WHAT IS ZINC CARNOSINE?

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.

GASTRIC MUCOSAL BALANCE: A NEW WAY OF THINKING ABOUT ULCER

DISEASE

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.

CONVENTIONAL PHARMACOTHERAPIES AND THEIR LIMITATIONS

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.

BASIC RESEARCH

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.

CLINICAL TRIALS: SAFE AND EFFECTIVE MONOTHERAPY

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.