kofi

In article
<09f5b6e5-e002-4b88-8e4d-2b3fa6ec279f@a17g2000prm.googlegroups.com>,


Chlorella and glutamine are helpful for "short bowel syndrome." That's
the condition you want to research. Zinc L-carnosine is a smart move -
since it works on the IGF-1 axis - but then so is pure growth hormone.
If your doctors haven't suggested growth hormone/IGF-1 or testosterone
(and you don't have a history of cancer) then fire them. They're
idiots. These things are standard treatments.

If you're going to use gh, you have to have adequate Vitamin D3 to make
it function optimally. D3 is vital for angiogenesis (cathelicidin -
blocked by glucocorticoids; see my post on anemia and HIF-1a) and
antimicrobial defense. Oral absorption and sometimes even depot shots
are notoriously mixed. I hate to say it but you might want to resort to
a UV lamp if pills and shots don't work. (Because you may already be
deficient in vitamin D3, the vitamin K idea may be extremely dangerous
since the two antagonize each other - although it's possible you might
be deficient in both K and D3.)

Butyrate and carnitine are vital for enteral nutrition. Since butyrate
is formed from the digestion of dietary fiber from gut bacteria, the
advice to avoid fiber will cause you to alter your GI tract native
bacteria. Taka can discuss the evils of fiber and omega-3 fats all he
wants but the truth is nobody knows what the effect of eliminating them
is on native gut bacteria and other aspects of your health. It's
possible the fiber may inhibit already low cholesterol absorption. If
so, then don't take, say, psyllium husk powder with your fats and
fat-soluble vitamins.

Let me just pause here a moment and say you probably don't know what's
really going on in your gut at all. Your best bet is to get one of
those broad-spectrum nutritional panels from a company like metabolic
maintenance and supplement whatever component in which you fall short.

The carnitine transporter in the gut - OCTN2 - can be upregulated by
PPARalpha agonists (olive oil), intermittent fasting, heavy exercise (at
least in the muscles and blood) and - I assume - anabolic steroids (the
later, of course, may give you prostate cancer and/or make your hair
fall out).

Treating anemia in a bowel problem is, well, problematic for reasons
I've outlined here before.

Alpha-ketoglutarate may be an LGR5 agonist/stanniocalcin mimetic and may
stimulate the stem cells that manufacture bowel. I'm still looking at
that which is why I haven't posted anything yet (picking stocks during
the market meltdown has kept me busy). You should research the part of
the bowel you're missing and see what stem cells it uses. LGR5 stem
cells are also responsible for hair growth so substances like ephrin A3
that regrow hair via stem cell stimulation may also work in certain
parts of the bowel. Hell, you might even be able to *use* cells in the
hair bulb to culture and inject into the ulcer site. No one's tried it
yet, but it's a logical hypothesis worthy of testing given other recent
research results.

It may be possible for you to try some sort of platelet-rich
prolotherapy or an autologous stem cell transplant back into your own
blood. Simply filter out your stem cells, expand them and inject them
back into your body. Somebody posted something on that to one of the
IBD groups a few years back. Again, a history of cancer would be a
concern in any regenerative effort. Trying PRP or Acell directly on the
ulcer might be brilliant (or disastrous). I'm not aware of anyone who's
ever tried it *or who would have the balls to* (and frankly, I have no
experience with ulcers; clearly you don't want to die from severe anemia
but too much iron will certainly aggravate your other problems).

Viagra or citrulline may improve blood flow. Do NOT try arginine as
that will oxidize your gut lining and turn on mTOR (which glutamine will
turn off).

Consider that you're now autoimmune for whatever reasons. Tregs are
trained in the gut. Try an allergy elimination diet if you have
symptoms of chronic inflammation (which is, frankly, dangerous for
someone with malnutrition). Gluten, casein, red meat and rice spring to
mind as chief suspects, as they are opioid ligands. Nightshades and
molds are suspect too. Also consider eliminating liver/other iron-rich
foods and turkey/other tryptophan-rich foods (IDO).

There's a guy who recently tried a gut bacteria transplant to treat his
intractable c diff infection. Might be worth a try with an ulcer.

Low-dose naltrexone may help.

Have you got neuropathy issues?

Your enterocolitis may have been caused by a virus that has yet to be
resolved. Various glucans from algae and fungi can modify your immune
reaction to that (as can gut bacteria which may have lived in the part
of your bowel that was removed). Furthermore, butyrate and carnitine
might be problematic. I won't rehash what I've said in the IBD groups
in the past. Run some titers for the herpes family. Cytomegalovirus is
a prime candidate.

You may have become vulnerable to those viruses because of metals
exposure or defective antibody response. The only thing to do about the
later is an antibody transplant (IVIG). That's expensive. The former
might result in molybdenum/selenium/zinc deficiency and other issues.
That will require a DMPS/DMSA challenge test.

Be very careful with generic antiinflammatories as you don't know what
infections you're fighting.

This is probably a monumental task you will want to peel like an onion
until you have an adequate resolution. I suggest you place the less
expensive solutions at the top of the queue.

I also suggest finding a doctor who knows all of the above - which is,
frankly, difficult. Medicine is not often practiced on the basis of
actual medical knowledge anymore. It's a cookbook engineering
discipline and most of the morons never get a new cookbook when they get
out of school (that would require some actual reading...).

I've got to go now. Capitalism is melting down (again).
<Sigh.>

Glad I cashed out two years ago...

George Bush can **** up anything, can't he? We should make him join the
Taliban when he leaves office. We'd win the war on terror overnight.

I sometimes think we should be grateful he went AWOL in Alabama. If
he'd actually shown up for duty, the whole damn state would probably be
speakin' Vietnamese to this day...

Which is fine by me, I suppose. I'm hardly a 'Bama fan...


http://www.eurekalert.org/pub releases/2008-10/wjog-ana101008.php

A new alternative in treating short bowel syndrome

SBS is a clinical condition characterized by diarrhea, dehydration,
electrolyte imbalance, malabsorption, and progressive malnutrition
related to a wide resection of the small intestine. The most important
the****utic objectives in the management of SBS are maintenance the
patient's calorie intake and nutritional status. However, some enteral
nutrition (EN) products use for energy supports in order to reduce
total parenteral nutrition (TPN) demand. The new treatment modalities
alternate the current ones are still under research with the
experimental and clinical studies. Chlorella is a species of green
algae that grows in fresh water. It has been consumed as a food source
for centuries in mainly Japan and other Far East countries, besides,
it's healing properties has enhanced it's consumption too. Several EN
products have been used for SBS.

A research article to be published on July 28, 2008 in the World
Journal of Gastroenterology addresses this question. The research team
was led by Mustafa Kerem from Gazi University Experimental Surgery
Center. In this original study, it has been seen that there's a
positive effect of chlorella crude extract (CCE) on intestinal
adaptation of rats which had undergone short bowel syndrome.
Administration of CCE lead significant increase in intestinal villi
height and villi width, intestinal protein and DNA amount, and serum
citruline levels which is a sign of improved intestinal absorption. As
being the first it's an important study. By this information algs
which are easily found widely in salt and fresh waters and can be
generated easily, can be used in clinical settings.

CCE has beneficial role in intestinal adaptation. It seems that it can
be an alternative to the other commercial enteral and parenteral
products.

###

Reference: Kerem M, Salman B, Pasaoglu H, Bedirli A, Alper M,
Katircioglu H, Atici T, Perçin EF, Ofluoglu E. Effects of microalgea
chlorella species crude extracts on intestinal adaptation in the
experimental short bowel syndrome. World J Gastroenterol 2008; 14(28):
4512-4517 http://www.wjgnet.com/1007-9327/14/4512.asp

olafur pall olafsson

Hi Kofi,

Thanks a lot for your comments. I am about to order more of the custom
whey protein blend I take, which has arginine in it. Given your
comment below I may pass on the arginine though. I need to look into
it more first before deciding. I will respond to the rest of your post
later.

I find it interesting that you recommend against arginine in this case
since I know glutamine inhibits mTOR and has been shown to be
beneficial for the gut while arginine in contrast can increase mTOR.
Do you have any direct evidence that arginine will oxidize my gut?

IIRC a lot of the glutamine ingested will end up being consumed by the
intestinal cells and thus will not show up in the blood. I haven't
looked into it specifically but I'd think supplemental arginine would
be almost completely absorbed in the intestine and thus would never
reach the colon and have a chance of exerting any systemic effects
there, positive or negative.

Some research suggests arginine may be beneficial for ulcer healing.
Here is a study on arginine's effect on ulcer healing in the stomach.
However as with so many things it may not be very useful for colonic
ulcers because, being easily absorbed, most of it will not reach the
colon.

Histol Histopathol. 2005 Apr;20(2):437-47.
Related Articles, Links
Click here to read
Administration of L-arginine reduces the delay of the healing
process caused by ibuprofen. Implication of COX and growth factors
expression.

Sánchez-Fidalgo S, Martín-Lacave I, Illanes M, Bruseghini L,
Esteras A, Motilva V.

Departament of Pharmacolgy, Faculty of Pharmacy, University of
Seville, Spain.

The objective of the present study has been to advance knowledge
of the gastric role played by the amino acid L-Arginine (L-Arg) in the
evolution of a chronic gastric ulcer. In order to clarify it, L-Arg
alone or together with Ibuprofen have been administrated in an
experimental acetic acid chronic ulcer, ****ysing characteristic
parameters of an active curative process, such as PGE2 production, COX
expression, and also angiogenesis, proliferation/apoptosis and growth
factors expression. Our results reveal that L-Arg is favourable in the
healing process improving the curative course. Ibuprofen caused a
delay in ulcer healing, more evident 14 days after ulcer induction;
COX-2 expression was increased at the 7th day although no signal of
protein could be detected after 14 days; PGE2 production was inhibited
in intact and ulcerated areas at both times assayed. In contrast,
treatment with L-Arg reduced the delay of the lesion, the increment in
COX-2 expression induced by Ibuprofen, and was able to maintain PGE2
levels similar to the control group after 14 days. Additionally, the
histological study showed that the healing effects of L-Arg might be
associated with an increased angiogenesis and FGF-2 expression. These
actions could be considered key factors in the healing response
associated with L-Arg administration. However, the proliferation study
assayed with the PCNA-immunostaining method did not reveal significant
differences, as the same as the apoptosis ****ysis. In conclusion, the
coupling of L-Arg to Ibuprofen is an attractive alternative to
Ibuprofen administration alone because it not only attenuates but also
improves the evolution of chronic lesions through mechanisms that
implicate endogenous PG and FGF-2-associated pathways, which allow an
increase of angiogenesis process.

Publication Types:

* Research Support, Non-U.S. Gov't


PMID: 15736048 [PubMed - indexed for MEDLINE]

news.chi.sbcglobal.net

Bananas and Plantains.
Saw a book called "The Food Pharmacy" by Jean Carper that says observant
Indians say unquestionably plantains contain some powerful medicinal stuff
that can heal the distressed cells of present ulcers and ward off the
appearance of new sores. Several noted researchers in India and Great
Britain have devoted years to pinning down the amazing biological changes
that plantain imposes in the stomach lining of animals. They conclude it
works the same way as an anti-ulcer drug carbenoxolone, but without that
drugs serious side effects.
New double blind studies in several medical centers in India find that
unripe plantain powder induces healing of duodenal ulcers in about seventy
percent of the patients. Go for the green. Unripe, green plantains are
the most potent against ulcers. And usually the larger the plantain, the
greater its protective effect.
Best of all against ulcers is the highly concentrated powder made from dried
unripe plantains.
I really know nothing about this, just some of what I read. Ask the
doctor or someone more knowledgeable than I would be. There is more to the
article, but too time consuming to write. Try to be certain that if
it doesn't help, it doesn't hurt. I know nothing of it.
Gail Michael

Hi Kofi,

Thanks a lot for your comments. I am about to order more of the custom
whey protein blend I take, which has arginine in it. Given your
comment below I may pass on the arginine though. I need to look into
it more first before deciding. I will respond to the rest of your post later.
On Nov 12, 2:54 pm, Kofi <k...@anon.un> wrote:

I find it interesting that you recommend against arginine in this case
since I know glutamine inhibits mTOR and has been shown to be
beneficial for the gut while arginine in contrast can increase mTOR.
Do you have any direct evidence that arginine will oxidize my gut?

IIRC a lot of the glutamine ingested will end up being consumed by the
intestinal cells and thus will not show up in the blood. I haven't
looked into it specifically but I'd think supplemental arginine would
be almost completely absorbed in the intestine and thus would never
reach the colon and have a chance of exerting any systemic effects
there, positive or negative.

Some research suggests arginine may be beneficial for ulcer healing.
Here is a study on arginine's effect on ulcer healing in the stomach.
However as with so many things it may not be very useful for colonic
ulcers because, being easily absorbed, most of it will not reach the
colon.

Histol Histopathol. 2005 Apr;20(2):437-47.
Related Articles, Links
Click here to read
Administration of L-arginine reduces the delay of the healing
process caused by ibuprofen. Implication of COX and growth factors
expression.

Sánchez-Fidalgo S, Martín-Lacave I, Illanes M, Bruseghini L,
Esteras A, Motilva V.

Departament of Pharmacolgy, Faculty of Pharmacy, University of
Seville, Spain.

The objective of the present study has been to advance knowledge
of the gastric role played by the amino acid L-Arginine (L-Arg) in the
evolution of a chronic gastric ulcer. In order to clarify it, L-Arg
alone or together with Ibuprofen have been administrated in an
experimental acetic acid chronic ulcer, ****ysing characteristic
parameters of an active curative process, such as PGE2 production, COX
expression, and also angiogenesis, proliferation/apoptosis and growth
factors expression. Our results reveal that L-Arg is favourable in the
healing process improving the curative course. Ibuprofen caused a
delay in ulcer healing, more evident 14 days after ulcer induction;
COX-2 expression was increased at the 7th day although no signal of
protein could be detected after 14 days; PGE2 production was inhibited
in intact and ulcerated areas at both times assayed. In contrast,
treatment with L-Arg reduced the delay of the lesion, the increment in
COX-2 expression induced by Ibuprofen, and was able to maintain PGE2
levels similar to the control group after 14 days. Additionally, the
histological study showed that the healing effects of L-Arg might be
associated with an increased angiogenesis and FGF-2 expression. These
actions could be considered key factors in the healing response
associated with L-Arg administration. However, the proliferation study
assayed with the PCNA-immunostaining method did not reveal significant
differences, as the same as the apoptosis ****ysis. In conclusion, the
coupling of L-Arg to Ibuprofen is an attractive alternative to
Ibuprofen administration alone because it not only attenuates but also
improves the evolution of chronic lesions through mechanisms that
implicate endogenous PG and FGF-2-associated pathways, which allow an
increase of angiogenesis process.

Publication Types:

* Research Support, Non-U.S. Gov't


PMID: 15736048 [PubMed - indexed for MEDLINE]

kofi

I can't find it, but I know it's true. The conversation I had with my
doctor revolved around arginase/ADMA. When I went home and looked on my
own, I stumbled on the mTOR stuff. I get sick from arginine (and even
pentofylline) but not citrulline - but then I've got several viruses I'm
fighting. (You might be too, by the way.)

Consider superoxide.

Inflammation => makes superoxide => makes eNOS oxidative by pumping out
OONO- instead of NO (which is where the folic acid/homocysteine comes
into play)

Stick arginine in the mix and you get OONO-.

Also, arginine will activate mTOR and inhibit TGF-beta - two signaling
pathways important to Treg function. TGF-beta is also important in
healing. Arginine enhances immune reactions by yanking the breaks on
the whole system - the Tregs. If your ulcer has a persistent infection,
you might want to do something similar to that but PRP would be much
better than arginine.

PGE2 is also necessary for Tregs, which is why taking a Cox-2 inhibitor
is going to block the resoolution of inflammation necessary for healing.
PGE1 is also necessary for mucosal healing which is why both Cox-1 and
Cox-2 inhibitors are contraindicated for ulcers - indeed they can
*cause* ulcers. Take a look at papers on zinc L-carnosine. In some
ways, it's the opposite of arginine. Don't outfox yourself taking
arginine. Just take growth hormone per se.

You cite a paper on arginine rescuing ulcer healing from Cox-2
inhibition. Well, they shouldn't have blocked Cox-2 in the first place.
Read the papers on zinc L-carnosine and PGE2.

Let me suggest something even more heretical: H Pylori may be in the
ulcer trying to kick start the healing process but something goes awry
and turns it into a pathological problem. We know now that H Pylori
helps activate regulatory T cells.

______________
Notes
______________

L-arginine can increase neuropathic pain and block the effects of
gabapentin through enhanced NO oxidation [PMID 12119449]

levels of arginine and tetrahydrobiopterin drop as part of the natural
aging process and as they do so, estrogen goes from being a nitric oxide
promoter to a superoxide promoter; blocking nitric oxide in general
turns estrogen into a vasoconstrictor; menopause may be an evolutionary
adaptation to lower estrogen levels in women to keep it from killing
her; drops in tetrahydrobiopterin parallel those in estrogen
<http://www.sciencedaily.com/releases/2005/02/050223131205.htm>; folic
acid not only reduces homocysteine but also enhances eNOS and helps
regenerate tetrahydrobiopterin, blocks O2- and increases the lifespan of
nitric oxide and increases the concentrations of omega-3 fats which also
enhance NO synthesis; vitamin C also increases intracellular BH(4) and
stabilizes it; insulin stimulates BH(4) synthesis and PUFA metabolism,
suppresses O2- and TNF-a; [PMID 12831960]; BH(4) is synthesized with the
aid of 5-methyltetrahydrofolate, magnesium, zinc and B12; BH4 levels
drop in hypertrophied hearts and eNOS turns dangerously oxidative and
fibrotic under these conditions
<http://www.sciencedaily.com/releases/2005/04/050426215140.htm>

homocysteine itself induces oxidative stress by uncoupling NO synthase
activity through reduction of BH(4) in human umbilical cord veins;
homocysteine dose-dependently inhibited thrombin-activated NO release
without affecting eNOS phosphorylation and independently of the
endogenous NOS inhibitor asymmetric dimethylarginine (ADMA); this
produced RNS/ROS independent of extracellular superoxide and this was
supressed by L-NAME, a NOS inhibitor; eNOS-dependent superoxide
synthesis was associated with reduced intracellular levels of both total
biopterins (-45%) and tetrahydrobiopterin (-80%) and increased release
of 7,8-dihydrobiopterin and biopterin in the extracellular medium
(+40%); also, homocysteine suppressed the activating effect of
sepiapterin on NO release but not that of ascorbate; oxidative stress
caused by homocysteine are due to eNOS decoupling from reduction of
BH(4) availability [PMID 15182855]; ADMA or homocysteine inhibited
population doublings of cultured endothelial cells and accelerated
senescence; co-incubation with arginine enhanced population doublings
and inhibited senescence-associated beta-galactosidase activity and
increased the activity of telomerase; it increased nitric oxide
generation, synthesis of NOS and generation of HO-1 while decreasing
oxidative stress; L-name blocked all the effects of l-arginine on ADMA-
or homocysteine-accelerated aging [PMID 16713997]; homocysteine triggers
oxidative stress and decreases nitric oxide by significantly elevating
iNOS, depressing eNOS (nNOS stayed the same) in microvascular
endothelial cells; Hcy elevated nitrotyrosine expression; Hcy caused
asymmetric dimethylarginine (ADMA) to ac***ulate partly because of
reduced dimethylarginine-dimethylaminohydrolase (DDAH); Hcy may also
activate protease-activated receptor 4, inducing production of ROS by
increasing NADPH oxidase and decreasing thioredoxin expression [PMID
16085680]; the primary metabolite of folate, 5-methyltetrahydrofolate,
is structually ****ogous to BH(4) and rescues the nitric oxide
vasorelaxation response from superoxide overproduction by restoring
normal NOS function; alone neither arginine nor BH(4) rescued
hypercholesterolemic mice from endothelial superoxide but together they
normalize it; this may explain which 5-10mg dosages of folic acid
improve endothelial dysfunction [PMID 15325022]; folate stimulates
endogenous BH(4) regeneration and increases the concentration of omega-3
fats which also enhances endothelial nitric oxide synthesis independent
of lowering homocysteine levels; Vitamin C also stimulate endothelial
NO; insulin stimulates BH(4) synthesis and PUFA metabolism, suppresses
TNF-a and O2- [PMID 12831960]

olafur pall olafsson

I think you erred a little above. Uncoupling of eNOS causes it to
synthesize more *superoxide* instead of NO. But I get your point that
arginine can be harmful under conditions where eNOS is uncoupled. Also
as you mention folic acid and homocysteine play a role here. As I
understand it homocysteine reduces the bioavailability of BH4. Since
BH4 is an essential cofactor for NO synthesis this leads to uncoupling
of eNOS which causes eNOS to produce superoxide rather than NO. Here
are my references for this for those interested: http://pmid.us/12841652
http://pmid.us/15182855 http://pmid.us/18724032

I do not see any good reason why I would suffer from low BH4 levels
causing uncoupled eNOS. I had a blood test in March this year at which
time I most certainly had the ulcer (it was discovered just a month
later with a colonoscopy). During that blood test my homocysteine
level came at rock bottom. It was 3,4mcmol/L which is extremely low.
My folic acid and B12 levels have also been measured twice here in
Iceland and were very high in both cases. In March the 4th my folate
level was >45,4 nmol/L on the scale of 6-35 nmol/L while my B12 level
was 804 pmol/L on the scale of 210-800pmol/L. And in October the 2nd
my folate level was 43,8 nmol/L and my B12 level was 706 pmol/L.
Clearly I do not appear to have low levels of the B vitamins, at least
not B12 and folate. And my homocysteine is excellent which is probably
attributed in most part to the fact that I do take a lot of
supplements that lower it. These include B6, B12, B2, folate,
creatine, lecithin, choline bitartrate and TMG.

In light of this information I doubt I have a problem with uncoupled
eNOS. And I have not noticed any negative effects from taking arginine
that would indicate so. However I may just stop taking arginine for a
couple of months in case it makes a difference, particularly because
it may have negative effects through mTOR and TGF-beta as you state below.


I haven't looked into TGF-beta before. Looking into TGF-beta and
healing I found this abstract http://pmid.us/16628336 . It's a review
abstract on it's role in wound healing. Here is a quote from the
discussion section of the full text:

"From a discussion of the effects TGF-3 has on monocytes, fibroblasts,
endothelial cells, and keratinocytes, one can
clearly identify that this growth factor has pivotal roles in each
phase of wound healing. In the inflammatory phase, it is necessary for
proper chemoattraction of monocytes. In the proliferative phase, it
stimulates ECM production and impacts angiogenesis and
epithelialization. Finally, it induces the formation of myofibroblasts
for wound contraction in the maturational phase."


Well I stopped taking my daily dose of aspirin (80mg daily) as soon as
I found out I had an ulcer. I am not taking any supplements or drugs
that have strong Cox-2 inhibitory effects. Some of the supplements I'm
taking may have weak COX-2 inhibitory effects though.

Your last comments fit exactly with this quote from http://pmid.us/18467372
:

"Together our data suggest that H. pylori induces a regulatory T cell
response, possibly contributing to its peaceful coexistence with the
human host, and that ulcers occur when this regulatory response is
inadequate."

BTW do you have any oppinion on glutamine for ulcer healing? It has
been shown to inhibit mTOR and to be beneficial for the intestines,
but I have not come across any direct evidence indicating it may help
the healing of ulcers in the colon. I do get glutamine from the diet
of course but am considering adding supplemental glutamine also.

kofi

BH4 per se has become useful as an antioxidant. The only problem is
that it increases dopamine and serotonin synthesis too. Long term use
may bring Parkinson's risk and it's not a good idea to mix it with
chronic pain problems for this reason.


Well, there you go. I didn't know that. (Too much B vitamins, by the
way, doesn't always mix well with a candidiasis problem.)

Creatine is useful via IGF-1, by the way. I had trouble with almost
every kind of creatine for some reason except kre-alkalyn, which is
specially buffered to survive digestion. Vitamin D3 is also helpful in
conjunction with IGF-1.


TGF-3 is NOT the same. In some ways, it's the opposite. I'm talking
about TGF-beta1 or -beta2. TGF-beta3 is completely different - and,
frankly, only really expressed in newborns.

There can be times when inhibiting TGF-beta1 or -beta2 can accelerate
wound closure in the skin. However, gut healing is different. I'm
unaware what a literature search on ulcers and TGF-beta inhibition would
show. I'm just warning you about it.

Both glutamine and butyrate are excellent for damaged epithelia, whether
burned skin or damaged gut. You should run a search against them with
ulcers to check. There might be something you can do with probiotics
but I don't know which strain will help and this problem is poorly
studied.

olafur pall olafsson

I take 3g of creatine daily and have been doing so for a long time.
Most of it will never make it to the colon though since creatine
monohydrate is absorbed very well. But with respect to getting more of
it to the colon intact, taking a higher dose might help of course. As
the full text of http://pmid.us/12793840 states:

"there is some evidence that faecal excretion of creatine is increased
with a higher creatine intake.[69]"

Also taking all the creatine in one large daily dose should logically
increase the chances that some of it will not be absorbed and will
reach the colon intact. So I may try adding some creatine, taking it
all at one dose.

Sorry, it was supposed to read TGF-beta not TGF-3. When I copied it
from the full text article, which was in pdf. form, the Greek
character Beta was replaced by the number 3 because html doesn't recognize Greek characters.

I've searched the literature on glutamine and ulcers but didn't find
much at all. Glutamine can enhance heat shock proteins. It has been
shown to increase HSP70. This is interesting since zinc can also
increase HSP70 http://pmid.us/15501017 as can zinc l-carnosine
12498304 . Activation of heat shock proteins appears to be one of the
methods by which zinc l-carnosine protects against ulcers http://pmid.us/6949620
.. So theorotically glutamine may be synergistic with zinc l-carnosine
with respect to the healing of ulcers, that is if it reaches the colon
intact. Most of it of course will likely be either absorbed to the
blood or consumed by the intestinal cells before reaching the colon. I
think I will try taking some glutamine even though I didn't find any
data on glutamine and ulcers, it probably won't hurt to try.

With respect to butyrate, I suppose my fiber rich diet should provide
plenty of butyrate from carbohydrate fermentation.

kofi

Try the kre-alkalyn.

The location of the ulcer makes me think that an I.V. or a direct PRP
injection might be the only sure way to target it. You might also reach
it through an enema.


I wouldn't make that assumption. Inflammatory insults tend to knock out
carnitine/butyrate uptake in the gut.

Have you ruled out the cytomegalovirus?

in colonocytes in a rat model of IBD induced by trinitrobenzene sulfonic
acid (TNBS), expression of carnitine transporters Octn2 and Atb0+
(required for beta-oxidation of butyrate; ATB0+ is also the glutamine
transporter which might explain the benefits of glutamine for bowel
disorders) decreased in inflammatory samples at translational and
functional level; butyrate oxidation, evaluated based on CO2 production
and acetyl-coenzyme A synthesis, was deranged in colonocytes from
TNBS-treated rats; treatment with carnitine-loaded liposomes corrected
the butyrate metabolic alterations in vitro and reduced the severity of
colitis in vivo; suggesting that carnitine depletion in colonocytes is
associated with the inability of mitochondria to maintain normal
butyrate beta-oxidation; carnitine is a rate-limiting factor for the
maintenance of physiological butyrate oxidation in colonic cells,
perhaps explaining the contradictory the****utic efficacy of butyrate
supplementation observed in clinical trials of IBD [PMID 17065219]
(liposomes are specially designed to penetrate cells and deliver their
payloads so simply taking powdered L-carnitine is not a guarantee of
effective delivery, especially if normal cellular transporters are
knocked out; I wonder if carnitine could potentiate the actions of
similar compounds like the HDAC inhibition of sodium butyrate, e.g.
beta-hydroxybutyrate¹s actions in seizure control or HMB for muscle loss)

LPS suppresses PPARalpha in the rat liver (so perhaps it suppresses
carnitine uptake in the gut via PPARalpha¹s effect on OCTN2) [PMID
18085354]

butyrate has anti-inflammatory properties in experimental colitis and on
Crohn¹s disease lamina propria mononuclear cells in vitro; of 13
patients with mild-to-moderate ileocolonic Crohn¹s, 4g daily butyrate in
enteric-coated capsules for eight weeks, caused remission in 7 patients
and partial recovery in 2 (one dropped out; three had no effect);
endoscopical and histological scores significantly improved; leucocyte
blood counts, erythrocyte sedimentation rates and mucosal levels of
NF-kappaB (NFKB) and IL-1beta dropped dramatically after treatment; oral
butyrate was well tolerated [PMID 16225487]

Creatine came up a lot in this discussion. Isn't is supposed to cause
kidney damage in long term use?

kofi

In article
<29a1f93c-5138-456e-ab8b-92f53e47d882@s1g2000prg.googlegroups.com>,

It has been linked [PMID 17046619, 16260971] - however I'm not
suggesting taking unbuffered creatine or anything near 21g/day.