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I love this lady... in fact she might be my hero

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Posted 9/29/2015 10:57 PM (GMT 0)
/www.youtube.com/watch?v=1eSiAUHDhyA

For the science and maybe not so science folks.

In keeping with the theme of amazing video's lately this one in my mind is simply the best. This woman is just.... remarkable does not do her justice.

For Old Mike:

I know you're big in oral tolerance. Go here: /www.youtube.com/watch?v=hxZQZ1zZVk0 and skip to 6:54 and watch the section until she speaks about oral polio vaccine. Spoiler alert - Inactivated polio virus given via injection in the blood really does only produce an IgG and IgM response - oral vaccination produces IgA which is much more effective.

Anyway - this lady's logic and thinking really applies to IBD. None of this self / non-self antigen nonsense.
Posted 9/29/2015 11:01 PM (GMT 0)
PS - Please at least watch until the 2 minute mark before turning it off and deciding it's not your cup of tea... just let her speak for a few minutes.

Thankx
Posted 9/29/2015 11:11 PM (GMT 0)
Excellent explanation!!!! She did a great job explaining this, now hopefully those who don't believe that IBD involves the immune system may finally understand what and how the immune system actually is and how it works, always shake my head when people say IBD isn't an autoimmune disease/issue...clearly they don't get what the immune system actually is.

Thanks for posting this CM!!
Posted 9/30/2015 12:03 AM (GMT 0)
Fascinating
Posted 9/30/2015 12:23 AM (GMT 0)
wow as a zennie i've done a good deal of study with self-vs-non-self SO INTERESTING from a scientific immunology standpoint. I love her!
Posted 9/30/2015 12:35 AM (GMT 0)
Gonna have to find the time to watch the whole thing. Didn't realize it was so long but it definitely looks like it will be worth watching. Thanks for posting.
Posted 9/30/2015 2:46 AM (GMT 0)
@zengirl - sorry for the length.

I just wrapped up a full non-credit (long story) immunology course - 3'rd year Intro to Immunology if you're in university would be the equivalent. So it's pretty detailed. How I stumbled upon her was this, which you may appreciate:

I understand the concept of self MHC (Class 1 and 2) restriction in antigen presentation to T-cells pretty well (I think) - i.e. if my macrophages phagocytized, degraded and loaded a 'foreign' peptide (antigen) onto a class 2 MCH molecule and expressed it on it's cellular membrane - then we took my macrophages and put them in with your helper t-cells, my macrophages would not be able to activate your helper T-cells because our MCH haplotypes are different. So your MCH is foreign to my immune system. Fine and dandy. I believe this is the correct way to word it and correct thinking. So this is the text book example that T-cells (CD4+ & CD8+) will only respond to antigen if it's presented in a self-MHC molecule. Otherwise they are not activated.

So they need dual recognition of self MHC and 'foreign' antigen to become activated and mount an immune response.

But what I could not wrap my head around is the 'foreign antigen' or peptide aspect... I didn't, and still do not get it. It just doesn't make sense deep down in the gut type feeling. I kept repeatedly asking what makes a peptide 'foreign'??? Or more specifically, since say a class 1 MHC molecule presents peptides that are 8-9 amino acids in length - How in the heck does our immune system say "hey this sequence of 8 or 9 amino acids are found nowhere else in our body so we need to attack"??? - or why? really as she states...

I mean really, honestly sit back and think about it... what is the difference between a bacterial produced amino acid and a human produced amino acid??? Is there any difference at all? Probably not. And are they telling me that if you string 8 or 9 of these amino acids together they make a peptide that is not found anywhere else in the body? Or they make a peptide that is just a little bit different from the same 'self' peptides?? I guess maybe but is this actually likely? ... And is the immune system is only supposed to respond to these? Well, yes so I am told... but does this really happen? Does it make sense?

As I asked these questions, I got answers like "no one knows for sure but there are studies looking into this". Or "maybe there is a bonding (structural) difference within the amino acids themselves that cause them to sit in the MHC molecule pocket just a little differently"... basically the answer was "we have no clue whatsoever, we just think this is the way it works".

Since MHC restriction is learned in the thymus... that is fine, but are they also really learning to distinguish between self and non-self peptides at the same time?? I don't know....

It doesn't sit well to be honest. But perhaps I still don't understand it enough yet.

The other night I was googling around trying to find some answers and stumbled upon a link to her paper... then I found the video...

For me I was like wow.... I can breathe again because THIS seems to make so much more sense.

I had no idea there was even a bit of controversy over this - and had never been told of her 'alternate' theory.

Anyway, the more I learned about her the more I realized just how much I admired her... I love the way she comes across. Not afraid to challenge the thinking and teachings of many - and she seems to be able to back it up.

Imagine getting up there and schooling a room full of immunologists and nano biologists or whatever you want to call them with no notes at all... just off the cuff like that... unreal. I was like wow, I love this lady!

Awesome for her... and I hope she has more of a chance to speak her mind like this. Maybe it will get people thinking...

Post Edited (Canada Mark) : 9/29/2015 9:06:46 PM (GMT-6)

Posted 9/30/2015 3:42 AM (GMT 0)
She is awesome!!! I must have sent lots of damaged signals from my gut!
Posted 9/30/2015 4:28 AM (GMT 0)
This lady is totally freaking me out tonight!

OLD MIKE - /www.youtube.com/watch?v=9fktuiLkTrw go to 32:30 and listen. You said on your peroxide thread that "you are being oxidized" I had no idea there was an injectable version. The common 'supplement' form is not going to do anything, but in blood injection... maybe... maybe a lot actually. Though really catalase would be used based on that excess peroxide theory I guess. ?

For others: Her take and description of Autoimmune Disease and what it really is according to her Damage Theory is just after this.

Gary and PB4 etc you might like the autoimmune part. It starts at 35.30 into it.
Posted 9/30/2015 12:28 PM (GMT 0)
Ok looked at the 3rd video first.

I took SOD in the past orally, made me much worse.

My reasoning is that it makes peroxide from the super oxide, so if you don't have enough catalase around

or are perhaps low on glutathione, then the peroxide does the damage.

I do like her comments on SOD being cheap and so it was shelved for other clinical trials.

I made the same comment in the other thread on DHEA and the 2003 UC/crohns trial where it worked pretty

good on refractory people, where the hell is the next clinical trial,I wonder.

I was just guessing, but now I know from her comments, that cheap drugs that might work are shelved.

No money in it, starting to get me a bit upset.

Hopefully other countries might pick up the slack on these types of cheap compounds.


On the oral polio vaccine not quite sure what she means, do we just shift immune response to Iga, or are we also actually tolerating polio and not having an immune response, therefore we don't get sick from it.


That is why I tend to think that oral FMT might be a better way to make FMT work.


She also brought up CFA,which is made from dead TB or perhaps other mycobacteria, so nasty

that not allowed for human use.

My point is that it activates the immune system.

So what about crohns and MAP,or even UC an MAP, where for some reason our immune system

is over activated from antigen acting as an adjuvant, wild speculation.

Of course all of us are exposed everyday to MAP, so why does not everyone get IBD.


https://en.wikipedia.org/wiki/Freund%27s_adjuvant



Old Mike

 

Post Edited (Old Mike) : 9/30/2015 8:03:33 AM (GMT-6)

Posted 9/30/2015 4:14 PM (GMT 0)
Maybe the same reason not everyone gets cancer just cuz they smoke? And some people that are exposed to MAP simply don't get the response of inflammation in the bowels just like not all women get breast cancer regardless if they smoke or not or are exposed to second-hand smoke, there's a gene that's specific to breast cancer (even some men can get it) and there are women getting their breast removed (Angelina Jolie for one example) based on the fact that she was tested and found to have the same gene that gave her mother breast cancer. They know that genetics plays a role with IBD as well, so maybe it's along the same lines as the breast cancer gene?
Posted 9/30/2015 11:15 PM (GMT 0)
I think she meant this in regards to the oral polio and myelin basic protein stuff:

She means that the idea of ‘tolerance’ developing in mice due to oral administration of myelin basic protein is perhaps not what it seems.

She is suggesting that by giving mice oral myelin basic protein they are really just teaching (pre-conditioning) the mice immune system to mount an IgA response to myelin basic protein which is less damaging and the type of immune response the brain tissue actually wants….

By adding all the nasty crap (adjuvants) and bypassing the oral route altogether they are simply forcing the immune response to be an IgG response which calls in the nasty heavy hitting immune cells and does all the damage in their 'desease model'. The result just ‘happens’ to somewhat resemble Multiple Sclerosis.

When they look at the mice that they gave myelin basic protein to orally first, they don’t see the damage… and they think that oral administration of myelin basic protein was inducing ‘tolerance’ and alleviating the disease or immune effects. BUT what she is pointing out is that they are simply looking at the effect “no lesions” and making this assumption and not realizing that these particular mice are pre-conditioned to mount an IgA response - not IgG by giving it to them orally first.

The gut tissue want's an IgA response otherwise there is to much risk of damage.. Just like what happens when you give an oral Polio vaccine - you get an IgA response to the virus and it works to kill the virus off.

Polio is an orally transmitted virus that the body naturally deals with by making IgA antibodies.

In essence, she is saying they forgot to measure the IgA in the poop of the orally treated mice and interpreted the lack of damage as them building up ’tolerance’ to the myelin basic protein - and then going further to say it's not actually 'tolerance' that was developed, it was the class switch to IgA that produced the effects and they just didn't measure it.

She is suggesting that in the brain (an immune privileged site), the 'tissue' should dictate that it only wants an IgA response as a protective measure, not the immune cells otherwise there would be to much damage.

It turns out they have tried this in humans with Multiple Sclerosis. They fed them oral myelin basic protein in hopes to alleviate the disease just like in the effects in the muse model.... and there was no change or noticeable effect in humans. Which is interesting.

----------------

This extends a little further to those of us with IBD... by her theory the gut really only wants an IgA response and dictates this to the cells of our immune system. BUT in those of us with IBD, we actually have a marked increase in IgG and IgM in our gut lumen and all these nasty cells going bonkers destroying tissue, releasing TNF-a, releasing oxygen radials etc etc etc - it's a blood bath of immune disaster..........

So just like her example of the eye that only wants IgA response otherwise it would do to much damage, when it cannot clear the virus it switches class and makes the sacrifice of the eye itself to deal with the pathogen it cannot clear - As she says, this type of response is useful because when the tissue is destroyed you also kill the infection. The question being do we have a chronic infection that we cannot clear and not an autoimmune response? Or is it as she says at the end of her other video:

Have they simply been asking the wrong questions about autoimmune disease? She thinks some auto-immune conditions might be caused by damage... and we sure have a lot of that going on in our guts.

I like her comment on the auto-immune diseases that 'flare' as having a good chance of being "you have an infection and don't know it'.

Post Edited (Canada Mark) : 9/30/2015 5:19:21 PM (GMT-6)

Posted 9/30/2015 11:39 PM (GMT 0)

Yea Mark I think I understand much of what she says. Very smart lady.

But at least in colitis I think Swidniski said the stool is covered in IGa.

Colitis also makes sense in terms of a mucus breach, = danger.

So we get a polymicrobial infection that cant be cleared, thus the immune system tries to destroy the organ.

But in this case if you don't cut it out, the organ destruction will also kill the whole organism.

Immune system doing its job,but killing us in the process.

Brings up the question how does rectal FMT work at all, in some people.

Perhaps it produces more of a weak Iga response,as opposed to just changing gut bacteria populations.

I still think oral is the way to go, or at least stomach tube,might make more of an Iga response.


OM


Post Edited (Old Mike) : 9/30/2015 5:46:43 PM (GMT-6)

Posted 10/1/2015 1:40 AM (GMT 0)
Here I'll just re-do this.

That's such a good thought OM. I scanned it and had the very same thought.

At the same time maybe perhaps someone else's antibodies for whatever reason trigger an immune response against them - just like rejecting a Remicade antibody and ultimately causing a negative reaction in some. Something to consider perhaps.

In thinking it through a little further just now, in a way they are sort of measuring the same as above - They are giving FT and measuring the success by the change in the bacteria population and the immune reaction - and not looking at the possible change in dominant antibody class.

Post Edited (Canada Mark) : 9/30/2015 9:00:04 PM (GMT-6)

Posted 10/1/2015 1:46 AM (GMT 0)
Immunoglobulin coating of faecal bacteria in inflammatory bowel disease:
www.ncbi.nlm.nih.gov/pubmed/15201580

This one was interesting compared to controls.
"Long-term-remission IBD patients had normal IgG and IgM but increased IgA (50 +/- 16%) coating."

As for if any of these tests are truly accurate - I have zero clue.
Posted 10/1/2015 10:42 AM (GMT 0)
"The principal function of secretory IgA may not be to destroy antigen but to prevent passage of foreign substances into the circulatory system" - Fisher Scientific Company

This was a new thought or suggestion to me. Was never mentioned.

So essentially just "bung" things up so it's more difficult to pass through mucus and such, but not necessarily mark them for destruction by the immune system - or mark then for a light immune reaction. Wonder if they have looked into this idea much further.

However the really bad guys would most likely get the big guns pointed at them in a sense.

I was looking the weight up for the different classes because of that one study where they fluoresced sIgA in IBD patients compared to normals and found it was not throughout the mucus but concentrated at the outer layer.

Anyways this was an intriguing statement in relation to her theory.

Post Edited (Canada Mark) : 10/1/2015 4:48:30 AM (GMT-6)

Posted 10/1/2015 10:55 AM (GMT 0)
Here is another.

Seems to tie in with her thinking.  Also interesting that the response is not to bacteria surface proteins

but cytoplasmic for some reason the bacteria are leaking internal components =  danger.

OM

http://www.ncbi.nlm.nih.gov/pubmed/8675088

here is a more modern one

http://www.ncbi.nlm.nih.gov/pubmed/25171403

Post Edited (Old Mike) : 10/1/2015 5:03:46 AM (GMT-6)

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