Zinc Carnosine: Nutraceutical Therapy for Ulcers

Excerpted from Holistic Primary Care, a Summer 2004 Special Report published by Metagenics.

Zinc carnosine, a patented combination of two nutrients that have beneficial effects on the gastrointestinal mucosa, represents an important advance in the management of peptic ulcers. Widely used in Japan, where it is recognized as a drug by regulatory authorities, zinc carnosine given alone was shown by endoscope to resolve ulcers by 60 to 70%, a result comparable to conventional drug therapies and with a safety profile as good as or better than commonly used pharmaceuticals.

This novel compound contributes to ulcer healing through a number of different mechanisms, including the inhibition of Helicobacter pylori (H. pylori)—a bacterial strain thought to be causative of ulcers. Zinc arnosine has been shown to promote wound healing, reduce inflammation, improve secretion of the protective mucosal lining, and possess antioxidant effects. It can be used as a natural therapy, an antibiotic, or an alternative to conventional pharmaceuticals, such as proton pump inhibitors (i.e., Nexium) and H2 receptor antagonists (i.e., Pepcid), both of which serve to decrease hydrochloric acid (HCl). It can also be used as adjunctive therapy in combination with conventional ulcer drugs. Moreover, patients can safely take zinc carnosine with non-steroidal anti inflammatory drugs (NSAIDs) as a way of preempting their adverse gastric effects.

In many ways, zinc carnosine is an ideal complementary therapy for ulcers. Conventional allopathic medicines are suppressive and address the problem of peptic ulcers by controlling the corrosive aspects of stomach function (i.e., reducing acid secretion and eliminating H. pylori). Zinc carnosine enhances and strengthens the stomach's natural defensive and self-protective capacities. It thus provides benefits characteristic of natural products and holistic strategies by treating the cause of the problem, but with the strong scientific pedigree of a pharmaceutical.


Elemental zinc is known to speed healing of mucosal wounds and damaged cells, particularly in the gut. Carnosine is a naturally-occurring dipeptide, comprised of the amino acids, beta-alanine and L-histidine. It is a strong free-radical scavenger capable of blocking free radical chain reactions, inhibiting cell damage. It is also essential for DNA and RNA polymerase activity to aid cell damage.

Zinc carnosine was developed in an effort to provide a therapy that bolsters the ability of the gastric lining to repair and protect itself. A chelate of elemental zinc and carnosine in a 1:1 ratio, zinc carnosine entered the Japanese market as a pharmaceutical for ulcer treatment in the early 1990s and has been marketed there under the trade name Polaprezinc.


The digestive tract has a curious challenge. It must produce caustic matter (stomach acid, pepsin, enzymes, bile) capable of breaking down many different substances, including animal tissue much like those comprising the digestive organs themselves. Consequently, the mucosa must produce sufficient quantities of mucus and other protective factors to keep digestive juices from going to work on its own walls. Digestive health hinges on the balance between secretions of digestive substances and maintenance of the mucosal wall.

Peptic ulcers are best understood as the net result of an imbalance between the caustic processes of digestion and stomach-wall maintenance. When the latter can't keep up with the former, the stage is set for stomach-wall disruption and ultimately ulceration.

And even with the best pharmacotherapy, ulcer recurrences are common, suggesting that acid suppression and eradication of microbial pathogens are insufficient.

Hyper-secretion of stomach acid may play a role in some cases and this is clearly stress-related. However, under-secretion of mucus and/or a breakdown in stomach cell repair mechanisms likely play an equal, if not more significant, role. The current therapeutic challenge is to restore the delicate balance by addressing the factors that impair healing of the gastric lining and improve mucosal integrity.


Pharmacologic treatment of ulcer disease is big business. Aside from costs, long-term treatment with acid-suppressing drugs can result in a number of untoward effects, many of which run counter to the primary objective of restoring digestive health.

Effective digestion is based upon maintaining strongly acidic pH in the stomach and a base pH in the intestines.Many people with heartburn and indigestion actually tend to have too little gastric acid, rather than too much, a condition especially common among the elderly. Thus, many older individuals with ulcers are already acidsuppressed before being given acid-suppressing drugs.

Further suppression via pharmacotherapy has downstream consequences, including poor digestion, malabsorption, and gradually deteriorating nutritional status. Acidsuppression therapy also reduces the secretion of gastric mucus, a natural response to reduced stomach acidity. However, when a patient discontinues acid suppression drugs and returns to normal acid secretion levels, the gastric lining is left even more vulnerable than it was initially. This accounts for the high recurrence rate following treatment cessation.

Bear in mind that stomach acid is among the body's primary defense strategies, providing a way to destroy pathogens ingested with food. By reducing HCl, suppressive therapies increase the possibility that pathogenic organisms will be able to pass through the gastric phase and colonize the lower GI tract.When stomach acid production is deficient and gastric digestion incomplete, it is more difficult to maintain a healthy intestinal ecology. Similarly, antibiotics that kill off H. pylori knock off a lot of friendly flora as well, increasing the chances of intestinal overgrowth with pathogenic bacteria or yeasts. Plus, gastric acid triggers the release of enzymes in the small intestine, and reducing this stimulus results in an inadequate release of digestive juices.


In rats subjected to aspirin-induced gastric mucosal injury, zinc carnosine markedly reduced lipid peroxidation, neutrophil accumulations, and inflammatory factors. The net result was significant reduction in mucosal erosions. A separate study, also in rats, showed that zinc carnosine could prevent the reduction in gastric mucus secretion that follows the exposure to alcohol, another ulcer trigger.


To date, there have been eight clinical trials of zinc carnosine for the treatment of peptic ulcers. Initial dose-ranging and safety studies evaluated doses of 75 to 600 mg per day, given under fasting conditions, as well as at meal times. The data indicate that zinc carnosine is entirely safe up to 600 mg per day. The only adverse effects were mild heartburn-like symptoms in two patients on the highest dose taken without food. There was no toxic accumulation of zinc in the lood, and the compound was readily excreted in urine and stool without adverse kidney or lower GI effects. Researchers demonstrate zinc carnosine to be highly effective when used continuously for 8 weeks. A fitting recommendation is one tablet, twice a day, of Zinlori 75 from Metagenics Inc. Beyond its applications in the management of peptic ulcers, zinc carnosine may have a role in treatment of gastritis and stomatitis.