Natural H. Pylori Treatment and a Brief Overview of its Ill Health Effects & the Scientific Debate About Whether its Eradication Would Necessarily be Good for Us

An H. pylori infection is not exactly a death sentence, but it can still have nasty consequences.

Over the past decade H. pylori has repeatedly been in the focus of scientific research. It has been linked with gastric carcinoma (Parsonnet. 1991; Huang. 1998). The summary of odds-ratio of a 198 meta-analysis by Huang et al. for example shows increases of cancer risk of 92%, 124% and 81% in infected patients for all studies, cohort, and case-control studies, respectively. The meta-analysis also found that "H. pylori–infected younger patients have a higher relative risk for gastric cancer than older patients with odds ratios decreasing from 9.29 at age ≤29 years to 1.05 at age ≥70 years." (Huang. 1998).

But cancer is only the "worst case" scenario, when it comes to the potential (ill) health effects of being infected with H. pylori.

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The Helicobacter pylori bacterium has also been associated with in cases of chronic gastritis, functional dyspepsia, peptic or duodenal ulcers, and cancer or gastric lymphomas.

"Because it can survive in acidic environments, it remains intact in the stomach and promotes the destruction of the gastric mucosa. This makes the organ sensitive and vulnerable to triggering of ulcerative lesions and blocks the sterilization of food, producing failures in the digestion process." (Bonifácio. 2014)

Atrophic gastritis, which is a common consequence of rampant H. pylori infections, may cause pernicious anemia because it interferes with the absorption of vitamin B12 from food. The symptoms of gastritis in general are burning, abdominal pain, loss of appetite, nausea, vomiting, feeling of satiety and gastrointestinal bleeding.

One question that arises is: How likely is it that you are infected?

With worldwide prevalence estimated at between 50 and 90%, this type of cancer frequently occurs in developing countries. And one of the most comprehensive reviews of the literature confirms, the answer to this question may well depend on where you live.

Table 1: Population-based studies of Helicobacter pylori prevalence according to detection method,
published between April 2008 and March 2009 (Azevedo. 2009).

As a brief glimpse at the data in Table 1 shows, the number of infected individuals is lowest in Japan (in kids) and highest in African immigrants to Australia.

How is H. pylori transmitted? Laboratory studies have yielded evidence in favor of both faecal-oral and oral-oral pathways. However, a role for either waterborne or zoonotic transmission has not been ruled out. Overall, "the failure of investigations to single out a mode of transmission for H. pylori signals the possibility of multiple transmission pathways." (Goodman. 1995)

A classic, pharmacological "H. pylori" eradication scheme that would of which recent studies show that it is more effective if a metronidazole-based therapy is chosen over the standard clarithromycin-based therapy (Nishizawa. 2014), is yet something you should only contemplate if you have actually been diagnosed with the nasty gram-negative, microaerophilic bacterium. If you only suspect being infected or want to reduce your risk of being affected, the following natural H. pylori treatments are certainly preferable to the nitroimidazole antibiotic medication metronidazole:

• 

  Feijoa sellowiana (O.Berg) is one of the natural anti-H. pylori agent (Basile. 2010)

  Feijoa sellowiana fruits have been shown to inhibit the growth of Helicobacter pylori by Basile et al. in 2010.
• Leaves of Strychnos pseudoquina ST. HIL. (Loganiaceae) or rather a methanolic extract from these leaves which have been used traditionally as malaria treatment has been shown to be effective in a rodent study by Silva et al. (2005).
• Chamomille or more specifically an extract from the inflorence of the camomille flower (Cogo. 2010).
• Achiote (Bixa orellana) or rather a tincture that's made from the seeds of this shrub or small tree originating from the tropical region of the Americas (Cogo. 2010).
• Green Yerba mate leaves are another effective H. pylori treatment as Schubert et al. point out in a 2006 paper. Whether drinking mate tea will do the same, has not been established, though.

Maybe H. pylori  is not always bad!? As strange as it may sound, some scientists argue that the contemporary evidence that "with modern life, for probably the first time in human history, there are large numbers of noncolonized persons" and that this decrease in H. pylori infections was associated with an increase in gastroesophageal reflux (GERD), Barrett's esophagus, and adenocarcinomas of the gastric cardia and lower esophagus. These diseases are not directly related to H. pylori, but "colonization with cag+ H. pylori strains appears protective against these diseases." Accordingly, the authors of one of the more recent papers elaborating on this hypothesis conclude: "[I]n the 21st century, the continuing decline in H. pylori may lead to the disappearance of duodenal ulcers and distal gastric cancers and toward a marked increase in GERD, Barrett's esophagus, and esophageal adenocarcinoma." (Blaser. 1999)

• Garlic extracts are another of the better-known H. pylori treatments (Cellini. 1996)
• Pistacios, or rather the mastic gum from Pistacia lentiscus (L.) var. chia (Duham) has been found to inhibit H. pylori growth by Paraschos et al. (2007).
• Malva sylvestris inflorences and leaves have been shown to inhibit the growth of H. pylori by Buffon et al. (2001)
• False rubarb, aka Rheum rhaponticum roots have been reported to be effective H. pylori killers (Cogo. 2010).
• Pomegranate peels exhibit anti-H. pylori activity, as well (Hajimahmoodi. 2011).

Table 2: Anti-Helicobacter pylori activity of essential oils (Bonifácio. 2014)

Next the aforementioned plants, fruit and fruit parts which are usually used as methanolic or aqueous extracts, there is a good dozen of essential oils of which a recent review by Bonifácio et al. (2014) indicates that all of them exert significant inhibitory effects on H. pylori (see Table 2).

As you can see in Table 1 the major problem is that in vivo studies, i.e. studies in which the oil was tested in intact organisms, in the case of the essential oil from Cymbopogon aka lemongrass the anti-H. pylori effects were observed in vivo, as well (in a mouse study by Ohno et al. (2003), to be precise).

Against that background it remains to be seen if any of the previously mentioned oils, fruits, plants and plant extracts are "strong" enough to eradicate a rampant H. pylori infection in a living human being. What appears to be likely, though, is that they could prevent it from becoming "rampant" in the first place.

H. pylori eradication is not the only thing pistachios can do for you - find out more in "The Pistachio Manifesto: Antioxidant, Metal Chelator, DNA Protector, Anti-Cancer Agent, Bug Killer  & More." | read more

Bottom line: While the is conclusive evidence that certain strains, but not all forms of H. pylori increase your risk of developing gastric cancer. There is (a) evidence that some strains may actually protect you from developing other gastrointestinal diseases (see red box) and (b) insufficient data from in vivo studies to recommend any of the previously listed agents as an "effective replacement" for the standard course of antibiotics doctors usually prescribe to eradicate H. pylori.

That being said, it is non unlikely that the regular consumption of garlic and pistacios or the use of essential oils from lemon grass could protect you from being infected or infections from flaring up | Comment on Facebook!

References:

• Azevedo, Nuno F., Janis Huntington, and Karen J. Goodman. "The epidemiology of Helicobacter pylori and public health implications." Helicobacter 14.s1 (2009): 1-7.
• Basile, Adriana, et al. "Antibacterial and antifungal properties of acetonic extract of Feijoa sellowiana fruits and its effect on Helicobacter pylori growth." Journal of medicinal food 13.1 (2010): 189-195.
• Blaser, Martin J. "Hypothesis: the changing relationships of Helicobacter pylori and humans: implications for health and disease." Journal of Infectious Diseases 179.6 (1999): 1523-1530. 
• Bonifácio, Bruna V., et al. "Antimicrobial Activity of Natural Products Against Helicobacter pylori: A Review." Annals of clinical microbiology and antimicrobials 13.1 (2014): 54. 
• Buffon, Marilene da Cruz Magalhães, et al. "Avaliação da eficácia dos extratos de Malva sylvestris, Calendula officinalis, Plantago major e Curcuma zedoarea no controle do crescimento das bactérias da placa dentária. Estudo" in vitro." Revista Visão Acadêmica 2.1 (2001): 31-38. 
• Cellini, Luigina, et al. "Inhibition of Helicobacter pylori by garlic extract (Allium sativum)." FEMS Immunology & Medical Microbiology 13.4 (1996): 273-277.
• Cogo, Laura Lúcia, et al. "Anti-Helicobacter pylori activity of plant extracts traditionally used for the treatment of gastrointestinal disorders." Brazilian Journal of Microbiology 41.2 (2010): 304-309.
• Goodman, Karen J., and Pelayo Correa. "The transmission of Helicobacter pylori. A critical review of the evidence." International Journal of Epidemiology 24.5 (1995): 875-887.
• Hajimahmoodi, M., et al. "In vitro antibacterial activity of some Iranian medicinal plant extracts against Helicobacter pylori." Natural product research 25.11 (2011): 1059-1066.
• Huang, Jia-Qing, et al. "Meta-analysis of the relationship between Helicobacter pylori seropositivity and gastric cancer." Gastroenterology 114.6 (1998): 1169-1179. 
• Nishizawa, Toshihiro, et al. "Clarithromycin Versus Metronidazole as First-line Helicobacter pylori Eradication: A Multicenter, Prospective, Randomized Controlled Study in Japan." Journal of clinical gastroenterology (2014).
• Parsonnet, Julie, et al. "Helicobacter pylori infection and the risk of gastric carcinoma." New England Journal of Medicine 325.16 (1991): 1127-1131. 
• Paraschos, Sotirios, et al. "In vitro and in vivo activities of Chios mastic gum extracts and constituents against Helicobacter pylori." Antimicrobial agents and chemotherapy 51.2 (2007): 551-559.
• Schubert, Alexandre, et al. "Variação anual de metilxantinas totais em amostras de Ilex paraguariensis A. St.-Hil.(erva-mate) em Ijui e Santa Maria, Estado do Rio Grande do Sul." Quim. Nova 29.6 (2006): 1233-1236.
• Silva, Marcelo Aparecido da, et al. "Evaluation of Strychnos pseudoquina St. Hil. leaves extract on gastrointestinal activity in mice." Chemical and pharmaceutical bulletin 53.8 (2005): 881-885.

True or False: High Volume + Nutrient + Low Energy Foods Keep You Lean. Bonus-Question: Will a High Volume Make Your Stomach Go Baggy & Mess Up Your Satiety Response?

There are millions of ways to con- sume 100kcal and volume isn't the only difference (img greatist.com)

I have repeatedly pointed out that filling yourself up on vegetables and other high volume, high nutrient (vitamins, minerals, polyphenols, etc.), low energy foods is one of the fundamental principles of weight management. The question that remains, though, is whether this principle is so effective because of the food we eat (tons of veggies), or rather due to the fact that there is no room for the foods we thusly don't eat (the typical processed junk)?

I guess, it's not debatable that replacing trashy foods with healthy ones is the most important factor. We have all heard about the beneficial effects "high volume foods" and the downsides of the average high energy + low nutrient 100kcal junk-food snack. But how important is the volume, actually? Isn't food "quality" (whatever that may be) all that counts?

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It's surprisingly difficult to answer this question and after reviewing the most important studies, I have to say that I still can't tell for sure how important the volume is.

Figure 1: Effects of pylorectomy (removal of the part of the stomach that contains the vagal nerves) and vagal deafferetation on the ability of CCK to affect liquid food intake in rats (Moran. 1988)

What I can tell you, though, is that it appears to be certain that the mechanical stretch will be detected by vagal affarent endings in the stomach (Phillips. 2000; Berthoud. 2001). These "stretch detectors" are hard-wired to your brain, where they are processed in the so-called "nucleus tractus solitarius" (Näslund. 2007). Unfortunately, the exact role of the "nucleus tractus solitarius" in the satiety response is not even partly understood.

What we do know is that electrophysiological recording studies as well as behavioral studies have found that the effect of a given dose of cholecystokinin (CCK) is increased in the presence of stomach stretch (Schwartz. 1993 & 1995) and disrupted, when the vagus nerve is damaged or the NTS lesioned (Edwards. 1986; Moran. 1988; Smith. 1985).

With CCK being a major satiety hormone (and on top one that actually does what it's name implies, i.e. signal satiety) it appears to be quite certain that the multiplying effect the mechanical stretch exerts on the satiety effect of CCK is one of the secondary mechanisms by which eating high volume foods keep you lean.

Do you remember? You've read about a couple of things that will increase the release of CCK and would thus synergize with the effects of what I would like to call "high volume eating": (1) The pre-ingestion of protein before a meal | learn more, (2) Arginine, lysine and glutamic acid | learn more, and lastly and unsurprisingly a gastric bypass operation | learn more. Another well-known trigger of CCK release is the ingestion of fatty acids (low amounts suffice; long chain polyunsaturated fatty acids are particularly effective; Gribble. 2012) - is not satiating.

In view of the fact that the NTR, ie. the nucleus tractus solitarius, integrates (adds up and processes) a whole host of signals from the gastro-intestinal tract, it's also hardly surprising that a gastric bypass surgery and the corresponding increase in stretch per volume unit of food that has just recently been shown to change not just the satiety response to food but also the way foods taste and smell for patients who have undergone Roux-en-Y gastric bypass surgery (learn more in the SuppVersity Facebook News).

Figure 2: Model depicting signals that influence food intake. Not all elements are relevant in the context of this article - focus on the way the satiety signals that are generated in the gastrointestinal (GI) tract during meals provide information about mechanical (e.g., stomach stretch, volume) and chemical properties of the food to the brain (Woods. 2004)

Other mechanisms by which the gastric stretch may contribute to an increase in satiety / reduction in food intake and, via the release of GLP-1 and other glucose regulating satiety hormones (learn more about GLP-1) are the reduction of gastric emptying (Read. 1994), and other interactions between the vagus nerve and the brain, which include aside from directly satiety related mechanisms also the activation of serotonergic neurons (remember: serotonin is the happy hormone) in the brain (Mazda. 2004).

Bonus question: Is high volume eating setting you up for obesity? You could argue that the constant gastric distension and consequently increased postprandial gastric accommodation will reduce the satiety response to small calorie dense meals. Now aside from the fact that you will get fat, no matter what if you eat those on a daily basis, a study from the Gastroenterology Research Unit in Rochester and the Mayo Clinic did not find a sign of increased postprandial gastric accommodation or reduced satiety in any of of their 13 obese subjects (Kim. 2012).

So, yes! There is more to eating tons of veggies than not eating tons of other food. Moreover, although we don't yet know exactly what this "more" is, we can already say that all the existing evidence appears to support that it the high food volume, the stretch of the stomach and the vagally mediated downstream effects on the release and effect of our satiety hormones (incretins) is one of the factors that contribute to the ability of high volume, high nutrient, low energy foods to keep you lean.

On it's own, the multi-layered stretch-response is probably significantly less important than the reduction in junk-food intake. In conjunction with the synergistic effects of a high protein diet, and a reasonable amount of long-chain fatty acids in the diet, it could yet be what distinguishes people who have to resort to a gastric bypass as a last resort to save their lives from those individuals, who manage to flip the switch, turn their life around and lose their life-threatening overweight without the help of a surgeon.

References:

• Berthoud, Hans-Rudolf, Penny A. Lynn, and L. Ashley Blackshaw. "Vagal and spinal mechanosensors in the rat stomach and colon have multiple receptive fields." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 280.5 (2001): R1371-R1381.
• Edwards, et al. "Dorsomedial hindbrain participation in cholecystokinin-induced satiety." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 251.5 (1986): R971-R977. 
• Gribble, Fiona M. "The gut endocrine system as a coordinator of postprandial nutrient homoeostasis." Proceedings of the Nutrition Society 71.4 (2012): 456. 
• Kim, Doe‐Young, et al. "Is there a role for gastric accommodation and satiety in asymptomatic obese people?." Obesity research 9.11 (2001): 655-661.
• Mazda, Takayuki, et al. "Gastric distension-induced release of 5-HT stimulates c-fos expression in specific brain nuclei via 5-HT3 receptors in conscious rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 287.1 (2004): G228-G235.
• Moran, Timothy H., et al. "Pylorectomy reduces the satiety action of cholecystokinin." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 255.6 (1988): R1059-R1063.
• Näslund, Erik, and Per M. Hellström. "Appetite signaling: from gut peptides and enteric nerves to brain." Physiology & behavior 92.1 (2007): 256-262.
• Phillips, Robert J., and Terry L. Powley. "Tension and stretch receptors in gastrointestinal smooth muscle: re-evaluating vagal mechanoreceptor electrophysiology." Brain research reviews 34.1 (2000): 1-26.
• Read, Nicholas, Stephen French, and Karen Cunningham. "The role of the gut in regulating food intake in man." Nutrition reviews 52.1 (1994): 1-10.
• Schwartz, Gary J., et al. "Gastric loads and cholecystokinin synergistically stimulate rat gastric vagal afferents." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 265.4 (1993): R872-R876.
• Schwartz, Gary J., Gervais Tougas, and Timothy H. Moran. "Integration of vagal afferent responses to duodenal loads and exogenous CCK in rats." Peptides 16.4 (1995): 707-711.
• Smith, Gerard P, et al. "Afferent axons in abdominal vagus mediate satiety effect of cholecystokinin in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 249.5 (1985): R638-R641.
• Woods, Stephen C. "Gastrointestinal satiety signals I. An overview of gastrointestinal signals that influence food intake." American Journal of Physiology-Gastrointestinal and Liver Physiology 286.1 (2004): G7-G13.