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Health Protocols

Peptic Ulcers

Integrative Interventions

Primary Support

Licorice and DGL. Licorice (Glycyrrhiza glabra) root has been used for centuries to treat a wide array of health problems, including peptic ulcers. Deglycyrrhizinated licorice, or DGL, is made by removing a component of licorice that has been associated with side effects such as fluid retention and high blood pressure (Shibata 2000; Borrelli 2000; UMMC 2016).

In a randomized, double-blind, placebo-controlled trial, 100 patients who tested positive for H. pylori were treated with 150 mg per day of a DGL preparation or placebo for 30 days. At the end of the treatment period, 56% of the DGL group and 4% of the placebo group tested negative for H. pylori (Puram 2013). The addition of licorice to standard treatment of H. pylori-positive ulcers has also been shown to be beneficial. In a randomized controlled trial, licorice extract improved the H. pylori eradication rate of standard triple therapy (the combination of two antibiotics plus a proton pump inhibitor [PPI]) (Hajiaghamohammadi 2016), while another controlled clinical trial found that triple therapy plus licorice extract was as effective as bismuth quadruple therapy (Momeni 2014).

Licorice root, DGL, and combinations of DGL and antacids have been studied for decades for the treatment of peptic ulcers, with many of these trials finding a positive therapeutic effect (Tewari 1968; Turpie 1969). One trial using a combination product of DGL plus antacids found this preparation to be nearly as effective as cimetidine in reducing recurrence of stomach ulcers over a two-year period (Morgan 1985). In a clinical trial, concurrent administration of DGL and aspirin significantly reduced aspirin-induced bleeding, as measured by fecal blood loss (Rees 1979).

In a rat model, the incidence of aspirin-induced ulcers was reduced by half when the aspirin was coated with different forms of licorice, including DGL (Dehpour 1994). In other animal research, a DGL preparation reduced gastric acidity and decreased ulceration due to NSAID exposure and stress (Mukherjee 2010), and both licorice root extract and omeprazole (Prilosec, a PPI) were effective in preventing NSAID-induced ulcers (Jalilzadeh-Amin 2015).

Licorice compounds present in DGL have demonstrated anti-inflammatory, free radical-scavenging, and anti-ulcer activities in preclinical research (Choi 2015; Mukherjee 2010). DGL has also been shown to increase the number of mucous-producing cells and enhance mucous secretion in the rat stomach (van Marle 1981). Animal and laboratory studies confirm that compounds in licorice and DGL have activity against H. pylori, including antibiotic-resistant strains (Kim 2013; Krausse 2004; Fukai 2002; Wittschier 2009).

Zinc-carnosine. Zinc-carnosine, also called polaprezinc, is a combination of the mineral zinc and L-carnosine, a compound composed of the amino acids beta-alanine and L-histidine. Zinc-carnosine is thought to help protect the gastrointestinal lining (Watari 2013; Mahmood 2007).

In a randomized clinical trial in 66 participants with symptomatic H. pylori infection, zinc-carnosine significantly improved the ability of standard triple therapy (two antibiotics plus a proton pump inhibitor) to eradicate H. pylori. In those who completed treatment, 86% treated with triple therapy alone achieved eradication while 100% treated with triple therapy plus zinc-carnosine (150 mg twice daily) were H. pylori-negative four weeks after treatment (Kashimura 1999). In 20 patients with injury to the small intestine caused by low-dose aspirin, treatment with 150 mg per day of zinc-carnosine for four weeks resulted in a significant reduction in mucosal injury and ulcers compared with no treatment (Watari 2013). In another trial, 10 healthy individuals were treated for seven days with 37.5 mg twice per day of zinc-carnosine, or placebo. During the final five days, study subjects also consumed the NSAID indomethacin (Indocin, Tivorbex). Those who received placebo experienced a three-fold increase in intestinal permeability (a sign of mucosal damage), while those treated with zinc-carnosine did not have a significant increase in gut permeability (Mahmood 2007).

Studies using animal models of gastrointestinal mucosal damage have also demonstrated the cell-protective and anti-ulcer effects of zinc-carnosine (Choi 2013; Cho 1991; Seiki 1990). Among zinc-carnosine’s possible mechanisms of action are a reduction in inflammation, neutralizing tissue-damaging free radicals, preventing intestinal cell death, and protecting the tight junctions that link mucosal cells together (Watari 2013; Choi 2013).

Probiotics. Probiotics are microorganisms that confer health benefits when ingested (Lesbros-Pantoflickova 2007). Lactobacillus species, commonly used in probiotics, have been shown in laboratory studies to inhibit the growth of H. pylori and reduce H. pylori-associated inflammation (Enany 2015), and numerous randomized controlled trials have found that the addition of probiotics to standard antibiotic therapy markedly improves the success of H. pylori eradication (Boltin 2016; Dang 2014; Ma 2015). In one randomized trial, probiotics combined with triple therapy (two antibiotics plus a PPI) was compared with triple therapy alone in patients with H. pylori-associated peptic ulcers. The addition of probiotics resulted in an H. pylori eradication rate over 24% higher, and a total treatment effectiveness rate over 13% higher, compared with triple therapy alone (Ma 2015).

An important potential benefit of probiotics is the reduction of antibiotic-associated side effects, particularly diarrhea (Boltin 2016). An analysis of randomized controlled trials determined that Saccharomyces boulardii, a probiotic yeast, decreased side effects of antibiotic treatment of H. pylori (Dang 2014).

Lactobacillus reuteri DSM17648 is a probiotic strain that specifically binds to H. pylori bacteria in the gut, preventing them from adhering to the gastric mucosa and reducing their numbers in the stomach. L. reuteri DSM17648 supplements have been shown to decrease the H. pylori load in healthy H. pylori-positive individuals, and may thus prevent future H. pylori-associated problems, including the need for antibiotic treatment. These clinical effects of L. reuteri DSM 17648 were also demonstrated by preparations in which the L. reuteri bacteria were killed by freeze-drying or spray-drying procedures (Holz 2015; Mehling 2013). Similarly, S. boulardii has been found to reduce gastric colonies of H. pylori in symptom-free H. pylori-positive subjects (Namkin 2016).

Lactoferrin. Lactoferrin is a component of milk (Vogel 2012). It has been the subject of numerous clinical trials investigating its ability to eradicate H. pylori. A meta-analysis examined five randomized controlled trials that evaluated whether lactoferrin treatment was effective for H. pylori eradication. A total of 682 subjects took part in these trials, 316 of whom received lactoferrin, with the remainder serving as controls. Those who received lactoferrin had more than 2.2-fold higher odds of eradication compared with controls (Sachdeva 2009).

A later review suggested a number of different mechanisms by which lactoferrin could have an anti-H. pylori effect, including a complementary action to antibiotics, inhibition of H. pylori growth, and a reduction in the rate of treatment side effects (Sachdeva 2014).

Flavonoids/polyphenols. Polyphenols, naturally occurring compounds present throughout the plant kingdom, are obtained in the diet mostly from fruits, vegetables, spices, grains, coffee, tea, and wine (Cardona 2013). Flavonoids make up the largest group of polyphenolic compounds. Evidence from numerous studies indicate polyphenols, including flavonoids, hold promise in the prevention and treatment of peptic ulcers (Farzaei 2015; Mota 2009). Extracts from tea, apples, pomegranate, and grape seed are especially good sources of polyphenols with possible anti-ulcer and anti-H. pylori activity (Farzaei 2015; Ankolekar 2011).

Curcumin, the principal active ingredient in the spice turmeric (Curcuma longa), is a flavonoid with strong free radical-scavenging, anti-inflammatory, and anti-bacterial properties. In particular, curcumin has been found to reduce symptoms in those with H. pylori-associated ulcers when used in combination with standard triple therapy (two antibiotics plus a PPI) (Khonche 2016; Di Mario 2007). Preclinical and animal studies have found that curcumin protects against NSAID-induced and stress-induced ulcers by increasing gastric blood flow, decreasing gastric acid secretion, protecting against mucosal injury, and reducing H. pylori-induced inflammatory tissue damage (Sharma 2012; Morsy 2013; Kim 2016; Santos 2015).

Quercetin is a flavonoid found in a wide variety of plants and plant foods (Suganthy 2016). Findings from animal studies suggest quercetin may help prevent and heal peptic ulcers (Suzuki 1998; Yan 2011; Zahorodnyi 2003). Quercetin’s antihistamine activity may reduce gastric acidity (Farzaei 2015; Kahraman 2003).

Additional Support

Cranberry. Cranberry (Vaccinium macrocarpon), a good source of anthocyanins and well known for its usefulness against urinary tract infections, has also demonstrated anti-H. pylori properties in preclinical, animal, and clinical models (NIH 2016; Matsushima 2008).

In a randomized controlled trial in a population at high risk for stomach cancer, 90 days of twice-daily consumption of cranberry juice was more effective than placebo at suppressing H. pylori infection (Zhang 2005). In another randomized controlled trial, the addition of cranberry juice to triple therapy (two antibiotics plus a PPI) markedly improved the rate of H. pylori eradication in women (Shmuely 2007).

In preclinical research, cranberry extract inhibited the growth and proliferation of H. pylori. This action was attributed to its polyphenol components (Matsushima 2008). A compound from cranberry has been shown to prevent H. pylori from attaching to stomach lining cells and to mucus (Burger 2002; Burger 2000).

Glutamine. Glutamine, the most abundant amino acid in the body, is a major metabolic fuel for cells of the intestinal lining and immune cells (Zuhl 2015; Lacey 1990). Preclinical, animal, and human studies have shown that glutamine supplementation can help repair the intestinal lining (Zuhl 2015; Wang 2016).

Glutamine supplementation may be beneficial in preventing injury due to H. pylori infection. In a study in mice infected with H. pylori, supplemental dietary glutamine protected the stomach mucosa by modulating the immune response to H. pylori and reducing inflammation (Hagen 2009). In another study, long-term supplementation with glutamine prevented cancerous change in gastric mucosa of H. pylori-infected gerbils (Amagase 2010).

Vitamin C. In multiple trials, vitamin C deficiency has been associated with peptic ulcer disease, gastritis, H. pylori infection, and bleeding from peptic ulcers (Aditi 2012). At least one author has proposed that vitamin C may help prevent reinfection in those who have been treated for H. pylori infection, based on experimental evidence that vitamin C inhibits growth and colonization of H. pylori (Pal 2011).

In a randomized controlled trial, the addition of oral vitamin C (500 mg per day) to bismuth quadruple therapy was compared with the same quadruple therapy alone. The addition of vitamin C resulted in a significantly higher H. pylori eradication rate (78% vs. 49%) (Zojaji 2009). In a randomized clinical trial in patients with H. pylori infection and chronic gastritis, high-dose vitamin C treatment (5 grams daily for four weeks) resulted in H. pylori eradication in 30% of patients (Jarosz 1998).

Magnesium. Magnesium salts are common ingredients in antacid formulations, but magnesium also appears to possess important anti-ulcer properties. In one animal study, rats were pre-treated with magnesium before administration of an NSAID (indomethacin) to induce ulcers. Compared with an untreated control group, the magnesium-treated rats had significantly reduced ulcer formation. The anti-ulcer effects of magnesium were attributed to its ability to decrease the number of acid-secreting cells and increase the number of mucous-producing cells in the stomach (Adewoye 2013).

Whey protein. In animal studies, whey and whey protein-derived compounds have demonstrated ulcer-protective properties (Castro 2010; Rosaneli 2004; Rosaneli 2002). These effects of whey protein may be related to its role in raising levels of glutathione, which shields the mucosal lining from free radical damage (Rosaneli 2002). Whey protein contains high levels of sulfur-containing amino acids such as cysteine, which is utilized in the synthesis of glutathione, a powerful scavenger of free radicals (Zavorsky 2007). Increased mucous production and lower plasma gastrin (an acid-stimulating hormone) may also help explain whey protein’s mucosal protection (Castro 2010).

Phospholipids. The prevalence of duodenal ulcers is higher in countries where the diet is based on refined plant foods such as milled rice and wheat. Conversely, the duodenal ulcer rate is lower in countries where staple foods consist of unrefined wheat, corn, soy, millet, and legumes. Experimental studies have determined that the lipid portion of these whole, unrefined foods (eg, oil from wheat germ or bran) protects the stomach and duodenal mucosa by increasing gastric mucous production and forming a protective barrier against stomach acid (Tovey 2015). Within the lipid portion, phospholipids have been identified as active components (Tovey 2015; Tovey 2013).

In a clinical trial, 204 subjects between 50 and 74 years old were given either aspirin (325 mg daily) or the same dose of aspirin complexed with phosphatidylcholine for seven days; those who received the phosphatidylcholine-aspirin complex had less evidence of gastric and duodenal mucosal damage and ulcers compared with those receiving aspirin alone (Cryer 2011). Animal studies suggest phospholipids may protect against the damaging effects of other NSAIDs such as naproxen and indomethacin as well (Tovey 2015).

Aloe vera extract. Aloe vera extracts have been shown to have healing and anti-inflammatory effects for skin damage, burns, pain, and edema. Preclinical and animal studies have found that Aloe vera also has gastroprotective and anti-ulcer properties (Keshavarzi 2014; Eamlamnam 2006).

In an early trial in 12 patients diagnosed with peptic ulcer disease, administration of a tablespoon of Aloe vera gel emulsion daily led to complete recovery (Blitz 1963). Results from animal studies indicate Aloe vera inhibits secretion of stomach acid (Keshavarzi 2014; Yusuf 2004), reduces gastric mucosal inflammation, and enhances stomach ulcer healing (Eamlamnam 2006; Park 2011). In a laboratory study, the inner gel of Aloe vera inhibited the growth of H. pylori bacteria, including antibiotic resistant strains (Cellini 2014).


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This information (and any accompanying material) is not intended to replace the attention or advice of a physician or other qualified health care professional. Anyone who wishes to embark on any dietary, drug, exercise, or other lifestyle change intended to prevent or treat a specific disease or condition should first consult with and seek clearance from a physician or other qualified health care professional. Pregnant women in particular should seek the advice of a physician before using any protocol listed on this website. The protocols described on this website are for adults only, unless otherwise specified. Product labels may contain important safety information and the most recent product information provided by the product manufacturers should be carefully reviewed prior to use to verify the dose, administration, and contraindications. National, state, and local laws may vary regarding the use and application of many of the treatments discussed. The reader assumes the risk of any injuries. The authors and publishers, their affiliates and assigns are not liable for any injury and/or damage to persons arising from this protocol and expressly disclaim responsibility for any adverse effects resulting from the use of the information contained herein.

The protocols raise many issues that are subject to change as new data emerge. None of our suggested protocol regimens can guarantee health benefits. The publisher has not performed independent verification of the data contained herein, and expressly disclaim responsibility for any error in literature.