Larry Smarr

[Karma]

Highlandsrock has already mentioned this guy in relation to calprotectin testing.

It's really worth watching his video on his website - I can't post it here because I've not posted enough. 'Calit2 tedmed 2013' will find it.

Basically he has colonic crohn's and has used sequencing and data mining to diagnose his disease. He then had stools sequenced and bacterial populations analysed. Very interesting results. E. coli, lots of other nasties at very high levels and more normal species decimated. He describes it as a great extinction rather than a disbiosis.

He then had Pred and antibiotic to thin out some of the monsters...

 

[wild_one353]

this guy IS AWESOME!!!

here is a link http://lsmarr.calit2.net/multimedia?vid=2EMzInPwDDQ

whats funny is i realized that we needed a new term to differentiate from dysbiosis to describe what is happening in microbiome research as far as IBD FLORA. the term, MASS EXTINCTION would be along those lines, thus far i haven't come across anyone coining a different term from dysbiosis until now.

this is why fecal transplants can restore these bacteria and likely cure these diseases. http://www.crohnsforum.com/showthread.php?t=52400

 

[sir.clausin]

This blew my mind, abscense of a lot of different strains of bacteria!!! Never seen it in black and White like this Before. So we don´t know exactly what bacteria a,b,c etc. does, but if we fill up on those missing, that would certainly improve / cure ibd.

Thanks so much for posting this, gives me hope.

 

[wild_one353]

This blew my mind, abscense of a lot of different strains of bacteria!!! Never seen it in black and White like this Before. So we don´t know exactly what bacteria a,b,c etc. does, but if we fill up on those missing, that would certainly improve / cure ibd.

Thanks so much for posting this, gives me hope.

this is only the second time ive seen someone attempt to measure the quantity of pathogens when compared to a healthy gut, but first time ive seen them carefully broken down into different species. we have previously known there are many pathogens and some good bacteria missing though,so that is not very new information, but good to reproduce this knowledge to solidify it as a indisputable scientific fact.

 

[mf15]

Interesting for sure,I wonder what mucosal testing would have shown.,stool of course
is much easier,but perhaps does not show the whole picture,or it may not matter.
I also might suspect that after the initial event,the immune system is killing off most of the good bugs, or some combination of the immune system and perhaps ingested toxins,
from modern diet,toothpaste, chlorinated water, or a million other xenobiotics.
What this also shows it would seem and it is good news, from the
graph at 7 minutes 40 seconds is that even though many species are mostly gone they are not totally dead. That gives me hope that somehow they can be brought back in larger numbers and shift the populations back to normal.
Old Mike

 

[Malgrave]

Extremely interesting! Thanks a lot for sharing!

 

[highlandsrock]

I'm amazed I'd never heard of Larry Smarr before. Will check out his websie. It was only the BBC documentary on self monitoring that brought him to my attention. The link to the iPlayer version is here (UK only as far as I know)

http://www.bbc.co.uk/iplayer/episode/b038p1pm/Horizon_20132014_Monitor_Me/

It inspired to start writing a post on my blog about self monitoring and has raised even more questions that I need to work through. Here's that link

http://www.crohnoid.com/2013/08/self-monitoring.html

 

[kiny]

I don't really agree with much of what he says, some things are wrong too. I think there is a lot of confusion and misinformation out there and he's just adding to it. The minute he calls crohn's disease an autoimmune disease he's off on the wrong foot, autoimmune requires an identifiable autoantigen, which to this day has never been shown in crohn's disease...and I disagree with his dysbiosis theory too.

I mentioned my support for people who don't jump to conclusions in the past, most studies don't simply "assume" that dysbiosis is causative since it's seen in plenty of other intestinal diseases, including intestinal TB. You can make lots of pretty graphs that show dysbiosis in other diseases too, but luckily for those sufferers, people don't assume that it's causative.

Instead of just showing the studies that show dysbiosis in CD or in his own body, he should show the ones where dysbiosis is present in countless other diseases, how any form of intestinal inflammation results in dysbiosis, how F Prau is actually found more in children with CD instead of less like in adults, pulling the rug out of the idea that it's causative. Nor does dysbiosis explain fistulae or the transmural inflammation so close to the mesentery. Nor does it explain why the peyer's patches would be involved. Nor does it explain why there is inflammation in other organs sometimes. Nor does it explain the aphthae (sp?) or "mouth ulcers" in crohn's disease that many of us are familiar with.

I also disagree with the idea of "firing" doctors just because they're not on board with your dysbiosis or other theories, many GI are just there to treat their patient the best they can, they're not there to agree with everything you say, he's not a doctor himself. He just discovered what CRP means and he's already firing doctors that aren't on board with him. Good luck with that approach.

Thanks for the link, I just disagree with him, most of his talk were assumptions, and I don't think we should spend another $10 billion on researching the microbiome before we know it's actually related to crohn's disease. So far it hasn't helped anyone.

 

[hugh]

I don't really agree with much of what he says, some things are wrong too. I think there is a lot of confusion and misinformation out there and he's just adding to it. The minute he calls crohn's disease an autoimmune disease he's off on the wrong foot, autoimmune requires an identifiable autoantigen, which to this day has never been shown in crohn's disease

Personally, I don't care if crohns is an autoimmune disease of which we have not yet identified the 'identifiable autoantigen' or if 'Crohn’s disease may reflect a breakdown in the normal immuno-suppression of gut immune cells, which then get out of control and react strongly to the gut flora. This, in turn, leads to a very severe inflammatory response with pathological consequences for the integrity of intestinal tissues.'
You might know something we don't, that this debate has been finally settled, but your assumption in favour of the most recent theory does not automatically invalidate anybody who still refers to it as an autoimmune disease just because they haven't kept up with the journal that you read.
In other words I am aware that one (possibly more likely) 'theory' is replacing another 'theory' , but that isn't even relevant to this guys talk,

I mentioned my support for people who don't jump to conclusions in the past, most studies don't simply "assume" that dysbiosis is causative since it's seen in plenty of other intestinal diseases, including intestinal TB. You can make lots of pretty graphs that show dysbiosis in other diseases too, but luckily for those sufferers, people don't assume that it's causative.

The graphs show correlation and I don't think he talks about causation. The talk was more about the medical profession's lack of interest in the science that in now available

Instead of just showing the studies that show dysbiosis in CD or in his own body, he should show the ones where dysbiosis is present in countless other diseases, how any form of intestinal inflammation results in dysbiosis,

Why should he show anything, It was a TedMed talk about the possibility of quantifying his own health, in which he uses himself to demonstrate some methods he has available to monitor his own health and symptoms.

Nor does dysbiosis explain fistulae or the transmural inflammation so close to the mesentery. Nor does it explain why the peyer's patches would be involved. Nor does it explain why there is inflammation in other organs sometimes. Nor does it explain the (sp?) or "mouth ulcers" in crohn's disease that many of us are familiar with.

That's not the talk he was giving.
I think that an imbalance or illness may promote other manifestations through mechanisms that we may not yet understand. Just because I haven't seen the link doesn't mean that it doesn't exist. Nor does it strengthen your arguement

I also disagree with the idea of "firing" doctors just because they're not on board with your dysbiosis or other theories, many GI are just there to treat their patient the best they can, they're not there to agree with everything you say, he's not a doctor himself. He just discovered what CRP means and he's already firing doctors that aren't on board with him. Good luck with that approach

Good on him, i'm sure he will do better than most with the resources and intelligence at his disposal.

Thanks for the link, I just disagree with him, most of his talk were assumptions, and I don't think we should spend another $10 billion on researching the microbiome before we know it's actually related to crohn's disease. So far it hasn't helped anyone.

Most of everything is assumption, and we keep using them until we disprove them (or improve them) because they are useful tools. That's called science. If you want absolutes then you should switch to maths

So we can only spend the money if we know it's gonna work? You don't understand science, do you?

The money is being spent, it is the hot new thing and being touted as the cure for everything, so I like your scepticism.
I too am sure that the microbiome will be overhyped, but I disagree about the extent of overhyping...

 

[rollinstone]

personally I am just glad people are pursuing more answers.

 

[Karma]

Kiny: I agree that correlation is not causation. However: it does provide a good fit for why EN works, yet often relapses quickly. Doesn't it also fit with the SSI company's working hypothesis?

I think he fired (changed GI) because they weren't receptive to stool testing. Lactoferrin seems to be a pretty good marker for intestinal inflammation AFAIK. I'm sure lots of us have wanted to switch from a GI who doesn't seem interested in different approaches!

 

[kiny]

Yes.

I don't know if EN works. They put it up against steroids and the group consisted of people with <150 CDAI scores. The likelyhood that they would have gone into remisison with or without EN is high when you start off with a very low CDAI score.

*IF* EN actually helps, there is more than one way suggested:

-one of them is that it acts on the intestinal flora like you said
-another is that it corrects nutritional deficiencies
-another is that it is low in microparticles
-another is that it uses medium chain triglycerides, which would avoid interaction with lymphatics

They don't know if it works, and if it works, they don't know why.


"SCD cured me"
"Fecal transplants cured me"
"probiotics cured me"
"EN cured me"

People read it, they try it, and a few months later they end up in ER.

EN is made to help people get the calories they need, it's not a treatment for crohn's disease.

I understand the position many GI are in now, we complain they don't give diet advice, probiotic advice, they didn't do this, they didn't do that .. they use what they know works, they don't want to experiment with things that aren't confirmed in the literature.

There's a lot of tests that aren't reliable, ASCA is one of them, many doctors won't do them. You can fire them, but they don't do them because they many have reasons not to. They're not bad doctors, they're often good doctors that don't want to risk the health of their patient.

 

[Karma]

I was under the impression that there have been a number of studies testing EN against placebo and some against steroids.

Isn't EN used as primary therapy for children in many hospitals?

Anyway, we're straying a little OT perhaps

 

[kiny]

Isn't EN used as primary therapy for children in many hospitals?

EN and TPN is used here to correct nutritional deficiencies, it's not used to control inflammation. You use pentasa, steroids or imuran for that.

EN might help someone with a very low CDAI score or someone who is already in remission. You can't give someone who is flaring EN and hope for the best, you give them anti-inflammatories.

 

[kiny]

I was under the impression that there have been a number of studies testing EN against placebo and some against steroids.

Yes, with very low CDAI scores, if the CDAI scores are low enough you can prove ketchup helps crohn's disease too.

I'm not saying EN might not help, but you should take studies that only rely on CDAI scores and use low scores and associate a drop in CDAI with clinical remission without doing a colonoscopy with a grain of salt.

Not all of those EN studies are reliable.

Many studies claimed for years that that acne medicine was related to crohn's disease, until there was a big study that showed there was no correlation at all.

 

[wild_one353]

i just wanted to say that there may be some confusion between what a theory and a fact is. the detection, identification and measurement of bacteria of the gi flora in IBD and normal healthy people would be considered objective facts. trying explain why these facts are the way they are and how they might be involved in disease is a theory.

this guy has some theories but he also has some facts. the fact that there is an imbalance of healthy bacteria from normal healthy people is a fact, not a theory. to say that this is either the cause or the result of the inflammation is a theory until some experiment/observations/fact might provide evidence to support, dispute or absolutely prove the theory correct or incorrect.

dysbiosis as i recall is a term to describe some imbalance of normal flora.
he coins a new term to describe a slightly different concept of bacteria that are no longer existent, rather then simply imbalanced, this term was mass extinction. in this case he created a new concept, not a new theory.


also, there have been experiments that tried to determine whether bacterial extinction remains after the inflammation is controlled and remission is induced, some abnormalitys correct themselves after remission and some abnormalitys remain after remission, suggesting again, dysbiosis/mass extinction could be a cause of disease state as full normalization of flora does not happen when inflammation is normalized.

i also realize there are tons of experiments, in rats/mice etc, that show dysbiosis/extinction after inflammation and as a result of inflammation and pathogen introduction which suggests the inflammation can be enough to change the flora, rather then the flora changes initiating the inflammation. these observation seem to contradict that flora abnormalitys came before diseases onset, but these are under experimental conditions and only animal models of diseases state, which may or may not accurately represent what happens in a human or in IBD.

then there is evidence that suggest certain bacteria regulate inflammation, which supports that extinction of certain bacteria brings on inflammation of the gut. i believe the only way to answer the question of whether dysbiosis/extinction can correct the disease state is to perform Fecal Transplants in people with ibd, and that's exactly what they are doing right now, and have already done years ago, and some appear to be cured.

 

[mf15]

Once you loose bacterial diversity it would seem to me that this is part of
the mechanism driving continued inflammation.
Old Mike
http://www.ncbi.nlm.nih.gov/pubmed/21937990