Sulphur and Ulcerative Colitis

What is the relationship between sulphur and ulcerative colitis?

Dietary measures are not widely accepted as a form of therapy for
ulcerative colitis, although withdrawal of milk has been shown to be
of benefit.1 Recent evidence has implicated fermentative formation of
sulphide in the disease process.2,3 Excess bacterial formation of
sulphide in the colonic lumen or failure of detoxification of sulphide
in the colonic mucosa could result in damage to colonic epithelial
cells, leading to inflammation. The chief sources of sulphur for
colonic fermentation and cellular function are the sulphur aminoacids
(SAAs) of animal and plant origin.3,4 A pilot study was undertaken to
observe whether reduction of intake of SAAs would benefit patients
with ulcerative colitis. Treatment with salazopyrin/prednisolone was
not changed.

Diet sheets were drafted to indicate foods with a high content of
SAAs.1 Intake of fats, sugar, and complex carbohydrates was not
curtailed. We advised patients to completely avoid eggs, cheese, whole
milk, icecream, mayonnaise, soya milk, mineral water, and sulphited
drinks (wine and cordials) as well as nuts and cruciferous vegetables
(cabbage, broccoli, cauliflower, brussel sprouts); to diminish intake
of red meat and to use chicken, fish, and skimmed milk. Patients were
encouraged to try the diet for four weeks before accepting longterm
dietary change. Following an acute attack of ulcerative colitis, four
patients aged 31, 32, 56, and 71 had colonoscopies, biopsies, and
stool culture before commencing salazopyrin and a 3-week course of
oral prednisolone. Diet and salazopyrin were maintained for 12 months
before repeat colonoscopy and biopsy was undertaken. Four patients
aged 35, 56, 60, and 71 with established ulcerative colitis for 11,
12, 15, and 20 years were asked to commence the diet. The number of
bowel motions, attacks and bleeding were recorded.

The combined observation period for the patients who had had an acute
attack was 56 months. No relapses, attacks, or adverse nutritional
changes were observed during this time where an expected relapse on
salazopyrin would be 22·6%. All showed marked histological improvement
based on the Truelove criteria. Of the four patients with chronic
ulcerative colitis, one ceased steroids and has not had a further
attack for 18 months compared to 4 attacks for the same period before
dietary change. Of the other three, all had microscopic improvement of
inflammatory changes. The number of bowel motions per day for all four
chronic patients diminished from 6 (SD 1·1) to 1·5 (0·3) (figure) and
their stools were more formed. Two patients stopped their diet and
when they noticed adverse changes in bowel habit, they resumed the
diet.

Reduced intake of SAAs-containing foods produced no harmful effects
after an acute attack of colitis and produced an improvement in
moderately severe ulcerative colitis. Challenge with an enriched SAA
diet was considered unethical. Decreased entry of sulphur into the
colon5 with less formation of bacterial sulphide could be the
explanation, although diminished intake of SAAs, essential for
cytokine production,5 could reduce cytokine formation in the inflammed
mucus. A controlled trial of diminished intake of SAA-containing
foods, with biochemical monitoring of compliance with the reduced
intake of SAAs, needs to be undertaken.