Remember all the discussion about the issues with too much IGg4? Well those suffering from Long Covid have a deficiency of IGg2 - fizable with an acid?

Dr John Campbell discusses chronic fatigue and Guillain Barre syndrome with Professor Robert Clancy in this 50 minute video here (excuse the “um’s” in the text of the transcript -  I don’t know how to blanket delete a specific erm with multiple occurrences and there are 47 of them!).:

Long covid and long vaccine (youtube.com)

Here is an except using the YouTube transcript generator from around the 22 minute mark:

“ (people) who are prone to getting fatigue never quite make the right sort of T-cell response and I'll give you two quick examples and these relate exactly to the situation in uh that I'm certainly seeing and has recently been published to some extent

with long Co um if you look at antibody production - the antibodies are made by a cell given the very imaginative title of a “b cell”

a b lymphocyte requires T lymphocytes to help them so we have these helper T cells

now it appears that there's a defect in the T helper cells in people with long Covid and this has been identified in different studies and certainly exact in the same in people with other chronic fatigue illnesses

and the way the T cell deficiency expresses itself is that the B cell has markers of not working as well as it should

now if you get a virus infection you make what's called an IGM antibody the IGM antibody is the first antibody but it's not a particularly “High Affinity” good effective antibody and so what the body does it replaces it with an IGG antibody

so you go from IGM to IGG which is a much Higher Affinity antibody and you make different subclasses of IGG - and there's four sub IGG 1 2 3 and four

now two things I noticed over the years looking after literally hundreds of people with chronic fatigue illnesses is that - number one - many of these patients never switch from the IGM to the IGG anybody

and so when you do a routine Epstein Barr bar virus in antibody - and every Doctor who’s watching this will know you look for IGM antibody because that tells you you've got a current infection - you've just got the infection

and suddenly and I used to get a phone call every couple of weeks from General Practitioners that I work with saying hey this is confusing I got a patient who's got IGM and IGG antibodies and they've had them for weeks and months

and of course these are the people who have got ongoing chronic fatigue and they're not actually eliminating or controlling their Epstein Barr virus by virtue of the fact they're not making a particularly effective immune response

 and the response defect goes back to the T-cell because it's not helping the B efficient effective IGG response and so when you do a routine test the IGM which should tell you it's a recent infection but it's not it's been there for weeks or years

and an IG and the second - and this is really interesting because only just a month or so ago this was found for long Covid - that in people with chronic fatigue syndrome one of the things that uh we noticed uh in our Clinic was that a number of these patients have IGG subclass deficiency particularly an iGG2 subclass

and it didn't - initially - it didn't make much sense and I started seeing both the IGM IGG confusion plus the IGG subclass deficiency both of which depend on good T cells working

um now different subclasses have different jobs and so iGG2 has a particular job and if it's very low then you've got a defective antibody response by virtual of this

so what a wonderful study I saw I think it was about a month ago John um where they looked at IGG subclasses in Long Co and lo and behold there's a highly significant reduction across the long Covid

 something that's never really been done for chronic fatigue syndrome uh the classics um significantly lower iGG2

so exactly the same things is occurring in Long Covid which brings all of these chronic fatigue illnesses collectively together

(Dr Campbell - so moving on to the sort of um management strategies that we going to use - Robert I mean I mean the question is of course what the heck do we do we do about this so um do we need to promote a more effective immunity within the respiratory tract and how would we do that)

well uh I don't have all the answers no one has all the answers but I think that if you understand the process that's going on you can see some sense in going forward now I can run through there are five things that that uh I do with my patients uh

or I I'm thinking about uh the first is that we've developed the idea and I I've talked briefly about this with you before of what I call - immune resilience - and that is um and I think in the context we discussed it before

 I said why is it 99% of people who get long Covid uh inconvenience for a few days they feel a little sick a fever sore throat and then they get better whether you treat them or not

but 1 or 2% get very sick H and some may die and yet you look at that Collective group and of course there are predisposing factors for getting very sick but many of them are just like you and me uh that we all ,look the same we think we're the same and yet we handle the virus differently

and this has been an area that my group's been interested in for a long period of time and um we developed the idea that there's a thing called “immune resilience”  and that there are ways of Shifting that immune resilience so that that 1% behaves like the 99%

now that that's something that that that my own we've been certainly working on and uh not available yet but I think is the way one of the ways to go in the future so in other words people who uh get uh airway infections uh handle it more effectively and don't run into the complications which obviously include long Covid because of a defective immune response

so I think that's uh for the soon future not a long term uh

the second is to understand the process as being persistent antigen uh now the spike protein um is I think without our question the persistent antigen both these cases uh and this is a practical area uh and there are two approaches currently uh being used um uh

 our friends and colleagues in America uh have developed various enzyme packages uh based on nattokinase which is a very interesting um uh orally uh an ingested enzyme that has specificity for Spike protein and I know studies are being done uh in uh in America uh using these um substances uh and we're really looking forward to seeing uh how they come out uh

the second thing you can do about the expression of Spike protein is blocking its effect um really exciting work has come out in the last few months about how ivermectin works and there's a complete relook now at ivermectin uh  about time I may add but um and I think one of the things that's bridged from the narrative that was very unkind to ivermectin

and the reality of science is the demonstration by uh a combination French and American groups showing that ivermectin blocks the uh blocks Spike protein so it blocks the spike protein getting into the cell and it blocks it aggregating red cells which is the reason that you get low oxygen saturation in patients who get significant Covid

uh and I was on one of the three papers that showed that it was amazing within 24 hours of taking ivermectin – oxygen saturation reversed - now that's not suppressing inflammation and now by virtue of these studies it's shown that uh you disaggregate the cells and so the oxygen can return very quickly

now I've been treating some of my own patients with moderately high dose of ivermectin for a month I think I've treated five or six and every one of those has improved now that doesn't mean a thing it's not a randomized control trial, it's what I call clinical medicine

you look uh at a problem you say this - is a process uh what logically can be done - now it's not necessarily going to change all the structural damage that's been done but certainly there's been some improvement

not necessarily dramatic Improvement - some improvement uh in a month or so of taking ivermectin I think what really is needed is people who um have access to um academic uh um academic situations where they can study and do these a randomized control of ivermectin in Long Covid properly done uh would be the most important thing that can happen uh in in Long Covid

the third thing that um that I think is really interesting in Long Co is that uh and particularly a couple Chinese groups have been promoting this and that is that people who get long Covid get a disturbance of the microbiome in the bowel

now you might say how on Earth can that relate to something that's going on in the airway well um I was lucky enough years ago to work with John Penstock in Canada uh who came up with the idea of the common mucosal system which has been underpinning my work over many years uh in humans

and uh it it's just suddenly I realized that all our focus on this common mucosal system was the immune expression not the microbial drive and when you think that the architecture of this common system that expresses control over all the different mucosal surfaces of the body

the architecture involves sensor systems all the way down the gut not just the small bowel with pair patches but all sorts of little patches with specialized M cells they're called over them that allows bacteria to come in and so I think the important thing to understand here is that the commonality of mucosal immunology and expression involves the microbiomes at the different sites

and so uh what happens uh in the airway by swallowing and affecting P patches can distort the microbiome in the gut and the microbiome in the gut can equally influence what's going on in the airway

and I'll just give you one exciting um observation and that is a group was looking at uh in mice they were looking at clepsimonial (sp?)l pneumonia which is a nasty bacteria that causes pneumonia and they couldn't understand why on Earth when they gave pneumonia to the mouse by putting the bug in the airway their microbiome changed

this is in the gut and of course um the reason is this commonality this communication system that's so effective so what they found was and this is exactly what was found in the patients with long Covid

(Ed: I think Peter McCullough interviewed a doctor several months ago – maybe the same – who pushed the approach of swallowing mucus regularly in large amounts to “cure” the microbiome).

a particular type of bacteria was depressed and these bacteria well bacteria that produce short chain fatty acids butyric acid um acetic acid propionic acid those three main one two and three um carbon short chain fatty acids

um now the people working with the mice and clepiella said well what happens if we um reduce these bacteria uh in the gut then the main product from the bacteria uh is things like butyric acid and so they measured butyric acid and found it was very low so very sens they just started feeding butyric acid to these mice and the eclipsial pneumonia became much uh improved

uh didn't completely cure them but it certainly improved - showing there was this connection between the two

so you have two ways in which the microbiome can change the expression of any form of chronic fatigue - one is - by metabolic transfer of receptors of um molecules that can move around through the blood stream - and secondly by changing the cell Delivery Systems through the aggregated infid issue of P patches um sequel patches and the various ones in the colon

so that to me is very exciting and again if you can bear with me for 20 seconds I I'll give you a very important example many years ago - Tom Barode who was the guy who discovered the uh the treatment for peptic ulcers to which eradicated them uh

he also was the person who um really developed the idea of full microbiome transplants by changing the microbiome by washing you out and giving you some healthy ones um

Tom is uh quite extraordinary um he Tom treated patients who came to him with fatigue and non-specific gut symptoms and was surprised to find not only did the gut symptoms improve with this treatment but so did the fatigue

now uh no one quite believed it so he went back 10 years later 10 years later and found something like 60% of the patients and most of those patients still had a resolution of their symptoms including their fatigue

now you don't see that in chronic fatigue illnesses - in other words by having a specific intervention there was some resetting of the system which we don't understand very well and so um I'm I I do a clinic in in in Tom's practice uh and uh he was is my PhD student and um he Tom uh I'm actually if he's watching this or I'm going to send him an email

Tom uh you've got to go back and start looking at uh how we can manipulate the microbiome and have outcomes in Long Co um so um I think the next thing that I think is really important

so we there are the three things that I think are really important the next thing is don't feed the syndrome don't keep giving people vaxx who have got Long Covid syndrome because um you look at the literature - and I just did a review for a journal last week on a meta analysis of all the studies done on vaccination and long Covid - and it blew me away I mean it was a very well done study and 20 there was a 20% reduction of long covid in people who have been vaccinated

but I looked at the number of people was 1 million if you're looking at probably a 100,000 or a couple hundred, thousand people they get lost in they're very different they're the people who have got a fatigue illness maybe phenotype that have develop this uh in the context of the vaccine and you give them more vaccine or they get Covid and they get worse t

this is a concept that I find nobody really or or most people have great trouble grasping I just noticed this morning while I was waiting to hear from you John that Peter McCullough wrote one of his um uh reviews and it was making exactly the same point

you know you don't vaccinate people with chronic fatigue syndrome you're just putting petrol on the fire and of course yeah

the final thing is you address the issues the person has um uh I noticed what some of my colleagues say a lot of these people have got issues  - uh they can't work - they lose their job  - they’re broke  they're going to have a touch of reactive depression and anxiety and

um it's not that they have a primary mental health problem they've got serious responses mental health responses of a normal type to a uh to a very uh incapacitating problem so that's our approach anyway to chronic fatigue illnesses

excellent updates and uh we'll um certainly keep an eye on this one but I think gives us real cause for hope here Robert that there is potential way ahead for people that are suffering in this way y

Yeah but for now thank you very much

End partial transcript

Note that only three things out of the five promised at the outset were covered.

Onwards!

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