Crohns and uc

February 22, 2012

Thanks everyone for the info on my crohns and uc email. Noel, others, have you ever tried LDN with any luck?Cheers,-- Sent from my Palm Pre

February 23, 2012

No,LDN is my last resort before going under the knife. I hope I don't reach to that stage but with this disorder and difficulty in finding nutritious food at reasonable price in this country, you never know where you will end up in future. I have decided that I will never take Remicade or Humira or similar immuno-modulators, so this is the only one I am left with before the surgery.

Plus, hardly any Gastroenterologists is really keen on prescribing it. It needs to be compounded and the dosing is pretty tricky.Hope this answers your question.

Noel

Thanks everyone for the info on my crohns and uc email. Noel, others, have you ever tried LDN with any luck?Cheers,

-- Sent from my Palm Pre

February 23, 2012

Noel,

You might be interested in checking out the BodyEcology website.

-Tammy

Sent from my Kindle Fire

February 23, 2012

Noel am sure u ve looked at gaps.me or even bought the book??? It sound like it would help u.. And uo little boy Sent from my iPod

No,LDN is my last resort before going under the knife. I hope I don't reach to that stage but with this disorder and difficulty in finding nutritious food at reasonable price in this country, you never know where you will end up in future. I have decided that I will never take Remicade or Humira or similar immuno-modulators, so this is the only one I am left with before the surgery.

Plus, hardly any Gastroenterologists is really keen on prescribing it. It needs to be compounded and the dosing is pretty tricky.Hope this answers your question.

Noel

Thanks everyone for the info on my crohns and uc email. Noel, others, have you ever tried LDN with any luck?Cheers,

-- Sent from my Palm Pre

February 23, 2012

@ Tammy,Are you talking about

http://bodyecology.com/ I have not but will look into it.@ ,Didn't get which book you are talking about. Could you please post Amazon link?

With the diet, I gave up on alcohol (I used to drink occasionally anyways), turned completely vegetarian and eat almost everything in moderation. For a period of 3 years, I did a lot of testing with food but none of the foods turned out to be the triggers for my ulcerative colitis or migraine. Actually, my UC is pretty much under control with the meds and lifestyle I have, its the migraine that wreaks havoc twice a month. Thats where the original reply came from as NSAID work well for my migraine but I had to use it for much for 3 years that it gives me serious reaction now.

Thankfully, DS doesn't have any gut issues and I am seriously hoping that he doesn't get one.Noel

Noel am sure u ve looked at gaps.me or even bought the book??? It sound like it would help u.. And uo little boy Sent from my iPod

No,LDN is my last resort before going under the knife. I hope I don't reach to that stage but with this disorder and difficulty in finding nutritious food at reasonable price in this country, you never know where you will end up in future. I have decided that I will never take Remicade or Humira or similar immuno-modulators, so this is the only one I am left with before the surgery.

Plus, hardly any Gastroenterologists is really keen on prescribing it. It needs to be compounded and the dosing is pretty tricky.Hope this answers your question.

Noel

Thanks everyone for the info on my crohns and uc email. Noel, others, have you ever tried LDN with any luck?Cheers,

-- Sent from my Palm Pre

February 23, 2012

Yep! That's the one. : ) Click around. Donna Gates has been at it a long time and really knows her stuff.

-Tammy

Sent from my Kindle Fire

February 23, 2012

Compounding LDN is not tricky at all. Any compounding pharmacy can do it and coastal happily gives the formula away to any pharmacy that asks if they don't have it.BUT you don't actually have to have it compounded. We tend to have it compounded because it's dosed at night and our kids are usually in bed by then. Adults can take a 5mg pill and be done with it.My son didn't have gut issues so I can't make any claims on how LDN did there. But LDN was good in this house. Not a wow, but still very good. Insurance covers it, too. We had ours compounded by a local compounder and they compounded it in regular hypoallergenic base but then I asked for them to do the emu oil and they had no problem with it.

~ Antiviral Therapy 101~~ Make a biomed book ~~ gryffinstail.wordpress.com ~~ @Gryffins_Tail ~

No,LDN is my last resort before going under the knife. I hope I don't reach to that stage but with this disorder and difficulty in finding nutritious food at reasonable price in this country, you never know where you will end up in future. I have decided that I will never take Remicade or Humira or similar immuno-modulators, so this is the only one I am left with before the surgery.

Plus, hardly any Gastroenterologists is really keen on prescribing it. It needs to be compounded and the dosing is pretty tricky.Hope this answers your question.

Noel

Thanks everyone for the info on my crohns and uc email. Noel, others, have you ever tried LDN with any luck?Cheers,

-- Sent from my Palm Pre

February 23, 2012

Noel,

I doubt your gastroenterologist has talked to you about this, but there actually

is a strong association between oxalate and Crohns disease. Some of the reasons

for that association have only been discovered in the last three years, and are

still probably sequestered in the " ivory tower " and not changing the way

gastroenterologists think about this disease.

If you do a search on Crohns and oxalate in pubmed, you will find 72 articles

coming up, so this is a strong association, but if you start reading the

articles, you will quickly get the impression that the lines of causality are

thought in this way:

Crohn's ----> high oxalate absorption in gut ---> renal problems

Gastroenterologists have heard from the renal people that there is no reason to

warn those with Crohns about the dangers of high oxalate food until they have

already developed renal problems. This would be like telling people not to

reduce cholesterol until they need vascular surgery to correct the clogged

arteries. That makes no sense!

This is the key reason when I was talking with the Polish team that designed the

first study of oxalate issues in autism, we knew that a PRIMARY issue to address

was the myth that people don't have oxalate issues until they have renal

problems. Our study showed that NONE of the kids in our study had renal issues,

and they also were missing key risk factors that would have been the only things

to raise suspicions, but those children with obvious risks were elminated from

the study so we only studied those whose doctor's would have thought couldn't

possibly have an oxalate issue. Not only were these children high in blood or

urine or both in oxalate, but some got into lofty territory that is only seen in

the genetic hyperoxalurias, that are as rare as one in a million persons.

So, it will not be a gastroenterologist who will begin to ask if there is any

chance the arrows might work back the other direction, that the oxalate that

gets high in Crohn's may happen before the disease shows up, and that the

oxalate problem may drive the GI disorder. He won't ask, because he has been

taught not to ask that question.

You may be aware that Trying_Low_Oxalates was set up to help anybody who wanted

to reduce oxalate, so we do get people with other risk groups known associated

with oxalate. That has included people with cystic fibrosis. The thinking there

was that the antibiotics given in treatment were the setup for developing

oxalate problems, but then scientific work in the last few years showed that the

cystic fibrosis transporter (that is broken in that disease) coordinates its

activity with a family of oxalate transporters. So we got listmates with cystic

fibrosis doing LOD before they developed renal issues, and low and behold,

instead of their lungs getting worse each year, as expected, their lungs got

better and better on the low oxalate diet. So, in other words, oxalate was

having effects on the disease itself that no one realized could be there.

I just suspect Crohn's may be similar. It is possible that shifts in oxalate

trafficking may be part of what causes the distressed reactions in the gut, but

sense GI docs don't know about oxalate trafficking, or what it would change (if

you wonder if he knows anything about oxalate transport, just ask). I don't

think scientists will figure this out if this is the case because case histories

are really what drives new investigations. That means patients, fed up with

waiting for the doctors to hear about the science, may just try reducing oxalate

and see if it produces the needed change. Diet is certainly something the

patient CAN control.

One thing that argues a bit for this connection is the success of VSL#3, a

probiotic you can buy on the web that can be bought with a prescription, or at

half the strength without a prescription. This product was developed for

ulcerative colitis and pouchitis, but it can reduce intestinal inflammation. A

scientist I know named Steve did a study a number of years back that

found VSL#3, among other commercially available probiotics, was the winner in

being able to degrade oxalate. It may help to reduce the inflammation.

Another source for help could be the product N-acetyl glucosamine. This is not

the same thing as glucosamine sulfate. Simon Murch, a colleague of Andy

Wakefield at the Royal Free Hospital years ago did a study looking at the

effectiveness of this product in keeping people from needing to go under the

knife who had Crohn's disease and related intestinal inflammation. I've put

that study below.

You may be aware that it was Andy Wakefield's work on the association of measles

with Crohn's disease that set him up for an interest in the gastrointestinal

disturbances in autism.

In past presentations, I have talked about a little boy with autism who went to

a DAN! doctor who was thoroughly into using the antifungal parade and the longer

this was used with him, the more sickly he became and his autism wasn't

improving, either. His parents, advised by a therapist whose child went to a

different doctor, shifted physicians and went to a doctor who recommended the

low oxalate diet and quit using the antifungals. This boy had already had an

intestinal biopsy and was measles positive (from vaccine), but he didn't start

getting better until he went LOD and quit getting the antifungal medication. He

did well, I think, for several years, but I heard recently heard that he had

again been given antifungals, and, unfortunately, he again crashed as he had

done years before.

I have no idea what therapies your son has received, but maybe the story of this

other little boy would interest you. Right now I am trying to get more updated

information to this boy's doctor that shows when these other therapies that make

a big hit on the liver, may backfire. These are people that don't speak

English, so things will need to be translated.

So, this is just food for thought with a wish that you can turn this around for

your child before they have to do surgery. It is often after the surgeries that

the more serious oxalate issues in Crohn's come on, now associated with short

bowel syndrome. At that point they will advise a low oxalate diet to protect

from renal issues which themselves can be fatal. I hope their is solution you

can find before the surgery, but please read the literature on what changes

after the surgery to understand its risks. Those are spelled out in pubmed.

Wouldn't it be better to try the diet change BEFORE the surgery was necessary to

see if it would help with the gut inflammation and maybe get rid of the need for

surgery? I wish I had more Crohn's people on our listserve to tell you their

stories, but they just haven't found us yet.

Please see the references below, but use them as a springboard to learn more,

and you are very welcome if you would like to join us on TLO to learn more about

how to do a low oxalate diet. Also, some resources are available at

www.lowoxalate.info.

Clin Nephrol. 2006 Mar;65(3):216-21.

Amelioration of anemia after kidney transplantation in severe secondary

oxalosis.

Bernhardt WM, Schefold JC, Weichert W, Rudolph B, Frei U, Groneberg DA,

Schindler R.

Source

Division of Nephrology and Hypertension, Friedrich University

Erlangen-Nürnberg, Erlangen, Germany. wanja.bernhardt@...

Abstract

INTRODUCTION:

In small bowel disease such as M. Crohn, the intestinal absorption of oxalate is

increased. Severe calcium oxalate deposition in multiple organs as consequence

of enteric hyperoxaluria may lead to severe organ dysfunction and chronic renal

failure. The management of hemodialyzed patients with short bowel syndrome may

be associated with vascular access problems and oxalate infiltration of the bone

marrow leading to pancytopenia. Although the risk of recurrence of the disease

is very high after renal transplantation, it may be the ultimate therapeutic

alternative in secondary hyperoxaluria.

CASE:

Here, we report a patient with enteric oxalosis due to Crohn's disease. He

developed end-stage renal disease, erythropoietin-resistant anemia, oxalate

infiltration of the bone marrow and severe vascular access problems. Following

high-urgency kidney transplantation, daily hemodiafiltration of 3 hours was

performed for 2 weeks to increase oxalate clearance. Despite tubular and

interstitial deposition of oxalate in the renal transplant, the patient did not

require further hemodialysis and the hematocrit levels normalized.

DISCUSSION:

Early treatment of hyperoxaluria due to short bowel syndrome is essential to

prevent renal impairment. Declining renal function leads to a further increase

in oxalate accumulation and consecutive oxalate deposition in the bone marrow or

in the vascular wall. If alternative treatments such as special diet or daily

hemodialysis are insufficient, kidney transplantation may be a therapeutic

alternative in severe cases of enteric oxalosis despite a possible recurrence of

the disease.

PMID:

16550754

Nutrition. 1999 Jul-Aug;15(7-8):633-7.

Management of patients with a short bowel.

Nightingale JM.

Source

Leicester Royal Infirmary NHS Trust, UK.

Abstract

Short bowel syndrome most commonly results after bowel resections for Crohn's

disease. The normal human small intestinal length ranges from about 3 to 8 m,

thus if the initial small intestinal length is short, a relatively small

resection of the intestine may result in the problems of a short bowel. Two

types of patient with a short bowel are encountered in clinical practice: those

with their jejunum anastomosed to a functioning colon, and those with a

jejunostomy. Both types of patient have problems absorbing adequate

macronutrients, and both need long-term vitamin B12 therapy. Patients with a

jejunostomy also have major problems with large stomal losses of water, sodium,

and magnesium. This high-volume jejunostomy output is treated by restricting

oral fluids, giving a glucose-saline solution to drink, and using drugs that

either reduce gastrointestinal motility (loperamide or codeine phosphate) or

secretions (H2 antagonists, proton pump inhibitors, or octreotide). Patients

whose jejunal length is less than 100 cm, and whose stomal output is greater

than their oral intake, benefit most from antisecretory drugs. In patients with

a retained colon, bacterial fermentation of unabsorbed carbohydrate in the colon

results in energy being salvaged. However, they have increased oxalate

absorption and a 25% chance of developing calcium oxalate renal stones. Thus

patients with a colon are advised to eat a high-energy diet rich in carbohydrate

but low in oxalate. Patients with a jejunostomy need a high-energy iso-osmolar

diet with added salt. Both patient types have a 45% prevalence of gallstones.

With current therapy most patients with a short bowel have a normal body mass

index and a good quality of life.

PMID:

10422101

Aliment Pharmacol Ther. 2000 Dec;14(12):1567-79.

A pilot study of N-acetyl glucosamine, a nutritional substrate for

glycosaminoglycan synthesis, in paediatric chronic inflammatory bowel disease.

Salvatore S, Heuschkel R, Tomlin S, Davies SE, S, - JA,

French I, Murch SH.

Source

University Department of Paediatric Gastroenterology, Royal Free, London, UK.

Abstract

BACKGROUND:

The breakdown of glycosaminoglycans is an important consequence of inflammation

at mucosal surfaces, and inhibition of metalloprotease activity may be effective

in treating chronic inflammation.

AIM:

To report an alternative approach, using the nutriceutical agent N-acetyl

glucosamine (GlcNAc), an amino-sugar directly incorporated into

glycosaminoglycans and glycoproteins, as a substrate for tissue repair

mechanisms.

METHODS:

GlcNAc (total daily dose 3-6 g) was administered orally as adjunct therapy to 12

children with severe treatment-resistant inflammatory bowel disease (10 Crohn's

disease, 2 ulcerative colitis). Seven of these children suffered from

symptomatic strictures. In addition, similar doses were administered rectally as

sole therapy in nine children with distal ulcerative colitis or proctitis

resistant to steroids and antibiotics. Where pre- and post-treatment biopsies

were available (nine cases), histochemical assessment of epithelial and matrix

glycosaminoglycans and GlcNAc residues was made.

FINDINGS:

Eight of the children given oral GlcNAc showed clear improvement, while four

required resection. Of the children with symptomatic Crohn's stricture, only 3

of 7 have required surgery over a mean follow-up of > 2.5 years, and endoscopic

or radiological improvement was detected in the others. Rectal administration

induced remission in two cases, clear improvement in three and no effect in two.

In all cases biopsied there was evidence of histological improvement, and a

significant increase in epithelial and lamina propria glycosaminoglycans and

intracellular GlcNAc.

CONCLUSIONS:

GlcNAc shows promise as an inexpensive and nontoxic treatment in chronic

inflammatory bowel disease, with a mode of action which is distinct from

conventional treatments. It may have the potential to be helpful in stricturing

disease. However, controlled trials and an assessment of enteric-release

preparations are required to confirm its efficacy and establish indications for

use.

PMID:

11121904

Eur J Paediatr Neurol. 2011 Sep 10. [Epub ahead of print]

A potential pathogenic role of oxalate in autism.

Konstantynowicz J, Porowski T, Zoch-Zwierz W, Wasilewska J, Kadziela-Olech H,

Kulak W, Owens SC, Piotrowska-Jastrzebska J, Kaczmarski M.

Source

Department of Pediatrics and Developmental Disorders, Medical University of

Bialystok, Poland.

Abstract

BACKGROUND:

Although autistic spectrum disorders (ASD) are a strongly genetic condition

certain metabolic disturbances may contribute to clinical features. Metabolism

of oxalate in children with ASD has not yet been studied.

AIM:

The objective was to determine oxalate levels in plasma and urine in autistic

children in relation to other urinary parameters.

METHOD:

In this cross-sectional study, plasma oxalate (using enzymatic method with

oxalate oxidase) and spontaneous urinary calcium oxalate (CaOx) crystallization

(based on the Bonn-Risk-Index, BRI) were determined in 36 children and

adolescents with ASD (26 boys, 10 girls) aged 2-18 years and compared with 60

healthy non-autistic children matched by age, gender and anthropometric traits.

RESULTS:

Children with ASD demonstrated 3-fold greater plasma oxalate levels [5.60

(5th-95th percentile: 3.47-7.51)] compared with reference [(1.84 (5th-95th

percentile: 0.50-4.70) & #956;mol/L (p < 0.05)] and 2.5-fold greater urinary

oxalate concentrations (p < 0.05). No differences between the two groups were

found in urinary pH, citraturia, calciuria or adjusted CaOx crystallization

rates based on BRI. Despite significant hyperoxaluria no evidence of kidney

stone disease or lithogenic risk was observed in these individuals.

CONCLUSIONS:

Hyperoxalemia and hyperoxaluria may be involved in the pathogenesis of ASD in

children. Whether this is a result of impaired renal excretion or an extensive

intestinal absorption, or both, or whether Ox may cross the blood brain barrier

and disturb CNS function in the autistic children remains unclear. This appears

to be the first report of plasma and urinary oxalate in childhood autism.

PMID:

21911305

> >

> > Thanks everyone for the info on my crohns and uc email. Noel, others, have

you ever tried LDN with any luck?

> > Cheers,

> >

> > -- Sent from my Palm Pre

> >

>

February 23, 2012

Hi ,Thanks a lot for taking efforts to write such detailed email with references. Just curious if you are a scientist by profession.Actually I know of oxalates issue with UC folks but my theory is different than yours. The way I learned is, its the intestinal pH thats the cause of the trouble and guess what, been to the ER twice last year for kidney stone. Still going to the urologist to check calcium and oxalate excretion. I posted message about my theory (thats where this all conversation began) Luckily the urology intern was aware of it and we discussed almost for 30 minutes on UC and renal issues.

The way he mentioned and I read around is, for some reason intestinal pH decreases, may be due to your incomplete digestion or affected intestinal linings do not secrete bicarbonate (as a result of inflammation) thats supposed to be there to keep pH alkaline. Majority of Oxalates are in insoluble form in alkaline pH, due to the acidity now, they become soluble and they get reabsorbed. Kidney tries to excrete them but as the inflammation increases, this re-absorption increases too. When it becomes too much for the kidney, it turns into a stone. This is not only with the kidney but can also happen with gall bladder. So essentially, low oxalate diet can help but will not guarantee that there will no stones in future, should the inflammation persists. After kidney stone issue, I started avoiding high oxalate foods though.

Glucosamine connection is new to me. I will check the article.With VSL#3, its the only probiotics that is super potent. There is no other. I considered VSL#3 many a times but the cost is prohibitive and my insurance does not cover it. They recently came up with patient assistance but I don't qualify for it.

If you look the other way around to this story, I found a weak connection between UC and Autism. There have been many pointers but scientifically its difficult to prove it. I am participating in one clinical trial for DS and one of the question on their questionnaire was, if any parents or first family members have Irritable Bowel Disease. I have been mining data for this reverse connection but the results are not what I would like to see.

With my son, I am really on the fence with the BioMed stuff. I read a lot but many of the things fail to convince me, so at the moment, all my son is getting is MB12 oral and some homeopathic stuff along with regular therapies. I am on the list to learn more from other parents and their experiences. Luckily, my son doesn't show any of the symptoms usually reported on this list. He is a happy kid with limited language and limited social skills, so I decided to concentrate on these issues through therapy. Plus, I am super hard-wired for not to do anything that doesn't come up with scientific evidence (Agreed that there is a LOT of bad science but I decided that I will trust Pubmed more than a DAN! doctor. Me and DW poked a lot of holes in Bock's book and his stories), and hence I said, I will prefer surgery to immuno-modulators, there is just not enough evidence that its a 'good' medication to 'treat' UC/Crohns. It just masks symptoms but underlying cause, whatever it is, remains.

Again, thanks a lot for the detailed mail and reference. I will make sure to check everything.Noel

Noel,

I doubt your gastroenterologist has talked to you about this, but there actually is a strong association between oxalate and Crohns disease. Some of the reasons for that association have only been discovered in the last three years, and are still probably sequestered in the " ivory tower " and not changing the way gastroenterologists think about this disease.

If you do a search on Crohns and oxalate in pubmed, you will find 72 articles coming up, so this is a strong association, but if you start reading the articles, you will quickly get the impression that the lines of causality are thought in this way:

Crohn's ----> high oxalate absorption in gut ---> renal problems

Gastroenterologists have heard from the renal people that there is no reason to warn those with Crohns about the dangers of high oxalate food until they have already developed renal problems. This would be like telling people not to reduce cholesterol until they need vascular surgery to correct the clogged arteries. That makes no sense!

This is the key reason when I was talking with the Polish team that designed the first study of oxalate issues in autism, we knew that a PRIMARY issue to address was the myth that people don't have oxalate issues until they have renal problems. Our study showed that NONE of the kids in our study had renal issues, and they also were missing key risk factors that would have been the only things to raise suspicions, but those children with obvious risks were elminated from the study so we only studied those whose doctor's would have thought couldn't possibly have an oxalate issue. Not only were these children high in blood or urine or both in oxalate, but some got into lofty territory that is only seen in the genetic hyperoxalurias, that are as rare as one in a million persons.

So, it will not be a gastroenterologist who will begin to ask if there is any chance the arrows might work back the other direction, that the oxalate that gets high in Crohn's may happen before the disease shows up, and that the oxalate problem may drive the GI disorder. He won't ask, because he has been taught not to ask that question.

You may be aware that Trying_Low_Oxalates was set up to help anybody who wanted to reduce oxalate, so we do get people with other risk groups known associated with oxalate. That has included people with cystic fibrosis. The thinking there was that the antibiotics given in treatment were the setup for developing oxalate problems, but then scientific work in the last few years showed that the cystic fibrosis transporter (that is broken in that disease) coordinates its activity with a family of oxalate transporters. So we got listmates with cystic fibrosis doing LOD before they developed renal issues, and low and behold, instead of their lungs getting worse each year, as expected, their lungs got better and better on the low oxalate diet. So, in other words, oxalate was having effects on the disease itself that no one realized could be there.

I just suspect Crohn's may be similar. It is possible that shifts in oxalate trafficking may be part of what causes the distressed reactions in the gut, but sense GI docs don't know about oxalate trafficking, or what it would change (if you wonder if he knows anything about oxalate transport, just ask). I don't think scientists will figure this out if this is the case because case histories are really what drives new investigations. That means patients, fed up with waiting for the doctors to hear about the science, may just try reducing oxalate and see if it produces the needed change. Diet is certainly something the patient CAN control.

One thing that argues a bit for this connection is the success of VSL#3, a probiotic you can buy on the web that can be bought with a prescription, or at half the strength without a prescription. This product was developed for ulcerative colitis and pouchitis, but it can reduce intestinal inflammation. A scientist I know named Steve did a study a number of years back that found VSL#3, among other commercially available probiotics, was the winner in being able to degrade oxalate. It may help to reduce the inflammation.

Another source for help could be the product N-acetyl glucosamine. This is not the same thing as glucosamine sulfate. Simon Murch, a colleague of Andy Wakefield at the Royal Free Hospital years ago did a study looking at the effectiveness of this product in keeping people from needing to go under the knife who had Crohn's disease and related intestinal inflammation. I've put that study below.

You may be aware that it was Andy Wakefield's work on the association of measles with Crohn's disease that set him up for an interest in the gastrointestinal disturbances in autism.

In past presentations, I have talked about a little boy with autism who went to a DAN! doctor who was thoroughly into using the antifungal parade and the longer this was used with him, the more sickly he became and his autism wasn't improving, either. His parents, advised by a therapist whose child went to a different doctor, shifted physicians and went to a doctor who recommended the low oxalate diet and quit using the antifungals. This boy had already had an intestinal biopsy and was measles positive (from vaccine), but he didn't start getting better until he went LOD and quit getting the antifungal medication. He did well, I think, for several years, but I heard recently heard that he had again been given antifungals, and, unfortunately, he again crashed as he had done years before.

I have no idea what therapies your son has received, but maybe the story of this other little boy would interest you. Right now I am trying to get more updated information to this boy's doctor that shows when these other therapies that make a big hit on the liver, may backfire. These are people that don't speak English, so things will need to be translated.

So, this is just food for thought with a wish that you can turn this around for your child before they have to do surgery. It is often after the surgeries that the more serious oxalate issues in Crohn's come on, now associated with short bowel syndrome. At that point they will advise a low oxalate diet to protect from renal issues which themselves can be fatal. I hope their is solution you can find before the surgery, but please read the literature on what changes after the surgery to understand its risks. Those are spelled out in pubmed.

Wouldn't it be better to try the diet change BEFORE the surgery was necessary to see if it would help with the gut inflammation and maybe get rid of the need for surgery? I wish I had more Crohn's people on our listserve to tell you their stories, but they just haven't found us yet.

Please see the references below, but use them as a springboard to learn more, and you are very welcome if you would like to join us on TLO to learn more about how to do a low oxalate diet. Also, some resources are available at www.lowoxalate.info.

Clin Nephrol. 2006 Mar;65(3):216-21.

Amelioration of anemia after kidney transplantation in severe secondary oxalosis.

Bernhardt WM, Schefold JC, Weichert W, Rudolph B, Frei U, Groneberg DA, Schindler R.

Source

Division of Nephrology and Hypertension, Friedrich University Erlangen-Nürnberg, Erlangen, Germany. wanja.bernhardt@...

Abstract

INTRODUCTION:

In small bowel disease such as M. Crohn, the intestinal absorption of oxalate is increased. Severe calcium oxalate deposition in multiple organs as consequence of enteric hyperoxaluria may lead to severe organ dysfunction and chronic renal failure. The management of hemodialyzed patients with short bowel syndrome may be associated with vascular access problems and oxalate infiltration of the bone marrow leading to pancytopenia. Although the risk of recurrence of the disease is very high after renal transplantation, it may be the ultimate therapeutic alternative in secondary hyperoxaluria.

CASE:

Here, we report a patient with enteric oxalosis due to Crohn's disease. He developed end-stage renal disease, erythropoietin-resistant anemia, oxalate infiltration of the bone marrow and severe vascular access problems. Following high-urgency kidney transplantation, daily hemodiafiltration of 3 hours was performed for 2 weeks to increase oxalate clearance. Despite tubular and interstitial deposition of oxalate in the renal transplant, the patient did not require further hemodialysis and the hematocrit levels normalized.

DISCUSSION:

Early treatment of hyperoxaluria due to short bowel syndrome is essential to prevent renal impairment. Declining renal function leads to a further increase in oxalate accumulation and consecutive oxalate deposition in the bone marrow or in the vascular wall. If alternative treatments such as special diet or daily hemodialysis are insufficient, kidney transplantation may be a therapeutic alternative in severe cases of enteric oxalosis despite a possible recurrence of the disease.

PMID:

16550754

Nutrition. 1999 Jul-Aug;15(7-8):633-7.

Management of patients with a short bowel.

Nightingale JM.

Source

Leicester Royal Infirmary NHS Trust, UK.

Abstract

Short bowel syndrome most commonly results after bowel resections for Crohn's disease. The normal human small intestinal length ranges from about 3 to 8 m, thus if the initial small intestinal length is short, a relatively small resection of the intestine may result in the problems of a short bowel. Two types of patient with a short bowel are encountered in clinical practice: those with their jejunum anastomosed to a functioning colon, and those with a jejunostomy. Both types of patient have problems absorbing adequate macronutrients, and both need long-term vitamin B12 therapy. Patients with a jejunostomy also have major problems with large stomal losses of water, sodium, and magnesium. This high-volume jejunostomy output is treated by restricting oral fluids, giving a glucose-saline solution to drink, and using drugs that either reduce gastrointestinal motility (loperamide or codeine phosphate) or secretions (H2 antagonists, proton pump inhibitors, or octreotide). Patients whose jejunal length is less than 100 cm, and whose stomal output is greater than their oral intake, benefit most from antisecretory drugs. In patients with a retained colon, bacterial fermentation of unabsorbed carbohydrate in the colon results in energy being salvaged. However, they have increased oxalate absorption and a 25% chance of developing calcium oxalate renal stones. Thus patients with a colon are advised to eat a high-energy diet rich in carbohydrate but low in oxalate. Patients with a jejunostomy need a high-energy iso-osmolar diet with added salt. Both patient types have a 45% prevalence of gallstones. With current therapy most patients with a short bowel have a normal body mass index and a good quality of life.

PMID:

10422101

Aliment Pharmacol Ther. 2000 Dec;14(12):1567-79.

A pilot study of N-acetyl glucosamine, a nutritional substrate for glycosaminoglycan synthesis, in paediatric chronic inflammatory bowel disease.

Salvatore S, Heuschkel R, Tomlin S, Davies SE, S, - JA, French I, Murch SH.

Source

University Department of Paediatric Gastroenterology, Royal Free, London, UK.

Abstract

BACKGROUND:

The breakdown of glycosaminoglycans is an important consequence of inflammation at mucosal surfaces, and inhibition of metalloprotease activity may be effective in treating chronic inflammation.

AIM:

To report an alternative approach, using the nutriceutical agent N-acetyl glucosamine (GlcNAc), an amino-sugar directly incorporated into glycosaminoglycans and glycoproteins, as a substrate for tissue repair mechanisms.

METHODS:

GlcNAc (total daily dose 3-6 g) was administered orally as adjunct therapy to 12 children with severe treatment-resistant inflammatory bowel disease (10 Crohn's disease, 2 ulcerative colitis). Seven of these children suffered from symptomatic strictures. In addition, similar doses were administered rectally as sole therapy in nine children with distal ulcerative colitis or proctitis resistant to steroids and antibiotics. Where pre- and post-treatment biopsies were available (nine cases), histochemical assessment of epithelial and matrix glycosaminoglycans and GlcNAc residues was made.

FINDINGS:

Eight of the children given oral GlcNAc showed clear improvement, while four required resection. Of the children with symptomatic Crohn's stricture, only 3 of 7 have required surgery over a mean follow-up of > 2.5 years, and endoscopic or radiological improvement was detected in the others. Rectal administration induced remission in two cases, clear improvement in three and no effect in two. In all cases biopsied there was evidence of histological improvement, and a significant increase in epithelial and lamina propria glycosaminoglycans and intracellular GlcNAc.

CONCLUSIONS:

GlcNAc shows promise as an inexpensive and nontoxic treatment in chronic inflammatory bowel disease, with a mode of action which is distinct from conventional treatments. It may have the potential to be helpful in stricturing disease. However, controlled trials and an assessment of enteric-release preparations are required to confirm its efficacy and establish indications for use.

PMID:

11121904

Eur J Paediatr Neurol. 2011 Sep 10. [Epub ahead of print]

A potential pathogenic role of oxalate in autism.

Konstantynowicz J, Porowski T, Zoch-Zwierz W, Wasilewska J, Kadziela-Olech H, Kulak W, Owens SC, Piotrowska-Jastrzebska J, Kaczmarski M.

Source

Department of Pediatrics and Developmental Disorders, Medical University of Bialystok, Poland.

Abstract

BACKGROUND:

Although autistic spectrum disorders (ASD) are a strongly genetic condition certain metabolic disturbances may contribute to clinical features. Metabolism of oxalate in children with ASD has not yet been studied.

AIM:

The objective was to determine oxalate levels in plasma and urine in autistic children in relation to other urinary parameters.

METHOD:

In this cross-sectional study, plasma oxalate (using enzymatic method with oxalate oxidase) and spontaneous urinary calcium oxalate (CaOx) crystallization (based on the Bonn-Risk-Index, BRI) were determined in 36 children and adolescents with ASD (26 boys, 10 girls) aged 2-18 years and compared with 60 healthy non-autistic children matched by age, gender and anthropometric traits.

RESULTS:

Children with ASD demonstrated 3-fold greater plasma oxalate levels [5.60 (5th-95th percentile: 3.47-7.51)] compared with reference [(1.84 (5th-95th percentile: 0.50-4.70) & #956;mol/L (p < 0.05)] and 2.5-fold greater urinary oxalate concentrations (p < 0.05). No differences between the two groups were found in urinary pH, citraturia, calciuria or adjusted CaOx crystallization rates based on BRI. Despite significant hyperoxaluria no evidence of kidney stone disease or lithogenic risk was observed in these individuals.

CONCLUSIONS:

Hyperoxalemia and hyperoxaluria may be involved in the pathogenesis of ASD in children. Whether this is a result of impaired renal excretion or an extensive intestinal absorption, or both, or whether Ox may cross the blood brain barrier and disturb CNS function in the autistic children remains unclear. This appears to be the first report of plasma and urinary oxalate in childhood autism.

PMID:

21911305

> >

> > Thanks everyone for the info on my crohns and uc email. Noel, others, have you ever tried LDN with any luck?

> > Cheers,

> >

> > -- Sent from my Palm Pre

> >

>

February 23, 2012

" Gut Solutions " is a WONDERFUL and quick, usable source on foundational and

holistic treatment (diet, supplement) of GI problems, with a section on

Chrohn's. A good, old friend from high school picked it up after my

recommendation. Her husband was essentially disabled from Chrohn's and in and

out of the hospital. He had some surgical intervention, and still had

significant issues. He is doing really well now, and found a mainstream but

" integrative " GI specialist in Washington D.C. who uses the tests recommended in

the book.

I have used this book to address our digestive system issues and we have

reversed eosinophilic disorder, mast cell activation disorder, duodenal ulcers

(all Mia), and advanced celiac (me, with MCAD). At the time I had advanced

celiac, I was losing weight no matter what I ate and had many severe, disabling,

chronic symptoms indicative of Chrohn's and UC. My GI specialist recommended

several invasive tests to confirm Chrohn's and UC. I scheduled the tests but was

worried because Mia had had anaphylaxis with anesthesia the year before, which

is a significant risk with MCAD. This, with some other troubling family history

related to contrast dyes, and at the end of the day I couldn't take the risk of

either dying or becoming completely handicapped for a period following the

testing. This was the start of our walk away from mainstream solutions and back

to integrative/holistic solutions. I still have some issues, and am reminded

when I waver from the few remaining diet restrictions (mainly gluten, which on

top of significant GI issues causes eruptions of a poison ivy like rash on my

hands, and a few other unmentionable things), but all in all, we have had life

changing, significant success with longterm recovery through diet and supplement

recommendations from this book. Using a LOT of glutamine powder, I feel, was a

life saver for us- of note- which we discoverd through a friend treating Autism

but is also recommended in the book.

I hope this helps. I truly feel your pain. There is nothing worse than Chrohns.

Here it is on Amazon, with some reviews:

http://www.amazon.com/Gut-Solutions-Natural-Digestive-Conditions/product-reviews\

/0971930929

One last note, Mia has been on LDN for over a year now and she has handled it

well. It has been a good one over all for her. We have found compounding

pharmacies nearby but also there are some that doctors use essentially mail

order.

Have you looked for an integrative GI specialist? In our experience if a doctor

assumes the label integrative, they are well versed in both standard medical

care and nutritional/supplemental therapies as well. A good balance.

>

> > **

> >

> > Thanks everyone for the info on my crohns and uc email. Noel, others, have

> > you ever tried LDN with any luck?

> > Cheers,

> >

> > -- Sent from my Palm Pre

> >

>

February 23, 2012

What is LDN?Sent: Thursday, February 23, 2012 11:29 AMTo: mb12valtrex Subject: Re: Crohns and ucCompounding LDN is not tricky at all. Any compounding pharmacy can do it and coastal happily gives the formula away to any pharmacy that asks if they don't have it.BUT you don't actually have to have it compounded. We tend to have it compounded because it's dosed at night and our kids are usually in bed by then. Adults can take a 5mg pill and be done with it.My son didn't have gut issues so I can't make any claims on how LDN did there. But LDN was good in this house. Not a wow, but still very good. Insurance covers it, too. We had ours compounded by a local compounder and they compounded it in regular hypoallergenic base but then I asked for them to do the emu oil and they had no problem with it. [The entire original message is not included]

February 23, 2012

Sent: Thursday, February 23, 2012 11:29 AMTo: mb12valtrex Subject: Re: Crohns and ucCompounding LDN is not tricky at all. Any compounding pharmacy can do it and coastal happily gives the formula away to any pharmacy that asks if they don't have it.BUT you don't actually have to have it compounded. We tend to have it compounded because it's dosed at night and our kids are usually in bed by then. Adults can take a 5mg pill and be done with it.My son didn't have gut issues so I can't make any claims on how LDN did there. But LDN was good in this house. Not a wow, but still very good. Insurance covers it, too. We had ours compounded by a local compounder and they compounded it in regular hypoallergenic base but then I asked for them to do the emu oil and they had no problem with it. [The entire original message is not included]

February 23, 2012

Of interest, I wrote a post about our GI issues in this thread. VSL is what was

prescribed for us. That and a low ox, gluten free diet, with Glutamine powder

daily, were life changers for us.

I apologize for thumping this bible, but I strongly feel that oxalate issues

point to parasite issues. When I treated for parasites I suddenly could eat

oxalates again. It was overnight. Oxalates are root crop protections against

being eaten by bugs and other soil organisms. Salicylates are similar

protections for the leaves of plants. So it seems to me that when the parasites

in our intestines get the oxalates and salicylates, they get aggravated or die,

releasing compounds that aggravate nearby mast cells, causing degranulation with

associated vessel permeability, among other things. Do you have any thoughts on

this ? I would love to hear an opinion.

Thanks,

>

> Noel,

>

> I doubt your gastroenterologist has talked to you about this, but there

actually is a strong association between oxalate and Crohns disease. Some of

the reasons for that association have only been discovered in the last three

years, and are still probably sequestered in the " ivory tower " and not changing

the way gastroenterologists think about this disease.

>

> If you do a search on Crohns and oxalate in pubmed, you will find 72 articles

coming up, so this is a strong association, but if you start reading the

articles, you will quickly get the impression that the lines of causality are

thought in this way:

>

> Crohn's ----> high oxalate absorption in gut ---> renal problems

>

> Gastroenterologists have heard from the renal people that there is no reason

to warn those with Crohns about the dangers of high oxalate food until they have

already developed renal problems. This would be like telling people not to

reduce cholesterol until they need vascular surgery to correct the clogged

arteries. That makes no sense!

>

> This is the key reason when I was talking with the Polish team that designed

the first study of oxalate issues in autism, we knew that a PRIMARY issue to

address was the myth that people don't have oxalate issues until they have renal

problems. Our study showed that NONE of the kids in our study had renal issues,

and they also were missing key risk factors that would have been the only things

to raise suspicions, but those children with obvious risks were elminated from

the study so we only studied those whose doctor's would have thought couldn't

possibly have an oxalate issue. Not only were these children high in blood or

urine or both in oxalate, but some got into lofty territory that is only seen in

the genetic hyperoxalurias, that are as rare as one in a million persons.

>

> So, it will not be a gastroenterologist who will begin to ask if there is any

chance the arrows might work back the other direction, that the oxalate that

gets high in Crohn's may happen before the disease shows up, and that the

oxalate problem may drive the GI disorder. He won't ask, because he has been

taught not to ask that question.

>

> You may be aware that Trying_Low_Oxalates was set up to help anybody who

wanted to reduce oxalate, so we do get people with other risk groups known

associated with oxalate. That has included people with cystic fibrosis. The

thinking there was that the antibiotics given in treatment were the setup for

developing oxalate problems, but then scientific work in the last few years

showed that the cystic fibrosis transporter (that is broken in that disease)

coordinates its activity with a family of oxalate transporters. So we got

listmates with cystic fibrosis doing LOD before they developed renal issues, and

low and behold, instead of their lungs getting worse each year, as expected,

their lungs got better and better on the low oxalate diet. So, in other words,

oxalate was having effects on the disease itself that no one realized could be

there.

>

> I just suspect Crohn's may be similar. It is possible that shifts in oxalate

trafficking may be part of what causes the distressed reactions in the gut, but

sense GI docs don't know about oxalate trafficking, or what it would change (if

you wonder if he knows anything about oxalate transport, just ask). I don't

think scientists will figure this out if this is the case because case histories

are really what drives new investigations. That means patients, fed up with

waiting for the doctors to hear about the science, may just try reducing oxalate

and see if it produces the needed change. Diet is certainly something the

patient CAN control.

>

> One thing that argues a bit for this connection is the success of VSL#3, a

probiotic you can buy on the web that can be bought with a prescription, or at

half the strength without a prescription. This product was developed for

ulcerative colitis and pouchitis, but it can reduce intestinal inflammation. A

scientist I know named Steve did a study a number of years back that

found VSL#3, among other commercially available probiotics, was the winner in

being able to degrade oxalate. It may help to reduce the inflammation.

>

> Another source for help could be the product N-acetyl glucosamine. This is

not the same thing as glucosamine sulfate. Simon Murch, a colleague of Andy

Wakefield at the Royal Free Hospital years ago did a study looking at the

effectiveness of this product in keeping people from needing to go under the

knife who had Crohn's disease and related intestinal inflammation. I've put

that study below.

>

> You may be aware that it was Andy Wakefield's work on the association of

measles with Crohn's disease that set him up for an interest in the

gastrointestinal disturbances in autism.

>

> In past presentations, I have talked about a little boy with autism who went

to a DAN! doctor who was thoroughly into using the antifungal parade and the

longer this was used with him, the more sickly he became and his autism wasn't

improving, either. His parents, advised by a therapist whose child went to a

different doctor, shifted physicians and went to a doctor who recommended the

low oxalate diet and quit using the antifungals. This boy had already had an

intestinal biopsy and was measles positive (from vaccine), but he didn't start

getting better until he went LOD and quit getting the antifungal medication. He

did well, I think, for several years, but I heard recently heard that he had

again been given antifungals, and, unfortunately, he again crashed as he had

done years before.

>

> I have no idea what therapies your son has received, but maybe the story of

this other little boy would interest you. Right now I am trying to get more

updated information to this boy's doctor that shows when these other therapies

that make a big hit on the liver, may backfire. These are people that don't

speak English, so things will need to be translated.

>

> So, this is just food for thought with a wish that you can turn this around

for your child before they have to do surgery. It is often after the surgeries

that the more serious oxalate issues in Crohn's come on, now associated with

short bowel syndrome. At that point they will advise a low oxalate diet to

protect from renal issues which themselves can be fatal. I hope their is

solution you can find before the surgery, but please read the literature on what

changes after the surgery to understand its risks. Those are spelled out in

pubmed.

>

> Wouldn't it be better to try the diet change BEFORE the surgery was necessary

to see if it would help with the gut inflammation and maybe get rid of the need

for surgery? I wish I had more Crohn's people on our listserve to tell you

their stories, but they just haven't found us yet.

>

> Please see the references below, but use them as a springboard to learn more,

and you are very welcome if you would like to join us on TLO to learn more about

how to do a low oxalate diet. Also, some resources are available at

www.lowoxalate.info.

>

> Clin Nephrol. 2006 Mar;65(3):216-21.

> Amelioration of anemia after kidney transplantation in severe secondary

oxalosis.

> Bernhardt WM, Schefold JC, Weichert W, Rudolph B, Frei U, Groneberg DA,

Schindler R.

> Source

>

> Division of Nephrology and Hypertension, Friedrich University

Erlangen-Nürnberg, Erlangen, Germany. wanja.bernhardt@...

> Abstract

> INTRODUCTION:

>

> In small bowel disease such as M. Crohn, the intestinal absorption of oxalate

is increased. Severe calcium oxalate deposition in multiple organs as

consequence of enteric hyperoxaluria may lead to severe organ dysfunction and

chronic renal failure. The management of hemodialyzed patients with short bowel

syndrome may be associated with vascular access problems and oxalate

infiltration of the bone marrow leading to pancytopenia. Although the risk of

recurrence of the disease is very high after renal transplantation, it may be

the ultimate therapeutic alternative in secondary hyperoxaluria.

> CASE:

>

> Here, we report a patient with enteric oxalosis due to Crohn's disease. He

developed end-stage renal disease, erythropoietin-resistant anemia, oxalate

infiltration of the bone marrow and severe vascular access problems. Following

high-urgency kidney transplantation, daily hemodiafiltration of 3 hours was

performed for 2 weeks to increase oxalate clearance. Despite tubular and

interstitial deposition of oxalate in the renal transplant, the patient did not

require further hemodialysis and the hematocrit levels normalized.

> DISCUSSION:

>

> Early treatment of hyperoxaluria due to short bowel syndrome is essential to

prevent renal impairment. Declining renal function leads to a further increase

in oxalate accumulation and consecutive oxalate deposition in the bone marrow or

in the vascular wall. If alternative treatments such as special diet or daily

hemodialysis are insufficient, kidney transplantation may be a therapeutic

alternative in severe cases of enteric oxalosis despite a possible recurrence of

the disease.

>

> PMID:

> 16550754

>

> Nutrition. 1999 Jul-Aug;15(7-8):633-7.

> Management of patients with a short bowel.

> Nightingale JM.

> Source

>

> Leicester Royal Infirmary NHS Trust, UK.

> Abstract

>

> Short bowel syndrome most commonly results after bowel resections for Crohn's