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Zinc-carnosine complex beneficial for stomach health

stomach A patented, molecular combination of L-carnosine and zinc bound by chelation (hereafter referred to as Zinc-carnosine complex) has been extensively studied in Japan both for its ability to boost mucus secretion and for its antioxidant effects. It is used there for treating gastric problems such as ulcers, dyspepsia and Helicobacter pylori infections, the bacteria that causes stomach ulcers. Zinc-carnosine complex boosts the stomach’s natural defence mechanisms, thus reducing the effects of stress, bacteria and lifestyle.

The theory behind its mechanism of action is that it disassociates slowly in the acid part of the stomach, adhering to the stomach wall specifically at ulcer sites, and releasing zinc ion and L-carnosine. It boosts normal mucus secretion and maintains the integrity of the gastric mucosal barrier1.
Studies on distribution in tissues have shown that Zinc-carnosine complex is metabolised like endogenous amino acids or zinc once it has disassociated in the body2. Zinc plasma concentrations peak one hour after taking Zinc-carnosine complex and then slowly fall, reverting to initial levels after 11 hours. In other studies, it has demonstrated antioxidant potency and membrane-stabilising effects in the stomach.

Boosts the health of gastric cells

Scientists have studied the ability of Zinc-carnosine complex to protect gastric cells from free radical damage. Rat gastric cells were exposed to ethanol and hydrogen peroxide, two substances known to cause radical damage in living cells. The cells were bathed in hydrogen peroxide, ethanol, Zinc-carnosine complex or a combination of Zinc-carnosine complex and either ethanol or hydrogen peroxide. While the cells bathed in ethanol and hydrogen peroxide all showed damage due to free radical production, those bathed in Zinc-carnosine complex were shown to have been significantly protected from such damage. The researchers concluded that the zinc compound directly protected the stomach’s mucosal cells from oxidative stress and alcohol-induced damage3.
Other research has confirmed the gastro-protective effects of Zinc-carnosine complex. Gastric lesions were induced in rats by the pro-oxidant monochloramine, with one group of animals given Zinc-carnosine complex before exposure to the chemical. The scientists found that lesion size was significantly smaller in this group than in those animals not given the compound 4. Further studies have corroborated these results, partially attributing the efficacy of Zinc-carnosine complex to its antioxidant properties5.

A study on a rat gastric mucosal cell line examined the inhibitory effect of Zinc-carnosine complex on apoptosis induced by indomethacin (IND), a chemical known to produce reactive oxygen species. The study showed Zinc-carnosine complex to confer protection, though it inhibited gastric cell apoptosis by blocking activation of the enzyme caspase-3, rather than through an antioxidant effect6.
Zinc-carnosine complex has also been shown to slow the development of aspirin-induced stomach lesions in rats. Lower levels of TNF-alpha, an inflammatory cytokine released in response to gastric lesions, were found in animals given Zinc-carnosine complex compared with controls. These results suggest that Zinc-carnosine complex may protect gastric cells by intermittently reducing levels of some cytokines in cases of minor stomach inflammation7. Other research has confirmed this anti-inflammatory effect. MKN28 cells were used as a model of gastric epithelial cells to study the effects of Zinc-carnosine complex on pro-inflammatory cytokines induced by expression of interleukin 8. Zinc-carnosine complex was also observed to exert effects on nuclear transcription factor-kappa B which regulates the expression of IL-8, suggesting that it reduces the inflammatory response of gastric mucosal cells.

Inhibitory effect on Helicobacter pylori

More than half the world’s population is thought to be infected with the bacteria Helicobacter pylori which is known to cause gastric ulcers. It is found in more than 80% of people suffering with these ulcers. Non-steroidal anti-inflammatory drugs (NSAIDs) are the second most common cause of peptic ulcers. Helicobacter pylori, like NSAIDs, disrupts the function of the stomach’s mucosal membrane, allowing acids to come into contact with the stomach wall.
Standard treatment for ulcers involves reducing levels of stomach acid, generally through the use of antacids or histamine-blockers combined with antibiotics to try and eliminate the bacterial infection.
Studies have primarily focused on the ability of Zinc-carnosine complex to fight Helicobacter pylori infection and to improve mucosal protection. A review of gastrointestinal ulcer medication examined the effects of Zinc-carnosine complex, noting that zinc directly suppresses the growth of Helicobacter pylori and inhibits activity of the urease produced by the bacteria9. The active site of urease contains a nickel ion essential to its enzymatic activity. When the nickel is replaced by zinc, the urease becomes considerably less active. Scientists have theorised that this is how Zinc-carnosine complex is able to inhibit the growth of Helicobacter pylori.
It has also been shown that Zinc-carnosine complex optimises the ability of antibiotics to eliminate the bacteria. One study showed that treatment combining antibiotics and Zinc-carnosine complex resulted in almost total elimination of Helicobacter pylori, while antibiotics alone had a failure rate of almost 20%10.
Other research has demonstrated that Zinc-carnosine complex inhibits GI inflammation as well as activation of the leucocytes associated with Helicobacter pylori11, 12. It stimulates expression of mucosal growth factor to heal lesions13 and also protects the stomach from NSAID-induced mucosal damage, probably through its antioxidant and anti-inflammatory properties14.

Boosts treatment of viral hepatitis

One human study examined the combined effects of Zinc-carnosine complex and interferon-alpha in the treatment of hepatitis C in a group of Japanese subjects infected with type 1b of the disease. Ten patients were given daily injections of 10 million units of interferon for four weeks, followed by the same injection three times a week for a further 20 weeks. Nine other patients took 300mg/day of zinc sulphate, and another fifteen took 150mg/day of Zinc-carnosine complex, in addition to the interferon treatment. The percentage of patients experiencing a complete response, ie, eradication of the virus, was 20% from the interferon alone, 11% from the interferon/zinc combination and 53.3% from the interferon/Zinc-carnosine complex combination15. The synergistic effects of zinc supplementation on interferon response were evaluated in a pilot study of patients with intractable hepatitis C. There was no clinical difference between the patients who received interferon alone and those given interferon combined with Zinc-carnosine complex.
All had more than 105 copies of the virus per ml of serum at the start of the study. Ten million units of natural interferon-alpha was administered daily to 40 of the patients for four weeks, followed by the same dose every other day for 20 weeks. Another group of 35 patients in addition received 150 mg/day of Zinc-carnosine complex over the 24 weeks. Complete response to treatment was defined as negative HCV RNA in serum and a normal aminotransferase level six months after therapy. Incomplete response was characterised by normal liver enzyme and positive serum HCV RNA.
Patients who began the study with the highest serum HCV levels (more than 5 x 105 copies per ml) responded poorly to both treatments. Patients with moderate serum HCV levels (105-4.99 x 105 copies per ml) had a better response to the combined treatment than to interferon alone, indicating that supplementation with Zinc-carnosine complex improves the response to interferon treatment in patients with chronic, intractable hepatitis C. 16.

1. Furuta S. et al., Jpn J. Pharmacol., 1995 Apr, 67(4) : 271-8.
2. Furuta S. et al., J. Pharma. Biomed. Anal., 1999, 19 : 453-61.
3. Hiraishi H. et al., Aliment Pharmacol. Ther., 1999, 13 : 261-9.
4. Kato S. et al., Dig. Dis. Sci., 1997, 42(10) : 2156-2163.
5. Nishiwaki H. et al, J. Physiol. Pharmacol., 1999 Jun, 50(2) : 183-95 ; Suzuki H. et al., J. Gastroenterol., 1999, 34 Suppl 11 : 43-6.
6. Fuji Y. et al., Jpn J. Pharmacol., 2000 Sept, 84(1) : 63-70.
7. Naito Y. et al., Dig. Dis. Sci., 2001, 46 (4) : 845-851.
8. Tadahiti S. et al., The J. Pharmacol. Experimen. Therap., 1999, vol 291 n° 1, 345-352.
9. Furuta S. et al., Nippon Rinshon., 2002, 60 Suppl 2,717-20.
10. Kashimura et al., Aliment Pharmacol. Ther., 1999 April, 13(4) : 483-7.
11. Suzuki H. et al., Aliment Pharmacol. Ther., 2001, 15 : 715-25.
12. Handa O., Can. J. Gastroenterol., 2002 Nov, 16(11) : 785-9.
13. Korokiewicz R. et al., Dig. Dis. Sci., 2000, 45 ; 6: 1200-9.
14. Naito Y. et al., Dig. Dis. Sci., 2001, 46 ; 4 : 845-71.
15. Nagamine T. et al., Biological Trace Elements Research, 2000, vol 75, issue 1-3 : 53-63.
16. Takagi H. et al., J. Vir. Hepat., 2001 Sept, 8(5) : 367-71.
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Zinc L-carnosine

Patented zinc-carnosine complex, protects the stomach from numerous irritants

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