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The Role of L.Reuteri DSM17648 and MANC in the Reduction of Helicobact


H.pylori is a gram-negative, spiral-shaped human pathogen infecting an estimated 60% of the global population.1. It has the ability to survive the acidic environment of the stomach and adhere to the gastric mucosa, colonizing the mucosal lining of the stomach. An estimated 104–107 H. pylori colony forming units (CFU) per g of gastric mucus can be found in infected persons 2. The spiral shape of H. pylori allows for penetration into the stomach lining where they are protected by the mucus lining.  While H. pylori reside in the mucus where it is present in its motile form, mucus is constantly produced by the epithelium and shed into the stomach lumen. This continuously releases planktonic H. pylori cells into the stomach.

H.pylori infections are usually harmless but are also associated with a number of gastrointestinal diseases, such as peptic ulcer disease and gastric cancer3. The infection can also lead to an inflammatory response, increased secretion of gastric acid, and type-B gastritis. Interestingly, the severity of the clinical manifestations of the infection is associated with bacterial load 4

Helicobacter pylori infection in humans can cause gastritis. The infection elicits a complex immune response in which the activation of mast cells and histamine release is of particular importance. Histamine further promotes the immune response and stimulates gastric acid secretion.9 This may further explain the role of Histamine in inflammation within the digestive tract.

Pharmaceutical therapeutic options for H. pylori-infection aiming at complete eradication include various combinations of proton pump inhibitors combined with two to three different antibiotics. This complex approach has inherently high risks of side effects and non-compliance as well as intestinal microbiota damage and the development of antibiotic resistance.  Therefore, there remains a therapeutic gap for persons infected by H. pylori. 



As mentioned earlier, H pylori are residing in the mucosal lining of the stomach and are continuously releasing H. pylori bacteria into the stomach.  Much research has been undertaken to find ways of capturing and reducing the bacteria within the stomach.  

In recent years, pieces of evidence have accumulated suggesting that H. pylori could be eradicated from the stomach through selective intercellular interactions by some particular Lactobacillus strains5. 

 But which strain is the correct one?

Again, research has been undertaken to find this out.  Tests were made on a large Lactobacillus strain collection. The in-house, private strain collection was assembled from wild-type strains of diverse origin, such as food sources, plants, vegetables or human skin. The strains were classified according to the physiological characteristics prior to being included in the screening process. Among over 700 Lactobacillus strains tested, only eight were found to co-aggregate with spiral forms of H. pylori strain. Of these eight, one showed the most beneficial results and was studied further. 

The results showed that Lactobacillus reuteri DSM17648 interferes with the mobility of H. pylori.  

The surface structures on L. reuteri DSM17648 contains adhesion molecules that recognise and adhere to the surface structures of H. pylori in the gastric mucosa. Once bound, the H. Pylori alongside the L. reuteri will be flushed from the stomach by a natural bowel movement. Interestingly, the aggregation activity was preserved when the cells were killed by freeze-drying or spray drying. It can, therefore, show that the binding is due to specific surface molecules of the Lactobacillus reuteri DSM17648 cells which are strain-specific and are resistant to such process steps.6.

These results have again been repeated in a small in vivo study of 22 people which showed a significant decrease of H. pylori stomach colonisation after Lactobacillus reuteri DSM17648 supplementation in asymptomatic subjects with detectable H. pylori infection7

A further study combined L. reuteri in association with extract of deglycyrrhizinated liquorice and calcium carbonate vs Triple Therapy.  They found that this combination was successful in eradicating H. pylori in over 50% of patients and had good tolerability and compliance8.  This could be an interesting protocol for practitioners to try with their patients.

Alternatively, using the Lactobacillus Reuteri DSM17648 on its own has shown beneficial results even with young children10



H.pylori releases the urease enzyme which divides urea into carbon dioxide and ammonia. H. pylori also produce histamine which it uses to increase the acidity in the stomach. Using a process called ‘protonation’, ammonia picks up the hydrogen to produce ammonium. This allows the H. pylori to use both the ammonia and ammonium as a shield to protect itself against the gastric acid. Ammonium is also now known to make the stomach lining more soluble which allows the H pylori to burrow through more easily.

MANC® absorbs and eliminates ammonium from the stomach and intestines. MANC® binds and eliminates histamine produced by the H.Pylori, thereby alleviating the associated digestive problems. This also stops histamine being absorbed by the body, where it would be free to circulate and cause other histamine modulated symptoms in other areas where histamine receptors are present e.g. lungs, heart, brain, skin.

MANC® also binds and eliminates the protective shield of ammonium which allows H. Pylori to survive in the stomach.

Over 5 days, the ammonium shield can be slowly broken down, leaving the bacteria exposed to the acidic stomach conditions. Gastric acid is then able to kill off the infestation and eliminate H. Pylori, stopping further production of ammonium and reducing the burden on the liver created from H. Pylori.

This also optimises the level of acid in the stomach, ensuring that there isn't too much acid, nor too little acid.  Once the MANC® has bound to toxins (such as ammonium), it travels through the digestive tract where it is passed out with the body’s natural bowel movement.



Carry out the following procedure each morning for 5 days:

8:00am: Stir 3 x Toxaprevent Medi PLUS Sachets into 200ml of water and drink slowly over the next hour, on an empty stomach

9:00am: Eat several small bites from a bread roll (or vegan substitute) to stimulate acid production in the stomach

10:00am: Stir 3 more Toxaprevent Medi PLUS Sachets into 200ml of water and drink slowly over the next hour

11:00am: Again, eat several small bites from a bread roll (or vegan substitute) to stimulate acid production in the stomach

Do not eat anything until 12:00pm (mid-day)

Do not eat or drink anything extra from 8:00am to 12:00pm (mid-day)

Over the 5 days, it is very important to eat light meals, preferably without meat, and avoid tea, coffee and alcohol. This is due to protein degradation from meat-producing ammonia and, consequently, ammonium, which would contribute towards neutralising gastric acid.

In addition, L. reuteri DSM 17648 can also be used in between 8am and 10am.



  2. Blaser, M.J. Helicobacters are indigenous to the human stomach: Duodenal ulceration is due to changes in gastric microecology in the modern era. Gut 1998, 43,721–727
  3. Ford, A.C.; Axon, A.T. Epidemiology of Helicobacter pylori infection and public health implications. Helicobacter 2010, 15, 1–6.
  4. Varbanova M, Malfertheiner P (2011) Bacterial load and degree of gastric mucosal inflammation in Helicobacter pylori infection. Dig Dis 29:592–599
  5. Tyagi AK, Prasad S, Commentary: probiotic and technological properties of Lactobacillus spp. Strains from the human stomach in the search for potential candidates against gastric microbial dysbiosis. Front Microbiol., 2015; 6: 433.
  6. Significant Reduction in Helicobacter pylori Load in Humans with Non-viable Lactobacillus reuteri DSM17648: A Pilot Study Caterina Holz et al 2014.
  7. Non-Viable Lactobacillus reuteri DSMZ 17648 (PylopassTM) as a New Approach to Helicobacter pylori Control in Humans Heidrun Mehling 1 and Andreas Busjahn 2.
  8. Mihai et al 2019 : Lactobacillus Reuteri – An alternative in the first-line of Helicobacter pylori eradication.
  9. Klausz G et al 2004: Effects of Helicobacter pylori infection on gastric inflammation and local cytokine production in histamine-deficient (histidine decarboxylase knock-out) mice.
  10. Parolova et al 2019 – Gastric microbiota and probiotic opportunities in Helicobacter Pylori eradication in children