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Posted 5/6/2015 10:30 PM (GMT 0)
Regarding teaching redox chem/biochem in school,

As a biochem student in the last few years, I personally was annoyed any time we went into redox biochemistry in class. It was a subject with lots of backwards terms so it was annoying to think about, and if I remember correctly, my friends thought similarly. I also taught intro chemistry labs and whenever redox chemistry came up, it was a subject students were not great at.

These are all people who are trying to get into medical school, so it would make sense to me that the disdain for redox biochem is an area that doctors could potentially be weak at.

We definitely learned about the electron transfer chain in our biochemistry classes, but it was more about the proper pathways, nothing about oxidative stress per se. It was touched on briefly, but more as "scientists believe that plays a factor in x,y, and z diseases". Didn't think it would be that way in medical school.

I could also find the explanation plausible when it comes to GI docs/researchers or immunology researchers. Couldn't see either group being particularly well versed in the intracacies of redox biochemistry beyond knowing how electrons are transferred in normal metabolism.

Regarding PHDs, MDs etc...yes, I definitely agree with the idea they can miss the forest for the trees and can lack common sense. No doubt all of them are smarter than me, but all are human and can be suggested to groupthink, confirmation bias, wanting to keep funding coming in for dead avenues of research, etc etc.

Personally, I think the biggest reason is that its so easy to ignore a single GI doc backing a theory out of left field when there is so much momentum and money behind microbiome, biologic, and immunologic research. Medicine is pretty conservative as it is, so a correct theory being 10 years old and relatively ignored means it has about 40 more years to be taken seriously, haha.

Also, that's really cool to hear that you are an industrial chemist, no wonder you have a great handle on this stuff. Have definitely learned a lot from you during my short time here on HW so far, OM!
Posted 5/6/2015 10:49 PM (GMT 0)
Thanks Tunnel:
I am retired so that is why I have the time to search all of this stuff out.
Still work 4 days a month,keeps my brain going,can see old friends at work and provides bowling money.
Actually was an aluminum lubricant chemist/management.
So anytime you fly,drink a can of beer, or coke,get into your car, wrap something in aluminum foil,
my hand is in somewhere in the finished product.
Better living through chemistry.

This is what happens when you get a Gilbert Chemistry Set before you can read.

http://en.wikipedia.org/wiki/Chemistry_set


Don't get me wrong, I applaud all the research docs/biochemists who have been trying to solve

UC for the past 100 plus years, but Pravda has finally put it together, IMO.

Without them we would have no data to form a picture.

I also believe that Pravda for some reason has missed the importance of the taurine chemistry,which

seems to me an integral part of the overall ROS quenching mechanism. Don't remember him discussing it.

Specifically, the MPO-Hydrogen Peroxide-Chloride/Bromide System.

You also have to understand one other thing.
My son lost his colon to UC,he is doing fine with a pouch.

I was, shall we say more than upset when he lost his colon.

I remember one day after the surgery I had to change his pad/diaper blood goo what ever was coming out.

Anyhow I thought to myself.

I changed you when you were a baby, and now doing it when you are 21.

Something is not right with this picture.
I have grandchildren,and two other kids who don't have IBD,even though they are in their 30's.
Therefore I am driven.
Old Mike

Post Edited (Old Mike) : 5/6/2015 5:35:33 PM (GMT-6)

Posted 5/6/2015 11:54 PM (GMT 0)
Part of the problem might simply be that students would really need to check the "immunology" box for course selection in their higher years before they would really get into it.


This probably does't help much but...

--------

In essence what happens is first the immune system has to encounter something it doesn't like. When it does the offending "item" (bacteria, fungi, virus, protozoa) is recognized by a receptor and this triggers the immune cell (phagocytes) to eat them (internalize). Then the immune cell (phagocyte) goes to work on the "item" in an internal compartment. The actual oxidative attack takes place in macrophages, neutrophils and dendritic cells specifically as far as I am aware. The clean up crew of the body.

It's the enzymes that the cells possess that ultimately govern the reaction and what is generated (what type of ROS) and isn't activated until something specific binds with it's (the phagocytes) receptor. The main "super duper killer" is superoxide ion O2- By adding enzymes to this reaction other ROS (reactive oxygen species) are produced like hydrogen peroxide and hypochlorus acid. Each phagocyte has it's own unique NADPH oxidase enzyme complex and it uses these enzymes to product the various ROS's. I think this is also highly dependant on what it encounters and what Pattern recognition receptors is triggered by the "item".

At the same time the immune cells (phagocytes) can also "release" ROS to kill external pathogens.

But in both cases one must first encounter someone intracellularly or extracellularly.... so there has to be a "bug" of sorts inside or outside....

-------

My personal take would be that that is in-line with the two studies he sent you. One is dealing with internal issues and one is dealing with external issues in a sense. So intracellular bacteria versus extra cellular bacteria - or virus etc etc.

Which then brings things back to well.... I don't know... It drives one mad.

But MAP, or even AIEC etc are good examples of intracullar bacteria that would trigger both ROS and the massive inflammatory response. Not sure what would trigger an extracellular response in UC though... other than of course an abundance of extra cellular bacteria - or even just a few of some type. Perhaps locking the colon into a permanent highly oxidative state.

Also MAP and AIEC screw with ROS and inflammation to promote uptake and subsequent infection. Not sure what would screw with extracellular ROS in UC though.

PS - obviously the fancy parts came from the immune text. Kuby Immunology.

Post Edited (Canada Mark) : 5/6/2015 5:57:34 PM (GMT-6)

Posted 5/7/2015 12:07 AM (GMT 0)
If the source of excess peroxide is from internal cellular process gone wonky and not due to an immune reaction per say to an "item". And the actual defect is "internal" within the colon epithelial cells then something has to "trigger" that defect.... or alter the process of butyrate oxidation.

It didn't happen to you until one day out of the blue I think... that's the frustrating thing.

So again MAP messes with this and perhaps has something to do with Crohn's... But what else does as well?

EDIT:

MAP

"Our results suggest that in MAP, reduced activity of leucine biosynthesis pathway leads to diminished levels of 2-oxoglutarate, acetyl-CoA, coenzyme A, NAD+, and NADH. These compounds are required to complete several steps in synthesis of mycolic acid and other fatty acids."


EDIT EDIT:

Maybe its a defect that isn't a major problem until something comes along and screws with it just that little bit more??? Past the tipping point.

The double whammy disease(s)

Why left sided colitis if the right side is also impaired?? I just jump to the double whammy thought.

Post Edited (Canada Mark) : 5/6/2015 6:43:56 PM (GMT-6)

Posted 5/7/2015 8:18 AM (GMT 0)

Yes Mark, MAP is always lurking in the back of my mind as a causative agent.

My history>

While in Korea 1971 had a case of the Korean craps for two weeks.

One day felt something tear, and burning sensation in rectum for about 3 days,back then I knew nothing about rectal abscesses, anyhow it went away and I thought no more about it.

Get back to the states 1972, big abscess/pus ball needed emergency surgery.

Healed, but then recurring, with fistula tracks.

Quit smoking 1977, new job lots of stress, moved into new house 1/4 mile from working dairy farm 1979,UC 1980,

still live in same house,dairy farm still there.

Old fart proctologist who used rigid scopes, I guess that is what they had back then, said he thought the proctitis

was due to all the abscesses. So for sure I have had a mucosal breach,and immune system exposed to lots of bacteria. My earlier history was, Eisenhower shook my hand when I was about 3 or so, he had Crohn's, this would have been around 1951. So I have a mechanical mucosal breach and live near a dairy farm.

But restarted smoking 1982 when meds/azulfadine was not working well, into remission.

Quit smoking again 1986, flared and still in same flare, still smoke.

My son get UC when he is 21, had to have colon ripped out.

So are we genetically predisposed, both have MAP from the dairy farm, or this crap is contagious.

Or all 3.

Old Mike


Post Edited (Old Mike) : 5/7/2015 2:28:44 AM (GMT-6)

Posted 5/7/2015 12:15 PM (GMT 0)
Will keep adding interesting stuff as I find it.

Bromine and basement membranes.

In the RIT paper the basement membranes are the first thing to go, in the UC induction phase.

Old Mike

https://www.sciencenews.org/article/bromine-found-be-essential-animal-life#

Posted 5/7/2015 12:17 PM (GMT 0)
I just meant anything really - and not necessarily MAP. Just like that pathologist said the other day:

"Autoimmune disease is basically a host response to an environmental agent(s), and this response is cross-react to the body's own tissue. It has a genetic element, but it is mostly acquired. EBV has been implicated in many conditions. As for Crohn's, MAP could be the pathogen, but it is clearly not the only player in pathogenesis."

So maybe there is something like a defect of mitochondrial acetoacetyl CoA thiolase in people with Ulcerative Colitis that is not a major problem really. Or has no immediate consequence. They are perhaps just fine until one day an injury and infection occurs and "something" is able to take advantage and manipulate this same pathway. Then the trouble starts.

So I was asking what else aside from MAP might be able to manipulate this pathway that has also been associated with uc?

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

On the plus side, at least you realized that antioxidant's really should yield some success. That might be pretty darn helpful to a lot of people on here.

Post Edited (Canada Mark) : 5/7/2015 6:22:29 AM (GMT-6)

Posted 5/7/2015 12:59 PM (GMT 0)
Well if UC is autoimmune, which I don't think it is, then.
The autoimmunity is probably downstream of the other events, such as a mucus breach,due to
weakened barrier function,resulting in the immune cascade.
OM


Have not looked at basement membranes much here is something on UC

http://www.ncbi.nlm.nih.gov/pubmed/10766090


more

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1770144/


something on rats and peroxide enema probably posted this earlier but now that I have

read if full, these rats don't heal well, it is not that they are not making enough new cells to repair the

ulcer, but the cells are being destroyed at a faster rate than new ones are made.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2072729/pdf/brjexppathol00408-0011.pdf


this one might go with the above for cell death.

http://www.medscape.com/viewarticle/819340_4


may have posted this one also diversion colitis oxidative stress, ties in with above I think

the longer it goes the more ROS the more starvation from lack of butyrate or SCFA.

http://www.jcol.org.br/pdfs/32_4/01.pdf


here is a NAC and oral mesalamine human trial again

seems like NAC might work locally

http://www.wjgnet.com/1007-9327/14/2851.asp


and here is what carrageenan does with leucocytes

http://www.ncbi.nlm.nih.gov/pubmed/3835323

Post Edited (Old Mike) : 5/8/2015 3:28:15 PM (GMT-6)

Posted 5/7/2015 5:35 PM (GMT 0)
My transit time has seemed to slow down a lot, as I can not feel an urge to go for about 5-6 hours now and when I do it's really easy to hold it in, but I think the slower transit time is not good to have before barrier integrity is fixed. I take it as both good and a bad sign. Good because I think it's a sign things are moving in the right direction, but bad because I think if slowing down occurs too much too soon, it would exacerbate the problem. Pravda states constipation exacerbates the disease, and it makes sense...greater exposure to luminal antigens for a longer period of time would stimulate an immune response in a broken mucus barrier.

I remember while I was in the hospital for pneumonia last November, the antibiotics they gave me made my stools firm and formed and my uveitis looked dreadful. The corners of my eyes were completely red, and it made no sense despite the better stools. Now I realize that the diarrhea is probably a protective response to limit exposure to antigens.

Been on the verge of constipation the last few days and my eyes went from being 85% clear to being mildly red all over again. Uveitis is a pretty good gauge for me about what is going on in my gut it seems like.

So I think refining my approach is warranted. I have been feeling a ton better since I've began supplementing all the vitamins I had been deficient in well over a year before I had UC symptoms at all. Never thought it would help, but now I know there are very plausible mechanisms at work here. Next, I think I'm going to supplement butyrate as I realized I don't get very much from my diet. Mark also said butyrate producing species are low in IBD, and my diet hasn't been sufficient in fiber since I was diagnosed so I think giving my colon the energy it needs to help rebuild and repair is a good idea. Pravda said in his patent that if energy deficient, epithelial cells will take away glutamine, which is a precursor to glutathione formation. Read butyrate will also reduce constipation and strengthen the barrier, which is what I'm thinking I need to do now.

Additionally, I'm thinking of adding ALA and some type of good quality whey supplement, as I don't think I'm getting enough protein or a wide variety of amino acids in my diet. Since I've been doing more and more outside of reading and writing about UC, I've been slacking on sufficiently feeding myself, plus my eating disorder history makes it plausible for me that I might not have the raw materials to build the proper antioxidant enzymes. Just an idea, probably couldn't hurt to add.

We'll see where things go from there before I try adding other things, but I think this will end up helping...hopefully give me that final push where the uveitis just disappears and my stools finally start to thicken.

EDIT: After much searching, i've determined whey is probably really good for raising glutathione levels, and it doesn't really matter too much what kind you buy. There is so much debate on denatured vs. undenatured but the digestive process breaks down all proteins, regardless of structure, into their individual amino acids and small peptides. Tons and tons of misinformation out there. Just gonna dive in and see, after all, the body just needs the raw materials (amino acids) to build whatever it needs.

Post Edited (Tunnelvisionary) : 5/7/2015 4:08:46 PM (GMT-6)

Posted 5/8/2015 6:47 PM (GMT 0)
I have not researched crohns much in terms of peroxides.

It is quite possible that both diseases are just a different phenotype of the same initial problem,namely

excess peroxides. Keep in mind that on enteral feeding crohns can go into remission, then when they start

a normal diet, it comes back. I can guess that perhaps serium lipid peroxides might be higher in crohns than

UC since they are absorbed in the small intestine, which is quite damaged with crohns.

I can also guess it might have something to due with the size difference if feet between the small intestine

and say distal colitis, what are we talking multiple feet vs like a foot of tissue.

Old Mike

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3801366/

dietary lipid peroxides interesting drink you red wine with high heat cooked meat

http://www.fasebj.org/content/22/1/41.long


Tunnel: This might be a good one to send to Pravds, see what he thinks is going on with UC and lower levels.


lipid peroxides in plasma actually seems worse for crohns than UC

looking at crohns and peroxides is providing some additional info

http://www.saudijgastro.com/article.asp?issn=1319-3767;year=2007;volume=13;issue=4;spage=187;epage=190;aulast=Alzoghaibi


another good one on crohns

http://www.biochemsoctrans.org/bst/039/1102/bst0391102.htm


just as an aside, a blog from another old chemist DMSO and melatonin

guess what, same theory

I also believe that Pravda might mention DMSO and or melatonin in on of his patents

http://krysalishealthnotes.blogspot.com/2011/03/proposed-biochemical-cause-and-remedies.html


riboflavin vitamin B2 needed for FAD as cofactor for glutathione reductase let alone MTHFR

http://breakingmuscle.com/nutrition/the-abcs-of-vitamins-vitamin-b2-riboflavin


I don't see how we can be deficient in B2 you don't need much and diet should provide easy access, but

look what it does to pigs.


LINK

 

Post Edited (Old Mike) : 5/10/2015 6:10:05 AM (GMT-6)

Posted 5/9/2015 12:02 AM (GMT 0)
I'll be sure to run it by him. He hasn't responded yet, but it seems he checks his emails every week or so.
Posted 5/9/2015 1:16 AM (GMT 0)
Maybe I should try adding vitamin C and vitamin E to my daily doses. So WOO 3x daily, Imuran daily, and a vitamin A,D,C & E. Se what that does for a few weeks. I cut back on Vitamin D a lot now that the sun is out. I recall reading that excessive vitamin D can be inflammatory - so I figured why not cut back some just in case during the summer.

Also had medium rare steak and a bad reaction yet again last night. Loose stool. Mild uncomfortableness approximately 12 hours after ingestion. Ground beef in the frying pan or meat loaf type thing always works great though. So something is up with medium rare/rare or just the BBQ factor perhaps. Excess peroxides as you suggest maybe.

I was going to write to the MAP guy and ask about MAP and peroxide (oxidation really). Was just trying tot think of the right question(s). MAP interference with acetoacetyl CoA and lipid metabolism was what I was thinking. See if he had any research experience/thoughts on this. Any ideas?
Posted 5/9/2015 4:51 AM (GMT 0)
I think I found what I was looking for tonight. I was becoming curious about this (excess peroxide) and this whole Radical Induction Theory in relation to Crohn's. And about the paper you posted in regards to not only excess peroxides but also in increase in inflammatory cytokines in Crohn's. And more so in relation to MAP as well. Also keep in mind MAP is tested for in the blood.

So circulating MAP would be a blood borne systemic infection. I think of this in relation to the paper you posted today.

So MAP possesses a gene for the production of catalase/peroxidase. These I believe are produced to disable peroxide. This is one of the ways they avoid destruction when residing 'inside' an immune cell or phagocyte. So this in a sense is more so "removing" peroxide.

While inside a cell MAP also utilizes the beta-oxidation pathway to oxidize fatty acids. They do this to provide a carbon source in order produce acetyl-CoA. Ultimately this provides them with an "energy" source for replication when inside a cell. So they steal from us to mature and reproduce.

But here is the interesting thing:

Once they mature and replicate inside a cell, either they trigger or the body triggers the cell to die (no one is sure which triggers it). They are released into either the blood or mucosa etc depending on where they are (or the location of the immune cell really) to begin to cycle again. Now the interesting part - Mycobacteria and as far as I understand mycobacterium avium subspecies paratuberculosis cell walls contain what is called lipoarabinomannan. Lipoarabinomannan does a few things 1) it enhances production of TNF-a. So the main inflammatory cytokine we're all familiar with. BUT what it also does is scavenge reactive oxygen intermediates............ Now, when the body is trying to deal with 'external' or extracellular pathogens as I mentioned in an earlier post - the immune cells start to pump out ROS (reactive oxygen species).

So my question is this: Because MAP cell walls not only enhance TNF-a but also scavenges reactive oxygen intermediates. Does this cause the immune cells to react by continually producing ROS and in turn excessive amounts of peroxide trying to rid the body of them?? And could this excessive amount of peroxide be the real damage doing in Crohn's disease as suggested by Dr. Pravada.

Alternatively could scavenging of reactive oxygen intermediates itself produce excessive peroxide simply by interfering with the chain reaction?

Also certain components of MAP trigger a TH2 response. Map Antigen. I forget what it is called specifically. MDS or something of that nature. So you have another dramatic increase in inflammatory cytokines in response when extracellularly. When MAP is intracellular you have more of a metabolic issue from their interference.

So I think I'd like to verify and ask some questions about this. Also I say 'inside us' but really this is just from studies on animal testing. Not humans. But I believe human isolated MAP have all these same characteristics.

Post Edited (Canada Mark) : 5/8/2015 11:00:36 PM (GMT-6)

Posted 5/9/2015 5:43 AM (GMT 0)
*** !!

OM - Did I read this wrong or misunderstand this ?????????????????

Identification of a secreted superoxide di****ase in Mycobacterium avium ssp. paratuberculosis (MAP): tinyurl.com/nfuf2k5

So if I am reading this correctly - aside from the above mentioned, MAP secretes superoxide di****ase.... an enzyme which in turn converts or mutates superoxide radicals (O2-) into hydrogen peroxide and molecular oxygen ???????

Tell me I misunderstand this one! I'm literally floored..............

And furthermore ONLY pathogenic strains do this???? Holy crap!

Post Edited (Canada Mark) : 5/8/2015 11:50:40 PM (GMT-6)

Posted 5/9/2015 6:20 AM (GMT 0)
I  get a forbidden error for that site.
But yes MAP secretes SOD, believe many bacteria use it as a defense mechansism.
Yes it seems the less virulent strains produce less SOD.

If supplement SOD I get worse, makes more peroxide.

On the subject of steak,try soaking it in red wine first,or try drinking red wine with the steak.

But I would tend to think that well done meat has more oxidized lipids if grilled at high heat.

So the rare meat makes you worse, I still have to go back to more foreign protein in raw meat,

where if cooked well done the protein is denatured and perhaps not immunogenic.

Pure speculation on my part.

Amazing where these threads can take you.


OM
http://www.ncbi.nlm.nih.gov/pubmed/8260663

this one covers a lot of ground perhaps the same one you found

http://vri.cz/docs/vetmed/49-5-161.pdf

Taucl will kill but it takes days taubr not sure

http://jac.oxfordjournals.org/content/65/3/399.full


Tunnel:Regardless of any conflicting info on RIT I might find, the proof perhaps is in the pudding.

Pravda's trial data had a 95% remission rate, which is unheard of.

Also in my above post in ulcers the cell death rate is faster than the replenishment rate.

Leading me to believe that excess ROS is killing the cells off too fast, and that is why ulcer healing is perhaps difficult.

Post Edited (Old Mike) : 5/9/2015 4:56:22 AM (GMT-6)

Posted 5/9/2015 11:50 AM (GMT 0)
Mark: Since you have crohns-colitis, here are a few more thoughts.

Crohns defective macrophage handling e coli

http://www.ncbi.nlm.nih.gov/pubmed/25809337

more

http://www.ncbi.nlm.nih.gov/pubmed/25805890

Here are some other thoughts which I copied from a post I made on the crohns forum,not healingwell.

This ties in with my research on taurine, which will protect macrophages from ROS but it will also protect the intercellular bacteria from being killed.
Arginine will make more NO from inos, is that what crohns people need.
I have UC arginine supplements make me worse.
A question might be, protect the macrophages in both diseases with taurine, to lower
inflammation, or not. In other words is the overwhelming inflammation
causing a problem with the macrophage clearance of bacteria, in crohns.
Vegetarians get little dietary taurine, would love to know if vegetarians get less crohns and more UC,when compared to just vegetarians,not the omnivore
population. See semi vegetarian diet and crohns.
So for UC take taurine for crohns arginine,perhaps.

With the rare meat that gives you problems, you are getting taurine, cooking to well done may lower it not sure on that, stewed meat probably has less.


http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3128366
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC303164/

semi vegetarian diet crohns
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2877178/[
old thread on this diet, hard to tell
http://www.crohnsforum.com/showthread.php?t=13170
Posted 5/11/2015 8:49 PM (GMT 0)
OM,

Had an idea about that 1995 study finding normal glutathione levels in UC patients and normal controls.

What if glutathione is upregulated in response to oxidative stress? You think upregulated peroxide production from the immune attack among other ROS species being created upregulates our normally low glutathione levels to normal levels but it is not enough to slow or stop the progressive damage?

A brief look at "oxidative stress upregulates glutathione" seems to yield some info. Haven't gone into much depth, but here's a study saying that that is exactly what happens: www.ncbi.nlm.nih.gov/pubmed/12441363

Exercise induced increase in oxidative stress seems to have a similar effect.

Maybe that study showed normal glutathione levels because our body was trying to produce as much as it could in response to the heightened peroxides/ROS species.

Just a thought. It would help explain the results of that study and combine it with the other evidence supporting RIT.
Posted 5/11/2015 10:34 PM (GMT 0)
Looks like we can find conflicting info.

OM

http://www.ncbi.nlm.nih.gov/pubmed/8582668

were you talking about this one

http://www.ncbi.nlm.nih.gov/pubmed/9590426

cant find much if any newer info there is of course info on mice,but human data is sparse

Posted 5/11/2015 10:40 PM (GMT 0)
Hmmm, interesting. Perhaps in the early stages of disease the body might upregulate glutathione and then in becomes depleted as active disease carries on, ROS load becomes too great, malnutrition becomes a factor, etc?

I was talking about the 1995 study where biopsies showed normal levels of glutathione but reduced levels of glutathione transferase that we discussed on the last page of this thread.
Posted 5/11/2015 10:59 PM (GMT 0)
It was this one.

Also notice that the myeloperoxidase is upregulated, while the glutathione transferase is low.

Also remember the neutrophiles come in once the mucus barrier is broken,then the myeloperoxidase will increase.

So this is a down stream part of the cascade some time after the induction phase I think.

There is a lot going on between the two phases,induction and propagation.

The colon is making every attempt to heal itself,but as we see it many times fails.

For instance if we are depleted in the amino acids that are used in core mucins, well it seems that

cytokines/other immune chemicals come first at the expense of mucins.

I think I have exhausted most of the studies I can find on the subject.

As far as I am concerned Pravda is correct, now we just need to implement some form of

supplements, perhaps ALA is enough don't know.

For me I am attempting it with no meds.

The question is if you slow down the destruction from ROS will you heal.

As we know one of the main mechanisms of healing with 5asa drugs is suppression of ROS, but it is

also biostatic.

If you quench immune cell bursts,wil the mucosa  bacteria be killed, will the biofilm grow as they do,

with immune suppressive drugs. Interestingly enough people go into remission with say Imuran, so

the immune cells are causing a lot of the damage.

OM

http://www.ncbi.nlm.nih.gov/pubmed/7787158

apheresis

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2981852/


Post Edited (Old Mike) : 5/11/2015 5:34:35 PM (GMT-6)

Posted 5/11/2015 11:31 PM (GMT 0)
Yes, lots of stuff going on. Just trying to make sense of the glutathione levels. Pravda has not responded to my second email, will try again in a week or two if no response. There is upregulation at least in the short term when oxidative stress comes into play, and who knows, maybe genetic differences and differences in case severity will lend to different levels of glutathione present at any given time.

Lots of other evidence makes sense and supports RIT and it's nice that there are studies that show reduced levels as well, but I'm just confused about the studies that show normal levels of GPx

---

Yeah, I'm tackling the problem from the point of view of reducing intracellular peroxide/increasing glutathione and healing the tight junctions and basement membrane as well. Added oral sodium butyrate last Friday and am noticing improvements, more solidity and like my colon is absorbing more water again. Still having an issue with constipation, but making improvements either way. It seems to be working but don't wanna say one way or the other until I know for sure.

I wouldn't recommend forgoing all meds until you know the inflammation has swelled down. I believe RIT would support the idea that meds can be very helpful to reduce the consequences of the propogation phase. Pravda even uses mesalamine and uceris for patients already having inflammation. Meds can only help here, I don't see any benefit in stopping them, I feel that would only further overwhelm the system.

So you've exhausted most of the glutathione/UC studies OM? That would be okay, as I still think a good chunk of evidence that supports RIT.

Post Edited (Tunnelvisionary) : 5/11/2015 5:37:05 PM (GMT-6)

Posted 5/12/2015 12:38 AM (GMT 0)
Tunnel I have not taken any meds since 1982, I don't go near GI docs, might kill me but, my choice.

Everyone should take their meds.

What I am trying to do is the no med remission, which has of course not worked for me since

1986, when I quit smoking again, my restart did not fix that flare of which I am still in.

And like most have boxes of supplements that did not work, I probably have more than most.

Yes butyrate is important, probably deficient in butyric acid produced by bacteria.

But we also need to fix the problem with beta oxidation of butyrate.

Think I have more on this somewhere in the thread.

http://www.ncbi.nlm.nih.gov/pubmed/21987487

ammonia and sulfides inhibit

http://www.ncbi.nlm.nih.gov/pubmed/23466063

here is my old 2012 beta oxidation inhibitor thread,but thought I has something newer in the current thread

https://www.healingwell.com/community/?f=38&m=2493840


Yes here it is took me a minute to find it,seems peroxides are the problem, this is why I post so many

studies in a thread, takes too long to find them again if they were not archived here.

It's the acetoacetyl CoA thiolase that is blocked by peroxides, so the butyrate cant be oxidized.

http://www.ncbi.nlm.nih.gov/pubmed/17483192


Seems to confirm what is going on with RIT.

We can question a lot of things but, low butyrate and impaired beta oxidation beyond dispute.

So far what might help.

R-ala, Se, taurine, butyrate, Vitamin B2, D,NAC,might need biotin if taking lots of ala. glutamine.

Possibly Bromine,through in some Mn for arginase perhaps,also Zn,curcumin,quercetin,rutin.


I did R-ala about 15 years ago, no help that I remember.

OM

 

Post Edited (Old Mike) : 5/11/2015 7:14:31 PM (GMT-6)

Posted 5/12/2015 1:25 AM (GMT 0)
Om you mention a 95% remission rate - where did you find this? Or more easily what is the treatment that was used?
Posted 5/12/2015 1:34 AM (GMT 0)
Personally, i'm doing a combination of finding out what will increase glutathione/reduce H2O2 inside the cell and what pravda is doing with his own patients. Beta oxidation is impaired but that doesn't mean butyrate metabolism is completely gone, so allowing myself to slowly increase butyrate supplements and perhaps supplement a little more than necessary might be a good course of action. That will free up colonocytes to use glutamate to create more glutathione instead, helping quell the peroxide concentration which should theoretically improve beta oxidation, according to Pravda.

As far as vitamins go, I feel that if you supplement one vitamin, you might as well supplement a little bit of everything (i.e. a multivitamin). They all work together and go hand in hand. I know Pravda is weary of some B vitamins, but again, they all have so many functions and all work together.

Regarding conventional drugs for UC, I would try to be open-minded about using them to induce remission, OM. I think they can be directly helpful to inducing remission under RIT. At this point, the whole system is overwhelmed with free radicals, reducing intracellular production or increasing glutathione is not likely to fix everything, but temporarily using these methods and conventional drugs might be enough to tip the balance. It's all up to you in the end, however. Those are just my 2 cents.

In any case, I'm just gonna continue this avenue of treatment. RIT gives an angle that can be worked with. If it works, then it works, if it doesn't then it doesn't. Just gonna see what happens. At the moment things are looking positive. Hope Pravda gets back to me soon, but for now, i'm just gonna focus on following his treatments/methodology and see where it takes me.
Posted 5/12/2015 10:22 AM (GMT 0)
OM, looking at your list of things that might/should help, I think there's something in it. (Also, I assume you've seen the Biotin MS study). Among the foods that I find the most effective for helping my symptoms are foods that are relatively high in butyrate and biotin--unpasturized cheese and butter, swiss chard, liver, shellfish. A few days of eating large quantities of the above foods and I usually have fully formed stools.

I think Tunnel has a point about taking a broader range of supplements. If they work in concert, taking only one at a time won't work.
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