15 replies to this topic

[kismet]

Helicobacter pylori: should we test-and treat in the very healthy? Points for discussion.

Herein I propose that it might be beneficial to treat the ”pathogen” even though there is no official recommendation for population-wide screening yet. A note of caution: this is based on a preliminary review, but I think it’s time to act. As a starter I recommend these two reviews, the authorative Maastricht IV/ Florence Consensus Report [1a] and a book chapter by Marshall et al. [1b].

H. pylori has been causally linked to atrophic gastritis, functional dyspepsia, peptic ulcer, gastric cancer and some rare conditions e.g. MALT lymphoma, iron loss, etc. The evidence for (other) extra-gastric benefits and harms is weak and inconsistent [1a, 1b]. The pathogen may promote auto-immune diseases, colorectal adenoma, pancreatic and lung cancer, CVD, disturbed glucose homeostasis, neurodegenerative disorders, etc. Whereas potential benefits from H. pylori infection include: reduced asthma, CVD(!), atopy, inflammatory bowel diseases, weight gain, diarrheal diseases etc. („commensal hypothesis“).

On gastric cancer: preclincal evidence, observational [1a], and non-randomized studies as well as secondary prevention RCTs* support a role [4]. Eradication also improves precancerous lesions at least somewhat - gastric atrophy may improve but metaplasia does not, Rokkas et al. 2007 [3]: point of no return hypothesis.
Recently, follow-up of a large trial and an updated meta-analysis of primary prevention trials was published and both showed a significant reduction in gastric cancer incidence RR=0.66, 0.46-0.95 with n=4 (see suplementary data, Ma et al. 2012) [2]. The meta-analysis looked at N=4+1+1 studies but even excluding the one secondary prevention (Fukase 2008) and another controversial trial (Leung 2004/Zhou 2008) the result was significant. This was an update of the (then-flawed) 2009 analysis[4b]. However, in this large study there was no decrease in all-cause mortality and a non-significant 30% decrease in gastric cancer mortality. This was mostly expected since the predicted decrease in all-cause mortality was ~ 6%. Nonetheless, this result is decent since their eradication treatment was outdated and reinfection rate must be high. OTOH, the Asian data is difficult to generalize and the study quality wasn’t perfect. If we compare it to the HPV vaccine, as an example of an approved treatment scheme, it still looks favorable in my opinion: HPV studies were better quality and larger, but the non-cancer benefits of HPV eradication are very modest vs. H. pylori eradication and all data concerns precancerous lesions only!
All in all, I think the weight of evidence supports population wide screening but the evidence is weak. And if we consider preliminary data on extra gastric effects the case for eradication is stronger, if anything.

But the incidence of gastric cancer is low in the west, particularly in the healthy, no?
Well, yes, but so is the risk of most other diseases, this shouldn’t affect the risk-benefit ratio that much since treatment is very safe.

*to be fair: in this case treatment may only slow cancer progression, if at all, as shown by a recent study (Maehata Y. 2012)

CVD: H. pylori has been linked to CVD e.g. stroke in (nested) case-control studies but prospective cohort studies have been mixed. In fact, the largest study to date found H. pylori to be protective against CVD mortality, but it suffered from multiple testing. (Schöttker et al. 2011) [7]

On esophagal cancer: This is the best supported problem with H. pylori eradication. Observational studies suggest a protective role in GERD, barret esophagus and adenocarcinoma but RCTs and meta-analyses do not support a net effect of eradication on GERD, which may even improve afterwards; or worsen in some cases [1a]. Confusingly, some observational studies even showed protection from esophageal cancer depending on the location of infection: “It is associated with a reduced risk of oesophageal adenocarcinoma when it induces gastric atrophy but an increased risk when it induced a non-atrophic antral-predominant gastritis. It is now also associated with squamous cell carcinoma when it induces atrophic gastritis.” (McColl 2007) [5]
On the other hand, the large experimental study cited above [2] did find a non-significant excess of esophageal cancers. This is not that concerning because GERD can be managed relatively well and, mechanistically, eradication should only worsen existing GERD. One should closely monitor for GERD symptoms, nevertheless. Since deaths from e.-adenocarcinoma are about as abundant as deaths from stomach cancer in the US, in the very worst case this might more or less offset gastric cancer benefits.

Other risks of killing H. pylori: interestingly, most diseases that H. pylori could prevent are relatively easily manageable, early onset and/or low mortality. Also, the harms of H. pylori are well supported, the benefits are not and they are balanced by other speculative extra-gastric harms, see the reviews.

So Is H. pylori a beneficial commensal? As far as I know a variation on this theme has been championed by Blaser [7]. However, commensal does not equal beneficial: drift, recent acquisition or antagonistic pleiotropy may explain negative effects of a commensal. "early benefits, late harms" is emerging as a plausible mode of action for the pathogen and Blaser indeed suggests something along this line.
This fact coupled with the problem that gastric atrophy/IM may be irreversible [1a, 3] means that early adulthood is the best time for treatment (this is the second good reason to get rid of H. pylori).



Interactions with dietary salicylates [8a, 8b]: early reports most probably over estimated salicylate content. In a recent systematic review [8b] the mean intake was 3.2/4.4mg mg in a UK population and South Indian vegetarian diets contain 12-13 mg. Dietary intakes vary greatly depending on what you consume. Spices and herbs, particularly those consumed in large quantities (say, ~100g), wine, tea, fruit/veg, grains, certain legumes are important contributors to one’s intake. Since I can’t access the systematic review (please, PM me the pdf), I am relying on this review as “secondary/tertiary source”. [8a]
Notably, top serum levels of vegetarians can be higher than those of south Indians and both overlap with low dose aspirin users. Top quartile serum levels in a recent adenoma study were also very high. Calculated intakes probably underestimate actual intakes because salicylate precursors e.g. benzoic acid are not included, organically grown food contains more salicylates and they are found in toothpaste and mouthwash (as per [8]). Now consider this: Aspirin– 1mg equals ~0.9mg salicylic acid – intakes as low as 10mg have been linked to GI damage (single RCT), also there is little or only a very flat does response relationship between ~80 and 300 mg of aspirin & GI side-effects (meta-analysis) - and to some extent this must extend downwards of 80mg. Obviously, the COX/prostaglandin pathway might also be inhibited and bleeding risk increased by other typically healthy foods and behaviours.
This could – I speculate–make the “very healthy” exceptionally susceptible to GI damage, enhanced by H. Pylori. As per recommendation, Aspirin (particularly naïve) users should benefit more from eradication than the general population [1a]:

“H pylori infection is associated with an increased risk of uncomplicated and complicated gastroduodenal ulcers in NSAID and low-dose aspirin (acetosalicylic acid (ASA)) users. Evidence level: 2a Grade of recommendation: B
Eradication reduces the risk of complicated and uncomplicated gastroduodenal ulcers associated with either NSAID or low-dose ASA use. Evidence level: 1b Grade of recommendation: A
H pylori eradication is beneficial before starting NSAID treatment. It is mandatory in patients with a peptic ulcer history. Evidence level: 1b Grade of recommendation: A”

I know this is quite speculative, but the evidence fits. (so this is the third good reason to get rid of H. pylori).

Key studies cited only:

[1a] Management of Helicobacter pylori infection—the Maastricht IV/Florence consensus report. Malfertheiner et al.
[1b]Practical Gastroenterology and Hepatology: Esophagus and Stomach. Chapter 44. Helicobacter pylori. Marshall et al. 2012
[2] Fifteen-Year Effects of Helicobacter pylori, Garlic, and Vitamin Treatments on Gastric Cancer Incidence and Mortality. Ma et al. 2012
[3] The Long-term Impact of Helicobacter pylori Eradication on Gastric Histology: a Systematic Review and Meta-analysis. Rokkas et al. 2007
[4] Clinical prevention of gastric cancer by Helicobacter pylori eradication therapy: a systematic review. Ito et al. 2009
[4b] Meta-analysis: can Helicobacter pylori eradication treatment reduce the risk for gastric cancer?
Fuccio L, Zagari RM, Eusebi LH, Laterza L, Cennamo V, Ceroni L, Grilli D, Bazzoli F.
Ann Intern Med. 2009 Jul 21;151(2):121-8. Erratum in: Ann Intern Med. 2009 Oct 6;151(7):516.
[5]Helicobacter pylori and oesophageal cancer – not always protective. McColl et al. 2007
[6] Atherosclerosis. 2012 Feb;220(2):569-74. Epub 2011 Nov 25.
Helicobacter pylori infection, chronic atrophic gastritis and major cardiovascular events: a population-based cohort study.
Schöttker B, Adamu MA, Weck MN, Müller H, Brenner H.
[7] Nature. 2011 Aug 24;476(7361):393-4. doi: 10.1038/476393a. Antibiotic overuse: Stop the killing of beneficial bacteria. Blaser M.
Or a longer review: http://www.ncbi.nlm....10/?tool=pubmed
[8a] Food Funct. 2011 Sep;2(9):515-20. Epub 2011 Aug 30. Natural salicylates: foods, functions and disease prevention. Duthie GG, Wood AD.
[8b] A systematic review of salicylates in foods: estimated daily intake of a Scottish population. Wood A, Baxter G, Thies F, Kyle J, Duthie G. Mol Nutr Food Res. 2011 May;55 Suppl 1:S7-S14. doi: 10.1002/mnfr.201000408. Epub 2011 Feb 23. Review.

Studies I would like to read but lack access:

Quality of RCTs exploring Helicobacter pylori eradication for the prevention of gastric cancer and preneoplastic lesions.
Sun TT, Wang JL, Fang JY.
Expert Rev Anticancer Ther. 2011 Oct;11(10):1509-19. Review.

Meta-analysis: can Helicobacter pylori eradication treatment reduce the risk for gastric cancer?
Fuccio L, Zagari RM, Eusebi LH, Laterza L, Cennamo V, Ceroni L, Grilli D, Bazzoli F.
Ann Intern Med. 2009 Jul 21;151(2):121-8. Erratum in: Ann Intern Med. 2009 Oct 6;151(7):516.

A systematic review of salicylates in foods: estimated daily intake of a Scottish population. Wood A, Baxter G, Thies F, Kyle J, Duthie G. Mol Nutr Food Res. 2011 May;55 Suppl 1:S7-S14. doi: 10.1002/mnfr.201000408. Epub 2011 Feb 23. Review.

Edited by kismet, 18 July 2012 - 06:00 PM.

[kismet]

reserved for updates

[Mind]

Please forgive my ignorance of the detailed science behind the pros/cons of "treating" helicobacter pylori, but I am going to approach this from a more holistic and anecdotal perspective.

Of all the people I have known who have had gastric ulcers (maybe a couple dozen), it appeared to be an opportunistic infection. Stress combined with a poor diet preceded the development of the ulcer. The typical medical advice was to reduce stress, get proper sleep, and eat a little better. All of those who followed the advice generally healed well. There are many different infections that occur in the population which are opportunistic (especially as we age) that could be "treated". Some people think infections are the sole cause of aging see here. These could all be treated or vaccinated against, however, I am wondering if it would be better to just remain healthy. I realize this is not the perfect solution as many people have little self-control, but it seems going down the treatment route, engages us in a war against all types of infections that we would absolutely have to win.

I hope I am making myself clear, but in case not..... When we are healthy, our immune system is absolutely the most powerful weapon we could ever possibly hope to leverage against microbes/bacteria/viruses/infection. Throughout most of our healthy life we are in a symbiotic balance with trillions of foreign cells all over the interior and exterior of our bodies (even our "human" cells are made up of ancient bacterial parts/cells), many of which are harmful when we are immune system malfunctions (most often due to aging). Our immune system is also highly adaptable so new infections that might make us sick are usually quickly neutralized. Therefore, I feel our best bet is to put more focus on maximizing our symbiotic balance with the trillions of foreign cells that we are in contact with every single day of our life. Otherwise we have to be prepared for a long battle with millions of known infectious agents. If the immune system is never challenged, it would likely become ill prepared for new infections (I know, this is an opinion, don't kill me for it).

An allegory would be the situation we find ourselves with antibiotic resistant bacteria. The bacteria have evolved quickly. The only defense we have is our intelligence (or going back to more natural treatment options that do not create super-bugs such as is the case in Norway). As long as we can figure out new defense mechanisms faster that the bacteria can evolve...we "win". If not, we have a huge problem on our hand. So that is the way I think about H. pylori. We could focus on staying healthy and devote more resources to curing aging, or we could start a war of treatments/vaccinations to try and eliminate hundreds or even thousands of (what I consider) opportunistic viruses (remember that some people are absolutely convinced that heart diseases and obesity are infectious diseases - these could be targets as well). I think we can win that war with our intelligence. Technological progress is happening fast. I just think that it would be a misallocation of resources.

Of course, having treatments and vaccines available for people with damaged or compromised immune systems would be an imperative, but I wouldn't want to make it standard across the entire healthy population because of the bad experience we have had with staph and antibiotic resistance.

[pmcglothin]

Thank you for this very provocative, and impressive post. It is obvious that you have done your research and come to a logical conclusion based on what you have found.

I have done a lot of testing of microbial health with two doctors who are specialists in that area. One of the tests I was very excited about initially was an opportunity to measure the RNA of hundreds of microbes in my stool.

When the results came back I was flabbergasted. H Pylori was one of many "pathogens" found. So I decided to look more deeply and submit to a colonoscopy where bacterial samples were taken from the wall of my colon and an endoscopy where samples were taken from my stomach. No sign of any of the pathogens were found.

My question is this. If indeed we should eradicate H Pylori, what testing mechanisms are available to accurately identify if it's present? What medicines are available that would not seriously affect other valuable microbes?

Rather than elimination, is perhaps better to plan a diet combined with the right supplements that tip the balance in favor of beneficial microbes? I predict that possibility will soon become a reality and that it will have significant life extension effects.

Wishing you extraordinary health,

Paul

[niner]

My question is this. If indeed we should eradicate H Pylori, what testing mechanisms are available to accurately identify if it's present? What medicines are available that would not seriously affect other valuable microbes?

Good question. It appears that the RNA test was very sensitive, and was something of a global measurement, while the samples taken endoscopically were from only a relatively few sites, and were measured with a less sensitive test- probably standard culturing. Perhaps there were pockets of H. Pylori somewhere that were missed. Another question is "How much H. Pylori is too much?"

[kismet]

@pmcglothin, all:

Even after erdication (or w/o primary gastric infection?), H. pylori is known to regularly persist in the oral cavity and DNA detected by PCR also persists. Gastric re-infection is rare, nonetheless. This may explain the results of your NON-VALIDATED screening test.
I think you should have undergone validated non-invasive testing afterwards, it’s just safer. Urea Breath Test (UBT), validated stool antigen test and as a close second validated IgG serology (not useful for follow-up! best test if you use acid-suppressing drugs).

„Several non-invasive H pylori tests are established in clinical routine. The UBT [Urea Breath Test (UBT)] using essentially [13C]urea remains the best test to diagnose H pylori infection, has a high accuracy and is easy to perform.76 During recent years new formats of the SAT [stool antigen test (]using monoclonal antibodies instead of polyclonal antibodies, which lead to a constant quality of the reagents have been developed. The two formats available are: (1) laboratory tests (ELISAs) and (2) rapid in-office tests using an immunochromatographic technique. A meta-analysis of 22 studies including 2499 patients showed that laboratory SATs using monoclonal antibodies have a high accuracy both for initial and post-treatment diagnosis of H pylori.77 These data have been confirmed by more recent studies.78 79 In contrast, the rapid in-office tests have a limited accuracy.80 81 Therefore, when a SAT has to be used the recommendation is to use an ELISA format with a monoclonal antibody as reagent.“

The Urea Breath Test (UBT) and stool antigen testing are acceptable non-invasive tests for H pylori infection in this setting. For UBT, sensitivity is 88-95% and specificity 95%-100%.4 Stool antigen testing may be somewhat less acceptable to patients in some cultures but is equally valid, with a sensitivity of 94% and a specificity of 92%.5

How to treat?

The standard is triple treatment including PPI(acid inhibition) clarithromycin, and amoxicillin (or metronidazole),but can be further improved. Talk to your gastroenterologist.

Proton pump inhibitor (PPI)-clarithromycin containing triple therapy without prior susceptibility testing should be abandoned when the clarithromycin resistance rate in the region is over 15-20%

The use of high-dose (twice a day) PPI increases the efficacy of triple therapy [esomeprazole preferred; perhaps slow phase-out vs rebound-reflux disease?]

Extending the duration of PPI-clarithromycin-containing triple treatment from 7 to 10-14 days improves the eradication success by approximately 5% and may be considered

Certain probiotics and prebiotics show promising results as an adjuvant treatment in reducing side effects [I'd recommend lactoferrin because of its safety]

Against inducing antibiotic resistance: hygiene and sanitation (don’t transfer the resistant germs), 100% compliance if possible, state oft he art therapy with high acid suppression (increases specificity fort he stomach), watch out for local patterns of resistance. This should help. See above.

--
I am not optimistic that considerably more specific PRO- and ANTI-biotic therapies will materialize any time soon. I do expect "probiotic" research to be quite fruitful in the next decade or two, however, but this seems orthogonal to the H. Pylori issue. you can fix your gut afterwards too.


[1a] Management of Helicobacter pylori infection—the Maastricht IV/Florence consensus report. Malfertheiner et al.
http://centrostudi.s...r-64_3179_1.pdf

Edited by kismet, 20 July 2012 - 12:33 PM.

[pmcglothin]

Thank you for your intelligent suggestions and insights on this matter. Over the years I have sought various ways to evaluate gastrointestinal health. Another test I had indicated high levels of Blastocystis hominis, a parasite that can be found in the gut of healthy people. Regrettably, I tried to eliminate that with antibiotics, which I now believe was a mistake.

My current low GI, low calorie regimen provokes high levels of NO -- making it more difficult for pathogens to survive.

For example:

Evaluation of the nitric oxide activity against Blastocystis hominis in vitro and in vivo.
J Egypt Soc Parasitol. 2008 Aug;38(2):521-36.
Eida OM, Hussein EM, Eida AM, El-Moamly AA, Salem AM.
Source

Department of Parasitology, Faculty of Medicine, Suez Canal University, Ismailia, Egypt.
Abstract

The effect of exogenous nitric oxide (NO) on growth, viability and ultra-structural of B. hominis was assessed in vitro by sodium nitrite (NaNO2) in 0.6 mM, 0.8 mM & 1 mM concentrations. The viability of B. hominis was identified using neutral red stain. The role of NO as an endogenous oxidant was assessed by identifying its level in cecum tissue, ileum tissue, blood and stool elutes of mice infected with B. hominis symptomatic human isolates using reactive nitrogen assay compared to control. In vitro study revealed that NaNO2 inhibited the growth and decreased viability of B. hominis with minimal lethal concentra-tion dose 1 mM on the 4th day while, minimal effects were detected with 0.6 and 0.8 mM. Transmission electron microscopy study proved that apoptotic-like features were observed in growing axenic culture of B. hominis upon exposure to NaNO2. These changes were not only found on the vacuolar (central body) form but also they were detected on granular, multi-vacuolar and cyst forms. In vivo study proved that high levels of NO were found in infected mice compared to low changes in control group. The high levels were in cecum tissue particularly. The mean levels of NO among infected mice were 211.8 +/- 20.7 microM in cecum, 90.4 +/- 11.6 microM in ileum, 60.1 +/- 4.7 microM in blood and 63.6 +/- 7.3 microM in stool elutes while, the mean levels of NO in control mice were 70.2 +/- 3.1 in cecum, 67.8 +/- 4.7 microM in ileum, 30.9 +/- 4.2 microM in blood and 28.1 +/- 2.9 microM in stool elutes. The differences were statistically highly significant. NO-donor drugs proved useful in treatment and increase the host resistance to B. hominis.

PMID:18853625


Further, I have been privy to a research breakthrough for improving gut health overall and ultimately extending life as a result. I am just waiting for the scientist to publish the results, so we can begin to raise funds for a human study. I have high hopes for more reliable assessments and an intervention with predictably positive results.

For the first time, I am optimistic that significant advances in GI health are neigh. I will report more as soon as I am given permission to do so.


Paul

Edited by pmcglothin, 21 July 2012 - 02:41 PM.

[kismet]

I re-published a slightly modified version of this on my blog.

Edited by kismet, 23 October 2012 - 01:09 PM.

[nowayout]

I think the answer is no. There is suggestive evidence now that H. pylori may be protective against certain chronic inflammatory diseases and allergies.

[kismet]

Allergies fall into the category "very low mortality, easily treatable, usually early-onset" so this is moot for adult-onset treatment. If it turns out to protect against important inflammatory diseases with a combination of high mortality, morbidity or incidence - this would matter. What good or suggestive evidence do you think has emerged on this topic?

Edited by kismet, 24 October 2012 - 09:54 AM.

[nowayout]

Allergies fall into the category "very low mortality, easily treatable, usually early-onset" so this is moot for adult-onset treatment. If it turns out to protect against important inflammatory diseases with a combination of high mortality, morbidity or incidence - this would matter. What good or suggestive evidence do you think has emerged on this topic?

I am not saying H. pylori shouldn't be treated if there are symptoms like GERD or ulcers that detract from quality of life or are associated with increased cancer risk. However, in the majority of the population with no symptoms, the risks are really too low to justify blanket eradication, for several reasons.

- These antibiotic treatments may eliminate uncounted other commensal bacterial species whose full importance we are just beginning to understand, and this disruption of commensal flora may cause all kinds of serious other conditions. For example, blanket antibiotic treatment might increase C. difficile incidence, fungal diseases, possibly Crohn's disease (according to some recent results), etc., not to mention the morbidity associated with antibiotic side effects themselves.

- As you mentioned, H. pylori seems to be protective against asthma, so eradicating H. pylori is likely to significantly increase the incidence of asthma, a serious chronic inflammatory disease with high morbidity and significant mortality.

- Allergies are not principally an early onset condition, and they are in many cases not easily treatable, as many, many of us who spend months of abject misery every year can attest. Sometimes I think cancer would be preferable (joking, but still). In any case, I am pretty sure many more man-hours are lost to allergies than to the cancers relevant here.

Edited by viveutvivas, 24 October 2012 - 04:44 PM.

[kismet]

- These antibiotic treatments may eliminate uncounted other commensal bacterial species whose full importance we are just beginning to understand, and this disruption of commensal flora may cause all kinds of serious other conditions. For example, blanket antibiotic treatment might increase C. difficile incidence, fungal diseases, possibly Crohn's disease (according to some recent results), etc., not to mention the morbidity associated with antibiotic side effects themselves.

- As you mentioned, H. pylori seems to be protective against asthma, so eradicating H. pylori is likely to significantly increase the incidence of asthma, a serious chronic inflammatory disease with high morbidity and significant mortality.

- Allergies are not principally an early onset condition, and they are in many cases not easily treatable, as many, many of us who spend months of abject misery every year can attest. Sometimes I think cancer would be preferable (joking, but still). In any case, I am pretty sure many more man-hours are lost to allergies than to the cancers relevant here.

That is not what proponents of the H. Pylori-asthma link say. The hygiene hypothesis (which they use) is primarily based on early childhood events, because that coincides with the onset of the common allergies.

"Although allergic rhinitis may have its onset at any age, the incidence of onset is greatest in children at adolescence, with a decrease in incidence seen in advancing age." with 80% beginning before 20yo.
The same is true for allergic asthma AFAIK. Other allergies are either rare or less important.
http://books.google....ies age&f=false

Therefore, I don't think that's a strong argument against eradication in adulthood, given there is speculative evidence linking H. Pylori to extra-gastric diseases too, which balances speculative harm. Additionally, some of the evidence you mention is based on simple antibiotic abuse (e.g. multiple AB courses to treat repeating colds in children), not comparable to a single eradication course.

I don't think there is strong evidence to claim that commensals (and non-commensals) must always have positive effects over a whole lifespan as you seem to imply, due to antagonistic pleiotropy, consitent with Blaser's hypothesis (early benefits, late harms). However, there is reason to be cautious, so I will try to review incoming evidence in the future.

Edited by kismet, 03 November 2012 - 03:30 PM.

[Logic]

http://grainfreeandf...-h-pylori-free/

[Sillewater]

http://www.crd.york....?ID=12009106662

I can't access the meta-analysis either but here is the CRDs take on the paper:

Implications of the review for practice and research

Practice: The authors stated that their findings supported the 2008 Asia-Pacific international guidelines, which recommend screening and treating patients for Helicobacter pylori as a gastric cancer risk reduction strategy in populations with a high incidence of the condition.
Research: The authors stated that further intervention studies are unrealistic and that future research should focus on the identification of people at higher risk of gastric cancer because of genetic susceptibility and environmental factors, who would benefit from preventative Helicobacter pylori eradication therapy.

So who is at risk for gastric cancer? Asians who eat salt?

Out of interest:

J Natl Cancer Inst. 2012 Mar 21;104(6):488-92. doi: 10.1093/jnci/djs003. Epub 2012 Jan 23.
Fifteen-year effects of Helicobacter pylori, garlic, and vitamin treatments on gastric cancer incidence and mortality.

Ma JL, Zhang L, Brown LM, Li JY, Shen L, Pan KF, Liu WD, Hu Y, Han ZX, Crystal-Mansour S, Pee D, Blot WJ, Fraumeni JF Jr, You WC, Gail MH.

Source

Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University School of Oncology, Beijing Cancer Hospital and Beijing Institute for Cancer Research, Beijing, China.

Abstract

In the Shandong Intervention Trial, 2 weeks of antibiotic treatment for Helicobacter pylori reduced the prevalence of precancerous gastric lesions, whereas 7.3 years of oral supplementation with garlic extract and oil (garlic treatment) or vitamin C, vitamin E, and selenium (vitamin treatment) did not. Here we report 14.7-year follow-up for gastric cancer incidence and cause-specific mortality among 3365 randomly assigned subjects in this masked factorial placebo-controlled trial. Conditional logistic regression was used to estimate the odds of gastric cancer incidence, and the Cox proportional hazards model was used to estimate the relative hazard of cause-specific mortality. All statistical tests were two-sided. Gastric cancer was diagnosed in 3.0% of subjects who received H pylori treatment and in 4.6% of those who received placebo (odds ratio = 0.61, 95% confidence interval = 0.38 to 0.96, P = .032). Gastric cancer deaths occurred among 1.5% of subjects assigned H pylori treatment and among 2.1% of those assigned placebo (hazard ratio   of death = 0.67, 95% CI = 0.36 to 1.28). Garlic and vitamin treatments were associated with non-statistically significant reductions in gastric cancer incidence and mortality. Vitamin treatment was associated with statistically significantly fewer deaths from gastric or esophageal cancer, a secondary endpoint (HR = 0.51, 95% CI = 0.30 to 0.87; P = .014).
PMID: 22271764 [PubMed - indexed for MEDLINE] PMCID: PMC3309129 [Available on 2013/3/21]

This is impressive considering that they were treated for only 2 weeks. Thus reinfection and such over that period would likely decrease the difference. It seems the garlic also has an effect (but not significant), requires GI release of allicin?

Edited by Sillewater, 12 December 2012 - 04:34 AM.

[Michael]

Thanks, Kismet. I'll make the salicylate review available to all full members in the Resource Sharing subforum.

[holdout]

I'm all for testing it in the healthy.  And by "healthy" I mean the "apparently healthy" until we discover something deleterious about carrying H. pylori.  Considering that 1 in 3 people in the world are infected, and that 85% are completely asymptomatic, this is one nasty bug people should rule out, based on the recent (Feb. 2014) implications with autoimmune disease, vasculitis, and even alopecia (balding): http://www.wjgnet.co...v20/i6/1510.htm

 

I personally went and had a blood antigen test plus a urea breath test done.  Glad to confirm both came back negative.

Edited by holdout, 11 July 2014 - 09:14 PM.