Monolaurin and Gastritis
Last Updated: January 8, 2019 | First Published: August 20, 2018
Reviewed by: Dr. Jennifer Meza, M.D.
Treating Stomach Ulcers (caused by H. Pylori) with Monolaurin
An ulcer is a sore area or a hole in the lining of the stomach. Ulcers of the stomach and the small intestine are mostly caused by a spiral-shaped bacteria called Helicobacter pylori (H. Pylori), and they can affect people from any age group (Ref #1). Gastritis is a disease that causes ulcers in the stomach through inflammation in the inner lining of the stomach. It can be caused by various factors including excessive consumption of alcohol or a normal dose of some medications like anti-inflammatory drugs.
Symptoms of Gastritis
The most common symptom is the pain in the upper abdomen area. When the lining of the stomach becomes inflamed, a burning sensation can be felt in this area of the body as it is in direct contact with the stomach. Patients may experience this pain in the early hours of the morning, on an empty stomach, and between meals. This pain may be relieved by using antacids, but not always. Accompanying symptoms can include hiccups, upset stomach, indigestion, vomiting and no appetite for days (Ref #2).
A diagnosis of an H. Pylori infection may take a long time, as doctors tend to omit these specific tests or assume that an ulcer is responsible for the overgrowth of the bacteria.
Monolaurin and H. Pylori Bacteria
Monolaurin is a medium chain fatty acid that can be extracted from coconut oil and has been shown to possess antibacterial properties (Ref #3). According to some laboratory studies, Monolaurin may kill H. Pylori bacteria, and in turn may be an effective treatment for gastritis.
Monolaurin displays a strong anti-bacterial behavior against H. pylori as compared to other chemicals. One study (Ref #4) showed that Monolaurin was the most effective of the fatty acids and monoglycerides tested in the killing of H. Pylori. Furthermore, the results were not impacted by pH, suggesting that Monolaurin might work in the hard acidity of the stomach.
A further study (Ref #5) shows that H. pylori is rapidly inactivated by medium-chain monoglycerides and lauric acid (Monolaurin) and exhibits a relatively low frequency of spontaneous development of resistance to the bactericidal activity of Monlaurin. Monolaurin was shown to be bactericidal agsint H. Pylori bacteria in as little as 15 minutes at neutral or acidic pHs.
Monolaurin does not appear to harm any useful gut bacteria. A research study of 2004 conducted in the Georgetown University Medical Centre of Washington DC revealed that Monolaurin could be very useful in treating infections as it is a safe compound that can be combined with other antibiotics as well (Ref #6). Since then, it has been used as an active ingredient in some anti-bacterial medicines. It is used to treat some common diseases like cold and swine flu.
In recent years, monolaurin has been studied for treating microorganisms, fungi, and bacteria that pose a threat to health. Research has indicated the potential of Monolaurin as an antibacterial agent as it has the power to inactivate bacteria in the laboratory. Like all dietary supplements, Monolaurin should be considered and administered under the supervision of a healthcare professional.
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IQWiG (Institute for Quality and Efficiency in Health Care) June 28, 2018 Accessed athttps://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0078820/
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Sun CQ, O'Connor CJ, Roberton AM. Antibacterial actions of fatty acids and monoglycerides against Helicobacter pylori. FEMS Immunol Med Microbiol. 2003 May 15;36(1-2):9-17. https://www.ncbi.nlm.nih.gov/pubmed/12727360
Petschow BW, Batema RP, Ford LL. Susceptibility of Helicobacter pylori to bactericidal properties of medium-chain monoglycerides and free fatty acids. Antimicrob Agents Chemother. 1996 Feb;40(2):302-6. https://www.ncbi.nlm.nih.gov/pubmed/8834870
Preuss HG, Echard B. Enig M. Brook I, Elliott TB. Minimum inhibitory concentrations of herbal essential oils and monolaurin for gram-positive and gram-negative bacteria. Molecular and Cellular Biochemistry April 2005, Volume 272, Issue 1–2, pp 29–34 https://doi.org/10.1007/s11010-005-6604-1