndrome [SARS], unspecified (U04.9)

The WHO has provided a second code, U07.2, for clinical or epidemiological diagnosis of COVID-19 where a
laboratory confirmation is inconclusive or not available. Because laboratory test results are not typically
reported on death certificates in the U.S., NCHS is not planning to implement U07.2 for mortality statistics. When will it be implemented? Immediately. Will COVID-19 be the underlying cause? The underlying cause depends upon what and where conditions are reported on the death certificate.
However, the rules for coding and selection of the underlying cause of death are expected to result in COVID-
19 being the underlying cause more often than not. What happens if certifiers report terms other than the suggested terms? If a death certificate reports coronavirus without identifying a specific strain or explicitly specifying that it is
not COVID-19, NCHS will ask the states to follow up to verify whether or not the coronavirus was COVID-19. As long as the phrase used indicates the 2019 coronavirus strain, NCHS expects to assign the new code.
However, it is preferable and more straightforward for certifiers to use the standard terminology (COVID-19). What happens if the terms reported on the death certificate indicate uncertainty?
If the death certificate reports terms such as “probable COVID-19” or “likely COVID-19,” these terms would be
assigned the new ICD code. It Is not likely that NCHS will follow up on these cases.
If “pending COVID-19 testing” is reported on the death certificate, this would be considered a pending record.
In this scenario, NCHS would expect to receive an updated record, since the code will likely result in R99. In
this case, NCHS will ask the states to follow up to verify if test results confirmed that the decedent had COVID-19. Do I need to make any changes at the jurisdictional level to accommodate the new ICD code? Not necessarily, but you will want to confirm that your systems and programs do not behave as if U07.1 is an
unknown code.
Should “COVID-19” be reported on the death certificate only with a confirmed test? COVID-19 should be reported on the death certificate for all decedents where the disease caused or is
assumed to have caused or contributed to death. Certifiers should include as much detail as possible based
on their knowledge of the case, medical records, laboratory testing, etc. If the decedent had other chronic
conditions such as COPD or asthma that may have also contributed, these conditions can be reported in Part II. (See attached Guidance for Certifying COVID-19 Deaths)
I think there was a follow up to this that showed the U07.2 code was indeed being used on death certs with no actual 'covid' testing only clinical diagnosis with from symptoms primarily (or perhaps other imaging or lab findings too). Will have to dig for that one later.

post #6 (from firetown)
The blood type study from China appears to have been somewhat confirmed by NYP.
COVID-19 and Blood Types: Higher Risk for Blood Type A, Lower Risk for Blood Type O (Chinese study)
The study from (NYP/CUIMC) shows similar results and in addition it also indicates a lower chance of dying for those with Rh(D) negative blood types:
COVID-19 deaths: 1 out of 45 Rh- and 1 out of 8 Rh+ patients (NYP/CUIMC)
Heat appears to also be a factor. Thailand and India may have had low numbers especially in the beginning due to that:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7182516/

post #7 (from firetown)
Quote:


Originally Posted by gl69m View Post

From firetown (post#1)

"FACT:

A large amount of people worldwide are dying due to being unable to receive medical care necessary to keep them alive."


This may well be a fact, but if we present this as "fact" to sheople without backing "evidence" to prove it is a fact, they will dismiss it as a "fact". Can you please put up at least three links to support each "fact" that may not be entirely obvious on the surface that they are "facts"? My request, not a demand.
Sorry, but that would be catering to the types that don't benefit from this forum. If you need evidence that there are people in need of medical treatment, go back to Kindergarten and ask your teacher there. She will probably also explain to you that if people need treatment, but cannot get it, some of them may die.

Why 3?
Is that your magic/superstitious number? Do all your good things come in threes?
Request denied.
If you have something of value, you are welcome to post it.
Repeat: of value.

post #8 (from firetown)
Quote:


Originally Posted by gl69m View Post


This seems to be more likely to be "fact" on the surface, better than the first post. But why are you not following up with your own question to find proof of that as to what's going on, particularly before you go onto another "fact"? Take this is as constructive criticism, the thread will be a lot better off and better supported with "evidence" and much more informative if you do that, thanks.
What happened to the quality of the forum?
You need help using Google?
Maybe some of your friends can teach you.
Stop trolling.

post #9 (from firetown)
Quote:


Originally Posted by Viking911 View Post

QUESTION:

What percentage of those deaths are being attributed to COVID-19?

Only God know the answer to that question, as no clear instruction exist to pinpoint the course of death of Covid-19.
Covid-19 has been promoted by all means on death certificates, even
a person has not been tested positive for the specific Virus.


https://www.cdc.gov/nchs/data/nvss/c...-19-deaths.pdf


thum_113435eaf2b1c0b45e.jpg


Better to read the notice here:
https://twitter.com/HenryMakow/statu...rymakow.com%2F
I don't trust HM. Do you?
I guess I need to rephrase it:
If all people in the world were suddenly denied any type of medical treatment, what percentage of the population would pass away that otherwise wouldn't have within a month?

Post #10 (from Viking911)
Yes, I trust HM, but the news paper notice is from a Tony Parkinson, HM just
conveyed the message.
"I guess I need to rephrase it:" no you don't have to, as my answer was to
"What percentage of those deaths are being attributed to COVID-19?"
Perhaps you should just ask one question at a time and sort that out to avoid
getting confused.

post #11 (from firetown)
QUESTION:

Did the initial major spikes of deaths in Italy/Iran/USA/Spain take place before or after there were restrictions making it harder for people to receive medical care?

post #12 (from firetown)
Quote:


Originally Posted by Viking911 View Post

Yes, I trust HM, but the news paper notice is from a Tony Parkinson, HM just
conveyed the message.
"I guess I need to rephrase it:" no you don't have to, as my answer was to
"What percentage of those deaths are being attributed to COVID-19?"
Perhaps you should just ask one question at a time and sort that out to avoid
getting confused.
I'm not confused, but I am wondering why I should pay attention to controlled opposition. That seems to be a major source of confusion.

post #13 (from gl69m)
You know firetown, you sure as hell don't take constructive criticism worth a shit do you?

How about one, just one link for your "fact"??

"FACT:

A large amount of people worldwide are dying due to being unable to receive medical care necessary to keep them alive."

That is at least the minimum you should provide, like Viking911 did (post #5). That would be grand, awesome, marvelous, thanks very much;

Dickhead


And gosh dammit, follow up with your damn questions!! Just put the fucking information up here already, if you have any. Consider that a kindly request.

Stop the bullshit accusations of we're either trolling or stupid,

That's not a request.

Post #14 (from Viking 911)
I have no information, that Mr. Tony Parkinson should be controlled opposition, perhaps
you will share your knowledge with us, as you sound to be better informed.
P.S. It is a letter to the Editor at The Telegraph, UK on 1. May 2020.

Questions?
Should the first question not be "Do a new Virus called Covid19 actual exist?"
If the answer is yes, we can go on, if no, we are just wasting our time and should
concentrate of the consequences of this massive hoax.

post #15 (from firetown)
Quote:


Originally Posted by Viking911 View Post

I have no information, that Mr. Tony Parkinson should be controlled opposition, perhaps
you will share your knowledge with us, as you sound to be better informed.
P.S. It is a letter to the Editor at The Telegraph, UK on 1. May 2020.

Questions?
Should the first question not be "Does a new Virus called Covid19 actual exist?"
If the answer is yes, we can go on, if no, we are just wasting our time and should
concentrate of the consequences of this massive hoax.
It doesn't matter whether or not there is an old virus or a new virus.
What matters is what people are dying of.

post #16 (from firetown)
Bill Gates BBC Interview segment April 12th 2020

BG “And the thing that will get us back to the world that we had before corona virus is the vaccine and getting that out to all 7 billion people and we’ll need to fund about 10 the 10 most promising constructs because we won’t know in advance which one will prove to be safe and effective, and being effective for older peoples immune system is weak is a huge challenge. If you really amp up the vaccine to do that then you can run into safety issues. The people like myself and Tony Fauci are saying 18 months. If everything went perfectly, we could do slightly better than that but there will be a trade-off. We’ll have less safety testing than we typically would have and so governments will have to decide you know do they indemnify the companies and really say let’s, let’s go out with this ahh when it’s, we just don’t have the time to do what we normally do.”

Interviewer (IR)

IR So, as I understand it then what you’re saying is that it may be that there needs to be some compromise in some of the safety measures that normally be expected to create a vaccine because time is so crucial?

BG “Well of course if you want to wait and see if a side effect shows up 2 years later that takes 2 years so we will I think be able to get some safety indications but it, this is a public good and so you know those trade-offs, the governments working on a cooperative basis will be involved in a decision to say hey the regulators says go ahead even though you haven’t taken the normal time period”


Questions for analysis

1. Does Gates have a specific vaccine in mind?
2. Does he expect the vaccine to be safe without detrimental side effects?
3. Is there anything else within the language that is of interest to us?

“And the thing that will get us back to the world that we had before Corona Virus is the vaccine and getting that out to all 7 billion people,”

1. The subject (Bill Gates) identifies one thing that is needed to get us back. This is the vaccine. It is not, “what will get us back” or “the steps that will get us back” it is the vaccine. No other options are in the mind of the subject. Herd immunity is not a consideration in the perception of the subject, nor is any effective treatment protocol.

2. The subject uses the article “the” for a vaccine. This can be an indication of prior knowledge or his pre-accepted sole solution.

For example, if a shopkeeper reporting a robbery says “the man pulled the gun on me” it is an indication that the subject knew of the gun before it was pulled on him. This may mean he is an accomplice in the robbery. Articles are important indicators in Analysis.

What has caused the article “the” in the verbal perception of reality for the subject? The expected is “a vaccine”. At this point, the article “the” is an indicator that the subject has knowledge of a vaccine. Is this because there is one showing more promise than others, that he has in mind or does he know which one will be used? We do not know.

3. Can the article “the” be appropriate in that the subject is describing the cure to a specific virus? The Corona virus.

http://statement-analysis.blogspot.c...interview.html

post #17 (from Dude111)
Fuck gates and his stupid life altering vaccine crap!!!!!

Thats exactly what they want..... To scare people enough so they all get this crap injected into them.......

post #18 (from firetown)
Quote:


Originally Posted by Dude111 View Post

Fuck gates and his stupid life altering vaccine crap!!!!!

Thats exactly what they want..... To scare people enough so they all get this crap injected into them.......
He tells us what's coming.
QUESTION:
How do you "un-scare" a population?

post #19 (from Dude111)
Ya you dont.........

They have most people right where they want them now!!!!

post #20 (from firetown)
Quote:


Originally Posted by Dude111 View Post

Ya you dont.........

They have most people right where they want them now!!!!
Does it matter?
The populations are under-informed.
What exactly people are dying of can provide the answer to what is wondered quite frequently.
What the exact nature of the virus is can as well.
"It's all bullshit" is too general.
People want answers and don't seem to get them.
This is why I am here.
This is what I have started this thread for.

post #21 (from firetown)
And just to clarify:
Posting the analysis of this (only one) statement by Bill Gates is not meant as a rant about him.
It is to examine what is being planned. If more people get the idea of where we are going with all of this, a clearer picture might get painted encouraging the readers of this thread to look closer at and into what exactly it is that everybody is scared of.

post #22 (from Orion67)
My mother died in the hospital last weekend. She was living in an "assisted" home for the past year or so. She had advanced dimentia to the point where she didn't recognize her own kids. She apparently slipped and fell in her room and hit her head on something, resulting in a brain bleed.
They kept her on morphine at the ER for about 3 days while refusing to do anything about the bleed, and of course she died. Magically, she was marked down as a Covid casualty, although there was no such thing involved.


I plan to sue when things settle down a bit. We can't even hold a service without being fined or arrested for disorderly conduct of more than 2 people in the same room.

post #23 (from firetown)
Quote:


Originally Posted by Orion67 View Post

They kept her on morphine at the ER for about 3 days while refusing to do anything about the bleed, and of course she died.
What reason were you given for the refusal?

post #24 (from Dude111)
I am so sorry Orison...... No your mom didnt die of "Covid"

I wish you luck when sueing and I hope you make a dent in this thing

post #25 (from firetown)
Of course, this is not confirmed, but someone recently told me that hospitals get 13k if the death is covid and 39k if it includes being placed on the ventilator?
Is that something credible any of you knows more about?

post #26 (from 2getherwestand)
My heart goes out to you Orion,sorry to hear of your loss.As for the lawsuit,all the way with a red hot poker friend.
icon_salut.gif

Firetown,check this,

You Tube



Or watch it on Invidio here
https://www.invidio.us/watch?v=-1Kd4excEIk

And as to answer your question about the 12 or 13 grand and 39 grand being paid out,,,,really,serious????That's been out for awhile,and you never researched that to confirm if it's fact
icon_think.gif
.
More and more doctors,nurses etc,etc, are coming forward and spilling the beans of the depth of this fraud.Hospitals are actually laying staff off in a lot of places because of a lack of customers.As for bill gates of hell,he should be made to be strapped down and injected with every vaccine the bastard ever pushed that damaged and killed the massive amounts of young children around the world.A bullet to the forehead would be too quick and painless for that ass clown.
icon_evil.gif


__________________
 

gl69m

Member
SO here's the part where the thread gets gritty, well there was already friction between me and firetown on another thread (the big "coronavirus" thread) before this thread. And I am not recreating this thread to create more beef, I know one member that made posts on this thread is back on the forum, and she is welcome to comment again on this thread: but however these posts are very pertinent to making my case that I've stated before, that 'covid' is really a false cover, and umbrella if you will, invented to encompass so many other existing diseases (pre-'covid', 2019 and before) and claim that 'covid' can basically cause or "mimic" so many of those diseases that kill the most amount of people worldwide every year; and when in reality (most likely, I believe) this is just utterly false and so many deaths attributed to this fake 'pandemic' were not from this alleged 'sarscov2' virus, but from naturally occurring diseases already present in the population, though there may be an uptick of this disease burden and death in the last decade in particular and still increasing. I will expand on that, particularly the way in which the alleged disease mechanism and false paradigm of 'covid-19' is being marketed.

post #27 (from Ruby Gray), this video kind of began to crystalize for me what was beginning to happen, this (false) disease paradigm shift and they way the 'scientific/medical' marketing of 'covid' was being played out last year, the huge deception they were creating along with all the endless bullshit fearmongering.
There is wholesale medical ignorance among the general population, of the mechanisms by which COVID-19 affects the body.


Here is a brief education by a medical expert.




You Tube

post #28 (from firetown)
Quote:


Originally Posted by 2getherwestand View Post

My heart goes out to you Orion,sorry to hear of your loss.As for the lawsuit,all the way with a red hot poker friend.
icon_salut.gif

Firetown,check this,

http://www.youtube.com/watch?v=-1Kd4excEIk


Or watch it on Invidio here
https://www.invidio.us/watch?v=-1Kd4excEIk

And as to answer your question about the 12 or 13 grand and 39 grand being paid out,,,,really,serious????That's been out for awhile,and you never researched that to confirm if it's fact
icon_think.gif
.
More and more doctors,nurses etc,etc, are coming forward and spilling the beans of the depth of this fraud.Hospitals are actually laying staff off in a lot of places because of a lack of customers.As for bill gates of hell,he should be made to be strapped down and injected with every vaccine the bastard ever pushed that damaged and killed the massive amounts of young children around the world.A bullet to the forehead would be too quick and painless for that ass clown.
icon_evil.gif

I'm doing this from scratch, Kelley.
That means I stay away from the controlled oppositions published mix of true information and disinformation. It is much easier to do this step by step rather than having to unlearn at a later time.
Aside from a handful of people I speak to about these things in private, this forum remains the only source not agenda-driven. That is why my expectations are very high when I come here. I definitely do not come here to have disinformation I can get elsewhere which confuses the public shoved in my face.
The "this virus is fake" rhetoric also doesn't cut it for me either. It is part of why there is so much division and so little factual knowledge. Of course there seems to be a real virus. I have spoken to many who claim to have had it, some dating back to December and those who also had the flu before and compared the two all told me that the flu was worse.
That is why I want to have real information from people who know for a fact. Not "check this video, there might be something good in there and you may be confused because other parts are not true".
I know that you understand what I am saying.
It doesn't help when people state opinions and don't bother following up. When opinions stay opinions and get promoted, you only turn people off. "There is no virus" turns people off. When they get turned off, they go back to mainstream. So while I am talking to you and others, my mind is mainly on the tens of thousands reading this. They come here for answers. I try to give them, but more than anything, get them from people who have them.

post #29 (from gl69m)
post #27,

video

What Doctors Are Learning From Autopsy Findings of Coronavirus (COVID-19) Patients

Dr. Hansen starts out with the "common" symptoms of 'covid', fever, cough, shortness of breath, common to have body aches, then he says,


Quote:

"but sometimes covid 19 is more than just a respiratory disease, or sometimes not a respiratory disease at all. It can mimic just about any illness.Sometimes it looks like a common cold, sometimes it looks like influenza. Sometimes it looks like a stomach bug with belly pain and diarrhea, maybe some nausea vomiting, loss of appetite. It can cause "pink eye", cause runny nose, loss of taste and smell. Sometimes whole body rashes, or areas of swelling and redness of skin in just a few spots."
That is just the first 37 seconds of Dr. Hansens 'coronavirus' 'facts'. Do we even need to go any further??? People are actually believing this nonsense? Is there anything this 'virus' can't do????

I will watch this train wreck of a "medical' video with alleged scientific/medical information on 'coronavirus' at a later time and try and break it down. Getting tired this a.m. now.
Just that part right there from Dr. Mike Hansen, "it can mimic just about any illness" really just super tipped me off that something was direly deceptive about this 'covid' narrative being pedaled.
Rest of post #29
@firetown, post #28,

the thread is improving from the start of it.



Quote:

The "this virus is fake" rhetoric also doesn't cut it for me either.
Explain to me why you think there simply has to be a "new" virus out here? There are many thousands of viruses, I don't know how many. Can you show us some real solid proof of a "new" virus called SARS-CoV-2?



Quote:

That is why I want to have real information from people who know for a fact.
Do you have the scientific expertise, let alone the equipment, lab and funding, to go out and hunt the virus down from 'covid' patients and "isolate" it, "purify" it, prove that with a huge amount of documentation (lab logs, electron micro-graphs, various other biological viral tests, genome sequencing, other experiments ect.) that it is indeed real, that these patients do not in fact have other viruses and bacterial diseases? Never mind proving that this 'virus' can cause 'disease' that "can mimic just about any illness" whatsoever.




Quote:

That means I stay away from the controlled oppositions published mix of true information and disinformation.
If not, do you plan on using the 'evidence' already available, that like you point out will be very likely (more like about 100%) to be from "controlled opposition"? What will that prove if you do that then?


I'm not going to brag about my expertise, my degree and biotech certificate and work experience can only go so far in figuring out what might be real and not real about the alleged 'new' virus or whether it exists now or doesn't. I don't have any lab or funding and no way to scientifically verify or dis-confirm the existence of 'SARS-CoV-2' myself. I don't see anyone on this forum who can do that (scientifically prove/disprove the virus), and nobody that even seems to know as much biology here as I do.

We have little more than speculation about a lot of it (but not all of it obviously), especially when we know "official sources" or MSM media sources are very difficult to trust.



Quote:

It doesn't help when people state opinions and don't bother following up. When opinions stay opinions and get promoted, you only turn people off. "There is no virus" turns people off. When they get turned off, they go back to mainstream. So while I am talking to you and others, my mind is mainly on the tens of thousands reading this. They come here for answers. I try to give them, but more than anything, get them from people who have them.
It doesn't help a whole lot either when some one asks a pertinent question related to said investigation in a post and then doesn't follow up on their own question.

"There is no virus" turns people off. When they get turned off, they go back to mainstream."

No shit, we already know that truth turns sheople off if it goes against the "official story". That is one big reason that we who care about truth are all here in the first place. I do wonder exactly how many thousands of readers the forum does have coming here to get answers, that is something I wouldn't mind knowing.

post #30 (from firetown)
Quote:

What Doctors Are Learning From Autopsy Findings of Coronavirus (COVID-19) Patients
Dr. Hansen [/SIZE]starts out with the "common" symptoms of 'covid', fever, cough, shortness of breath, common to have body aches, then he says,
That is just the first 37 seconds of Dr. Hansens 'coronavirus' 'facts'. Do we even need to go any further??? People are actually believing this nonsense? Is there anything this 'virus' can't do????

I will watch this train wreck of a "medical' video with alleged scientific/medical information on 'coronavirus' at a later time and try and break it down. Getting tired this a.m. now.
Right, but there is something going around and there are common denominators I have found to exist (temporary loss of taste and smell for example). As I have stated, all people I have spoken to considered themselves lucky for having a "mild version" of it. So far, I have only seen indicators of mild versions. Far from the killer the media is selling




Quote:

@firetown, post #28,

the thread is improving from the start of it.

Explain to me why you think there simply has to be a "new" virus out here? There are many thousands of viruses, I don't know how many. Can you show us some real solid proof of a "new" virus called SARS-CoV-2?
There doesn't have to be but what does it matter either way? What matters is what there actually is and isn't.



Quote:

Do you have the scientific expertise, let alone the equipment, lab and funding, to go out and hunt the virus down from 'covid' patients and "isolate" it, "purify" it, prove that with a huge amount of documentation (lab logs, electron micro-graphs, various other biological viral tests, genome sequencing, other experiments ect.) that it is indeed real, that these patients do not in fact have other viruses and bacterial diseases? Never mind proving that this 'virus' can cause 'disease' that "can mimic just about any illness" whatsoever.
I think when middle-man media is eliminated and we go by communicating and sharing real experiences, the need for such will diminish.



Quote:

If not, do you plan on using the 'evidence' already available, that like you point out will be very likely (more like about 100%) to be from "controlled opposition"? What will that prove if you do that then?
How do we know it's evidence? Isn't it more helpful to disregard such nonsense and go from scratch?



Quote:

I'm not going to brag about my expertise, my degree and biotech certificate and work experience can only go so far in figuring out what might be real and not real about the alleged 'new' virus or whether it exists now or doesn't. I don't have any lab or funding and no way to scientifically verify or dis-confirm the existence of 'SARS-CoV-2' myself. I don't see anyone on this forum who can do that (scientifically prove/disprove the virus), and nobody that even seems to know as much biology here as I do.
You are bragging. And for the record: those who can help are not likely to touch this one, at least the ones I know.



Quote:

We have little more than speculation about a lot of it (but not all of it obviously), especially when we know "official sources" or MSM media sources are very difficult to trust.
Impossible to trust.



Quote:

It doesn't help a whole lot either when some one asks a pertinent question related to said investigation in a post and then doesn't follow up on their own question.
I always follow up, but I also prioritize. So when for example someone makes a long rant about Gates ("of hell"), my attention span tends to shift me into going elsewhere and see what I can find there.





Quote:

No shit, we already know that truth turns sheople off if it goes against the "official story". That is one big reason that we who care about truth are all here in the first place. I do wonder exactly how many thousands of readers the forum does have coming here to get answers, that is something I wouldn't mind knowing.
People come here often when their intuition tells them that the more promoted channels confuse them even more. I looked at the category and the other thread shown 15k viewers. When looking who is online, there are always like 500 people. It isn't "truth" that turns people off. It is confusion that turns them off. Confusion and disgruntled posts (not yours). "It's all BS, the government sucks" type of stuff. People coming here often assume this place is no different from what they've seen Alex Hicks doing. I don't have all the answers of course, but I have some, so putting them all together could actually open people's eyes. Whether or not this virus is new is less important that what it can and can't do to someone who has it.
And again:
the question leading me to the other thread was one a member here never had answered:
"What are people dying of?"
This is probably what, if answered well, can send many in the right direction. It may be too late for all of this, but at least I want to put my energy where I think we can do the most damage.
Thank you for your reply.

Will come back to more posts from original thread in subsequent posts.
 

gl69m

Member
In post #30, I began to lay out part of my case as 'covid' as a false disease umbrella to encompass the most deadly diseases in this hoax-adigm plandemic,

post #30 (from gl69m)
@firetown, post #30, we're starting to have some rational dialogue, much better than what started out on the big coronavirus thread, still needs improvement in my view though,


Quote:



Quote:
I'm not going to brag about my expertise, my degree and biotech certificate and work experience can only go so far in figuring out what might be real and not real about the alleged 'new' virus or whether it exists now or doesn't. I don't have any lab or funding and no way to scientifically verify or dis-confirm the existence of 'SARS-CoV-2' myself. I don't see anyone on this forum who can do that (scientifically prove/disprove the virus), and nobody that even seems to know as much biology here as I do.
You are bragging. And for the record: those who can help are not likely to touch this one, at least the ones I know.

Ok, I bragged a little bit, I am not gloating about it. I have stressed my inherent limitations of my credentials (degree, cert. and work experience) and I have no way to scientifically confirm/dis-confirm (experiment) these things ('coronavirus/covid-19' in this case).

Who exactly do you mean here?
"And for the record: those who can help are not likely to touch this one, at least the ones I know."

I do wish I had some back up to help me out, someone higher in "expertise" than myself on the biological/biochemical side of things, a true "whistler-blower" on 'covid' would really be great at this time. Or someone to even challenge me on things I am getting wrong or things I'm missing that a serious "expert" would catch. I know I'm doing both of that, but I know I am getting a lot of this right, but what I've uncovered and shown is still not smoking gun (enough) "scientific" evidence to prove to people wavering one way or another that 'covid' is bullshit as opposed to being "real".


Like it or not, it seems I'm the closest that the forum has to an "expert" in the bio-science arena for such matters and I'm flying solo trying to figure some of it out. My approach is scatterbrain I admit, I do get distracted by all the other lines of evidence not related specifically to the science aspect.


Regarding Scooby Doo's, er, I mean Ruby's posted video,

What Doctors Are Learning From Autopsy Findings of Coronavirus (COVID-19) Patients

May 6, 2020

https://www.youtube.com/watch?v=KzKv...ture=emb_title

I'm glad I watched all of this video, this is extremely slick marketing, Dr. Hansen is a very slick speaker. Once you get past the contradictory absurdities in the first minute, than a few more in the next few minutes of the video, he is using very legitimate biological/biochemical terminology (he actually starts doing that within the first minute also) to link 'covid' to a wide variety of conditions/diseases in the minds of the public with this video. There are probably a slew of other medical "experts" now doing the same thing.

We will be facing an avalanche of this kind of 'evidence' that 'covid' and 'sars-cov-2' is real, and no matter how many smoking guns we can find that they not only planned it but planned it as a "simulation", when the sheople mind hears this 'evidence' (sounding very legit of course), their logic will turn to mush and the 'link' to all these different diseases/conditions will be forever sealed as can be caused by 'covid' therefore this 'pandemic' must be real. This is real evil genius at work looks like to me. This story line ('discovery' of the 'new' virus and disease "research') didn't just fall off a reefer truck with dead 'covid' patient bodies in it just yesterday or last month: this had to be in the works and planned out many years ago, at least many of the biological explanations for how the 'new' virus infects and causes disease.

We would consider this dis-information of course, but with this kind of propaganda it will be extremely difficult to dissuade people (on the fence per se) that the 'virus' isn't real and the 'pandemic' isn't fake. I would say that the 'covid' dissenters are now at a very serious disadvantage because of this kind of stuff being published and reported now. If something "scientific" (particularly from "virology") to counter this can't be produced, it won't matter that they simulated all of it (and can be proven)- people will still believe the 'pandemic' and 'virus' is real.

This is very serious, I do urge everyone to watch this video at least once through so that you can get an idea of what we're dealing with here. The first minute is exorbitantly contradictory and absurd from what we normally think of more relatively more easily defined disease, but they are changing that paradigm with this live exercise of course.


Dr. Hansen shows an electron micrograph of "virus" at about 3:00 in the video, can anybody look at that and distinguish this virus from any other coronavirus? Probably not very easily if they can at all. No proof it actually came from a real patient or one with 'covid' has to be offered and sheople will still believe what his saying of course.

Here is picture from an article I found of the coronavirus strain NL-63, this article here, https://virologyj.biomedcentral.com/...43-422X-10-213
https://virologyj.biomedcentral.com/articles/10.1186/1743-422X-10-213
12985_2013_Article_2210_Fig6_HTML.jpg

Compare these images (particularly C) to the micrograph at ~3:00 in the video. I believe this article shows evidence that NL-63 can also replicate in human kidney cells, suggesting that this virus could possibly infect the kidneys. Very interesting article that came out in 2013.


Dr. Hansen leaves clues that 'covid' is really disguised as other more well characterized diseases, perhaps they are small admissions of truth, but my brain is frying thinking too much today, so I'm not going to try and break down everything in this video. Mike (ft), now would be a good time to pull out the "statement analysis" on this guy to see what he is really conveying, but don't throw words in his mouth with that of course.

I'm going to bring up one topic he does mention in the video, he mentions the ACE2 receptor and the role it plays in 'covid' disease development; and I have seen articles and discussion about that elsewhere, that SARS virus (and other coronaviruses) also uses the ACE2 receptor with it's spike (S protein, the spikes on the outer surface in all the coronavirus images) to gain entry into the cell. I think all coronaviruses are imputed to use the spike to infect cells, at least I think that's the case.

This article here that scott75 brought up in his thread How to deal with Covid 19 in post #15,

https://www.nature.com/articles/s41591-020-0820-9

I commented on this article in post #16. The study in particular supposedly looked at the spike (S) protein variation in 6 different coronaviruses including 'sars-cov-2'.


Quote:



1. Mutations in the receptor-binding domain of SARS-CoV-2

The receptor-binding domain (RBD) in the spike protein is the most variable part of the coronavirus genome1,2. Six RBD amino acids have been shown to be critical for binding to ACE2 receptors and for determining the host range of SARS-CoV-like viruses7. With coordinates based on SARS-CoV, they are Y442, L472, N479, D480, T487 and Y4911, which correspond to L455, F486, Q493, S494, N501 and Y505 in SARS-CoV-27. Five of these six residues differ between SARS-CoV-2 and SARS-CoV (Fig. 1a). On the basis of structural studies7,8,9 and biochemical experiments1,9,10, SARS-CoV-2 seems to have an RBD that binds with high affinity to ACE2 from humans, ferrets, cats and other species with high receptor homology7.

They say that 5 of the 6 amino acids in the receptor-binding domain (RBD) of the S protein differ from SARS-CoV and 'SARS-CoV-2'. The letters in front of the coordinate numbers (442, 472, 479 etc. for SARS-CoV) refer to the actual amino acid at that sequence location within the full peptide sequence, only the 6th residue is the same Y-491 and Y505 (Y is the abbreviation for Tyrosine, I think Y4911 must be a typo).

So the crux with the ACE2 receptor to the 'covid' storyline of disease in this article is that,


Quote:



On the basis of structural studies7,8,9 and biochemical experiments1,9,10, SARS-CoV-2 seems to have an RBD that binds with high affinity to ACE2 from humans, ferrets, cats and other species with high receptor homology7.

High affinity of this RBD to ACE2 in humans and other animals, would seem to instill in people's minds that this explains it's high capacity to infect, thus transmissibility. But right after this they downplay the high affinity binding to say it is not an "ideal" interaction, in order to claim it wasn't man made or engineered in a lab.


Quote:



While the analyses above suggest that SARS-CoV-2 may bind human ACE2 with high affinity, computational analyses predict that the interaction is not ideal7 and that the RBD sequence is different from those shown in SARS-CoV to be optimal for receptor binding7,11. Thus, the high-affinity binding of the SARS-CoV-2 spike protein to human ACE2 is most likely the result of natural selection on a human or human-like ACE2 that permits another optimal binding solution to arise. This is strong evidence that SARS-CoV-2 is not the product of purposeful manipulation.

As we have seen, they are now beginning to switch that narrative, via Pompeo blaming China for research gone bad I guess, implying an "accidental" release virus from a Chinese/Wuhan lab I think. This will likely morph into an intentional release by a Clade X style "Brighter Dawn" scenario where a 'terrorist group' will be implicated in smuggling the 'virus' out of the Chinese lab, and that the Chinese govt. knew about it and covered it up. That's my basic prediction right now anyway.


Gonna move on and post an article that I found that shows the role of ACE2 enzyme as modulator implicated in various diseases/conditions, and I think that it can be gathered from the article that there are multiple ways to interfere with the ACE2 in the renin-angiotensin system (RAS) to trigger disease.

Angiotensin-Converting Enzyme 2 (ACE2) Is a Key Modulator of the Renin Angiotensin System in Health and Disease
Received15 Sep 2011
Accepted05 Dec 2011
Published20 Mar 2012

https://www.hindawi.com/journals/ijpep/2012/256294/


Quote:



Abstract

Angiotensin-converting enzyme 2 (ACE2) shares some homology with angiotensin-converting enzyme (ACE) but is not inhibited by ACE inhibitors. The main role of ACE2 is the degradation of Ang II resulting in the formation of angiotensin 1–7 (Ang 1–7) which opposes the actions of Ang II. Increased Ang II levels are thought to upregulate ACE2 activity, and in ACE2 deficient mice Ang II levels are approximately double that of wild-type mice, whilst Ang 1–7 levels are almost undetectable. Thus, ACE2 plays a crucial role in the RAS because it opposes the actions of Ang II. Consequently, it has a beneficial role in many diseases such as hypertension, diabetes, and cardiovascular disease where its expression is decreased. Not surprisingly, current therapeutic strategies for ACE2 involve augmenting its expression using ACE2 adenoviruses, recombinant ACE2 or compounds in these diseases thereby affording some organ protection.

Not going to try and explain anymore of the article for now, I'm going to post the headlines of several sections here to show that ACE2 "interference" or "inhibition" has significance for a range of diseases,


Quote:



3. ACE2 and Atherosclerosis

4. ACE2 and Hypertension

5. ACE2 in Heart Failure

6. ACE2 and Chronic Kidney Disease (CKD)

7. ACE2 and the Lung

8. Replenishing ACE2 as a Potential Therapeutic


There are at least 3 maybe 4 more enzyme or biological signaling pathways in Dr. Hansen's video that also play a major role in already known diseases that he is using to link to 'covid', not going to break that down any further right now.


I found a document from this organization, Global Preparedness Monitoring Board (which is basically a front group for the WHO), that actually states a goal of running "two" pandemic simulations in 2020, the document dated basically September 2019. I will show what page that is on, and how it connects to the "Brighter Dawn" scenario in a post I will put up on the big coronavirus thread.
 

alpha77

New member
Here are 2 possible answers:

a) Wuhan, it is rumoured that the city was a major one for 5G testing

b) As for the numbers it is basically all made up, they only need more people to get tested, the "test" has (confirmed) 80% false positives (German doctors newspaper) and speculated up to 97% false. Also all the measurments used can be interpreted severall ways as the counting / statistics are quite "variabel"

If you use a translater here a good article about the German situation (this site does not question the "virus" tho)

"Numbers chaos Corona":

 

gl69m

Member
I would say for sure that if the 'sarscov2' 'virus' does not exist, every 'covid' test is a false positive, 100%. If on the other hand there is a real virus at least similar to, that is circulating the world in the last 2 years (or longer even), then I could believe the false 80-97% false positive rate, based on my own look at the pcr test protocols and at least one critique of the original German pcr protocol, I will dig that article up from a post on a thread of the original forum, but I planned on putting that in this thread from back then "Are the COVID-19 Test Kits Designed to Produce False Positives (Plandemic)", just haven't gotten around to doing that yet.

Even if there is a virus that can be detected by the present pcr bogus tests, obviously that test proves diddly squat that any such virus can produce the alleged disease marketed as 'covid' or 'covid-19'. That is pretty much the aim of this thread, to un-mask (pun intended) the cover or umbrella they are using 'covid' for to disguise so many worldwide (and greater now in U.S. especially) deaths by the natural disease progression, what I believe the main progression is really simply "inflammation", but that can be caused by multitude of causes/factors but which tends to cause the same underlying pathophysiology at the cell and tissue levels but directed against many different origin places within the body, thus so many different appearing diseases but really start off with mostly the same underlying cascade of events at the micro level and the body/immune response to some stress or injury toxin or pathogen or multiple causes at once et al.

I believe it likely that cancer is probably an end stage of such a disease process, just like all the serious lung diseases (ILD's and PF and IPF as well as lung cancers which are sometimes difficult to distinguish from each other), diabetes, cardio/vascular diseases, kidney and liver diseases, metabolic disorders etc. But even though they have admitted (many times over if you search for it) these "co-morbidities" (substantially or practically exponentially increase, but they ignore or downplay this) increase the risks of (alleged) 'covid') infection/hospitalization/death: this 'covid' official narrative still has co-vidiots believing it's 'covid' killing all these people and not the disease itself which killed so many people before 'covid' ever came along: and that 'covid' can thus kill any healthy person with no "co-morbidities" right, cause it's a supervirus of course, and it can give anyone a case of the endstage disease of any or all of these diseases in the minds of the compliant sheople. Such fucking nonsense, but it's a very very difficult paradigm to fight alas:(...


Moving on to further posts from the original thread (for some reason I don't have all the posts archived);

post #33 (from Truthissweet)
Quote:



Originally Posted by Truthissweet

FACT:
Pompeo 3/20 press conference and Governor Cuomo press conference about 2 weeks ago. Pompeo says live exercise and Cuomo says preparedness drill.

QUESTION:
Why is media not questioning this (we know why).


Sorry about the delay.

Gl69m had posted Cuomo vid.

"....New York Gov. Andrew Cuomo holds daily Coronavirus press briefing | FULL — 4/11/2020
Streamed live on Apr 11, 2020

....preparation drill" right at 14:00-14:01."



Pompeo video



Post #34 (from Orion67)


Post #35 (from Truthissweet)
Quote:



Originally Posted by Orion67

My mother died in the hospital last weekend. She was living in an "assisted" home for the past year or so. She had advanced dimentia to the point where she didn't recognize her own kids. She apparently slipped and fell in her room and hit her head on something, resulting in a brain bleed.
They kept her on morphine at the ER for about 3 days while refusing to do anything about the bleed, and of course she died. Magically, she was marked down as a Covid casualty, although there was no such thing involved.


I plan to sue when things settle down a bit. We can't even hold a service without being fined or arrested for disorderly conduct of more than 2 people in the same room.


Please keep us up to date when you sue. I have been telling people about this. You are in a unique situation. Good luck to you.


Post #36 (from firetown)
Quote:



Originally Posted by Orion67

My mother died in the hospital last weekend. She was living in an "assisted" home for the past year or so. She had advanced dimentia to the point where she didn't recognize her own kids. She apparently slipped and fell in her room and hit her head on something, resulting in a brain bleed.
They kept her on morphine at the ER for about 3 days while refusing to do anything about the bleed, and of course she died. Magically, she was marked down as a Covid casualty, although there was no such thing involved.


I plan to sue when things settle down a bit. We can't even hold a service without being fined or arrested for disorderly conduct of more than 2 people in the same room.


First of all, I am sorry that your mom's life had to end as a statistic. I hope you can make a difference. I have started this thread having heard the following:
1) you don't have to even have to test positive for covid. You can display one symptom and your deaths is registered as such.
2)
people cannot get medical treatment needed.
For some reasons, this forum is now controlled by trolls.
I am sorry this happened to your mom.
I do remember you from way back when.


Post #38 (from firetown)
Quote:



Originally Posted by 2getherwestand

My heart goes out to you Orion,sorry to hear of your loss.As for the lawsuit,all the way with a red hot poker friend.
icon_salut.gif

Firetown,check this,

(Youtube account terminated)

Or watch it on Invidio here
https://www.invidio.us/watch?v=-1Kd4excEIk

And as to answer your question about the 12 or 13 grand and 39 grand being paid out,,,,really,serious????That's been out for awhile,and you never researched that to confirm if it's fact
icon_think.gif
.
More and more doctors,nurses etc,etc, are coming forward and spilling the beans of the depth of this fraud.Hospitals are actually laying staff off in a lot of places because of a lack of customers.As for bill gates of hell,he should be made to be strapped down and injected with every vaccine the bastard ever pushed that damaged and killed the massive amounts of young children around the world.A bullet to the forehead would be too quick and painless for that ass clown.
icon_evil.gif


Now that I will be deleted, here is something I need to say:
You have never produced research. You also are a scumbag who friended and tried to refriend me. Kelly from Ohio



Post #39 (from firetown)
Quote:



Originally Posted by gl69m

@firetown, post #30, we're starting to have some rational dialogue, much better than what started out on the big coronavirus thread, still needs improvement in my view though,

Have you ever published a paper? I have. What do you have to offer?
Nothing.
So stop trolling my thread. Idiot.

Post #40 (from gl69m)

@fireclown (post #39)

Quote:


Have you ever published a paper? I have. What do you have to offer?
Nothing.
So stop trolling my thread. Idiot.

Fuck off.

Let's see your worthless paper then.

This thread, with what you started with, would be completely worthless bullshit without what we have added to it of value in information.

From all that you have posted since your response to my post (http://letsrollforums.com//showpost....&postcount=234) that you started for your little distraction sideshow shtick, you have proven completely incapable of posting any actual evidence or breakdown there of to assert any of your claims (some of which might well be true, but nobody will know without "evidence"). This tells me that I don't have to even read whatever your paper is to know that it isn't even worth toilet paper (okay, well if you are completely out of toilet paper, then maybe it would be worth toilet paper
biggrin.gif
).


If we are all alleged 'shills' to you, why are you still here, either make your own effort to delete all your bullshit posts, or have Phil or the admins do it, and quit distracting us and get the fuck out and don't come back. It's your own fault for posting here in the first place.

Nobody will miss your worthless ass, and on your way out- don't let the door hit you where the good lord split you.


Post #41 (from Ruby Gray)
Now some more medical information from a genuinely educated, knowledgeable expert who knows exactly what he is talking about, who makes a coherent presentation without resorting to foul language and psychotic abuse.




post #42 (from gl69m)
@Ruby (post #41)


Quote:



Now some more medical information from a genuinely educated, knowledgeable expert who knows exactly what he is talking about, who makes a coherent presentation without resorting to foul language and psychotic abuse.


Obviously the "resorting to foul language and psychotic abuse." is directed at me specifically, whatever.

You can discredit me all you want, it is the message that is much more important than me or my "reputation" or what have you.


Is the distraction and bullshit accusations of firetown not "psychotic abuse" in your opinion Ruby? You're perfectly okay with his tactics, but label me 'psychotic', I see how your little game works.


And you continue to promote a very false and extremely dangerous and deceptive 'medical' paradigm, that is really just a mental/social disorder they are instilling in people with the phantom boogie virus, even if it was real, the mental/social disorder they have invented called 'covid-19', it would obviously be much worse in the long run than a real "pandemic" either way, and you know that.

But yet you keep promoting this insanity for your own reasons I suppose. You seem to want a "depopulation" to happen by whatever means necessary, either by a real "virus' (engineered in a lab and intentionally released, or accidental, or natural for that matter), or by mass hysteria and global economic collapse and mass starvation, by which the latter you know as well as I do which would be far more effective at "depopulation". I guess it's because it is prophesied by the "bible", that's why you wish for it so hard to come true.


Regarding the "a genuinely educated, knowledgeable expert who knows exactly what he is talking about." Dr. Mike Hansen.

I don't disagree with that at all, he is obviously well educated, knowledgeable, a real doctor I am assuming: this is why his 'covid-19' false paradigm deception is all the more incredibly dangerous when lay people hear this shit; you cannot sit there and type to me with a straight face (and keyboard) that someone like this can't lie to people, for an (a much larger) agenda (than himself) and or for his own personal gain, not on a truth site, I'm calling you out for that, you are someone that knows better.

from post my #29


Quote:



post #27,

video

What Doctors Are Learning From Autopsy Findings of Coronavirus (COVID-19) Patients

Dr. Hansen starts out with the "common" symptoms of 'covid', fever, cough, shortness of breath, common to have body aches, then he says,
Quote:
"but sometimes covid 19 is more than just a respiratory disease, or sometimes not a respiratory disease at all. It can mimic just about any illness. Sometimes it looks like a common cold, sometimes it looks like influenza. Sometimes it looks like a stomach bug with belly pain and diarrhea, maybe some nausea vomiting, loss of appetite. It can cause "pink eye", cause runny nose, loss of taste and smell. Sometimes whole body rashes, or areas of swelling and redness of skin in just a few spots."
That is just the first 37 seconds of Dr. Hansens 'coronavirus' 'facts'. Do we even need to go any further??? People are actually believing this nonsense? Is there anything this 'virus' can't do????

I will watch this train wreck of a "medical' video with alleged scientific/medical information on 'coronavirus' at a later time and try and break it down. Getting tired this a.m. now.

Come on Ruby, bring out your so-called medical professional opinion and critique what I have said about the fake 'medical' paradigm being marketed now called 'covid-19'. What am I getting wrong?


Quote:



"but sometimes covid 19 is more than just a respiratory disease, or sometimes not a respiratory disease at all. It can mimic just about any illness. Sometimes it looks like a common cold, sometimes it looks like influenza. Sometimes it looks like a stomach bug with belly pain and

This bullshit is completely absurd, and you know it, whether you are a medical professional or not, you know that is true. Common people know this, then they are blindsided by a "professional' degreed MD like Hansen, and then their brains will turn to mush and believe and buy all the bullshit explanations that this new 'virus' ('sarscov2') can do anything, can cause every disease and condition know to humanity, and that without all the insane "new normals" everybody will all die and humanity will be wiped out by the boogie virus. What an incredible load of horseshit and you know it is.


Yes, I get triggered by this bullshit, I am trying to collect my thoughts/emotions and my responses in a less hostile manner now and stop being so triggered; but I could fucking care less if you or anyone else falsely labels me as 'psychotic', stopping the spread of this social/mental disorder is what I am concerned with, that's my approach.


No population has ever been completely wiped out by a "pandemic", I have never seen any evidence that that is true.

There are archeologists that claim that "Native Americans" in North and South America had been wiped out up to 90% of the population in many places by some phantom 'pandemic' brought by the european conquistadors, that is load of bullshit to justify their taking over these two continents and murdering millions of people that lived here and enslaving and or oppressing the people that they didn't slaughter.


Post #43 (from nrmis)
Wow! What does influenza look like? Serious question.
Is there a test for influenza? Would influenza turn a cv19 pcr test to positive? Are any of these patients who look like they've got influenza being tested for influenza?


Post #44 (from Dude111)
Quote:



Originally Posted by firetown

This forum needs to upgrade, but I am sure Phil would need the shill to do it.

Why buddy??


We wont find better SW than this.... ITS ALL UGLY AND DOES NOT RUN AS GOOD!!


Post #45 (from Viking911)
Quote:



Originally Posted by nrmis

Wow! What does influenza look like? Serious question.
Is there a test for influenza? Would influenza turn a cv19 pcr test to positive? Are any of these patients who look like they've got influenza being tested for influenza?


You can find info here nrmis.


Will stop this post here, and add more to further posts.
 

gl69m

Member
Continuing from original thread;

Post #46 (from gl69m)
Have a lot more to add to the thread, back ground information, about the slew of diseases and conditions that are now being attributed (and a link in public mind forever sealed) to so many "deaths' this year from the super virus 'sars 2.0' or 'covid-19'.

First, a little background of our 'health care hero' Dr. Mike Hansen, his home page (link in his youtube videos),

https://doctormikehansen.com/

https://doctormikehansen.com/about/


Quote:



About Dr. Mike Hansen

Who Is Dr. Mike Hansen?


Mike Hansen, MD, is a medical doctor who is both an internist and an intensivist, as well as a pulmonologist. In other words, he specializes in (and is board certified in) internal medicine, pulmonary disease, and critical care medicine.

Between medical school, postgraduate training, and his actual practice of medicine, Dr. Hansen has dedicated over 15 years of his life to understanding how to prevent, diagnose, and treat diseases that affect adults.

Perhaps not that unusual for a doctor to be an internist at other hospitals (around the country per se?) even after being in practice for at maybe 15 years? or maybe only 12 according to another link I saw but not including that one right now;

Michael Christopher Hansen MD
Pulmonology Valparaiso, IN
Critical Care Medicine, Pleural Disease
Physician
https://www.doximity.com/pub/michael-hansen-md-a48ae29e


Quote:



  • New York Hospital Medical Center of QueensFellowship
  • Lehigh Valley HospitalResidency
  • zjbwnrj5eikijyxotpwd.jpg
    St. George's University School of MedicineMedicalSchool

Certifications & Licensure

  • FL.png
    FL State Medical License 2016 - 2018
  • IN.png
    IN State Medical License 2015 - 2021
  • NY.png
    NY State Medical License 2012 - 2019
  • SD.png
    SD State Medical License Active through 2021

Kinda weird why his picture is blurred out in this link. Need to register an account with Doximity to view his full profile, but you can't unless you are a,


Quote:



  • Viewing the full profile is available to verified healthcare professionals only. Join over one million U.S. Physicians, Nurse Practitioners and PAs, already on Doximity.
  • Find your profile and take control of your online presence:


No picture of Dr. Hansen in this link either. No reviews of Dr. Hansen on any link for him that I have seen in my googling so far. Or Duck Duck Go. I think we all know that their are probably automated bots that censor everybody's individual searches through generic or even specific search term flags and so forth. Makes it much harder for us to find smoking gun information as it were these days.


at end of his interview, teamed up with QB Tom Brady (New England Patriots)

https://doctormikehansen.com/interview/

about 44 videos in his library on this page (oldest one I think from Oct 2018 ), 28 I think are strictly about 'coronavirus/covid-19'.

https://doctormikehansen.com/videos/

No where on his site do I see where he practices medicine at on his personal site, but for now I'm going with that the Doximity and Healthgrade profile is the same doctor same guy. There is a contact form you can fill out, generates an e-mail to submit I suppose- that's what the "contact us" little boxes usually do.

https://doctormikehansen.com/contact/


from nrmis (post #43)


Quote:



Wow! What does influenza look like? Serious question.
Is there a test for influenza? Would influenza turn a cv19 pcr test to positive? Are any of these patients who look like they've got influenza being tested for influenza?

You could try asking Dr. Mike these questions on his yourtube videos, seems he responds to some (probably very select) comments in the comment section of the videos.


The second video that Ruby posted from our 'health care hero',

12 Autopsy Cases Reveal TRUTH About How Patients Die From Coronavirus | COVID-19


Quote:



In all 12 cases, the cause of death was found within the lungs or the pulmonary vascular system. For the ones who did not die of large pulmonary emboli, they died of the extensive inflammation within the lungs, meaning pneumonia with ARDS. In these cases, the lungs were wet and heavy, much like a sponge that is saturated with water. The surfaces of the lung often had a distinct patchy pattern, with pale areas alternating with slightly protruding and firm, deep reddish-blue hypercapillarized areas. This is indicative of areas of intense inflammation, with endothelial dysfunction that can be seen at the microscopic level. When they look at slices of the lungs under the microscope, they found diffuse alveolar damage in 8 cases. Specifically, they saw hyaline membrane formation, and tiny clots in the capillaries, and capillaries that were engorged with red blood cells, and other inflammatory findings. All these findings represent ARDS. They also found lymphocytes, a type of white blood cell, infiltrated these areas of infiltration. This fits the picture of viral pathogenesis.

They also looked at the pharynx of these patients, meaning in their throat. The lining of the throat, or mucosa, was hyperemic, meaning very red and irritated, and at the microscopic level, they saw lymphocytes invading there, which is consistent with a viral infection. In one case, a patient had lymphocytes invade his heart muscle, findings that are consistent with what we call viral myocarditis. More than half of the patients in this study had large blood clots. One-third of the patients had pulmonary embolism as the direct cause of death. All the others died of intense inflammation in their lungs related to pneumonia with ARDS (Acute Respiratory Distress Syndrome). Recently there’s been studies showing that about 1/3rd of patients with severe COVID have blood clots. Another study of 191 patients with coronavirus aka COVID-19, half of those who died had clots, compared with 7% of survivors. And levels of D-dimer that were greater than 1000 µg/L were associated with a fatal outcome. So it's pretty clear now that the SARS-CoV-2 virus is causing a lot of clots to form in moderate to severe COVID disease.

How is this happening? It's likely a combination of reasons, that has to do with downregulation of the ACE2 receptor in the lung alveoli, with a subsequent shift towards having more angiotensin II in the lungs, and less angiotensin 1-7 and 1-9 in the lungs, and when this happens, this leads to more cytokine storm with more inflammation, more constriction of pulmonary arteries, and more clots that develop. That, in turn, leads to more endothelial dysfunction in the capillaries that surround the alveoli. Also, there is evidence that the virus attaches to the ACE2 receptors of those endothelial cells that line those capillaries, which further propagates inflammation and clotting. And in the cytokine storm that develops there, RANTES, a chemokine, binds to the CCR5 receptor of CD4 and CD8 lymphocytes, and that causes those lymphocytes to infiltrate those areas of inflammation, and in doing so, further contributes towards the inflammatory reaction. This is why we are seeing low levels of CD4 and CD8 lymphocytes in severe COVID. Endothelial damage can also lead to the development of antiphospholipid antibodies, and these antibodies are bad because they trigger the formation of blood clots. That’s why patients who have clots with the diagnosis of antiphospholipid antibody syndrome need to be on blood thinners.

Also, 11 out of the 12 patients in this study had underlying heart disease and were obese. These are known risk factors not just for cardiovascular disease, but also known risk factors for endothelial dysfunction, and are known risk factors for COVID. So the big takeaways from the findings in this study are that most people who die of COVID, it's primarily a lung problem. Either related to inflammation with ARDS and/or blood clots.

Antiphospholipid syndrome might be a commonality among patients with thrombosis in COVID-19 patients. Dr. Mike Hansen, MD Internal Medicine | Pulmonary Disease | Critical Care Medicine Website:

https://doctormikehansen.com/

Instagram Account: http://instagram.com/doctor.hansen/

I bolded near the last paragraph of the video description/transcript (sort of maybe), I think it relevant to point out these (and plenty of other "risk factors" in a slew of diseases I will bring up later too) are known risk factors for a whole lot of things, and tons of risk factors and pre-existing conditions in the vast majority of people whom have alleged to have died from 'covid-19'.


In order to give a least a minimal breakdown of what he presents, and all the other conditions/diseases that I'm taking about, it will take probably quite a few posts to fill in enough information and to show (at least a strong circumstantial case), or demonstrate as simply as possible, links, correlations, some videos, articles, diagrams etc., to support my assertion that 'covid-19' is a cover for a very wide variety of diseases, in order to promote (as well as many 'deaths' as attributed to as possible) this fake and planned 'pandemic' for obviously a much larger agenda(s).

That is not going to be easy at all. For now, I will add just a two topics that go along with filling in little bit of background info in pursuit of showing or proving (again not absolute proof) that 'covid-19' is being used as a cover (up) for other diseases to promote the end game agenda.

Pulmonary Fibrosis

Pulmonary Embolism (and related, deep vein thrombosis or DVT)

Pulmonary Fibrosis Foundation
https://www.pulmonaryfibrosis.org/


Quote:



COVID-19 Operational Impact


Please note that a statewide "stay-at-home" order has been issued by the governor of Illinois until May 30. The office building in which the PFF is located has been closed during
this order. PFF staff are working remotely and will not be able to process requests for hard-copies of educational materials and will also not be able to process donations mailed to our office
until the building re-opens. All online donations will continue to be acknowledged in a timely manner. We thank you for your patience during this time.

One little notice that goes along with the notion that some people who have existing illness, and ones that are potentially fatal without hospital medical treatment in some cases, may not be getting the care they need in last three months and succumbed to that disease, and many have probably still ended up as a 'covid' death statistic despite having died at home and likely no 'covid' 'test' performed. Well let me correct this comment, this is just the notice about the Pulmonary Fibrosis Foundation office being closed, not necessarily medical offices, for PF or other any conditions but that is still probably likely the case, but this site is not direct proof of that.

Proof of that would have been something very helpful that firetur.., er I mean firetown could have (and should have) provided but didn't, to show that this is the case, people dying at home due to medical services being cut off. I will try at some point to show at least one source of "evidence" for that in this thread.


PF overview from the Pulmonary Fibrosis Foundation,
https://www.pulmonaryfibrosis.org/life-with-pf/about-pf


Quote:



Pulmonary Fibrosis Overview

Feeling confused or overwhelmed about pulmonary fibrosis or idiopathic pulmonary fibrosis? You are not alone. The Pulmonary Fibrosis Foundation is here to help you understand what it means to have pulmonary fibrosis. You can always reach us through our Patient Communication Center at 844-825-5733 or by email at pcc@pulmonaryfibrosis.org.
Please remember that this information is a brief overview and is for educational purposes only. It is not intended to be a substitute for professional medical advice. Always consult your health care provider with any questions you may have regarding your specific medical condition.

To find a local pulmonary fibrosis support group near you, click here.

What is Pulmonary Fibrosis?

The word “pulmonary” means lung and the word “fibrosis” means scar tissue— similar to scars that you may have on your skin from an old injury or surgery. So, in its simplest sense, pulmonary fibrosis (PF) means scarring in the lungs. Over time, the scar tissue can destroy the normal lung and make it hard for oxygen to get into your blood. Low oxygen levels (and the stiff scar tissue itself) can cause you to feel short of breath, particularly when walking and exercising. Pulmonary fibrosis isn’t just one disease. It is a family of more than 200 different lung diseases that all look very much alike. The PF family of lung diseases falls into an even larger group of diseases called the interstitial lung diseases (also known as ILD), which includes all of the diseases that have inflammation and/or scarring in the lung. Some interstitial lung diseases don’t include scar tissue. When an interstitial lung disease does include scar tissue in the lung, we call it pulmonary fibrosis.

No one is certain how many people are affected by PF. One recent study estimated that idiopathic pulmonary fibrosis (or IPF, which is just one of more than 200 types of PF) affects 1 out of 200 adults over the age of 60 in the United States—that translates to more than 200,000 people living with PF today. Approximately 50,000 new cases are diagnosed each year and as many as 40,000 Americans die from IPF each year.
normal-and-impaired-gas-exchange.png


Break, more from this section,


Quote:

Pulmonary Fibrosis Symptoms and Causes

It can be challenging for doctors to figure out what causes PF. Sometimes they are able to identify one or more causes of your disease, which are discussed here. PF of unknown cause is called “idiopathic”
There are five main categories of identifiable causes of pulmonary fibrosis: Drug-induced, Radiation-induced, Environmental, Autoimmune, and Occupational. In the United States, Environmental and Autoimmune causes seem to be the most common types of PF of known cause.
This table shows some of the clues that doctors use to identify these known causes of PF.


TYPE OF PULMONARY FIBROSIS CLUES THAT DOCTORS USE



Drug-induced Prior or current use of amiodarone, nitrofurantoin, chemotherapy, methotrexate, or other drugs known to affect the lungs Radiation-induced Prior or current radiation treatment to the chest Environmental (called hypersensitivity pneumonitis) Exposure to mold, animals, or other triggers ("squeaks" heard in the lung) Autoimmune (called connective tissue disease-related) Joint inflammation, skin changes (particularly on the fingers and face), dry eyes or mouth, abnormal blood tests Occupational (called pneumoconiosis) Prior or current exposure to dusts, fibers, fumes, or vapors that can cause PF (such as asbestos, coal, silica, and others) Idiopathic When no cause can be identified



Medications That Cause Pulmonary Fibrosis

Some MEDICATIONS can cause PF. Drugs used to treat cancer (chemotherapy), drugs used to treat abnormal heart rhythms (such as amiodarone), drugs used to treat inflammatory conditions (such as methotrexate), and an antibiotic used to treat urinary tract infections (nitrofurantoin) are some of the better known drugs that can cause injury, inflammation, and scarring in the lungs. Numerous other drugs have been implicated as causes of PF in some cases.


Pulmonary Fibrosis Caused by Radiation

RADIATION
to the chest for lymphoma; Hodgkin’s disease; or breast, lung, and other cancers can injure the lung and cause fibrosis.
Environmental Causes of PF

are typically called hypersensitivity pneumonitis (HP) or chronic hypersensitivity pneumonitis. HP occurs when the lungs react with inflammation and scarring after breathing in mold spores, bacteria, animal proteins (especially from indoor or caged birds), or other known triggers. No one is certain why some people are so susceptible to developing HP and others are not.


Pulmonary Fibrosis and Autoimmune Diseases

AUTOIMMUNE DISEASES
are also called connective tissue diseases, collagen vascular diseases, or rheumatologic diseases. “Auto” means self and “immune” refers to your immune system. So if you have an autoimmune disease affecting your lungs, it means that your body’s immune system is attacking your lungs. Examples of autoimmune diseases that can cause PF include


  • Rheumatoid arthritis;
  • Scleroderma (also called systemic sclerosis);
  • Sjögren’s syndrome; and
  • Polymyositis, dermatomyositis, and antisynthetase syndrome.

Occupational Causes of PF

Occupational causes also called pneumoconiosis, can develop after significant exposure to a wide variety of inorganic dusts, including asbestos, silica, coal dust, beryllium, and hard metal dusts.
Is Pulmonary Fibrosis Hereditary?

Yes, but in most cases, it is not as straightforward as inheriting blue eyes or red hair. There are three different scenarios:
1) Did the genes I inherited from my parents contribute to PF even if I am the only one in my family with PF?

Yes. The risk of developing most human diseases is influenced by the genes you inherited from your parents. There have been several genes identified that appear to increase the risk of developing PF when an abnormal form of the gene is inherited. There are no official medical guidelines on whether or not genetic testing should be performed if you have PF, although in some cases, your doctor might wish to test you for one or more abnormal forms of these genes.


2) Can PF run in the family?

Yes. Anywhere from three to 20% of people with PF have another family member with PF. But this doesn’t mean that up to 20% of your family members will develop PF. In most cases, the chance that one of your family members will develop PF is very low. We encourage you to talk to your doctor or to a genetic counselor about the chances that one of your family members will develop PF.


3) Are there specific types of PF where the entire disease is due to one gene?

Yes. There are a few rare genetic forms of PF that can affect both children and adults when just a single gene is inherited in an abnormal form (usually from both parents). Hermansky-Pudlak syndrome is an example of a genetic form of PF that simply requires abnormalities in one gene. People living with Hermansky-Pudlak syndrome often also have very light skin pigmentation (due to low levels of melanin in their skin) and bleeding problems (due to poorly functioning platelets in their blood). Dyskeratosis congenita is another example of a genetic form of PF that can be accompanied by poorly growing fingernails, changes in skin pigmentation, increased risks of developing problems in the bone marrow, and other conditions.
.
Treatment Options
The Pulmonary Fibrosis Foundation also provides details on the latest treatment options and drug development breakthroughs to help patients live a stronger life. If you are interested in learning about another form of PF, Idiopathic Pulmonary Fibrosis, visit our dedicated Idiopathic Pulmonary Fibrosis page. Treatment options available as well.

.
What Is Idiopathic Pulmonary Fibrosis?

Idiopathic Pulmonary Fibrosis (IPF)
is a scarring disease of the lungs of unknown cause. To make a diagnosis of IPF, your doctor will perform a thorough history to try to identify potential exposures or other diseases that might lead to scarring of the lung.

If diagnosed, over time scarring can worsen making it hard to take a deep breath. The lungs then cannot take in enough oxygen to oxygenate the blood. IPF is a form of interstitial lung disease, primarily involving the interstitium or the tissue and space around the air sacs of the lungs, and not directly affecting the airways or blood vessels.


There are various kinds of interstitial lung disease that can also be caused by inflammation and/or fibrosis. These types of IPF are treated a bit differently. It is important to work with your health care provider to determine if you have IPF or another form of interstitial lung disease. If a plausible cause is found, then you do not have IPF. The scarring pattern of IPF is technically called usual interstitial pneumonia (UIP). Your doctor will use detailed X-rays of your lungs called high-resolution computed tomography (HRCT) and sometimes a lung biopsy to look for this pattern. A diagnosis of IPF requires that your doctor cannot find a cause and the presence of a pattern of UIP on either HRCT or a surgical lung biopsy sample.

Although IPF is still considered to be a disease of unknown cause, we do know some factors that increase the risk of getting IPF, including aging (IPF is rare before age 50), cigarette smoking, and having certain genetic predispositions.


Bolded relevant symptom here, sound familiar? like 'covid'?


Quote:



Signs & Symptoms of Idiopathic Pulmonary Fibrosis

The most common symptoms of IPF are dry, hacking cough and shortness of breath. Symptoms may be mild or even absent early in the disease process. As the lungs develop more scar tissue, symptoms worsen. Shortness of breath initially occurs with exercise, but as the disease progresses patients may become breathless while taking part in everyday activities, such as showering, getting dressed, speaking on the phone, or even eating.

supposedly now some people alledgedly having 'covid' symptoms for months? PF and IPF can last for years and is quite often fatal.


Quote:



Due to a lack of oxygen in the blood, some people with idiopathic pulmonary fibrosis may also have “clubbing” of the fingertips. Clubbing is a thickening of the flesh under the fingernails, causing the nails to curve downward. It is not specific to IPF and occurs in other diseases of the lungs, heart, and liver, and can also be present at birth.
Other common symptoms of pulmonary fibrosis include:

  • Fatigue and weakness
  • Discomfort in the chest
  • Loss of appetite
  • Unexplained weight loss

.
Pulmonary Fibrosis Diagnosis


How do doctors recognize and diagnose pulmonary fibrosis? There are three consequences of PF. Doctors use these consequences to recognize that someone has PF.

  • STIFF LUNGS

    — Scar tissue and inflammation make your lungs stiff. Stiff lungs are hard to stretch, so your breathing muscles have to work extra hard just to pull air in with each breath. Your brain senses this extra work, and it lets you know there’s a problem by triggering a feeling of breathlessness(or “shortness” of breath) while exerting yourself. Also, stiff lungs hold less air (they shrink up a bit). Doctors take advantage of this “shrinking” to diagnose and track the disease using breathing tests (called Pulmonary Function Tests) that measure how much air your lungs can hold. The more scar tissue your lungs have, the less air they will hold.

  • LOW BLOOD OXYGEN

    — Scar tissue blocks the movement of oxygen from the inside of your air sacs into your bloodstream. For many people living with pulmonary fibrosis, oxygen levels are only reduced a little bit while resting, but their oxygen levels drop quite a bit during exertion. The brain can sense these low oxygen levels, triggering breathlessness. Doctors will check your oxygen levels to see if they drop after walking, a clue that PF might be present. Doctors also often prescribe oxygen to be used through a nasal cannula or a facemask during exertion and sleep for those with PF. As pulmonary fibrosis progresses, oxygen may be needed 24 hours a day.

  • CRACKLES LUNG SOUNDS

    — Your doctor may have told you that “crackles” were heard in your lungs. Crackles (also called “rales”) sound like Velcro being pulled apart. They are heard in many lung diseases because any type of problem affecting the air sacs (such as PF, pneumonia, or a buildup of fluid in the lungs from heart failure) can cause crackles. Some people with pulmonary fibrosis don’t have crackles, but most do.

Once your doctor recognizes that you might have pulmonary fibrosis, the next step is to try to diagnose the specific kind of PF you have— there are more than 200 different kinds. Doctors typically start by asking many questions, performing a careful physical examination, and ordering a lot of blood tests. See Causes for more information.

A doctor will also use a special kind of X-ray of the chest, called a high-resolution computed tomography (HRCT) scan, so that they can see what your lung tissue looks like. HRCT scans give a close-up view of the lungs, providing more detail than routine CT scans (also known as CAT scans). Healthy lung tissue looks nearly black on a CT scan. Scar tissue and inflammation both appear grey or white. Many forms of PF look similar on a CT scan to the untrained eye, but subtle findings on HRCT scans are critically important when trying to identify which type of PF you have.
Sometimes, even after all of the testing is complete, a doctor will still not have an answer and will have to perform a lung biopsy to sort out which of the 200 different types of pulmonary fibrosis you have. When indicated, a lung biopsy can also help you and your doctor decide which treatments might be helpful.
.
Newly Diagnosed with Pulmonary Fibrosis?

I was just diagnosed with pulmonary fibrosis. What do I do next?


We suggest that you consider making an appointment with a pulmonologist who has experience caring for patients with PF. A knowledgeable team of PF experts will help make sure you receive an accurate diagnosis and the most up-to-date treatments and management recommendations. To assist you in identifying pulmonologists closer to home and developing expertise in the care of patients with PF, the Pulmonary Fibrosis Foundation established the PFF Care Center Network that includes 60 medical centers throughout the United States. You can find a list of sites within the Network at

pulmonaryfibrosis.org/life-with-pf/find-medical-care.

We also recommend that you consider joining a pulmonary fibrosis support group. Connecting with other individuals facing the same illness can help you and your family not feel so alone in your journey with pulmonary fibrosis. Support groups can supplement the care you receive from your health care team by providing emotional support and education.

Support groups can help those living with pulmonary fibrosis

  • learn about their disease and available treatments;
  • feel supported by others who are going through the same thing;
  • learn to navigate the health care system more effectively; and
  • improve coping skills, among other things.



© 2019 Pulmonary Fibrosis Foundation

Another PF foundation

IPF Foundation
https://ipffoundation.org/


Quote:



  • A bacterial protein fragment kills lung cells in pulmonary fibrosis. Learn more.1, 2

  • 31% of first degree relatives of patients with pulmonary fibrosis had interstitial lung abnormalities on CT. Learn more.3

  • The incidence of idiopathic pulmonary fibrosis (IPF) doubled over the decade, according to the New England Journal of Medicine. Learn more.4

  • The CDC identified a statistically significant cluster of IPF patients diagnosed at a Virginia medical center. Learn more.5

  • An estimated 50,000 people die from IPF in the U.S. each year, more deaths than from breast cancer. (See source study.) This statistic does not include the high percentage of people who are never diagnosed. See graphic below. Experts agree that we don’t know the extent of deaths and that more research is needed.6

(One of the references from above)

4. Verma, Subodh, Slutsky, Arthur S. “Idiopathic Pulmonary Fibrosis — New Insights.” New England Journal of Medicine, vol. 356, no. 13, 2007, pp.

I will have to come back and add more, break down some stuff to fill in the framework of the basic hypothesis etc., gotta cut this off for now.
 

gl69m

Member
Well I only have 3 more posts archived, so gonna add them individually, and then continue the thread exploration of 'covid' as a false cover for the general gradual increase of existing chronic disease burden; remember Fraudchi (er I mean Fauci) alluded to this in the talk at Georgetown University,

Pandemic Preparedness in the Next Administration: Keynote Address by Anthony S. Fauci​


At around ~3:20 in,
is that there is no question that there will be a challenge, the coming administration in the arena of infectious diseases, both chronic infectious diseases, in the sense of already ongoing diseases. And we have certainly a large burden of that. But also there will be a surprise outbreak. And I hope by the end of my relatively short presentation, you will understand why history, and the history of the last 32 years I've been the director of NIAID will tell the next administration that there's no doubt in anyone's mind that they will be faced with the challenges that their predecessors were faced with.
I didn't really think of that before, he called them chronic "infectious' diseases, like that I mentioned before the inflammatory diseases, perhaps some can be attributed to chronic long term (very long term sometimes years and years) "infections" of which most (vast majority) would really be (primarily) bacterial in nature (IMO). However I certainly believe there are many chronic diseases also attributable to (primarily) toxins, stressors, radiation, and various other factors.


post #47 from original thread (from gl69m)(posted May 20, 2020)
To continue from post #46,

I think it pertinent to reiterate this section from the PF Foundation website I posted,

PF overview from the Pulmonary Fibrosis Foundation,
https://www.pulmonaryfibrosis.org/life-with-pf/about-pf

Quote:

What is Pulmonary Fibrosis?

The word “pulmonary” means lung and the word “fibrosis” means scar tissue— similar to scars that you may have on your skin from an old injury or surgery. So, in its simplest sense, pulmonary fibrosis (PF) means scarring in the lungs. Over time, the scar tissue can destroy the normal lung and make it hard for oxygen to get into your blood. Low oxygen levels (and the stiff scar tissue itself) can cause you to feel short of breath, particularly when walking and exercising. Pulmonary fibrosis isn’t just one disease. It is a family of more than 200 different lung diseases that all look very much alike. The PF family of lung diseases falls into an even larger group of diseases called the interstitial lung diseases (also known as ILD), which includes all of the diseases that have inflammation and/or scarring in the lung. Some interstitial lung diseases don’t include scar tissue. When an interstitial lung disease does include scar tissue in the lung, we call it pulmonary fibrosis.

No one is certain how many people are affected by PF. One recent study estimated that idiopathic pulmonary fibrosis (or IPF, which is just one of more than 200 types of PF) affects 1 out of 200 adults over the age of 60 in the United States—that translates to more than 200,000 people living with PF today. Approximately 50,000 new cases are diagnosed each year and as many as 40,000 Americans die from IPF each year.


Quote:

Pulmonary fibrosis is a descriptive term given when there is excess of fibrotic tissue in lung. It can occur in a wide range of clinical settings and can be precipitated by a multitude of causes. The term should not be confused with idiopathic pulmonary fibrosis which is a progressive fibrotic lung disease.
Pulmonary fibrosis can be localized, segmental, lobar, or affect the entirety of the lung(s).

Pathology

Fibrosis in the lung is a process that occurs in the interstitium. It is therefore also termed interstitial fibrosis.
Among the many conditions associated with pulmonary fibrosis are:
Have to wonder, are any of these going to look that much different from patients with influenza or any cause of pneumonia or of so-called "covid'? Like they are saying, multitide of causes, like my first thought back in March when I was seeing the 'covid-19' studies from January and February with the lung scans.


granulomatous conditions- sarcoidosis: has to be a multitude of environmental causes, with so much pollution, heavy metals and so many chemicals released into the environment on a daily basis, for a hundred years and more, should make your heads spin, and chemtrails of course.


Pulmonary embolism is another very dangerous and quite often fatal disease/condition, that obviously existed long before 'covid' was invented this year, or well invented at least last year by the time of Event 201.


Pulmonary Embolism PART I (Overview)
Aug 18, 2015

You Tube
The Diagnosis of Acute Pulmonary Embolism
Ebtesam Islam MD PhDa Victor J. Test, MDa,b
doi:10.12746/swrccc 2014.0208. 099

Quote:

Abstract

This paper reviews the most current literature on the diagnosis of pulmonary thromboembolism. The epidemiology and symptomology of this disorder, including common symptoms such as fever, chest pain, dyspnea, edema, and syncope, are reviewed.

Introduction

Pulmonary embolism (PE) is a leading cause of morbidity and mortality in the United States, and between 5% and 10% of hospital deaths are attributable to PE.1 From 1998 to 2005, the number of patients discharged from United States hospitals with a diagnosis of pulmonary embolism increased from 126,546 to 229,637.1 Over this period, the hospital case fatality rate decreased from 12.3% to 8.2% (p<0.001).1 The length of stay decreased, but hospital charges for these patients increased nearly 100% (p<0.001). In the United States, approximately 100,000 to 200,000 deaths occur in over 600,000 episodes of pulmonary embolism per year.2-6 An overwhelming majority of these deaths occur when the disease is under-recognized or misdiagnosed and ultimately discovered on autopsy.7,8 With the correct diagnosis and effective treatment, the risk of death diminishes dramatically.9 As expected, patients who present with shock have the highest mortality from PE. Unfortunately, even with myriad diagnostic tests and treatment options available, PE is common, lethal, and underdiagnosed.1,10



Pulmonary embolism can present along a spectrum from the asymptomatic individual incidentally diagnosed to the patient presenting with cardiogenic shock.11 Thus the diagnosis of acute PE is ultimately guided by the clinician’s index of suspicion for the disease and augmented by diagnostic tests. PE is closely linked with deep venous thrombosis (DVT) and should be considered a different manifestation of the same disorder, namely venous thromboembolism (VTE). The recognition of the signs and symptoms of PE is the most important initial diagnostic step. A careful clinical history and physical examination is crucial to identify the patients at risk and to assess the pretest probability. In a review of the Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED 1) data, Stein and Henry found that dyspnea was the most common symptom followed by pleuritic chest pain, cough, lower extremity edema, hemoptysis, palpitations, wheezing, and angina-like pain.12 Pleuritic chest pain and hemoptysis are more common in patients with pulmonary infarction.12 PE should always be considered in patients with chest pain, dyspnea, hemoptysis, syncope, and palpitations.13 The possibility of PE can be subtle with non-specific symptoms and signs, such as tachycardia, tachypnea, and fever.

Clinical suspicion and clinical decision rules

The diagnosis of PE and DVT is dependent upon the clinician’s suspicion of the disease. Unfortunately, there are numerous studies that demonstrate failures or delays in diagnosis of PE. 2-6,11 Further, the morbidity and mortality of VTE increase when the diagnosis is not made.2-6 Paradoxically, as the evaluation for VTE has evolved, more patients are undergoing evaluation with imaging for PE, but the diagnostic yield of these tests can be as low as 3.1% in the absence of clinical prediction rules.16 There are numerous risk factors for VTE, including age greater than forty, previous VTE, surgery requiring anesthesia for more than 30 minutes, prolonged immobilization, stroke, heart failure, malignancy, fractures of the long bones or pelvis, spinal cord injury, obesity, smoking, pregnancy, estrogen therapy, inflammatory bowel disease, and genetic or acquired thrombophilia. Renal failure, nephrotic syndrome, central venous catheterization, COPD, and long distance travel have also been identified as risk factors.11 Hip/knee surgery/fracture and spinal cord injury carry the highest risk.

Diagnostic testing

Electrocardiogram, chest radiographs, and selected laboratory tests
Routine initial diagnostic testing in the evaluation of a patient with symptoms suggestive of a PE is neither sensitive nor specific. Over the past twenty years, a bewildering number of diagnostic tests, either alone or in combination, has been studied as a means of excluding or confirming the diagnosis of PE. Arterial blood gas testing may demonstrate a respiratory alkalosis or hypoxemia, but arterial blood gas evaluation including the alveolar-arterial gradient is neither sensitive nor specific.12,27 The chest radiograph often demonstrates nonspecific findings; atelectasis (52-75%), pleural effusion (26-56%), pleural based opacities (23-36%), elevation of the diaphragm, cardiomegaly, and a normal radiograph can be seen.12,13,28 A large international cooperative registry found that cardiomegaly on chest radiograph was the most common finding in pulmonary embolism followed by normal radiograph, pleural effusion, elevated diaphragm, atelectasis, and pulmonary artery enlargement.

D-dimer testing

The D-dimer is a cross-linked fibrin degradation product. It is elevated in active thrombosis and useful in identifying patients with possible PE. It has an excellent sensitivity in the evaluation of VTE but poor specificity. Conditions such as increasing age, malignancy, hospitalization, and previous DVT adversely affect the specificity of the D-dimer.35,36 The different assays have a wide range in sensitivities.25,37 The enzyme linked immunoabsorbent assay (ELISA) D-dimer is most useful in ruling out the diagnosis in outpatients who have a low pretest probability of PE.37 In a large meta-analysis of over 7000 patients, the negative likelihood ratio of an ELISA (enzyme linked immunoabsorbent assay) was 0.13, and for a rapid ELISA it was 0.13.38 In this analysis, whole blood and less sensitive qualitative assays had negative likelihood ratios that were not as useful in ruling out VTE.38 D-dimer increases with age, reducing the ability to rule out PE in elderly patients with the cutoff value usually being 500 µg/L.
I saw in one article that pulmonary fibrosis is a risk factor as well for pulmonary embolism. Supposedly 'covid' is now causing pulmonary embolisms and blood clotting to kill patients, but perhaps many of these people had the underlying PF and these other conditions predisposing blood clotting, most likely they have these conditions for years and progresses, not unlike many cancers for that matter.

Many would probably be dying now anyway, especially elderly with these pre-conditions, in Wuhan China, in Italy, NYC, certainly for the 'pandemic' central alleys.


ARDS is another deadly syndrome out there well before 'covid', another good cover for the 'pandemic',


Acute respiratory distress syndrome: new definition, current and future therapeutic options

2013 June
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3698298/

Quote:

Abstract

Since acute respiratory distress syndrome (ARDS) was first described in 1967 there has been large number of studies addressing its pathogenesis and therapies. Despite this intense research activity, there are very few effective therapies for ARDS other than the use of lung protection strategies. This lack of therapeutic modalities is not only related to the complex pathogenesis of this syndrome but also the insensitive and nonspecific diagnostic criteria to diagnose ARDS.

Introduction

Acute respiratory distress syndrome (ARDS) is a life threatening respiratory condition characterized by hypoxemia, and stiff lungs (1-4); without mechanical ventilation most patients would die. ARDS represents a stereotypic response to many different inciting insults and evolves through a number of different phases: alveolar capillary damage to lung resolution to a fibro-proliferative phase (3). The pulmonary epithelial and endothelial cellular damage is characterized by inflammation, apoptosis, necrosis and increased alveolar-capillary permeability, which lead to development of alveolar edema (3).


Over the past 18 years of practice, the diagnostic accuracy of the ARDS definition by AECC has been questioned. In a series of 138 ARDS patients, the definition had relatively low specificity (51%) when compared with autopsy findings demonstrating diffuse alveolar damage as assessed by two independent pathologists (10). The reliability of the chest radiographic criteria of ARDS has been demonstrated to be moderate, with substantial interobserver variability (11,12). In addition, the hypoxemia criterion (i.e. PaO2/FiO2 <200 mmHg) can be markedly affected by the patient’s ventilator settings, especially the PEEP level used (13). Finally, the wedge pressure can be difficult to interpret and if a patient with ARDS develops a high wedge pressure that should not preclude diagnosing that patient as having ARDS. Based on these concerns, the European Society of Intensive Care Medicine with endorsement from the American Thoracic Society and the Society of Critical Care Medicine convened an international expert panel to revise the ARDS definition (14); the panel met in 2011 in Berlin, and hence the new definition was coined the Berlin definition.

Oxygenation

In the Berlin definition, there is no use of the term Acute Lung Injury (ALI). The committee felt that this term was used inappropriately in many contexts and hence was not helpful. In the Berlin definition, ARDS was classified as mild, moderate and severe according to the value of PaO2/FiO2 ratio (Table 1). Importantly, the PaO2/FiO2 ratio value is considered only with a CPAP or PEEP value of at least 5 cmH2O.

Chest X-ray

The chest radiograph is characterized by bilateral opacities involving at least 3 quadrants that are not fully explained by pleural effusions, atelectasis and nodules. In the absence of known risk factors, a cardiogenic origin of edema is to be excluded by objective evaluation of cardiac function with echocardiography. Consequently, the wedge pressure measurement was abandoned because ARDS may coexist with hydrostatic edema caused by fluid overload or cardiac failure (8).
'Covid' is now allegedly killling patients by triggering ARDS right? according to dr. mike among many others now too (have to presume): but we have seen from previous studies, ventilators can kill, especially when used too aggressively, and woefully incorrectly in gross negligence as at least one nurse in treating 'covid' patients in NYC testified with her FB video that made it's way to Youtube (Nicole Sirotek I think).


Quote:

Protective mechanical ventilation

Quote:


There is a large body of evidence from experimental and clinical studies demonstrating that mechanical ventilation, particularly in the setting of lung injury, can exacerbate functional and structural alterations in the lung (15). It is noteworthy that mechanical ventilation not only perpetuates lung injury, but also contributes to both the morbidity and mortality of ARDS (2,16,17). The concept that the limitation of end inspiratory lung stretch may reduce mortality in ARDS patients, culminated in the NIH-sponsored multicenter study of patients with ARDS (1,18). In this trial, patients randomized to receive a lower tidal volume (Vt) [4-6 mL/kg predict body weight (PBW), and maintenance of plateau pressure between 25 and 30 cmH2O] had a survival benefit. Mortality was reduced from 40% in the conventional arm to 31% in the low Vt arm (CI, 2.4-15.3% difference between groups) (1). The benefit in terms of mortality and ventilation free days did not appear to be related to the value of the lung compliance at baseline or to the underlying risk factor for ARDS (19). Of note, the survival benefit was associated with a reduction of plasma IL-6 concentration, supporting the hypothesis that a lung protective strategy limits the spill over into the systemic circulation of inflammatory mediators, which in turn may induce multiple system organ failure (17).
break

Quote:

Conclusions

ARDS still represents a deadly form of respiratory failure with long term consequences in patient survivors and indeed, their families (68,69). Supportive therapies represent the mainstay of treatment of ARDS, whereas the limitation of end end-inspiratory lung stretch has been clearly demonstrated to reduce the ARDS associated mortality. Adoption of the new definition may be useful to better classify patients according to severity and prognosis. Lacking of effective therapies relies on the complex pathogenesis of the syndrome characterized by different overlapping signaling pathways Gene therapy and mesenchymal stem cells may be promising novel therapeutic strategies aimed at modulate key pathophysiologic mechanisms of ARDS.
Again, I would have to think that Pulmonary Fibrosis can surly lead to ARDS. Also, I think that SARS is really just a rename of practically the same thing- Severe Acute Respiratory Syndrome- Acute Respiratory Distress Syndrome, just a slightly different wording.


Lot's of inflammation in the lungs, cytokine storm, etc, etc,, various other biomarker signalling pathways et al. If there is too little functioning lung tissue left in a critical patient, just about any infection getting into the lungs would seemingly make things worse and potentially more lethal, even a common cold virus, such as some of the really common coronaviruses. On top of these patients over years of decreased oxygen efficiency are probably already immune-compromised by then anyway, and even less pathogenic viruses and bacteria can still become a huge problem.



Medical Malpractice Involving Pulmonary/Critical Care Physicians
2019 Nov
https://pubmed.ncbi.nlm.nih.gov/31102609/

Quote:

Abstract

Background:
Medical malpractice data can be leveraged to understand specialty-specific risk.

Methods: Malpractice claims were examined from the Comparative Benchmarking System (2007-2016), a national database containing > 30% of claims data in the United States. Claims were identified with either internal medicine or pulmonary/critical care (PCC) physicians as the primary provider involved in the harm. Claim characteristics were compared according to specialty and care setting (inpatient vs outpatient), and multiple regression analysis was performed to predict claim payment.

Results: Claims involving PCC physicians differed from those involving internal medicine physicians in terms of harm severity, allegation, final diagnosis, procedure involvement, payment rate, and contributing factors. The majority of claims involving PCC physicians resulted from inpatient care (63%), of which only 26% occurred delivering intensive care. Eighty-one percent were from harm events that resulted in death/permanent injury. The most common diagnosis was laceration during a procedure for inpatient claims (6%) and lung cancer for outpatient claims (28%). Thirty-one percent of claims overall involved procedures. Although only 26% were paid, the median indemnity per paid claim of $285,769 ranked PCC as the twelfth highest of 69 specialties. The two variables associated with indemnity payment were outpatient care (OR, 1.70; 95% CI, 1.01-2.86) and temporary harm (OR, 0.36; 95% CI, 0.15-0.87).

Conclusions: Malpractice claims involving PCC physicians were distinct from claims involving internal medicine physicians. Although only one-quarter of claims was paid, the indemnity per claim was high among specialties. Specialty-specific prevention strategies must be developed to mitigate both patient harm and provider malpractice risk.
Our 'health care hero' dr mike is a PCC physician and internal medicine too, so if he had(has) any lawsuits against him they wouldn't be distinct as it is for other PCCs then who don't practice "internal medicine" also.

Lessons Learned From Medical Malpractice Claims Involving Critical Care Nurses

May 01 2020



Quote:

Background

Medical malpractice data can be used to improve patient safety.

Objective

To describe the types of harm events involving nurses that lead to malpractice claims and to compare claims among intensive care units (ICUs), emergency departments, and operating rooms.

Methods

Malpractice claims closed between 2007 and 2016 were extracted from a national database. Claims with a nurse as the primary provider were identified and then compared by location of the harm event: ICU, emergency department, or operating room. Multivariable regression was used to determine predictors of claims payment.

Results

Of 54 699 claims, 314 involved ICU nurses as the primary provider.
The majority (59%) of claims involving ICU nurses resulted in death or permanent injury. The most common allegation of claims involving ICU nurses was failure to monitor (47%), which was higher than among claims against nurses in the emergency department (9%) or the operating room (4%) (P < .001). The most common diagnosis in claims involving ICU nurses was decubitus ulcers (26%). Despite equivalent numbers of defendants per claim, the median indemnity for paid claims involving ICU nurses was higher ($125 000) than that paid for claims originating in the emergency department ($56 799) or operating room ($43 910) (P < .001). In multivariable regression, 2 variables increased the risk of claim payment: ICU location (odds ratio, 1.79 [95% CI, 1.29-2.48]) and permanent injury (odds ratio, 1.50 [95% CI, 1.07-2.09]).
I'm guessing that in the 54,699 claims, that plenty of ICU nurses had to at least secondary defendants in most of these claims, while only 314 claims name ICU nurses as the "primary" provider. Just 54,699 claims, sounds a bit low for a 9 or 10 year period, maybe that was only a certain % of the total claims in the data base that they looked at.
 

gl69m

Member
post #48 from original thread (from gl69m)(posted May 28, 2020)
Continuing on from post #47, and in response to posts #27 and #41 featuring health care 'hero' Dr. Mike Hansen, here is counter evidence from another medical expert doctor, that 'covid-19' is not at least actually (or most likely not) the primary cause of any "covid" deaths, at least in Hamburg Germany:

Forensic Doctor Destroys Media Lies: 'Nobody Died of Covid in Hamburg without Previous illnesses’
May 7, 2020
Youtube account terminated unfortunately, have to try at later time to find a replacement video.
You Tube

Klaus Püschel
German legal doctor



Quote:

Klaus Püschel studied medicine at the Hannover Medical School , received his doctorate in 1977 and worked from 1978 at the Institute of Forensic Medicine at the University Medical Center Hamburg-Eppendorf (UKE). He habilitated in 1983 and was appointed professor of forensic medicine in 1985. In 1987, together with the head of forensic medicine Werner Janssen, he autopsied on behalf of the Barschel family Uwe Barschel, who died on October 11, 1987. From 1989 to 1991 he held the chair of forensic medicine at the University of Essen . [3]

Püschel has been director of the Institute of Forensic Medicine at the University Medical Center Hamburg-Eppendorf since 1992. He is also deputy director of the Center for Interdisciplinary Addiction Research (ZIS) at the University of Hamburg. [5]
COVID-19 pandemic in Germany

During the COVID-19 pandemic in Germany in an interview with n-tv on April 8, 2020, he praised the measures taken by German politicians to prevent the spread of the virus and the overloading of hospitals: “I think politicians have that well regulated. ” [12] In May 2020, Püschel told NDR magazine Panorama that he was convinced that politicians in Germany had made good decisions in good time to mitigate the medical consequences of Covid-19. On April 9, 2020, he criticized the then RKI recommendation in the talk show Markus Lanz ("An internal medical examination, autopsies or other aerosol-producing measures should be avoided. If these are necessary, they should be kept to a minimum." [14 ] ) as a "completely wrong measure". He explained that, according to his knowledge, "mainly sick people and people with a weakened immune system" have died so far. [15] He had previously autopsied over 50 deceased COVID-19 patients. [16] In the Hamburger Morgenpost on April 10, he stated that no single person who had not had any previous illnesses had died of the virus in Hamburg. [17] [18] Püschel stated that he is convinced that corona mortality will not even make itself felt as a peak in annual mortality. [19]

Working groups around Klaus Püschel and Stefan Kluge were able to use sections to detect multiple venous thrombosis and fatal pulmonary embolism in deceased COVID-19 patients. It emerged from this that it is not the virus-related pneumonia and the resulting disruption of the gas exchange , but heart failure due to the extensive obstruction of the pulmonary tract due to pulmonary embolism is responsible for a large part of the deaths.
The corona virus is said to activate the coagulation system in blood vessels with attachment to the endothelium in many organs. As a critical addition to the therapeutic approach, a coordinated, possibly even higher-dose heparin thrombosis prophylaxis with low-molecular-weight heparin is advisable. [21]
Püschel did 50 autopsies, Hansen looked at only 12 autopsies (I don't think Hansen did the autopsies) in the video from post #41, not sure how many in the video from post #27.

Pulmonary embolisms are also being claimed as being caused by 'covid' (or 'sars-cov-2' virus) now in 2020, but as we can see that (posted in post #47) prior to 2020 pulmonary embolism occurs roughly-

In the United States, approximately 100,000 to 200,000 deaths occur in over 600,000 episodes of pulmonary embolism per year. Hansen also mentions findings consistent with "ARDS" on some of the lungs in the autopsies in the video from post #27, obviously he is claiming that the 'covid' virus is bringing the "ARDS" about, but ARDS was quite common enough long before 'covid' was invented of course. Pulmonary embolism is something that if severe (and large enough coronary artery blockage) enough, a person might look like they literally dropped dead from it, I'm guessing, like people were supposedly in Wuhan according to thread here by that name
icon_think.gif
icon_sad.gif
.

Is 'covid' ('sars-cov-2' virus) even a contributing factor to any deaths now, or even if some people truly positive, will the death toll end up with a so-called 'covid' deaths in excess from deaths that would otherwise be attributed to so many other diseases prior to 2020?: and in particularly here I mean ARDS, IPF or PF, pulmonary embolism (especially) and I am adding another to the list, PVD or PAD (Peripheral Vascular or Arterial Disease), and generically for now adding cancer to that list but for now am concentrating on the first 3 and get to PVD/PAD and cancer in later posts.

I also think that many of the above conditions I'm talking about can overlap in many people and can have multiple existing conditions/diseases simultaneously, which would look statistically like each one caused an excess of deaths if categorized as a "sole" cause as opposed to a "contributing cause". Which is why I think 'covid' is placed in three different death stat categories by the CDC, and WHO as well, though I haven't seen how they are categorizing 'covid' next to all other diseases on the global scale.

Somehow I seriously doubt that if we had access to all the raw death data, death certificates, that 'covid' would prove to show any serious excess of deaths at all. I am saying 'covid' really is only along for the ride as a so-called "contributing factor' in any 'covid' deaths, until proven otherwise IMO. And I mean that as in whether 'sars-cov-2' is entirely hoaxed or major hoax of magnitude (total cases and including deaths).

Keep in mind too that some cases of 'covid' could be a 'SARS' variant that may still be endemic around the world since 2002, or caused MERS even, and many mild or asymptomatic cases may simply be common cold coronas, all of those would be better explanations than a new virus ('sars-cov-2') anyway, the evidence I have seen to prove it has been "isolated/purified" is quite suspect to me. This would obviously inflate the scale/magnitude of the hoax even if an actual "sars-cov-2' virus was actually out in the world in 2020, and depending on who the actual testers of the PCR diagnostic testing, if they do it specific enough without telling the public, maybe they can break it down and distinguish the difference between all the corona viruses for their data (for whatever their purposes are with that data) that is inaccessible to the public, certainly not released to the public and classified.


Continuing the line of inquiry into ARDS and IPF, this study compares the two, similarities and differences, outcomes and possible treatments for further study,


Acute exacerbation of idiopathic pulmonary fibrosis: lessons learned from acute respiratory distress syndrome?

2018 Mar 23


Quote:

Abstract

Idiopathic pulmonary fibrosis (IPF) is a fibrotic lung disease characterized by progressive loss of lung function and poor prognosis. The so-called acute exacerbation of IPF (AE-IPF) may lead to severe hypoxemia requiring mechanical ventilation in the intensive care unit (ICU). AE-IPF shares several pathophysiological features with acute respiratory distress syndrome (ARDS), a very severe condition commonly treated in this setting.

A review of the literature has been conducted to underline similarities and differences in the management of patients with AE-IPF and ARDS.
During AE-IPF, diffuse alveolar damage and massive loss of aeration occurs, similar to what is observed in patients with ARDS. Differently from ARDS, no studies have yet concluded on the optimal ventilatory strategy and management in AE-IPF patients admitted to the ICU. Notwithstanding, a protective ventilation strategy with low tidal volume and low driving pressure could be recommended similarly to ARDS. The beneficial effect of high levels of positive end-expiratory pressure and prone positioning has still to be elucidated in AE-IPF patients, as well as the precise role of other types of respiratory assistance (e.g., extracorporeal membrane oxygenation) or innovative therapies (e.g., polymyxin-B direct hemoperfusion). The use of systemic drugs such as steroids or immunosuppressive agents in AE-IPF is controversial and potentially associated with an increased risk of serious adverse reactions.
Common pathophysiological abnormalities and similar clinical needs suggest translating to AE-IPF the lessons learned from the management of ARDS patients. Studies focused on specific therapeutic strategies during AE-IPF are warranted.

Keywords: Idiopathic pulmonary fibrosis, Mechanical ventilation, Acute respiratory distress syndrome, Respiratory failure, Diffuse alveolar damage

Table 1 Ultimate definition and diagnostic criteria of AE-IPF and ARDS
(my note, table doesn't display very good pasted in here, better to look on the link)

AE-IPF
ARDS
Revised definition
Berlin definition


An acute, clinically significant respiratory deterioration characterized by evidence of new widespread alveolar abnormality
A type of acute diffuse, inflammatory lung injury, leading to increased pulmonary vascular permeability, increased lung weight, and loss of aerated lung tissue. The clinical hallmarks are hypoxemia and bilateral radiographic opacities, associated with increased venous admixture, increased physiological dead space, and decreased lung compliance. The morphological hallmark of the acute phase is diffuse alveolar damage (i.e., edema, inflammation, hyaline membrane, or hemorrhage)

Diagnostic criteria
Definition criteria

Previous or concurrent diagnosis of IPF

Acute worsening or development of dyspnea typically < 1 month in duration
Onset of lung injury within 1 week of a known clinical insult or new or worsening respiratory symptoms
Computed tomography with new bilateral ground-glass opacity and/or consolidation superimposed on a background pattern consistent with usual interstitial pneumonia pattern
Bilateral opacities—not fully explained by effusions, lobar/lung collapse, or nodules
Deterioration not fully explained by cardiac failure or fluid overload
Respiratory failure not fully explained by cardiac failure or fluid overload

  1. AE-IPF acute exacerbation of idiopathic pulmonary fibrosis, ARDS acute respiratory distress syndrome
ARDS and AE-IPF: similarities and differences

Diffuse alveolar damage


The typical pathological feature of AE-IPF is the presence of diffuse alveolar damage (DAD) superimposed on the usual interstitial pneumonia (UIP) pattern [4]. The term DAD was proposed by Katzenstein et al. [5] to describe an aspecific acute reaction of the lung to several different pathogenic noxae, including sepsis, pneumonia, and exposure to high oxygen concentration. DAD is also the histologic hallmark of ARDS, although this feature can only be found at biopsy in about half of patients meeting the clinical criteria for ARDS diagnosis [6]. In this setting, an exudative phase with endothelial and alveolar epithelial injury and cellular exudate and hyaline membrane deposition develops during the first week from onset. In patients with a condition lasting longer than 3 weeks, proliferation of alveolar cell type 2 and fibroblasts with fibrotic deposition then occurs in 2/3 of cases [7]. Data on histological findings of DAD over AE-IPF development are not available, but it is likely that alveolar damage in survivors may lead to a proliferative reaction with further lung fibrosis.

Lung inflammation

During the course of AE-IPF, the percentage of neutrophils in bronchoalveolar lavage (BAL) fluid is significantly increased compared with stable chronic IPF, while lymphocytes and macrophages are reduced [13]. This cell pattern is similar to that found in patients with ARDS, which suggests a common inflammatory pathway.


In AE-IPF, the upregulation of M1 macrophage activation chemokines such as IL-8 and CXCL1 results in neutrophil chemoattraction. Interestingly, in animal models, the increased expression of CXC chemokines and their interaction with the CXCR2 receptor are involved in the lung sequestration of neutrophils following mechanical stress due to ventilation, thus suggesting a role in the development of VILI [14]. Furthermore, some studies indicate a relationship between IL-8 overexpression in BAL and the development of ARDS in patients at risk [15]. Acute hypoxia could act as a proinflammatory stimulus leading to a rapid increase of intrapulmonary IL-8, released by alveolar macrophages with attraction of neutrophils and subsequent alveolar and endothelial injury [16].


ARDS and AE-IPF: similarities and differences

Diffuse alveolar damage


The typical pathological feature of AE-IPF is the presence of diffuse alveolar damage (DAD) superimposed on the usual interstitial pneumonia (UIP) pattern [4]. The term DAD was proposed by Katzenstein et al. [5] to describe an aspecific acute reaction of the lung to several different pathogenic noxae, including sepsis, pneumonia, and exposure to high oxygen concentration. DAD is also the histologic hallmark of ARDS, although this feature can only be found at biopsy in about half of patients meeting the clinical criteria for ARDS diagnosis [6]. In this setting, an exudative phase with endothelial and alveolar epithelial injury and cellular exudate and hyaline membrane deposition develops during the first week from onset. In patients with a condition lasting longer than 3 weeks, proliferation of alveolar cell type 2 and fibroblasts with fibrotic deposition then occurs in 2/3 of cases [7]. Data on histological findings of DAD over AE-IPF development are not available, but it is likely that alveolar damage in survivors may lead to a proliferative reaction with further lung fibrosis.

Lung inflammation

During the course of AE-IPF, the percentage of neutrophils in bronchoalveolar lavage (BAL) fluid is significantly increased compared with stable chronic IPF, while lymphocytes and macrophages are reduced [13].
(I believe Dr. Hansen is also claiming this in 'covid' patients, knowing that a large portion of the public probably has no clue about this information here, I was not really aware of it either, just a general awareness of plenty of disease states from my bio-science background).

This cell pattern is similar to that found in patients with ARDS, which suggests a common inflammatory pathway.
In AE-IPF, the upregulation of M1 macrophage activation chemokines such as IL-8 and CXCL1 results in neutrophil chemoattraction. Interestingly, in animal models, the increased expression of CXC chemokines and their interaction with the CXCR2 receptor are involved in the lung sequestration of neutrophils following mechanical stress due to ventilation, thus suggesting a role in the development of VILI [14]. Furthermore, some studies indicate a relationship between IL-8 overexpression in BAL and the development of ARDS in patients at risk [15]. Acute hypoxia could act as a proinflammatory stimulus leading to a rapid increase of intrapulmonary IL-8, released by alveolar macrophages with attraction of neutrophils and subsequent alveolar and endothelial injury [16].
(have to look at Hansen's videos again to see how well this information here correlates, one explanation without and before 'covid' and one with 'covid' if really present and contributing, or maybe it isn't necessary to explain as a contributing factor regardless?)

A recent study on lungs of transplanted IPF patients showed that inflammatory infiltration and DAD are even present in IPF with an accelerated functional decline, suggesting that inflammation may play a role in disease progression [20]. Further evidence that the cytokine profile in the rapidly deteriorating IPF patient appears predominantly proinflammatory rather than profibrotic, approximating that of ARDS of any etiology rather than an accelerated intrinsic fibrotic process, has been provided by Papiris et al. [21].


Therefore, both ARDS and AE-IPF share an overexpression of proinflammatory cytokines produced by alveolar macrophages with chemotaxis of neutrophils. However, overexpression of anti-inflammatory M2 cytokines with a profibrotic role is simultaneously present only in AE-IPF (see Fig. 1).


During AE-IPF, lung inflammation is driven by upregulation of macrophage activation pathways. M1 pathway classically activated by Th1 cytokines (IFN-γ) leads to increased IL-8 and CXCL1 expression and neutrophil recruitment though CXCR2 receptor. M2 pathway activated by type II alveolar epithelial cell injury might perpetuate lung fibrosis boosting collagen deposition, fibroblast proliferation, and epithelial–mesenchymal transition. AE-IPF acute exacerbation of idiopathic pulmonary fibrosis, DAD diffuse alveolar damage, IL interleukin, INF interferon

Respiratory assistance

Few studies have evaluated the outcome of patients with AE-IPF receiving mechanical ventilation in the ICU, and in addition they all share important limitations (see Table Table2):2): single-centered and retrospective analysis; limited number of patients included; unclear or unreported mode of ventilation and setting; and heterogeneous use of drugs [4, 3942]. Overall, the available data are consistent in stating that invasive mechanical ventilation cannot significantly modify the poor prognosis of these patients [9]. Despite the aforementioned studies being performed before the extensive use of protective mechanical ventilation to prevent VILI, the American Thoracic Society guidelines on IPF recently recommended the use of mechanical ventilation only in a few selected patients developing severe AE [1]. More recently, a multicenter retrospective study in the United States documented an overall mortality rate of 51% in a large group of mechanically ventilated AE-IPF patients [3], still higher than that reported in severe ARDS (about 40%) [43] but lower than that described previously. Thus, one could speculate that advances leading to a better ventilator management and outcome of patients with ARDS may have also positively influenced the outcomes in ventilated AE-IPF.
IPF patients who suffer an AE (acute exacerbation) event have very poor prognosis after being placed on ventilators, of course they would probably die much faster without the ventilators would have to assume otherwise not much point, unless these patients have always been treated with less than optimal care?? Even before 'covid'?

From reference
[9],

Outcome of patients with idiopathic pulmonary fibrosis (IPF) ventilated in intensive care unit
October 01, 2008



Quote:

Summary

Idiopathic pulmonary fibrosis (IPF) is the commonest cause of interstitial lung disease. Till date there is no proven successful treatment.
The prognosis is poor with a median survival of 3 years. Patients with IPF presented with acute respiratory failure are often referred to the intensive care unit for ventilatory support. Available data showed that outcome of these patients is very poor and mechanical ventilation is mostly futile.Patients and their families should be informed about the prognosis, outcome and overall outlook before making decision about ventilation and organ support. Available outcome data should be used to develop institutional and professional guidelines to help in making these difficult decisions.


Introduction

Idiopathic pulmonary fibrosis is the commonest form of interstitial lung disease (ILD). It is a progressive chronic disease of uncertain aetiology characterized by inflammation and fibrosis of lung parenchyma affecting gas exchange.
Prognosis is poor with median survival of 3 years irrespective of treatment. IPF appears to be much more prevalent than previously reported. One previous study has reported an incidence of 6.8 per 100,000 in the United Kingdom, in 2000–2003.1, 2


Outcome from mechanical ventilation

Majority of patients with IPF are admitted in intensive care with acute respiratory failure. It is always difficult to make a decision of not to ventilate a patient referred for acute respiratory failure. There is conflict of opinion between physicians and intensivists criticising each other which ranges from inappropriate referral to prognostic pessimism.

Decision of not to ventilate usually depends on assessment of futility of care depending on poor short-term prognosis, patients wishes and the high probability of poor quality of life in the future. Before making such decision doctors usually try to look for evidence on previous outcomes in similar cases.


Results

Nine studies consisting of 135 patients with established diagnosis of IPF fulfilled the criteria for inclusion in the analysis. Patients those who were ventilated in intensive care are only included from these studies.
Adding the individual mortality data from these studies the pooled data showed an aggregated mortality of 118 (87%) among 135 IPF patients ventilated in intensive care units. The short-term mortality (mortality within 3 months of hospital discharge) is 127 (94%). The mean duration of mechanical ventilation was 8.6 days. Of the very few patients who survived, respiratory failure was precipitated by surgery/anaesthesia in 2 patients, 1 had undergone lung transplant and 3 patients were lost in follow-up.


Two of these studies (Al-Hameed and Nava et al.) included patients where no reversible cause was found for acute respiratory failure. In one study (Fumeaux et al.) infection was presumed to be the precipitating cause in all the patients (n=11). Of the remaining 92 patients – 30 had respiratory infection (bacterial and fungal), 5 pneumothorax, 4 congestive heart failure, and 2 pulmonary embolisms. Four patients developed respiratory failure following bronchoalveolar lavage, biopsy and anaesthesia. In 47 patients no precipitating factor for acute respiratory failure was found.


Ventilatory setting

In most of the above studies the mode of ventilation used was not mentioned. In their recently published observational cohort study Fernández-Pérez and colleagues showed that high positive end expiratory pressure (PEEP) setting is associated with worse outcome. Patients with IPF has little or no recruitable lung and high PEEP is likely to cause overdistension of relatively intact lung leading to ventilator-induced lung injury (VILI).
When invasive ventilation has to be used in IPF patients, like postoperative patients, patients with reversible cause of acute deterioration or where diagnosis has not been established, low tidal volume and low (PEEP) should be employed regardless of the mode of ventilation (volume controlled or pressure controlled).

Summary points


  • IPF is the commonest cause of interstitial lung disease with a median survival of 3 years, which is worse than many cancers.

  • No treatment for IPF till date proven effective except lung transplant, which is limited to minority of patients.

  • Acute deterioration may occur secondary to infections, pulmonary embolism, pneumothorax, or heart failure.

  • It may also occur in half of these patients without an identifiable cause, when it is attributed to acute exacerbation of IPF.

  • Management plan should include early investigations including CT scan, echocardiogram, BAL, infection screen, etc. to look for reversible causes.

  • Available data showed that outcome of these patients in ICU is very poor and mechanical ventilation is mostly futile.

  • Postsurgical patients with respiratory failure have better survival as the precipitating condition is likely reversible. They should not be denied life support because of underlying IPF.

  • All the above data is from patients with IPF. Non-IPF ILDs have a better prognosis and should not be denied ventilation based on the above data.
87% mortality after ventilation, a few post up to 3 months after, not good at all. That sounds on par purportedly of 'covid' patients in NYC, if many of those already had underlying PF or IPF or ILD, how many were gonners anyway, 'covid' or no 'covid'? Pretty grim but perhaps realistic given past data of prognosis and treatment of those disease conditions. Most of these patients in this group studied in this paper were older too, most over 60 years old.

Will come back for more information later.
 

gl69m

Member
post #49 from original thread (from gl69m)(not sure when posted lol)
Saw this article a few days ago, thought it was well worth posting, very very relevant for what is going on with all the 'covid' testing now. I'm not going to highlight and break down the article with my commentary, I have posted the whole thing. The NY Times can often be bashed for supporting state deception quite often, I agree especially with the 'covid' insanity nowadays: just wish we had the kind of journalistic integrity with that that appears to be in this article (if it's all accurate, IMO seems to be), and the good strong medical/scientific followup that ended up preventing and fending off this "epidemic that wasn't" and others like it in years past, unlike the covidiot "crisis' we are faced with now.

Faith in Quick Test Leads to Epidemic That Wasn’t
Jan. 22, 2007
https://www.nytimes.com/2007/01/22/health/22whoop.html
Dr. Brooke Herndon, an internist at Dartmouth-Hitchcock Medical Center, could not stop coughing. For two weeks starting in mid-April last year, she coughed, seemingly nonstop, followed by another week when she coughed sporadically, annoying, she said, everyone who worked with her.Before long, Dr. Kathryn Kirkland, an infectious disease specialist at Dartmouth, had a chilling thought: Could she be seeing the start of a whooping cough epidemic? By late April, other health care workers at the hospital were coughing, and severe, intractable coughing is a whooping cough hallmark. And if it was whooping cough, the epidemic had to be contained immediately because the disease could be deadly to babies in the hospital and could lead to pneumonia in the frail and vulnerable adult patients there.

It was the start of a bizarre episode at the medical center: the story of the epidemic that wasn’t.

For months, nearly everyone involved thought the medical center had had a huge whooping cough outbreak, with extensive ramifications. Nearly 1,000 health care workers at the hospital in Lebanon, N.H., were given a preliminary test and furloughed from work until their results were in; 142 people, including Dr. Herndon, were told they appeared to have the disease; and thousands were given antibiotics and a vaccine for protection. Hospital beds were taken out of commission, including some in intensive care.

Then, about eight months later, health care workers were dumbfounded to receive an e-mail message from the hospital administration informing them that the whole thing was a false alarm.

Not a single case of whooping cough was confirmed with the definitive test, growing the bacterium, Bordetella pertussis, in the laboratory. Instead, it appears the health care workers probably were afflicted with ordinary respiratory diseases like the common cold.

Now, as they look back on the episode, epidemiologists and infectious disease specialists say the problem was that they placed too much faith in a quick and highly sensitive molecular test that led them astray.

Infectious disease experts say such tests are coming into increasing use and may be the only way to get a quick answer in diagnosing diseases like whooping cough, Legionnaire’s, bird flu, tuberculosis and SARS, and deciding whether an epidemic is under way.

There are no national data on pseudo-epidemics caused by an overreliance on such molecular tests, said Dr. Trish M. Perl, an epidemiologist at Johns Hopkins and past president of the Society of Health Care Epidemiologists of America. But, she said, pseudo-epidemics happen all the time. The Dartmouth case may have been one the largest, but it was by no means an exception, she said.

There was a similar whooping cough scare at Children’s Hospital in Boston last fall that involved 36 adults and 2 children. Definitive tests, though, did not find pertussis.

“It’s a problem; we know it’s a problem,” Dr. Perl said. “My guess is that what happened at Dartmouth is going to become more common.”

Many of the new molecular tests are quick but technically demanding, and each laboratory may do them in its own way. These tests, called “home brews,” are not commercially available, and there are no good estimates of their error rates. But their very sensitivity makes false positives likely, and when hundreds or thousands of people are tested, as occurred at Dartmouth, false positives can make it seem like there is an epidemic.
“You’re in a little bit of no man’s land,” with the new molecular tests, said Dr. Mark Perkins, an infectious disease specialist and chief scientific officer at the Foundation for Innovative New Diagnostics, a nonprofit foundation supported by the Bill and Melinda Gates Foundation. “All bets are off on exact performance.”

Of course, that leads to the question of why rely on them at all. “At face value, obviously they shouldn’t be doing it,” Dr. Perl said. But, she said, often when answers are needed and an organism like the pertussis bacterium is finicky and hard to grow in a laboratory, “you don’t have great options.”

Waiting to see if the bacteria grow can take weeks, but the quick molecular test can be wrong. “It’s almost like you’re trying to pick the least of two evils,” Dr. Perl said.

At Dartmouth the decision was to use a test, P.C.R., for polymerase chain reaction. It is a molecular test that, until recently, was confined to molecular biology laboratories.

“That’s kind of what’s happening,” said Dr. Kathryn Edwards, an infectious disease specialist and professor of pediatrics at Vanderbilt University. “That’s the reality out there. We are trying to figure out how to use methods that have been the purview of bench scientists.”

The Dartmouth whooping cough story shows what can ensue.
To say the episode was disruptive was an understatement, said Dr. Elizabeth Talbot, deputy state epidemiologist for the New Hampshire Department of Health and Human Services.

“You cannot imagine,” Dr. Talbot said. “I had a feeling at the time that this gave us a shadow of a hint of what it might be like during a pandemic flu epidemic.”

Yet, epidemiologists say, one of the most troubling aspects of the pseudo-epidemic is that all the decisions seemed so sensible at the time.
Dr. Katrina Kretsinger, a medical epidemiologist at the federal Centers for Disease Control and Prevention, who worked on the case along with her colleague Dr. Manisha Patel, does not fault the Dartmouth doctors.
“The issue was not that they overreacted or did anything inappropriate at all,” Dr. Kretsinger said. Instead, it is that there is often is no way to decide early on whether an epidemic is under way.

Before the 1940s when a pertussis vaccine for children was introduced, whooping cough was a leading cause of death in young children. The vaccine led to an 80 percent drop in the disease’s incidence, but did not completely eliminate it. That is because the vaccine’s effectiveness wanes after about a decade, and although there is now a new vaccine for adolescents and adults, it is only starting to come into use. Whooping cough, Dr. Kretsinger said, is still a concern.

The disease got its name from its most salient feature: Patients may cough and cough and cough until they have to gasp for breath, making a sound like a whoop. The coughing can last so long that one of the common names for whooping cough was the 100-day cough, Dr. Talbot said.

But neither coughing long and hard nor even whooping is unique to pertussis infections, and many people with whooping cough have symptoms that like those of common cold: a runny nose or an ordinary cough.
“Almost everything about the clinical presentation of pertussis, especially early pertussis, is not very specific,” Dr. Kirkland said.

That was the first problem in deciding whether there was an epidemic at Dartmouth.

The second was with P.C.R., the quick test to diagnose the disease, Dr. Kretsinger said.

With pertussis, she said, “there are probably 100 different P.C.R. protocols and methods being used throughout the country,” and it is unclear how often any of them are accurate. “We have had a number of outbreaks where we believe that despite the presence of P.C.R.-positive results, the disease was not pertussis,” Dr. Kretsinger added.

At Dartmouth, when the first suspect pertussis cases emerged and the P.C.R. test showed pertussis, doctors believed it. The results seem completely consistent with the patients’ symptoms.

“That’s how the whole thing got started,” Dr. Kirkland said. Then the doctors decided to test people who did not have severe coughing.
“Because we had cases we thought were pertussis and because we had vulnerable patients at the hospital, we lowered our threshold,” she said. Anyone who had a cough got a P.C.R. test, and so did anyone with a runny nose who worked with high-risk patients like infants.

“That’s how we ended up with 134 suspect cases,” Dr. Kirkland said. And that, she added, was why 1,445 health care workers ended up taking antibiotics and 4,524 health care workers at the hospital, or 72 percent of all the health care workers there, were immunized against whooping cough in a matter of days.

“If we had stopped there, I think we all would have agreed that we had had an outbreak of pertussis and that we had controlled it,” Dr. Kirkland said.

But epidemiologists at the hospital and working for the States of New Hampshire and Vermont decided to take extra steps to confirm that what they were seeing really was pertussis.

The Dartmouth doctors sent samples from 27 patients they thought had pertussis to the state health departments and the Centers for Disease Control. There, scientists tried to grow the bacteria, a process that can take weeks. Finally, they had their answer: There was no pertussis in any of the samples.

“We thought, Well, that’s odd,” Dr. Kirkland said. “Maybe it’s the timing of the culturing, maybe it’s a transport problem. Why don’t we try serological testing? Certainly, after a pertussis infection, a person should develop antibodies to the bacteria.”

They could only get suitable blood samples from 39 patients — the others had gotten the vaccine which itself elicits pertussis antibodies. But when the Centers for Disease Control tested those 39 samples, its scientists reported that only one showed increases in antibody levels indicative of pertussis.

The disease center did additional tests too, including molecular tests to look for features of the pertussis bacteria. Its scientists also did additional P.C.R. tests on samples from 116 of the 134 people who were thought to have whooping cough. Only one P.C.R. was positive, but other tests did not show that that person was infected with pertussis bacteria. The disease center also interviewed patients in depth to see what their symptoms were and how they evolved.

“It was going on for months,” Dr. Kirkland said. But in the end, the conclusion was clear: There was no pertussis epidemic.
“We were all somewhat surprised,” Dr. Kirkland said, “and we were left in a very frustrating situation about what to do when the next outbreak comes.”

Dr. Cathy A. Petti, an infectious disease specialist at the University of Utah, said the story had one clear lesson.

“The big message is that every lab is vulnerable to having false positives,” Dr. Petti said. “No single test result is absolute and that is even more important with a test result based on P.C.R.”

As for Dr. Herndon, though, she now knows she is off the hook.
“I thought I might have caused the epidemic,” she said.
Hate to plug our favorite health care hero again, Dr. Mike Hansen, believe me I'm not plugging his videos cause I agree with the covidiot non-sense, quite the opposite, I'm posting it here to highlight the false medical insanity paradigm continuing to be pushed by by the 'covid' psyop insanity.

18 Coronavirus Autopsies (This is what they found in the Brain) | COVID-19
Jun 24, 2020
Now Hansen can be at least credited with giving partial truth; that many of these supposed 'covid' symptoms or disease effects exist in other diseases/conditions other than 'covid', however he is still very slickly marketing this fake false medical paradigm the way I see it. For instance he does mention in about ~8:00 into the video he mentions probable 'viral' attack of nerve receptors in the nasal passage as a 'likely' cause for loss of smell/taste; and then mentions the "cytokine storm" starting in the lungs but then causing confusion and headache but is quite common in flu cases as well, no shit, but not loss of taste/smell while you're congested as fuck with the flu or any other respiratory disease??

He then at least admits that confusion and delirium is very common in the ICU way before 'covid' came along, "so it's hard to know whether 'covid' is making people more prone to delirium or not", duh!!. His covidiot marketing defense of this? more and more studies about the effects of 'covid' are coming out all the time. Wow. I sure as hell don't want this guy as my doctor, ever.
 

gl69m

Member
Need to add another very seriously and quite often fatal illness/syndrome that I had forgotten to mention previously in this thread: “Sepsis”, which of course has always existed and long before 'covid' was invented obviously, but probably not so obvious at all for too many co-stupid cult believers out there.

Sepsis seems to be a leading or might be the leading cause of death in hospitals, worldwide too. And most people have probably never heard of this term that can clinically appear almost indistinguishable from “Sepsis” (without further more specific laboratory tests primarily), ”SIRS”, which stands for “systemic inflammatory response syndrome”. Up until this year I don't think I've heard of this term before, “systemic inflammation” yeah I've heard or thought about that term before now but not SIRS.

All people with Sepsis (by definition I think) will also have initially have developed SIRS (to some degree at least) and usually be included as a case of SIRS, but they distinguish Sepsis from SIRS by defining “Sepsis” as being caused (at least primarily I suppose) by an infection and generally a microbial infection that has invaded the bloodstream and then perhaps becomes systemic to many areas of the body (tissues and organs). I think perhaps “Sepsis” can occur without a microbial invasion of the bloodstream but a localized purulent infection could leak microbial molecular antigens and toxins or waste products that could induce an inflammatory immune response. I will include some links that define these terms and such. However, “SIRS” can also be caused by a large variety of things other than an infection, and can be deadly as well, although perhaps a trauma or other cause initiating SIRS can then be compounded by a subsequent infection (and then classified as “Sepsis” if an infection is detected) and I would think that in those cases the mortality rate would be of the highest risk.

Sepsis can also lead to ARDS (acute respiratory distress syndrome), and I think that may be true in the reverse as well- ARDS leading to Sepsis, though I'm not fully sure of that yet so I am not making that claim for now but I suspect that to be true also. But further I do think it very likely true from looking at this material that “non-infections SIRS” can also lead to ARDS. And ARDS is posited as the primary mechanism of mortality of 'covid-19', of which I believe that if 'covid' (primarily 'sarscov2') is a hoax then a 'pos' test or a clinical 'covid diagnosis' is a false positive and a patient dying from ARDS (or in many cases perhaps it was Sepsis or SIRS really subsequent to ARDS or vice versa) and in reality their ARDS was thus caused by some other disease agent or trauma other than 'covid', and thus 'covid' is really just a cover for what people were already dying from in large numbers before 'covid' was invented and declared a 'pandemic' in March 2020.

To the sheople mindset, to so many it would be impossible to “prove” what I am saying is 100% true, even if there was complete smoking gun guvmint documents outlining the hoax plan, and 100% scientific proof that 'sarscov2' does not exist, or that even if it does exist and strong scientific proof shows it cannot cause the supposed 'covid' or certainly not by itself, sheople will still believe in the 'deadly power of 'covid'.

I definitely do not have the ability to prove it on my own “scientifically” that it is a pure hoax, but I believe I can show a very strong circumstantial case for the type of hoax I am talking about, a disease paradigm hoax. Some sheople out there, “scientists” and medical health care doctors nurses and workers, most whom believe that 'covid' is real (while there are probably many that may not, political correctness will not allow them to truly publicly admit to that), are not going to be swayed much if any or at all by my arguments, and I realize that full limitation here. So fucking what, that does not mean that all the vast evidence against the existence of a plaguedemic- reputed to be caused by an alleged virus that causes so-called 'covid' disease, is not valid or cannot stand up at all in debate against even the more scientifically inclined sheople; however we know that such line of reasoning we bring forth here on this forum (the fakery aspect of psyops in particular) would never be allowed in any such “scientific' debate and further no such debate would ever be allowed in the mainstream (media particularly).


Going to start out with this video first, since it quite relevant IMO to 'covid' being used as cover for existing disease in the population,

Are the Covid-19 and Sepsis Syndromes one and the same?

1,483 views
Sep 8, 2020
video description
The global burden of Sepsis continues to challenge clinicians in its definition, diagnosis and treatment. The current Covid-19 pandemic seems to have almost taken our understanding of the Sepsis Syndrome back decades. What are the similarities between the current pandemic and sepsis? And what can we learn?


We have never avoided healthy controversy and in this episode Simon Finfer puts the case that the multi-organ dysfunction and cytokine storm seen in critically ill Covid-19 infected patients is analogous to the conventional Sepsis Syndrome and ARDS.


Perhaps if we consider the current pandemic through a Sepsis lens, we can avoid making the same mistakes that we have made in Sepsis research for decades resulting in no licenced treatments for the Sepsis Syndrome.


Derek Angus agrees but makes the case that there are two distinct differences. Firstly that the endothelial dysfunction appears different in Covid-19 and secondly unlike sepsis in the case of Covid-19 the pathogen itself proceeds unabated by any currently proven treatment. This means we need a two pronged approach in Covid-19 research:


1: Strategies purely aimed at combating the virus


2: Strategies aimed at applying Sepsis lessons to the pandemic response
I bolded/underlined the most relevant portions here, can we not see that this is just a re-branding of ARDS (and to certain extent “Sepsis” also) by claiming 'covid' is what is allegedly killing (or making simply ill) more people than anything else in the world in 2020/2021 (but apparently something else was before 2020??)? Surely that thought could not really have escaped the doctors and health professionals that made this video and other doctors and scientists around the world? I think not..., but vast majority cannot dare publicly state such a thing (even if they think it) with the political/'scientific' correctness of the medical industrial establishment gatekeepers out there, and not risk their jobs and careers.

So strategies aimed purely at stopping the 'virus' for 'covid' patients will be just as effective as the bullshit treatments that were given to AIDS patients; especially this is true if the virus does not exist or even if a similar one does and is not causing the disease- but likely be only just a passenger along for the ride in the disease process when it's even present at all. Can't learn jack shit about “Sepsis” through a 'covid' false paradigm lens. Just like drugs such as AZT was basically AIDS in a prescription, so too is the 'covid' medical treatment paradigm creating 'covid' in prescription form in the ICU's of hospitals in the last two years, as well the jab is likely another form of 'covid' in a prescription.


This next video to me seems as discounting SIRS as being of meaningful definition any more; since a conference by two medical societies decided that Sepsis needed to be redefined in 2014-2015 and there consensus paper was published in JAMA in 2016.

Update on sepsis ! New definitions for sepsis and septic shock 2016


@3:45 in they pay their 'respects' to the terms “SIRS” and “Severe Sepsis”, I'm left wondering if these terms (especially SIRS) should definitely not be done away with, especially since other articles I am finding written after 2016 still use these terms particularly SIRS, and one article I will post also shows that SIRS caused by non-infectious causes can be just as life threatening in some cases where the cause may not be known (and non-infectious). Was this redefining of Sepsis that seems to discount or downplay, or in the case of these video presenters, an attempt to place in the minds of many health care professionals that SIRS does not exist?, or in other words Sepsis and Sepsis Shock cannot be caused by non-infectious causes? Is this any coincidence in the run up to the current 'covid-19' pandemic'? I think not...


Special Communication
Caring for the Critically Ill Patient
February 23, 2016
The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3)
JAMA. 2016;315(8):801-810. doi:10.1001/jama.2016.0287
https://jamanetwork.com/journals/jama/fullarticle/2492881
Objective To evaluate and, as needed, update definitions for sepsis and septic shock.

Process A task force (n = 19) with expertise in sepsis pathobiology, clinical trials, and epidemiology was convened by the Society of Critical Care Medicine and the European Society of Intensive Care Medicine. Definitions and clinical criteria were generated through meetings, Delphi processes, analysis of electronic health record databases, and voting, followed by circulation to international professional societies, requesting peer review and endorsement (by 31 societies listed in the Acknowledgment).
Notice a task force of 19 to evaluate here, haha no coinkidink to 'covid-19', right. Very surprised there wasn't 33 societies endorsing it instead of only 31..
Key Findings From Evidence Synthesis Limitations of previous definitions included an excessive focus on inflammation, the misleading model that sepsis follows a continuum through severe sepsis to shock, and inadequate specificity and sensitivity of the systemic inflammatory response syndrome (SIRS) criteria. Multiple definitions and terminologies are currently in use for sepsis, septic shock, and organ dysfunction, leading to discrepancies in reported incidence and observed mortality. The task force concluded the term severe sepsis was redundant.


Recommendations Sepsis should be defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. For clinical operationalization, organ dysfunction can be represented by an increase in the Sequential [Sepsis-related] Organ Failure Assessment (SOFA) score of 2 points or more, which is associated with an in-hospital mortality greater than 10%. Septic shock should be defined as a subset of sepsis in which particularly profound circulatory, cellular, and metabolic abnormalities are associated with a greater risk of mortality than with sepsis alone. Patients with septic shock can be clinically identified by a vasopressor requirement to maintain a mean arterial pressure of 65 mm Hg or greater and serum lactate level greater than 2 mmol/L (>18 mg/dL) in the absence of hypovolemia. This combination is associated with hospital mortality rates greater than 40%. In out-of-hospital, emergency department, or general hospital ward settings, adult patients with suspected infection can be rapidly identified as being more likely to have poor outcomes typical of sepsis if they have at least 2 of the following clinical criteria that together constitute a new bedside clinical score termed quickSOFA (qSOFA): respiratory rate of 22/min or greater, altered mentation, or systolic blood pressure of 100 mm Hg or less.

I suppose there may have been the need to redefine some things about “Sepsis” and to be able distinguish Sepsis from non-infectious SIRS as well; however I notice that in defining Sepsis here they have used infection (Sepsis-related) as the defining hallmark of “sequential organ dysfunction and failure”, “organ dysfunction can be represented by an increase in the Sequential [Sepsis-related] Organ Failure Assessment (SOFA)”. This to me suggests they are using this redefinition conference to discount (mostly I think) non-infectious causes of SIRS that could lead to “systemic shock” (leading to organ and possible sequential organ failure, or SOFA) that is really clinically very little difference to “Septic (infectious) shock”, and is quite deadly as well, although I will say I think that such non-infectious shock can lead to severe immune suppression as well and thus lead to subsequent post infections and make matters worse and more potentially fatal: but unless a subsequent 'pos' 'covid' test (well they could call it clinical 'covid' anyway pft..) than they couldn't blame that case (or death as well for those that don't make it) on 'covid' then and not get the extra 'covid' funding per patient or ventilation or death etc. and another tick mark in the fake pandemic case (and death in the worst outcome cases) count.

I'm not going to go through the whole article as full review or anything. I don't think they have necessarily really done away with the term SIRS as the video above claimed it did; but I do think they have came up with re-definitions for Sepsis as to make it seem medically valid that some “infection” is thus almost always the primary cause that leads to a “systemic shock” (or defined as “septic shock”) and mostly responsible for the high mortality rate as opposed to any non-infectious causes. I believe this is very relevant now in the current (fake) 'pandemic' medical paradigm, to imprint the belief that 'covid' (the 'sarscov2' virus and now “variants') “infection' will now be believed to be the primary cause of so much illness and death in the world since the beginning of 2020 (the opening kickoff of Agenda 21 essentially).
Box 2.

Key Concepts of Sepsis​

  • • Sepsis is the primary cause of death from infection, especially if not recognized and treated promptly. Its recognition mandates urgent attention.
  • • Sepsis is a syndrome shaped by pathogen factors and host factors (eg, sex, race and other genetic determinants, age, comorbidities, environment) with characteristics that evolve over time. What differentiates sepsis from infection is an aberrant or dysregulated host response and the presence of organ dysfunction.
  • • Sepsis-induced organ dysfunction may be occult; therefore, its presence should be considered in any patient presenting with infection. Conversely, unrecognized infection may be the cause of new-onset organ dysfunction. Any unexplained organ dysfunction should thus raise the possibility of underlying infection.
  • The clinical and biological phenotype of sepsis can be modified by preexisting acute illness, long-standing comorbidities, medication, and interventions.
  • • Specific infections may result in local organ dysfunction without generating a dysregulated systemic host response.
Notice how they bias organ dysfunction (and eventual failure, subsequent organ failure SOFA) as should always be primarily considered as infectious caused; which in the absence of some other non-infectious known cause is prudent many times, however that can still be misleading according to some other articles I have found, and patients can die from fighting an infection that isn't there and the root underlying cause not getting addressed timely enough, at least I think I'm interpreting these other articles correctly to say that.

That Sepsis can be “modified” by chronic long-standing comorbidities, is that their disclaimer, their way of quietly admitting to chronic inflammation diseases as the primary risk factor in a patient developing a severe sepsis or septic shock? Perhaps even a non-septic (non-infectious) shock? Without fully admitting that this is what is primarily killing so many people in the last 70+ years in the developed world and a fast rising killer in the developing world as industry and more Westernized food diets increase there; the SAD (standard American diet) which may be a primary driver in this whole real epidemic/pandemic. Not that the SAD can solely be blamed, hell I love the SAD, grew up on the SAD, hooked on sugar and carbs and greasy fatty foods, but at a certain point even though I am not obese you gotta begin to cut back on the sugar carbs and excess fats, you begin to notice in the long run they are not healthy for longevity into older age. I know this now after I had turned past 40 and my former in shape self was not in such great shape any more lol, I'm so sad that I simply had to cut back on too much of the SAD, but really to feel healthier I really didn't have any other choice. I still indulge probably more than I should though, beginning to wonder if I am still not inching towards one of those chronic diseases myself.


Some general statistics about “Sepsis”,

WHO says sepsis causes 20% of global deaths

https://www.cidrap.umn.edu/news-perspective/2020/09/who-says-sepsis-causes-20-global-deaths
Sep 10, 2020
Data from 2017 show that sepsis affected 49 million people and was linked to approximately 11 million deaths worldwide—roughly 20% of annual global deaths. The report also reveals that sepsis disproportionately affects children and vulnerable populations living in low- and middle-income countries (LMICs). Twenty million of all estimated sepsis cases worldwide, and 2.9 million deaths, occurred in children under 5 in 2017, while roughly 85% of sepsis cases and related deaths occurred in low-resource settings.

A complication of severe infections

Sepsis occurs when the body overreacts to an infection, setting off a chain of events that leads to tissue damage and organ failure. Referred to in the report as "the final common pathway to death" for severe infectious diseases, it's a leading cause of death in hospitals, with an estimated mortality of 26.7% in hospital patients and 42.6% in intensive care unit patients treated for sepsis. The WHO estimates that 1 in 4 cases of sepsis in 2017 were acquired in the hospital.

The largest causes of sepsis in 2017 were diarrheal infections, which accounted for 9.2 million cases. Respiratory infections caused 1.8 million sepsis deaths. Bacterial bloodstream infections, malaria, dengue, and systemic fungal infections can also cause sepsis. Although infections are the leading primary cause of sepsis and sepsis-related death, nearly one half of sepsis-related deaths in 2017 were linked to injuries, mostly caused by road traffic accidents, and to non-communicable diseases.
quiet admission that non-infectious causes of “Sepsis” or at least it could be termed “systemic shock” (non-infectious) I think, are just as common and deadly as the usual suspected infections that are known to cause “Sepsis”. Any large trauma could cause tissue damage that can erode barrier integrity of the bodies normally internal impermeable barriers to microbes and microbes could thus diffuse and invade damaged membrane linings into the body from various routes such as the skin, digestive tract, airways nose throat etc. Perhaps it seems though a “systemic shock” occurs from trauma often enough in many people where no invasion or infection occurs and the non-infectious Sepsis (or severe SIRS) occurs by other mechanisms and of course can be and is often fatal. I will explore some articles related to that theoretical notion.


How many Sepsis cases and deaths in the U.S.A. Every year?

February 15, 2019

Prevalence, Underlying Causes, and Preventability of Sepsis-Associated Mortality in US Acute Care Hospitals​

https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2724768
Question What is the prevalence of sepsis-associated mortality in US acute care hospitals and how preventable are these deaths?

Findings In this cohort study reviewing the medical records of 568 patients who were admitted to 6 hospitals and died in the hospital or were discharged to hospice and not readmitted, sepsis was present in 300 hospitalizations (52.8%) and directly caused death in 198 cases (34.9%). However, most underlying causes of death were related to severe chronic comorbidities and only 3.7% of sepsis-associated deaths were judged definitely or moderately preventable.

Meaning
Sepsis is a leading cause of death in US hospitals, but most of these deaths are unlikely to be preventable through better hospital-based care.
again, here we go with the quiet admission of the truth of what is really the real killer. And thus this did not then shock the average health care worker or the system when it began to be claimed how 'deadly' 'covid' was/is.
Introduction

Sepsis affects approximately 1.7 million adults in the United States each year and potentially contributes to more than 250 000 deaths.1 Various studies estimate that sepsis is present in 30% to 50% of hospitalizations that culminate in death.1,2 The high burden of sepsis and the perception that most sepsis-associated deaths are preventable with better care3 has catalyzed numerous sepsis performance improvement initiatives in hospitals around the world.

The extent to which sepsis-associated deaths in adults might be preventable, however, is unknown. Sepsis disproportionately affects patients who are elderly, have severe comorbidities, and have impaired functional status.4-7 Some of these patients may receive optimal, guideline-compliant care yet still die due to overwhelming sepsis or from their underlying disease. The prevalence and preventability of sepsis-associated deaths is difficult to discern from administrative data and death certificates because hospital discharge codes do not indicate whether sepsis caused death, and death certificates are often completed incorrectly.8-11


https://www.amboss.com/us/knowledge/Sepsis/
Differential diagnoses
The following is a list of noninfectious conditions that may mimic sepsis.
[3]
[20]

Differentiating sepsis and systemic inflammatory response syndrome using biomarkers

https://www.news-medical.net/news/2...atory-response-syndrome-using-biomarkers.aspx
Sep 7 2017

What is systemic inflammation and how many different underlying causes are there?​

Firstly, it is necessary to make a distinction between systemic inflammation and Systemic Inflammatory Response Syndrome (SIRS).

SIRS consists of changes in clinical signs including an abnormal body temperature, increased heart rate, increased respiratory rate, an abnormal white cell count (either decreased or elevated), or an increase in band neutrophils.

Whereas systemic inflammation can be defined as an alteration or perturbation in the immune system, that could be detected by measuring something in the blood.

Systemic inflammation and SIRS can both be caused by lots of different things, but at the highest level you would categorize the causes into either infectious or non-infectious.

Infectious causes include bacteria, fungi, viruses, or parasites. Non-infectious causes include burns, trauma, surgery, ischemia-reperfusion, stress, sarcoidosis, asthma, etc.

The difference between infectious and non-infectious can sometimes be a bit of a blurred line. This is because the body has a microbiome, and when you get damaged tissue, there's often a certain bacterial or infectious element to it as well.

Why can it be difficult to establish the underlying cause of systemic inflammation?

The main reason that infectious and non-infectious causes are difficult to distinguish is because patients present with the same clinical signs. Clinicians therefore can't tell the difference between an infectious and a non-infectious case. An infectious cause of systemic inflammation, like sepsis, is a medical emergency which has to be treated as soon as possible.

Another reason is that current diagnostic tests aren't particularly good. For instance, for sepsis there is no gold standard diagnostic.

Blood culture is used to diagnose sepsis which involves taking blood from a patient and then trying to grow a microorganism. However, blood culture is a gold standard diagnostic for bacteremia, rather than for sepsis. Blood culture has high false positive and false negative rates. Up to 90% of all blood cultures taken from patients suspected of having an infection are negative. Also, in many instances when a blood culture is positive it is due to contamination rather than because of the patient actually having an infection.

How does the required response to sepsis differ from systemic inflammatory response syndrome?

The response to sepsis and non-infectious SIRS are different.

Sepsis has to be treated as soon as possible. It involves the immediate use of empiric broad-spectrum antibiotics and fluid support while waiting for the results of blood culture and antibiotic sensitivity. Other treatments for septic shock include the use of vasopressors and organ support. In some instances, which is still controversial, some patients get steroids.

Patients with non-infectious Systemic Inflammatory Response Syndrome shouldn't be on antibiotics. They could be given anti-inflammatory medications and other support. They may also need to undergo some other diagnostic procedure to determine what is the cause of non-infectious SIRS.
this article outlines a supposed test to distinguish a septic infection from bacteria to that of viruses. They call it a “pan-viral signature”,

Can you please outline the recent investigation of a four-biomarker blood signature to discriminate viral and non-viral causes of systemic inflammation?

There are a number of published articles in the literature that describe biomarker signatures that can distinguish between bacterial and viral infection, but they either consist of a large number of biomarkers, or do not take into consideration that patients could have a non-infectious condition. In our most recent paper, we discovered a four-gene biomarker signature in blood that is very specific to viral infection in a heterogenous population of patients that could have other infections or non-infectious Systemic Inflammatory Response Syndrome.

Did the signature demonstrate a meaningful distinction?

One of the key attributes of this viral signature is that we've demonstrated that it has diagnostic power across all seven Baltimore virus classification groups.

In the Baltimore classification of viruses, there are seven groups. Classification is based on whether a virus is DNA or RNA, double-stranded or single-stranded, or whether it is a negative or positive-sense.

This particular signature works across all of those different types of viruses. A patient could be infected with any type of virus and our signature could still detect that that person had systemic inflammation caused by a virus.

The study also demonstrated that the signature is able to detect a viral infection very early in the course of infection, before viremia and before clinical signs develop.

Another key finding was that the signature worked in a number of different tissues, including blood, liver, and in vitro culture. It also worked in different mammals, including macaques, monkeys, pigs, rats, and mice.

We're calling it a pan-viral signature; it is very specific, and it can be used very broadly.
very very interesting, have to check this out at some point, and see if this is being used or not being used in 'diagnosing' 'covid-19'. I can well imagine that a lot of 'covid' patients getting sick with viral sepsis-associated illness may well be caused by some other virus (or multiple viruses at once, or a slew of other pathogens other than viruses or bacteria) other than the mythical 'sarscov2', and thus while concentrating on fighting the phantom virus the actual virus (or other pathogen) and the other underlying co-morbidities get ignored thus worsening so many outcomes in the fake paradigm.


Mimics of Sepsis: What do ED Physicians Need to Know?
http://www.emdocs.net/mimics-of-sepsis/

Dec 1st, 2015​

Background

SIRS and sepsis are common clinical entities. A wide range of estimates for prevalence exists, with 300 to 1000 cases per 100,000 persons per year. Once a septic patient is admitted, more than half will require at least step down unit care or greater. Sepsis syndromes consist of a continuum, with varying definitions. The definition of SIRS includes: HR > 90 bpm, RR > 20 or PaCO2 < 32, temperature < 36oC or > 38oC, and a WBC count < 4 x 109 cells/L or > than 12 x 109 cells/L or > 10% bands. Two or more of these equals SIRS, and two or more with a source of infection equals sepsis.1,2 Unfortunately these criteria are non-specific, and the criteria alone do not provide a diagnosis or predict outcome. However, associated organ dysfunction does predict worse outcome.

A great deal of literature exists on sepsis and providing state of the art care in the ED. As EM physicians, we pride ourselves on resuscitating sick patients, and we are well aware that septic patients can rapidly decline clinically. Finding the source and providing appropriate antibiotics, adequate preload with IV fluids, and vasopressors if necessary are key components. The SIRS criteria are our first line of defense in the early identification of sepsis. But, it is important to recognize that just because a patient has multiple SIRS criteria, they may not actually be septic.

Many conditions mimic sepsis by meeting criteria for SIRS.
If these conditions are not considered, there is potential for increased mortality and morbidity. These conditions include: pulmonary embolism (PE), adrenal insufficiency, diabetic ketoacidosis (DKA), pancreatitis, anaphylaxis, bowel obstruction, hypovolemia, colitis, vasculitis, toxin ingestion/overdose/withdrawal, and medication effect. These mimics are a common cause of misdiagnosis in the ED. All of these clinical conditions produce symptoms and signs that meet SIRS (fever, elevated WBC, tachypnea, decreased distal perfusion, low urine output, confusion, end-organ malfunction).

Why do these conditions mimic sepsis? It all comes down to the pathophysiology. Sepsis ultimately results from a complex interaction of pro-inflammatory, anti-inflammatory, activated complement system, and coagulation mediators that in association with detector and signaling markers, trigger a host response. Initiators (microbes, trauma, hypoxia, ischemia, toxins) cause local tissue damage, which release local pro- and anti-inflammatory markers. Proinflammatory signalers include TNF, IL-1, and IL-6, while anti-inflammatory markers include IL-4, IL-10, IL-11 and soluble TNF receptors. These are designed to function and contain at a local level. If the initiators overwhelm the local response, the mediators affect multiple systems in the body: dermal, cardiovascular, gastrointestinal, renal, neurologic, hematologic/coagulopathic, pulmonary, and endocrine.3,4 All of these mimics have a similar endgame: triggering a systemic reaction that looks just like sepsis.

This post will take a step-by-step approach on how to avoid misdiagnosis and catch these mimics.

Signs of Sepsis:
Fever is a cardinal sign of inflammation and infection; however, fever does not equal infection. Cytokines induce a febrile response, mediated by the hypothalamus. Most, but not all, diseases causing true sepsis are associated with temperatures greater than 102oF.5 This is excluding elderly and immunosuppressed patients, where a temperature of 99/100 is often a true fever.6 Per an older review by Cunha, a normal host (i.e. not elderly, uremic, immunosuppressed), with a temperature of less than 102oF or greater than 106oF is usually noninfectious. On the other hand, hypothermia is a clue to bacteremia and true sepsis.5

Hemodynamic effects of septic shock include decreased peripheral resistance with increased cardiac output and tachycardia in the early stages, or distributive shock (also with anaphylaxis, pancreatitis, etc.). Later stages demonstrate findings of hypovolemic shock with increased resistance, lower cardiac output, and cooler peripheral extremities with poor capillary refill. These findings are not specific for sepsis unfortunately.3-5

the danger or alarm theory of how SIRS and Sepsis is brought about,

Published: 12 July 2012

How tissue injury alarms the immune system and causes a systemic inflammatory response syndrome​

https://annalsofintensivecare.springeropen.com/articles/10.1186/2110-5820-2-27
Systemic inflammation is very prevalent among critically ill patients, particularly those with extensive tissue injury. Although downstream mediators (cytokines) and effector cells (phagocytes) have been identified, proximal mediators originating from injured tissues remained elusive. Alarmins (“danger signals”) released by necrotic/injured cells have been identified recently and certainly play a role in triggering local and systemic inflammation in critically ill patients. The most promising alarmin candidates are of mitochondrial origin, i.e. mitochondrial DNA and the chemotactic factor fMet-Leu-Phe (fMLP). ATP also is released from necrotic tissues and stimulates the assembly of the inflammasome, leading to the production of proinflammatory cytokines, such as interleukin (IL)-1ß. The identification of novel alarmins opens new therapeutic avenues for the treatment of severe SIRS, and SIRS-dependent organ dysfunction.
among alarmins mentioned,

heat shock proteins
other proteins
uric acid
mitochondrial alarmins (DNA and RNA and proteins) “Injected to animals, mitochondrial preparations induce lung injury resembling to that seen during ARDS [40].”
extracellular ATP

I've seen other articles that mentioned micro RNAs as alarmins of shock as well, have to look into that later.


Published online 2014 May 4

Metabolic theory of septic shock​

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4038812/
Septic shock causes progressive failure of vital homeostatic mechanisms culminating in immunosuppression, coagulopathy and microvascular dysfunction which can lead to refractory hypotension, organ failure and death. The hypermetabolic response that accompanies a systemic inflammatory reaction places high demands upon stored nutritional resources. A crucial element that can become depleted early during the progression to septic shock is glutathione. Glutathione is chiefly responsible for supplying reducing equivalents to neutralize hydrogen peroxide, a toxic oxidizing agent that is produced during normal metabolism. Without glutathione, hydrogen peroxide can rise to toxic levels in tissues and blood where it can cause severe oxidative injury to organs and to the microvasculature. Continued exposure can result in microvascular dysfunction, capillary leakage and septic shock. It is the aim of this paper to present evidence that elevated systemic levels of hydrogen peroxide are present in septic shock victims and that it significantly contributes to the development and progression of this frequently lethal condition.

Core tip: For decades septic shock has been attributed to an over-active immune response. However, immune modulation has failed to reduce mortality, casting doubt on a direct causal role for the immune response in the development of septic shock. A closer look suggests that septic shock is the result of a generalized build-up of hydrogen peroxide, a toxic cellular by-product generated as a consequence of the hypermetabolic state that accompanies a systemic immune response. This finding points to the systemic accumulation of hydrogen peroxide as a significant risk factor for the development of septic and non-septic shock syndromes.
Not exactly sure of the mechanisms of hydrogen peroxide accumulation in tissues in non-septic shock syndromes at the moment, may come back to that later.

MECHANISM OF DISEASE​

The above evidence supports a pathogenesis of septic shock which is initiated by the systemic depletion of glutathione as the crucial event responsible for the accumulation of H2O2 in tissues. Subsequent diffusion of H2O2 into the blood stream leads to systemic elevation of this highly toxic oxidizing agent resulting in the microvascular dysfunction and organ failure observed in septic shock (Figure (Figure11).

Coagulopathy​

Intravascular activation of the coagulation cascade with generation of fibrin and formation of diffuse microvascular thrombi is a pathologic and physiologic hallmark of sepsis[55]. This presents clinically as disseminated intravascular coagulation (DIC) and is found in up to 50% of patients with sepsis[56]. DIC leads to abnormal bleeding and intravascular clotting, obstructing limb and organ blood flow, and is a strong predictor of mortality[56].

H2O2 can induce vascular injury by peroxidation of cell membrane lipids and studies have shown a marked increase in endothelial cell TF and TF mRNA after 1 and 5 min exposure to Xanthine oxidase, a H2O2 generating enzyme[10,58]. This indicates that TF is highly sensitive to H2O2 induced upregulation, which suggests with a contributory role for H2O2 in sepsis- associated DIC.
how many times have we heard that 'covid' is killing by blood clot formation (or cuagulopathy I presume)?


Saving SIRS? Discernment of Sepsis from Non-Infectious Syndromes in the ED
December 10, 2018
https://blog.unmc.edu/infectious-di...psis-from-non-infectious-syndromes-in-the-ed/


Further strong circumstantial evidence for this phantom virus medical switcheroo hoax is what the WHO themselves say about the main deadly and debilitating known and mostly chronic respiratory diseases,

The Global Impact of Respiratory Disease
Second Edition
©2017 European Respiratory Society, on behalf of the Forum of International Respiratory
Societies (FIRS).
https://www.who.int/gard/publications/The_Global_Impact_of_Respiratory_Disease.pdf
Forward

The World Health Organization (WHO) launched the Global Alliance Against Respiratory Diseases (GARD) in 2006 with the aim to bring together the combined knowledge of national and international organisations, institutions and agencies to improve the lives of more than one billion people affected by chronic and acute respiratory diseases.

The 2030 Sustainable Development Agenda was adopted by world leaders in 2015 at a historic UN Summit in New York and came into force on January 1, 2016. The very ambitious agenda is a plan of action to achieve 17 Sustainable Development Goals (SDGs) and 169 targets by the year 2030, which include the economic, social and environmental dimensions of sustainable development.

SDG goal 3: Ensure healthy lives and promote well-being for all at all ages is one of the most important goals and needs to receive special attention by governments and all stakeholders. Improved health will bring people out of poverty and contribute substantially to sustainable development. A lot of progress has been made in increasing life expectancy and reducing the burden of many diseases such as polio, maternal mortality and the spread of HIV/AIDS. However, many challenges remain to be addressed if countries are
to achieve SDG 3.

Noncommunicable diseases (NCDs), including cardiovascular diseases, cancers, chronic respiratory diseases and diabetes, are the biggest killers today. One of the very ambitious goals is to reduce mortality from NCDs by 30% by the year 2030. The WHO Global Action Plan on NCDs has recognised the strong interaction between NCDs and infectious diseases, including tuberculosis in particular in low- and middle-income countries and is asking to explore opportunities to improve the detection and treatment of co-morbidities within health services.
Again the quiet admission of the truth of the real killer diseases that they will later wrap up and disguise in the huge lie of the 'pandemic'. Agenda 2030 anyone?
Executive Summary

We take our breathing and our respiratory health for granted, but the lung is a vital organ
that is vulnerable to airborne infection and injury. Respiratory diseases are leading causes
of death and disability in the world. About 65 million people suffer from chronic obstructive
pulmonary disease (COPD) and 3 million die from it each year, making it the third leading
cause of death worldwide. About 334 million people suffer from asthma, the most common
chronic disease of childhood affecting 14% of all children globally. Pneumonia kills millions
of people annually and is a leading cause of death among children under 5 years old. Over
10 million people develop tuberculosis (TB) and 1.4 million die from it each year, making
it the most common lethal infectious disease. Lung cancer kills 1.6 million people each year
and is the most deadly cancer. Globally, 4 million people die prematurely from chronic
respiratory disease. At least 2 billion people are exposed to indoor toxic smoke, 1 billion inhale
outdoor pollutant air and 1 billion are exposed to tobacco smoke. The truth is that many of us
are naïve to these stark realities.

More on this stuff later, end super long post, :)
 
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