Inflammatory bowel disease mystery
? cause ? best treatment.

Paediatric Crohn's inflammatory bowel disease is increasing - progressively from the 1970's, and we don't know why.

The other one, ulcerative colitis, hasn't increased. (Hadn't that is, but now it has, quite dramatically - 2013 note.)

Genetic studies have put that contribution to the incidence of IBD as 17%, leaving 83% for environmental factors.

Crohn's disease may be the human equivalent of Johne’s disease.
This is a chronic, wasting disease of cattle caused by the bacterium Mycobacterium paratuberculosis.
The bacteria live in the animal’s intestines and cause thickening of the bowel wall which interferes with the normal absorption of food.

Treatment based on this proposition with a combination of three antibiotics (Rifabutin, clarithromycin, and clofazimine) had a clinical response of almost 95% in a Phase II clinical trial of human Crohn's disease.

Another trial⁴ using rifaximin 800 mg twice a day, saw two thirds of people improve, half to complete remission. This was not statistically different from the placebo however, so this treatment remains of uncertain value.

A literature review published in 2011 has been more positive, see reference 8 below.

Whatever the cause, the bowel damage definitely causes "leaky gut", which definitely aggravates the condition.

Testing intestinal permeability with lactulose and mannitol³, shows the leaky gut - damage allowing the passage of increased quantities of large molecules into the bowel wall. Healthy gut doesn't allow this.

This test predicted most of the recurrences in a group of people with quiescent Crohn's disease, in a trial reported in Lancet¹.

Those with increased permeability, were more likely to relapse.

Hypo-allergenic enteral feeding (eg. Emsogen, Vivonex) can give remission rates of 50% in adults, 50 to 80% in children.

This is a diet avoiding the normal foods, to which a person may be allergic or intolerant. It is called an elemental diet, consisting of foods broken down into their elements (components) of sugars, amino acids and short chain fatty acids.

As mentioned above, their leaky gut would otherwise allow greater passage of these foods, undigested or partly digested, into the bowel wall.
Aggravation of the Crohn's disease would follow from the immune reaction in the bowel wall.

Ed, the author of, has a really interesting story, and his great inflammatory bowel disease response to Dr. Kwasniewski's "optimal diet" may well have an instance of avoiding food intolerances, or because it resulted in a healthy gut flora. site

In my experience, emotional stress has been a major aggravating factor when people have trouble with their Crohn's.

This certainly fits with all immune problems - stress aggravates.

Endoscopy in Crohn"s inflammatory bowel disease

The pediatricians do gastroscopy and colonoscopy on all children with this diagnosis. they take biopsies from multiple sites, in duodenum, stomach and oesophagus as well.

They often find histological granulomatous disease in areas which are macroscopically normal - less severe disease not visible to the naked eye, can be quite extensive.

You are likely to be advised to have endoscopy yearly. This is the best way to decide on treatment, as you can have active disease without causing much discomfort.

Faecal transferrin tests for granulocyte white blood cells (pus cells)

This substance is stable enough even after white cells are unrecognizable on microscopy of stool samples.

It is useful for showing inflammation of the bowel, of the degree and type seen in IBD colitis.

Faecal tests for calprotectin and lactoferrin are also very useful. A combination of these all negative may help your doctor enough to avoid the need for endoscopy.

Regular blood tests

Iron, folate, calcium, leucocyte ascorbic acid⁵ and vitamin D tests will give a measure of the function of your small bowel.

And check your bones

A study of 161 people with inflammatory bowel disease, such as ulcerative colitis and Crohn's disease, found 22% had low bone mineral density (osteopenia or osteoporosis.) Half of them were younger than 40.

"Bone loss is generally uncommon below the age of 40 in the normal population, so I was a little surprised to see a high number of my patients below that age with abnormal bone density. I do believe that it is further evidence of the effects of IBD," said Bincy P. Abraham, MD, MS, lead author of the study.

This could be due to poor absorption of vitamins and minerals, and/or cortisone treatments.

Nutrients and herbs as part of treatment

Herbs such as turmeric and licorice are worth looking into.

The anti-inflammatory bioflavonoid quercetin may have a role.

The tripeptide glutathione (GSH) Glu–Cys–Gly is absorbed to some degree, and is low in IBD².

It is now for the first time, available in a readily absorbed form (Lypo-Spheric GSH from LivOn laboratories.)

One component of GSH is the amino acid glutamine. This may have a dual role, as it is a fuel for the cells lining our small intestine as well.

In animal experiments, glutamine has been shown to downregulate nuclear factor kappa B (NFkB) and tumor necrosis factor-alpha (TNF-alpha.) These are two key players in the inflammation.

Glutamine is not one of the 10 essential amino acids, but becomes "conditionally essential" during inflammatory states. Then a functional deficiency can result, as the increased requirement may not be available.

This lack of glutamine may result in deterioration of the intestinal barrier (leaky gut.)

Another glutathione precursor treatment is Immunocal (Immunotec, Montreal.)

Other diets as part of treatment of IBD

Elaine Gottschall's "Specific Carbohydrate Diet"⁷ aims to regulate the intestinal microbial population by control of its' food supply.

Different carbohydrates support different germ populations.

From inflammatory bowel disease to home page.

From inflammatory bowel disease back to abdominal pain page

References for inflammatory bowel disease.

1. Wyatt et al Lancet 341 June 5 1993 p. 1437

2. Sido et al Impairment of intestinal glutathione synthesis in patients with inflammatory bowel disease Gut 1998;42: p.485-492
These researchers also found that abnormally low plasma cysteine and cystine levels were associated with inflammation in IBD.

3. Lactulose and mannitol are both are absorbed into our bloodstream by passive seepage through the wall of our small intestine. Lactulose is a bigger molecule so is only slightly absorbed here.

Once absorbed, neither is altered in our body, and both are passed out in our urine.

The ratio of lactulose to mannitol in the urine is increased if we have damaged "leaky" small intestine, as then more lactulose gets into our bloodstream.

4. C. Prantera Antibiotic Treatment of Crohn's Disease: Results of a Multicentre, Double Blind, Randomized, Placebo-Controlled Trial With Rifaximin Alimentary Pharmacology & Therapeutics 2006;23(8):1117-1125

5. B. D. Linaker Scurvy and vitamin C deficiency in Crohn's disease. Postgrad Med Journal 1979;55: pp 26-29

6. American College of Gastroenterology 2010 Annual Scientific Meeting: Poster P290. Presented October 17, 2010.




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