Above; Demonstration of Helicobacter pylori by the four staining methods: (A) modified Giemsa, (B) anti-H pylori antibody immunostain, (C) modified McMullen's method, (D) H pylori silver staining (HpSS) method.
From Barry Marshall the ‘male volunteer’ who implicated helicobacter pylori in gastritis and stomach ulcer (my comments in brackets and italics);
‘However, I had been arguing with the skeptics for two years and had no animal (pig) model that could prove H pylori was a pathogen. If I was right, then anyone was susceptible to the bug and would develop gastritis and maybe an ulcer years later.
I could see that bismuth (affects H pylori) was healing gastritis, albeit temporarily, but I had no convincing data to prove the bacteria were indeed pathogens. The experiment was planned with a culture from a patient with dyspepsia and confirmation that it was sensitive to metronidazole. The paper was published in the third person, but it gradually became known that the ‘male volunteer’ was me.
Then I underwent endoscopy in early July 1984 to confirm that I was negative for H pylori. Three weeks later, I drank the ‘brew’ which was a suspension of two culture plates of the organism. (NB THERE WAS NO CONTROL EXPERIMENT of a cell culture ‘infected’ with a different bacteria or minus bacteria.) If only I knew that people would be so interested, I would have taken a photograph! I omitted my breakfast but took 400 mg of cimetidine, believing that the infection might be easier if my stomach acid level was lowered. Two hours later, Neil Noakes scraped a heavily inoculated 4 day culture plate of Helicobacter and dispersed the bacteria in alkaline peptone water; a kind of meat broth used to keep bacteria alive. I fasted until 10 am when Neil handed me a 200 ml beaker about one quarter full of the cloudy brown liquid. I drank it down in one gulp (NOT ANYTHING THAT WOULD EVER HAPPEN IN NATURE).
After five days, I started to have bloating and fullness after the evening meal, and my appetite decreased. My breath was bad and I vomited clear watery liquid, without acid, each morning at approximately 06:00. Then, a follow-up endoscopy showed severe active gastritis with polymorphonuclear infiltrate and epithelial damage. Evidently, H pylori was a pathogen for normal people. To my joy, spiral bacteria were present on the Gram stain of the first biopsy. The next day Ross Glancy showed me a pathology specimen teeming with Helicobacter and pus cells. The experiment had succeeded – Helicobacter was a proven pathogen. (NB THERE IS NO EVIDENCE FOR THIS STATEMENT BASED ON DRINKING A BEAKER OF CELL CULTURE CONTAINING LARGE AMOUNTS OF BACTERIA; THEN FINDING THEM AGAIN).
The ulcer did not merely set you up for catching the infection. (HE DID NOT HAVE AN ULCER HE HAD TEMPORARY (and entirely unsurprising) INFLAMMATION OF THE STOMACH LINING). People with asymptomatic H pylori were ‘carriers’ and most people did not have ulcers from the bacterium (50-60% ‘infected’ with H pylori are ‘asymptomatic’). Gastritis was explained. (No it wasn’t).
The two biopsies taken on day ten were not enough to really define the pathology, so I scheduled another endoscopy four days later. However H pylori were not seen on that biopsy so I might have already had a spontaneous cure.(THERE IS NO EVIDENCE THAT HE WAS EVER ‘INFECTED’). At the next endoscopy the stomach seemed normal and, surprisingly, we could not find Helicobacter in any of the eight samples which were taken. Cultures, histology and electron micrographs were all bacteria-free, with the appearance of healing gastritis being the only abnormality.
I had apparently eradicated the Helicobacter myself, without antibiotics. Serum samples taken at the time and a few months later were negative for Helicobacter antibody. Whatever happened to cause the Helicobacter to disappear continues to be a mystery to this day. (D’ah)
Ulcers that result from nonsteroidal anti-inflammatory drug use now make up more than 50% of the cases.
With a healthy diet, acid levels are maintained throughout life and may protect from cancer.’ (yes!)(1)
This is now me.
The clincher is he was awarded the Nobel prize for services to germ theory.
The H pylori bacteria is present in 50-60% of the world population. It is strongly associated with ulcer, and therefore eradication with antibiotics or bismuth may temporarily ameliorate the symptoms, but as the bacteria is not the cause, they will return if the causes are not addressed. The chief causes appear to be NSAIDS and diet.
Triple therapy has been said to have said many lives by irradiating H. pylori however studies merely observe the reduction in deaths from peptic ulcer disease (PUD) in the 1990s. There could be many reasons for this; changes in medications, avoiding NSAIDS, changes in diet, changes in how deaths are recorded, changes in diagnostic criteria, temporary removal of bacteria at time of death (which would have come back if changes in life style were not made) (and they hadn’t died), perhaps tripe therapy itself was causing people to die of other diseases not PUD
Regarding cancer; only 2% of ‘infected’ individuals develop gastric cancer. It is estimated that 75% of gastric cancer cases are associated with H. pylori infections(4). H pylori presence is therefore not necessary for or predictive of gastric cancer.
A 2014 meta-analysis showed eradication by antibiotics gave only a 0.8% reduction in gastric cancer in healthy asymptomatic ‘infected’ individuals.(3)
In one study eradication of H pylori by antibiotics showed 5.5% less metachronous (at another site) gastric carcinomas developing after resection of ‘early cancer’, compared to uneradicated although there was no indication it improved overall survival and one serious side- effect was that it caused diarrhoea. Cancer still developed in 3.3% of H pylori free cases (2). In another study there was no significant difference between eradicated and control (6).
Diets high in methionine, which has sulphur containing amino acids producing sulphuric acid when they’re broken down, such as those high in animal products increase the stomach pH. High pork consumption was associated with 80% (7.6% absolute) increase in gastric cancer compared to no risk in low consumers even though both groups were ‘infected’ with H pylori.(5)
H pylori is able to survive high pH in the stomach by urease activity which produces urea and maintains an internal neutral pH. It may well be functioning to protect the body; not harm it.
The presence of the bacteria is associated with inflammation, ulceration and cancer due to high pH and carcinogens from a diet high in salt, animal products and N-nitroso compounds in cheese, fish bacon and other cured meats, and low in alkaline forming fresh fruit and vegetables.
There is no evidence in the literature that Helicobacter pylori is causative of stomach ulcer or gastric cancer.
Jo
Figure Journal of Clinical Pathology Histological identification of Helicobacter pylori: comparison of staining methods FREE
O Rotimi1, A Cairns1, S Gray1, P Moayyedi2, M F Dixon1
1).doi: 10.1155/2008/459810
PMCID: PMC2661189
PMID: 19018331
Helicobacter pylori: A Nobel pursuit?
Barry Marshall, MD1 and Paul C Adams, MD2 and
HELICOBACTER CONNECTIONS
Nobel Lecture, December 8, 2005
by
Barry J. Marshall
NHMRC Heliobacter pyroli Research Laboratory, QEII Medical Centre, Nedlands, WA 6009, Australia.
2).Randomized Controlled Trial Lancet
. 2008 Aug 2;372(9636):392-7. doi: 10.1016/S0140-6736(08)61159-9.
Effect of eradication of Helicobacter pylori on incidence of metachronous gastric carcinoma after endoscopic resection of early gastric cancer: an open-label, randomised controlled trial
Kazutoshi Fukase 1 , Mototsugu Kato, Shogo Kikuchi, Kazuhiko Inoue, Naomi Uemura, Shiro Okamoto, Shuichi Terao, Kenji Amagai, Shunji Hayashi, Masahiro Asaka, Japan Gast Study Group
3). 2014; 348: g3174.
Published online 2014 May 20. doi: 10.1136/bmj.g3174
PMCID: PMC4027797
PMID: 24846275
Helicobacter pylori eradication therapy to prevent gastric cancer in healthy asymptomatic infected individuals: systematic review and meta-analysis of randomised controlled trials
Alexander C Ford, associate professor and honorary consultant gastroenterologist,1,2 David Forman, head of section,3 Richard H Hunt, professor of gastroenterology,4 Yuhong Yuan, research associate,4 and Paul Moayyedi, director of Gastroenterology Division4
4).ScientificWorldJournal
. 2020 Jul 12;2020:3018326. doi: 10.1155/2020/3018326. eCollection 2020.
Helicobacter pylori Oncogenicity: Mechanism, Prevention, and Risk Factors
Muzaheed 1
Affiliations expand
PMID: 32765194 PMCID: PMC7374235 DOI: 10.1155/2020/3018326
Free PMC article
5). doi: 10.3748/wjg.v20.i25.8151.
Interactions between pork consumption, CagA status and IL-1B-31 genotypes in gastric cancer
Xiao-Qin Wang 1 , Paul D Terry 1 , Li Cheng 1 , Hong Yan 1 , Jian-Sheng Wang 1 , Wen-An Wu 1 , Sen-Ke Hu 1
Affiliations expand
PMID: 25009387 PMCID: PMC4081686 DOI: 10.3748/wjg.v20.i25.8151
6).doi: 10.1016/j.cgh.2013.09.057. Epub 2013 Oct 5.
Eradication of Helicobacter pylori after endoscopic resection of gastric tumors does not reduce incidence of metachronous gastric carcinoma
Jeongmin Choi 1 , Sang Gyun Kim 2 , Hyuk Yoon 1 , Jong Pil Im 1 , Joo Sung Kim 1 , Woo Ho Kim 3 , Hyun Chae Jung 1
The story of Helicobacter pylori, ulcers and cancer
Dear Jo,
This is... astonishing. I had, of course, heard the 'mythological' version of this story. I hadn't realized that the symptoms were so vague.
Of course: now I've heard that doctors have ingested *cholera* with no adverse effects.
What to make of all of this?!?! I come from the 'hard' sciences, but, although people shy away from the *math*, I feel like I can explain everything that I know quite easily, because the experiments are very extremely controlled and unambiguous. Even 'control experiments' aren't really necessary because, to be frank: either your lights turn on.... or they don't.
I always respected the *other* side of academia out of professional courtesy.
I suppose that I no longer extend that courtesy.