There are some interesting developments in research around the role of nutrition in ulcerative colitis. Recent studies have singled out sulphur as a possible culprit in exacerbating some of the symptoms associated in some individuals with ulcerative colitis.
What is sulphur?
Sulphur is found in a wide range of foods such as eggs, cheese, whole milk, ice cream, mayonnaise, and soy milk just to name a few. It is present in proteins and is vital in stabilizing protein structures. Sulphur-based substances (sulphides, sulphites) are also used as food additives.
In general, sulphites are quite useful compounds as they perform many functions – particularly in food preservation – such as:
- prevention of changes in pigment of food (browning reactions), especially cut food
- discouragement of microbial growth during wine or beer fermentation
- bleaching of food starches, and
- maintaining the stability and potency of some medication.
The downside of sulphur is that about 1% of the population is sulphite sensitive – they have mild to severe reactions when they consume sulphites, usually constriction of the airway. Sulphite sensitivity can occur at anytime and the trigger is unknown. Corticosteroid-dependent asthmatics, or those with severe symptoms, are at a high risk of becoming sulphite sensitive.
And now, it seems, these substances may negatively affect ulcerative colitis patients.
How can sulphur cause harm?
Bacteria that live in the bowel convert the sulphur in food into hydrogen sulphide, in a process known as fermentation. This highly toxic product is responsible for the foul odour associated with passing gas, can cause abdominal pain, and frequent, urgent trips to the toilet. Normally, the cells lining the colon absorb and detoxify the gas but in people with ulcerative colitis, there is a two-fold problem. Firstly, ulcerative colitis patients appear to produce more hydrogen sulphide than normal, and they have a more difficult time breaking down the gas (possibly due to existing inflammation of the bowel lining). The extra gas present may further damage the lining of the colon.
Hydrogen sulphide may have a number of adverse effects on the bowel and may contribute to the pathogenesis of ulcerative colitis. Hydrogen sulphide has been shown to increase the epithelial permeability and barrier function. In other words, it reduces the protective function of the cells lining the bowel. Other animal studies indicate high concentrations of the product can produce cell death, goblet cell loss, crypt architectural distortion, and superficial mucosal ulceration. It has also been shown to reduce the effectiveness of the immune system in trapping and killing unwanted bacteria. All of these examples point to the possible toxic effects of hydrogen sulphide on the cells lining the colon.
Other research supporting these finding has shown that increasing reduced-sulphur compounds causes a reversible inhibition of butyrate oxidation. Butyrate acid, a shot chain fatty acid, is also a product of colon fermentation, but unlike hydrogen sulphide, is vital in providing up to 70% of the energy metabolism required by the cells lining the large bowel (the small bowel uses different energy sources). Studies indicate that butyrate oxidation is impaired in the biopsies of cells lining the colon of ulcerative colitis patients.
There have been a number of clinical trials using topical short chain fatty acids, especially butyrate, in distal ulcerative colitis in order to overcome this deficiency of butyrate in the colon. The data in this area has shown some promise and supports the ideas of impaired short chain fatty acids metabolism by the presence of high levels of sulphur amino acids.
The physiological basis for this process is that there is competition between the bacteria that reduce the sulphur and the bacteria that produce the necessary short chain fatty acids. They compete for the available hydrogen in the bowel and the success of either is mediated by the amount of sulphur available.
Another interesting area of research has shown that 5-ASA actually reduces concentration of sulphide in the faeces. It was shown that ulcerative colitis patients have a higher level of sulphite in the colon and that in vitro studies have shown there is a dose-dependent reduction of sulphite in the presence of 5-ASA. The work in this area is very preliminary and further research is required.
In another study, researchers found that bismuth (Pepto-Bismol®) locks sulphides into solid waste as it passes through the intestines, and thus prevents the release of irritating hydrogen sulphide gas. However, although occasional use of the bismuth product may give short-term relief, long-term use is not recommended. If too much bismuth accumulates in the bloodstream, it may damage nerves. A delivery system of bismuth directly to the colon may avert this problem but it has not been developed.
Therefore, instead of trapping sulphur once it is in the system and preventing excessive accumulation in the bowel, the alternative is to reduce the amount of sulphur going into the digestive tract.
What happens when dietary intake of sulphur is reduced?
There has been one pilot study undertaken to see if a reduction in sulphur amino acids of animal and plant origin would benefit patients with ulcerative colitis. There were two groups consisting of only 4 individuals. One group had recently had an exacerbation and the other group had not had a recent attack.
Those patients who began the project with a recent exacerbation reported no acute attack after 56 combined months of observation. Expected relapse on a 5-ASA medication for such a group would be 22.6%. All showed marked histological (biopsies of the colon) improvement. Three members of the chronic group also showed histological improvement with at reduced number of bowel movements from 6 to 1.5 per day, with a more formed stool. The fourth member of the chronic group was able to stop steroids and had no further acute episodes compared to 4 attacks of the same period prior to beginning the diet.
Conclusion
These research projects indicate that there is an increase in the net luminal (within the bowel) production of hydrogen sulphide and amino acid fermentation in ulcerative colitis. These processes mediated by the level of sulphur in the luminal contents, and the presence of 5-ASA in the bowel. An overproduction of sulphide may impair the production of necessary short chain fatty acids such as butyrate, and lead to the onset of epithelial inflammation.
While these studies show that sulphur plays a role in ulcerative colitis, the nature and number of research studies completed so far are too small to be scientifically significant. What the research does indicate, however, is that there is a need for further controlled studies in the role that sulphur plays in the pathogenesis of ulcerative colitis.
Throughout history, sulphur has been utilized for a variety of tasks. Since the 17th century, it was used to sanitize wine and cider vessels. It has also been used to prevent undesirable microbial growth in wet milling of corn, and as an antioxidant in cured meat and in the prevention of rancidity.
Click here for information on Sulphite-Restricted Diets.
