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This book, which covers Visions and hallucinations, explains what causes them and summarises how many hallucinations have been caused by each event or activity. It also provides specific help with questions people have asked us, such as ‘Is my medication giving me hallucinations?’.

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Heartburn and ulcers

Category: Illness or disabilities



Introduction and description


The section Stomach disease provides an overview of both how the stomach works, the general threats it encounters and the diseases of the stomach.  This section, however, provides us with a chance to show you some specific research related to heartburn and ulcers.

  • Peptic ulcer disease (PUD), also known as a peptic ulcer or stomach ulcer, is a break in the lining of the stomach, first part of the small intestine, or occasionally the lower esophagus. An ulcer in the stomach is known as a gastric ulcer while that in the first part of the intestines is known as a duodenal ulcer.
  • Gastroesophageal reflux disease (GERD), gastro-oesophageal reflux disease (GORD), gastric reflux disease, acid reflux disease, or reflux (in babies and young children) is a chronic condition of mucosal damage caused by stomach acid coming up from the stomach into the esophagus (chronic reflux).
  • Heartburn, also known as acid indigestion, is a burning sensation in the central chest or upper central abdomen.  The pain often rises in the chest and may radiate to the neck, throat, or angle of the jaw.  Heartburn is usually due to regurgitation of gastric acid (gastric reflux) into the esophagus and is the major symptom of gastroesophageal reflux disease (GERD).



Heartburn and ulcers produce stomach pain (stomach ache).  There may be nausea, there may even be vomiting.  There can be bloating, belching, and headache.  Stools may be abnormal.

Additional symptoms, especially of GERD include regurgitation of semi digested food and acid, pain with swallowing/sore throat, increased salivation, chest pain, and coughing.

The pain of very bad heartburn may even travel up to the face and result in eye pain, ear pain and muscle pains in the face.  But here care is needed.....

Heart disease - One of the early indicators of heart disease is a pain which is almost identical to heartburn. It starts in the chest and travels up and can reach the face and neck where it manifests as pain in the jaw, the eyes and between the eyes. It can be excruciatingly painful. Interestingly there may be no pain down the arms and none of the tight chested feeling that comes later with angina.
Heartburn treatments are not a great deal of help here!  Go to a cardiologist.



One of the old medical chestnuts prevalent when I was young, was that coffee caused ulcers and heartburn.  Thankfully that wrong thinking has been squashed, but an excess of strong coffee drinking - enough to send the adrenaline racing in false panic - just might, because it simulates stress

Stress and fear and Overeating

Any emotion or environmental stressor that invokes the sympathetic nervous system – the fight or flight system - can result in heartburn and indigestion.  The flight and fight system is geared to halting the digestion of food whilst the fighting and flighting is going on.  The logic is obvious - if we are  fighting or 'flighting', our energy needs to be concentrated in our limbs not our stomach and thus digestion is put on hold.  All our energy is needed to metaphorically flee, so the stomach – a muscle – stops working.  The sympathetic nervous system also stops us weeing and pooing, as if we are fleeing a dinosaur, the weeing and pooing would be a distraction – and a bit messy.  The larger the meal and the more stressed, frightened, grief stricken agitated or angry we are, the more we will suffer.  If we eat when this stressed, we end up with a full stomach and nothing happening, which causes pain. 

Physiologically this was known as far back as the 1800s.  Claude Bernard, in his lectures in 1860, showed that

...taking the two nerves of which the solar plexus is composed — the vagi and the sympathetic — as those which influence the digestive process, galvanism of the vagi [parasympathetic nervous system] excited secretion of the gastric juice [helping digestion], while the same stimulus applied to the sympathetic arrested it [stopped digestion].
" We therefore meet with two orders of nerves in the stomach as in the case of all other glands : motor nerves which accelerate the secreting process, and organic nerves which oppose it."

The solution here is thus smaller meals and the adoption of methods of stress reduction.  As such the answer is to calm down before we eat - meditation, listening to nice music and not to eat in a hurry and when over wrought.  Furthermore, after a meal we need to sit down somewhere very comfortable and take the time to relax - calm down.

Sketches from the Case-Book to illustrate the Influence of the Mind on the Body. By R. Fletcher, M.B.C.S. 1833
….. a barrister enjoyed perfect health except when anxious during the assizes. Then the tongue became brown, the appetite vanished, and if food was taken, severe pain in the stomach succeeded. His anxiety once removed, his tongue cleaned, and his appetite, a distinguished one, returned with such uncontrollable force, that this limb of the Law stops at a half-way house in his return home, when the limb of an animal less dangerous than himself satisfies, in some measure, the capricious humour of his otherwise most respectable and certainly very capacious stomach ( p. 19).

Any form of antacid is by definition not just unhelpful, it is counter-productive.

On the odd occasion when very rich or over rich food, excessive consumption of fat, irritant spices or alcohol and other abuses of the stomach have occurred, doctors may say that a case has been made for their use. But the stomach is actually doing its best to handle this abuse by secreting gastric acids, as such to neutralise them does not help. The pain is there to tell you you have been a twerp and it may be better to grin and bear it.

A cup of coffee should help.

In conclusion, caffeine-induced gastric acid secretion helps digestion; there are no significant relationship between coffee consumption and the four major acid-related upper gastrointestinal disorders.  PMID:  23776588

Food Allergies


Food allergies such as gluten intolerance or dairy product intolerance, result in exactly the same sort of symptoms as other forms of heartburn – bloating, pain, wind and burping, headaches, occasional nausea and vomiting and fatigue, for example:

For the purpose of the analysis of risk factors of formation of a gastroesophageal reflux disease (GERD) in children's population of the Republic of Tyva examination of school students of Kyzyl is conducted. 2185 pupils (1746 schoolchildren of radical and 439 schoolchildren of the alien population) took part in research. … 203 schoolchildren with complaints to heartburn the fibro-esophagogastroduodenoscopy is carried out. … School students with complaints to heartburn in most cases have no endoscopic signs of damage of a gullet….. The risk of emergence of GERD is higher [with] early artificial feeding, existence of food allergy; ……PMID:  25916129

Severe stomach pain with bloating and wind is a well recognised symptom of coeliac disease and gluten and wheat intolerance.

Antacids applied if you have a food allergy can make you feel extremely ill.



Perhaps the best known bacteria to be implicated in the development of ulcers is Helicobacter pylori, a Gram-negative, microaerophilic bacterium naturally found in the stomach.  It was identified in 1982 by Australian scientists Barry Marshall and Robin Warren, who found that it was present in a person with chronic gastritis and gastric ulcers, conditions not previously believed to have a microbial cause. It is also linked to the development of duodenal ulcers and stomach cancer. What has always been confusing, however, is that over 80% of individuals ‘infected’ with the bacterium are asymptomatic – simply not ill.  Furthermore there is additional evidence that H. pylori is part of our gastro-intestinal flora.  And there is extra evidence that it may play an important role there:

Most cells in our body are not human but microbial: the ratio of ‘them' to ‘us' is about 10:1 (Savage, 1977). In addition to being numerous, our microbes also are enormously varied—more than 1,000 bacterial species abound in a variety of niches in our bodies. This immediately raises the question of who we are. Newborn babies are essentially sterile at birth; however, from the moment they pass through the birth canal and draw their first breath, they are colonized by successions of microbes that form the communities found in adults (Savage, 1977). The most numerous bacterial populations are in the gastrointestinal tract, on the skin, in the upper respiratory tract and inside the vagina. ……………..  microbes produce essential metabolites, such as menaquinone (vitamin K2); they aid organ development and metabolism, for instance by affecting fat storage (Backhed et al, 2004); and they protect against intrusions by exogenous pathogens (Bohnhoff & Miller, 1962). Overall, their beneficial activities affect many metabolic, physiological and immunological functions in our bodies……

Studies of the gastric helicobacters in other mammals, and of human migration patterns over time (Ghose et al, 2002; Falush et al, 2003), suggest that the forebears of modern H. pylori have been present in our ancestors since well before we became humans. There is now considerable evidence that H. pylori has colonized the stomach of humans for more than 100,000 years.

The bacterium is also of interest because diagnostic tools are now able to determine its presence or absence in the human stomach, and epidemiological methods can study its effects on human health….  Although H. pylori was once present in almost every adult human, the bacterium is now rapidly disappearing from human populations owing to changes in sanitation, demographics and antibiotic usage. Today, fewer than 10% of children in the USA harbour this bacterium in their stomach. When present, H. pylori is the single dominant species in the stomach (Bik et al, 2006), so its disappearance is potentially significant.

Through its pro-inflammatory effects, H. pylori modulates immunological, endocrine and physiological functions in the stomach (Blaser & Atherton, 2004), with both local and systemic manifestations.

The biological costs of carrying H. pylori include peptic ulcers and adenocarcinoma of the distal stomach. The (cag+) strains that interact to the greatest extent chemically with their hosts convey the highest risks. Conversely, these strains also protect against gastroesophageal reflux disease (GERD) and its consequences, including oesophageal adenocarcinoma, owing in part to their effects on gastric-acid secretion (Peek & Blaser, 2002). These observations are consistent with the rise of these diseases wherever H. pylori is disappearing, and therefore provide the first definitive example of a group of chronic diseases caused by changes in the human microbiota. GERD has been linked to asthma, and preliminary results now support a link between the disappearance of H. pylori and the increase in asthma cases. In addition, H. pylori affects gastric hormones that have a role in energy homeostasis, such as leptin and ghrelin; a link between its disappearance and the increasing prevalence of metabolic syndrome, type II diabetes and obesity has also been postulated (Blaser & Atherton, 2004).   PMID 17016449


So by giving anyone antibiotics you increase the chances of giving them asthma, diabetes, metabolic syndrome and obesity.  We can add to this paper results from other papers, which show that the presence of this bacteria in the stomach, reduces the prevalence of rhinitis, dermatitis, and inflammatory bowel disease.

As Professor Blaser says, however, the theoretical costs of carrying H. pylori include peptic ulcers and adenocarcinoma of the distal stomach.  But again one must ask the question, why do some people carrying the bacteria develop ulcers and others not?

Up to 85% of people harbouring H. pylori never experience symptoms or complications.  At least half the world's population is known to harbour the bacterium, making it the most widespread so called infection in the world.  The so called developing world has much higher rates of colonisation than the West (Western Europe, North America, Australasia).  But it is the peoples of the west that have the ulcers and the stomach cancer.

Furthermore, individuals with H. pylori have only a 1 to 2% risk of acquiring stomach cancer.  Perhaps of equal importance , H. pylori if it plays a role at all, only has an effect in the first stage of chronic inflammation, but not in further stages leading to carcinogenesis.  Let us put this another way.  H.  pylori does not actually cause the cancer, something else does.

So the big question is, what is that something?

H. pylori migrates to the stomach lining.  In addition to using chemotaxis to avoid areas of low pH, H. pylori also neutralizes the acid in its environment by producing large amounts of urease, which breaks down the urea present in the stomach to carbon dioxide and ammonia. The ammonia, which is basic, then neutralizes stomach acid.  If there is not enough stomach acid then the ammonia can become a problem.  There is a possibility that H pylori actually helps provide a protective barrier for the stomach lining, meaning that if H pylori is weakened or not present more acid can attack the stomach lining and heartburn and ulcers will result.

In effect, the very antibiotics and other pharmaceuticals used to supposedly help us, may actually be providing the environment in which the real pathogens – mostly it appears being viruses, can flourish.  By using an antacid, you could be disrupting the bacteria’s normal effects and the ammonia that results could be the culprit.  So the answer to the question ‘what is the true cause’ is viruses aided by doctor or self administered pharmaceuticals.

It is worth mentioning that the outer membrane of this bacteria contains cholesterol glucosides, which are found in few other bacteria.  So any pharmaceutical that directly attacks cholesterol may kill the bacteria.


Although viruses are less frequently mentioned as a problem, there appears to be every reason to consider them a major cause.  They become a problem in the ‘immunocompromised host’, but we should not forget that this is not a person with, for example, HIV.  Anyone who has been prescribed immunosuppressants is immunocompromised.  But viruses are a problem in the immunocompetent too.  The herpes virus is one culprit:

The aim of this study was to delineate the characteristics of herpes simplex virus esophagitis (HSVE) in the immunocompetent host….. A prodrome of systemic manifestations preceded the onset of esophageal symptoms in nine subjects (23.6%). Manifestations included acute odynophagia (76.3%), heartburn (50%), and fever (44.7%). …. Endoscopically, extensive involvement was common, showing friable mucosa (84.2%), numerous ulcers (86.8%), and whitish-exudates (39.5%). The distal esophagus was most commonly affected (63.8%). Microscopic examination showed characteristic viral cytopathology in 26 (68.4%) cases. Virus was recovered from esophageal-brushes or biopsies in 23 of 24 (95.8%) patients ….HSVE in the immunocompetent host is a rare but distinct entity, and is significantly more common in male subjects. …. Histopathological examination alone may miss the diagnosis; adding tissue-viral culture optimizes the diagnostic sensitivity. It is usually self-limiting; whether antiviral therapy is beneficial remains unknown.  PMID:  11007213

A number of other viruses are also starting to be implicated:

Although chronic liver disease is associated with gastroesophageal reflux disease (GERD), the impact of chronic hepatitis B virus (HBV) infection on this association remains unclear. We thus aimed to evaluate the relationship between chronic HBV infection and GERD…….FINDINGS:  Chronic HBV infection was associated with heartburn sensation ... and erosive esophagitis.  Our findings indicate a close association between chronic HBV infection and GERD, especially in female subjects and those with higher aspartate aminotransferase to platelet ratio index (APRI)  levels. Moreover, HBV carriers with higher aspartate aminotransferase (AST) and triglyceride (TG) levels have higher incidence of erosive esophagitis. PMID: 21063481


Human cytomegalovirus-induced lesions resembling malignancies have been described in the gastrointestinal tract and include ulcerated or exophytic large masses. PMID: 25776966


Esophageal squamous papilloma (ESP) is considered to be a rare finding during endoscopy or autopsy. … The presenting symptoms are mostly dyspepsia and heartburn. [in this patient study] All the ESPs were single growth, most of which were located in the lower segment of the esophagus. Immunoperoxidase staining was negative for human papilloma virus in all the tissue samples. It is calculated that ESPs may not be very rare in the Saudi population.  PMID:  17587924

A squamous cell papilloma is a papilloma that arises from the stratified squamous epithelium of the skin,or some other bodily membrane.  Squamous cell papillomas according to Wikipedia “are a result of infection with human papillomavirus - types HPV-6 and HPV-11”.  But in the paper the virus is unknown:


The one area that has received only minor attention is that of the bacteriophage.  Bacteriophage are viruses that colonise bacteria, and H.  pylori attracts a number of phages.

We saw that Helicobacter pylori is associated with ulcers and the development of gastric cancer – but only sometimes. Several genes, including cytotoxin-associated gene A (CagA) and vacuolating cytotoxin A (VacA), are associated with increased gastric cancer risk. And one recent finding is that these strains of H. pylori also contain sequences related to bacteriophage phiHP33.

We assessed the extent to which phiHP33-related sequences are present in 335 H. pylori strains using homology searches then mapped shared genes between phiHP33 and H. pylori strains onto an existing phylogeny.  One hundred and twenty-one H. pylori strains contain phage orthologous sequences, and the presence of the phage-related sequences correlates with the presence of CagA and VacA. Mapping of the phage orthologs onto a phylogeny of H. pylori is consistent with the hypothesis that these genes were acquired by horizontal gene transfer….phiHP33 phage orthologous sequences might be of significance in understanding virulence of different H. pylori strains.  PMID: 26612095

It is worth adding that phages are still being identified and some appear to be new :

Helicobacter pylori inhabits the stomach mucosa and is a causative agent of stomach ulcer and cancer. In general, bacteriophages (phages) are strongly associated with bacterial evolution, including the development of pathogenicity. Several tailed phages have so far been reported in H. pylori. We have isolated an H. pylori phage, KHP30, and reported its genomic sequence. In this study, we examined the biological characteristics of phage KHP30. Phage KHP30 was found to be a spherical lipid-containing phage with a diameter of ca. 69 nm. Interestingly, it was stable from pH 2.5 to pH 10, suggesting that it is adapted to the highly acidic environment of the human stomach. Phage KHP30 multiplied on 63.6% of clinical H. pylori isolates. The latent period was ca. 140 min, shorter than the doubling time of H. pylori (ca. 180 min). .. This evidence suggests that phage KHP30 is a new type of spherical phage that cannot be classified in any existing virus category.  PMID: 23475617


peptic ulcers and gastric cancer, … lead to significantly higher morbidity in Japan than elsewhere in the world. … Here we report two complete genome sequences of H. pylori phages KHP30 and KHP40, which were released spontaneously from the most pathogenic East Asian-type isolates from Japanese patients. PMID: 22997420

So, as we have seen, antibiotics and other pharmaceuticals used to supposedly help us, may actually be providing the environment in which the real pathogens – the viruses, can flourish.  The antibiotic may actually kill the bacteria and release the bacteriophage.  So the answer to the question ‘what is the true cause’ is viruses – both non phages and phages -  aided by doctor or self administered pharmaceuticals.

Fungal infections

So far we have only found the cause to be a fungal infection in immunocompromised patients, and the patients were immunocompromised as a result of being administered immunosuppressants:

Oropharyngeal candidiasis is a well-described side effect of inhaled corticosteroids. Nevertheless, few cases of esophageal candidiasis have been reported.
Our patient is a 70-year-old white woman with a 20-year history of intrinsic asthma, controlled on triamcinolone acetonide 400 micrograms, ipratropium bromide 36 micrograms, and pirbuterol acetate 400 micrograms, each inhaled four times daily. ….. The patient had gastritis with peptic ulcer disease in the past and developed worsening dyspeptic pain and heartburn. Following discontinuation of cimetidine and initiation of ranitidine without improvement, esophagogastroduodenoscopy was performed. Several small white patches in the mid and distal esophagus could not be removed with pressure. A biopsy confirmed the diagnosis of candidal esophagitis. ……There was strong in vitro lymphocyte transformation and a positive immediate skin test response to Candida. ELISA for human immunodeficiency virus was negative.  PMID:  9357379


First we will take a look at eHealthme and the statistics they have collected in the USA from doctor submitted Adverse drug reports to the FDA and SEDA.  The links should take you to the condition.  We have had problems with the eHealthme site reorganising and breaking the links we have set up, so if the link does not work, use the symptom charts on their site to find the symptom.  Then scroll down until you find the section 'Drugs that could cause'.

  • Heartburn - the drugs can be found by following this LINK.  As of Dec 2016, 1,200 drugs were implicated in causing heartburn
  • GERD - the drugs implicated in causing GERD can be found by following this LINKAs of Dec 2016, 1,200 drugs were implicated in causing heartburn
  • Peptic ulcer - the drugs implicated in causing peptic ulcer can be found by following this LINK . As of Dec 2016, 2,000 drugs were implicated in causing heartburn
  • Indigestion - the drugs implicated in causing indigestion can be found by following this LINKAs of Dec 2016, 2,150 drugs were implicated in causing indigestion

The following chart shows the trend for pharmaceuticals having caused indigestion, from eHealthme.

As we can see from the above sections on viruses, bacteria and so on, three major classes of pharmaceuticals are implicated, but there others:

In addition, as we we can see from looking at the eHealthme website statistics, NSAIDs are also significant contributors.

NSAIDs are a leading cause of drug-related morbidity, especially in the elderly and patients with comorbidities. Most adverse effects are related to generalized inhibition of the major targets of NSAIDs: cyclooxygenases I and II.  These enzymes are not only involved in pain and inflammation pathogenesis but are also required in the gastrointestinal (GI) tract for mucosal protection and gut motility, and in the kidneys for functional integrity.  Thus, the mechanisms of NSAID toxicity are well understood, but the consequences are largely uncontrolled in clinical practice. GI ulcers, including bleeding ulcers, may occur in several percent of all chronic unprotected, high-dose NSAID users. Renal side effects may precipitate renal failure, resulting in acute dialysis and chronic retention. This includes sodium retention, resulting in arterial hypertension, heart failure, and atherosclerotic events. Cardiovascular risk may be tripled by chronic high-dose NSAID use.  PMID:  25163793

And a significant source of problems come from osteoporosis treatments, beta blockers, benzodiazepines, statins, anti-depressants and so on.  And we also have the ‘cholesterol’ attacking drugs.


The following case study does not actually prove that either parasites or bacteria are the cause, but it shows some interesting statistical correlations.  It also shows how far these organisms can spread if the immune response of the stomach is in any way compromised:

The study involved 160 patients with chronic cholecystitis associated with chronic gastroduodenitis. Obtaining biopsy specimens of gastric mucosa and bile samples allowed to compare the microbial picture and the morphological structure of gastric mucosa in the same patient, to identify patterns of colonization of the stomach, 12 duodenal ulcer and gall bladder various microorganisms. At cytological examination G. lamblia was detected:

  • in the gall bladder in 47.5 +/- 3.95% of cases
  • in the stomach--in 29.09 +/- 6.12% of cases.

The frequency of H. pylori detection in biopsy of

  • gastric mucosa amounted to 98.18 +/- 1.8% of cases,
  • in 12-duodenum--93.75 +/- 1.9%,
  • in the gall bladder--to 54.38 +/- 3.94%,
  • in the bile duct--in 54.38 +/- 3.94%.

It was found strict association between the detection of H. pylori and G. lamblia in the stomach--100% of H. pylori-infection combined with giardiasis. Morphological changes of gastric mucosa in the form of lymphoid infiltration detected mainly in the mixed-infection H. pylori and G. lamblia.  PMID:  20731162

Many different sorts of parasites are implicated we have not listed them all, but here is another example:

Strongyloidiasis is a parasitosis caused by the female nematode of the Strongyloides stercoralis. S. stercoralis causes a chronic infection that is asymptomatic in 50% of chronically infected patients, and it can also affect the stomach. Gastric involvement causes symptoms mostly mimicking gastritis. We report herein a case of gastric perforation in a 37-year-old woman, which was caused by S. stercoralis.  PMID: 21341143



So what causes an upset stomach? Well, as we have seen it may be a bacteria, but is more likely to be viruses, fungi, toxins – a pathogen in other words. What do we want our stomach to do in this case? 
The answer is to secrete as much acid as possible so that the pathogen is killed or disabled.  We may get temporary discomfort, but on the whole, better to suffer a bit of discomfort than to have the pathogen enter the body.  So the treatment is to grin and bear it.

What else can cause an upset stomach – so called GERD gastric acid reflux, when the stomach contents regurgitate, or even when you just get heartburn or indigestion?

Well another cause can be food intolerance, so the obvious answer here is to get yourself tested for any allergens – any, as they will all do the same thing.  The body thinks it is being poisoned so it tries to either make you sick, or creates a lot of acid to try to get rid of it through the intestines.  Quick throughput.

Anything else?  Indeed yes – stress.

Stress of all sorts invokes the sympathetic nervous system – the flight or fight response.  People get upset stomachs from fear, loneliness, grief, panic, and depression.  Unable to cope, at a very low ebb their sympathetic nervous system is working overtime to help them flea, but sadly the ‘threat’ cannot in many case be flown from that easily.

Indigestion means just that, the body cannot digest its food because we are so stressed it has gone into 'lack of activity' mode.  It is not too much acid, the body under stress is not actually secreting any, so we have lack of digestion, which feels like a big lump in our stomachs that lasts for a very long time and gives us pain.

And what do we find if we take a look at the statistics for just one drug - Nexium, used to supposedly treat heartburn? The top conditions involved for these people, according to the eHealthme web site were:

  1. Pain (97 people, 23.15%)
  2. Depression (87 people, 20.76%)

So the answer is clearly to solve the stress problem, the sadness, the loneliness, the hurt.  There are all sorts of kindly ways of helping the lonely, the fearful, the grief stricken and the depressed and they do not involve and should not involve pharmaceuticals.  They need to involve people helping people.

References and further reading

  • Am J Gastroenterol. 2000 Sep;95(9):2171-6.  Herpes simplex virus esophagitis in the immunocompetent host: an overview.  Ramanathan J1, Rammouni M, Baran J Jr, Khatib R.
  • Hepatol Int. 2010 Jul 1;4(3):585-93. doi: 10.1007/s12072-010-9184-4.  Increased incidence of gastroesophageal reflux disease in patients with chronic hepatitis B virus infection.  Hsu CS, Wang CC, Wang PC, Lin HH, Tseng TC, Chen CH, Su WC, Liu CJ, Chen CL, Lai MY, Chen PJ, Chen DS, Kao JH.
  • EMBO Rep. 2006 Oct; 7(10): 956–960. doi:  10.1038/sj.embor.7400812  PMCID: PMC1618379; Science and Society Viewpoint Who are we? Indigenous microbes and the ecology of human diseases - Martin J Blaser, Frederick H. King Professor of Internal Medicine, the Chair of the Department of Medicine and a Professor of Microbiology at New York University School of Medicine, New York, USA. martin.blaser@med.nyu.edu
  • Blaser M (2011). "Antibiotic overuse: Stop the killing of beneficial bacteria". Nature 476 (7361): 393–4. doi:10.1038/476393a. PMID 21866137
  • Salama N. R.; et al. (2013). "Life in the human stomach: persistence strategies of the bacterial pathogen Helicobacter pylori". Nature Reviews Microbiology 11: 385–399. doi:10.1038/nrmicro3016
  • Blaser MJ, Chen Y, Reibman J (May 2008). "Does Helicobacter pylori protect against asthma and allergy?". Gut 57 (5): 561–7. doi:10.1136/gut.2007.133462. PMID 18194986.
  • Chen Y, Blaser MJ (August 2008). "Helicobacter pylori colonization is inversely associated with childhood asthma". J. Infect. Dis. 198 (4): 553–60. doi:10.1086/590158. PMID 18598192
  • Helicobacter. 2015 Nov 27. doi: 10.1111/hel.12282. [Epub ahead of print]  The Presence of Phage Orthologous Genes in Helicobacter pylori Correlates with the Presence of the Virulence Factors CagA and VacA.  Kyrillos A1, Arora G1, Murray B1, Rosenwald AG1.  1Department of Biology, Georgetown University, Washington, DC, USA.
  • Ann Allergy Asthma Immunol. 1997 Oct;79(4):333-8.  Esophageal candidiasis as a complication of inhaled corticosteroids.  Simon MR1, Houser WL, Smith KA, Long PM.  1Department of Pediatrics, Wayne State University School of Medicine, Detroit, Michigan, USA.
  • Ann Saudi Med. 1995 Mar;15(2):140-2.  Squamous papilloma of the esophagus - a clinicopathologic study of 10 cases and review of the literature.  Al-Sohaibani MO1, Al-Rashed RS.
  • Appl Environ Microbiol. 2013 May;79(10):3176-84. doi: 10.1128/AEM.03530-12. Epub 2013 Mar 8.  Characterization of Helicobacter pylori bacteriophage KHP30.  Uchiyama J1, Takeuchi H, Kato S, Gamoh K, Takemura-Uchiyama I, Ujihara T, Daibata M, Matsuzaki S.
  • Eksp Klin Gastroenterol. 2010;(6):30-4.  [Gastrointestinal giardiasis associated with Helicobacter pylori].  [Article in Russian] - Isaeva GSh, Efimova NG.
  • Ulus Travma Acil Cerrahi Derg. 2011 Jan;17(1):90-2.  Gastric perforation caused by Strongyloides stercoralis: a case report.  Oztürk G1, Aydınlı B, Celebi F, Gürsan N.  1Department of General Surgery, Atatürk University Faculty of Medicine, Erzurum, Turkey. gurkanoztrk@yahoo.com
  • PLoS One. 2013 Jun 12;8(6):e65996. doi: 10.1371/journal.pone.0065996. Print 2013.  No association of coffee consumption with gastric ulcer, duodenal ulcer, reflux esophagitis, and non-erosive reflux disease: a cross-sectional study of 8,013 healthy subjects in Japan.  Shimamoto T1, Yamamichi N, Kodashima S, Takahashi Y, Fujishiro M, Oka M, Mitsushima T, Koike K.
  • Korean J Parasitol. 2015 Feb;53(1):95-9. doi: 10.3347/kjp.2015.53.1.95. Epub 2015 Feb 27.  Comorbid gastric adenocarcinoma and gastric and duodenal Strongyloides stercoralis infection: a case report.  Seo AN1, Goo YK2, Chung DI2, Hong Y2, Kwon O3, Bae HI1.
  • J Virol. 2012 Oct;86(20):11400-1.  Complete genome sequences of two Helicobacter pylori bacteriophages isolated from Japanese patients.  Uchiyama J1, Takeuchi H, Kato S, Takemura-Uchiyama I, Ujihara T, Daibata M, Matsuzaki S. 1Department of Microbiology and Infection, Kochi University, Kochi, Japan.
  • J Med Virol. 2015 Jun;87(6):1041-5. doi: 10.1002/jmv.24152. Epub 2015 Mar 16.  Human cytomegalovirus induced pseudotumor of upper gastrointestinal tract mucosa: effects of long-term chronic disease?  Reggiani Bonetti L1, Barresi V, Bertani A, Maccio L, Palmiere C.

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