Homocysteine contributes to inflammatory bowel disease

May 14, 2005

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In this issue
	Life Extension Update Exclusive:
		Homocysteine contributes to inflammatory bowel disease
	Protocol:
		Crohn's disease
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Life Extension Update Exclusive

Homocysteine contributes to inflammatory bowel disease

Researchers from Catholic University in Rome reported in the April 2005 issue of the American Journal of Gastroenterology that homocysteine is increased in inflammatory bowel disease (IBD) and may contribute to the inflammation that characterizes the condition. Crohn's disease and ulcerative colitis are among the most common forms of IBD.

Homocysteine is an amino acid produced during metabolism which has been found to be a risk factor for cardiovascular disease when elevated, and may play a role in other conditions such as Alzheimer's disease.

Eighty-three men and women with Crohn's disease, 83 ulcerative colitis patients and 70 individuals without IBD took part in the current study. Blood samples were analyzed for homocysteine and folate, and homocysteine levels were measured in mucosal biopsy samples obtained via colonoscopy.

Subjects with IBD had significantly lower blood folate levels and higher homocysteine levels in plasma and colon mucosa than control participants. When cells known as lamina propria mononuclear cells derived from the subjects' mucosa were studied, those of the IBD patients were found to release more homocysteine than those derived from the control group, demonstrating that these cells are a source of this proinflammatory compound.

When cultured human intestinal microvascular endothelial cells were treated with homocysteine and/or the pro-inflammatory compound TNF-alpha, homocysteine produced a similar inflammatory reaction to that of TNF-alpha, yet a greater reaction was induced by both compounds given together than by either alone. This inflammatory effect was blocked in the homocysteine-treated cells by the addition of folic acid.

The authers observed, "In our in vitro studies we found that folic acid, a homocysteine scavenger, was very effective in inhibiting the homocysteine-triggered inflammatory effects . . . Moreover, as folic acid is able to reduce in vivo the inflammatory effect of homocysteine and to normalize homocysteine levels in patients with hyperhomocysteinemia, it could be reasonable to hypothesize a beneficial effect of folic acid supplementation in IBD patients to eliminate the homocysteine-mediated inflammatory events."

Protocol

Crohn's disease

Crohn's disease is a long-term, chronic disorder of the intestine. The etiology is unknown. Crohn's disease causes the gastrointestinal tract to become inflamed and weak, making digestion difficult and causing general debility.

Traditional treatments for Crohn's disease depend on the location and severity of disease, complications, and response to prior treatments. The goals of therapy are to control inflammation, correct nutritional deficiencies, and relieve symptoms like abdominal pain, diarrhea, and rectal bleeding. This may include drug therapy, nutrition supplementation, surgery, or a combination of approaches. Though treatment can help control the disease, there is no cure.

Aminosalicylates that disrupt colonic inflammation are the first line of conventional treatment for Crohn's disease. Steroids are often administered during acute outbreaks.

The most optimal approach for the overall management of the broad range of symptoms of Crohn’s disease is to utilize a range of nutritional therapies each of which addresses a specific type of problem related to the disease. The benefit of nutrient-based therapies is that they are free of serious side effects and can be used indefinitely.

Replacement of depleted antioxidants. The primary function of antioxidants is to help to eliminate harmful free radicals and oxidants. The intestinal mucosa contains an extensive system of antioxidants. Absolute levels of these antioxidants and the balance between the most important antioxidants are seriously impaired in intestinal mucosa during inflammatory bowel disease. Supplementation with antioxidants can improve symptoms of Crohn’s disease.

Replacement of depleted vitamins and minerals. Depletion occurs as a result of Crohn’s disease so it is vitally important to correct this disease-related malabsorption. Minerals often lacking in those suffering from Crohn’s disease include iron, magnesium, selenium, and zinc. Vitamins that are most lacking are the B-complex vitamins, folic acid, vitamin B6, and particularly, vitamin B12. Supplementation with these vitamins improves symptoms of Crohn’s disease by improving endothelial function.