Alternative Medicine for Stomach Ulcers Discovered

Beat Ulcers

The system is all natural and easy to use. You are just minutes away from taking your first steps to having painless days and nights. In less than 2 weeks, you can be totally free from ulcers, living without the pain and feeling free to eat without the thought of pain. All you need do is follow the plan. Beat Ulcers is a step by step guide that shows you how you can eliminate ulcers in as little as 10 days. All you need do is use the readily available natural products in the correct proportions at the correct times. Here is what you will learn in the Beat Ulcers guide: How to Eliminate an Ulcer without the use of medication. How to rid your body of the ulcer causing bacteria and keep it away. How to stop the aching. How to eliminate the burping and bloating. Focus on the root cause of ulcers rather than the symptoms. How to be totally free from pain and sleep soundly at night. How to stop using dangerous medications that are prescribed over and over. Learn the causes of ulcers and how to eliminate them forever.

Beat Ulcers Summary


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Author: Tammy Myers
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This is one of the best ebooks I have read on this field. The writing style was simple and engaging. Content included was worth reading spending my precious time.

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Gastritis and Peptic Ulcers

Peptic ulcers are erosions of the mucous membranes of the stomach or duodenum produced by the action of HCl. In Zollinger-Ellison syndrome, ulcers of the duodenum are produced by excessive gastric acid secretion in response to very high levels of the hormone gastrin. Gastrin is normally produced by the stomach but, in this case, it may be secreted by a pancreatic tumor. This is a rare condition, but it does demonstrate that excessive gastric acid can cause ulcers of the duodenum. Ulcers of the stomach, however, are not believed to be due to excessive acid secretion, but rather to mechanisms that reduce the barriers of the gastric mucosa to self-digestion. It has been known for some time that most people who have peptic ulcers are infected with a bacterium known as Helicobacter pylori, which resides in the gastrointestinal tract of almost half the adult population worldwide. Also, clinical trials have demonstrated that antibiotics that eliminate this infection help in the treatment of...

Perforated peptic ulcer

Complications of peptic ulcer disease are now much less common than 20 years ago due to improved medical management (see Peptic Ulcer, below), but perforations still imply a mortality of approximately 10 (higher in older patients). The well-recognised risk factors for developing a perforation are long-term non-steroidal anti-inflammatory drug (NSAID) use, and Helicobacter pylori infection. Once the perforation has been successfully dealt with, the peptic ulcer must be treated with full medical management as described below. This will include eradication of H. pylori if present, stopping NSAIDs as appropriate (or switching to alternative analgesia), and a healing course of anti-secretory medication.

Peptic ulcer

The management of peptic ulcer disease has changed dramatically in the last 20 years as the aetiology of peptic ulceration has become more clearly understood, and more powerful and effective medical treatment has evolved. At the same time there has been a dramatic decrease in both elective and emergency surgery for peptic ulceration. Aetiological factors in peptic ulceration include H. pylori infection, NSAID ingestion, smoking, renal failure, liver disease, and ZollingerEllison (ZE) syndrome. H. pylori is by far the most important, and adequate management of H. pylori is the mainstay of modern ulcer therapy. H. pylori is a spiral, gram-negative bacteria which is spread by direct contact, and infects up to 60 of the population, though only 5-10 of those infected develop ulceration. H. pylori causes increased gastrin levels, a rise in gastric acid production, and also has a direct effect on gastric and duodenal mucosa. NSAIDs have both a localised and systemic effect on gastric and...

Helicobacter pylori infection

Rates after eradication of H. pylori from the stomach of peptic ulcer patients has been reported (Marshall et al., 1988 Hantschel et al., 1993). It has been established that H. pylori infection is a major cause of chronic gastritis and peptic ulcer disease. H. pylori was designated a first class definite carcinogen for stomach cancer in 1994 following epidemiological investigation by the International Agency for Research on Cancer (IARC, 1994), a subordinate organization of the World Health Organization. Furthermore, association of primary malignant gastric lymphoma with H. pylori has been reported in a large-scale cohort study (Parsonnet et al., 1994).


Cholinergic agonists, such as pilocarpine and carbachol, should be avoided in conditions where pupillary constriction and intraocular vascular congestion are undesirable, such as in acute iritis or visually significant lens changes. These agents should also be avoided where there is a history of, or predisposition to, retinal detachment, or a proven sensitivity to these agents, or, for the membrane delivery dosage form, the presence of acute infectious conjunctivitis or keratitis. Patients with severe asthma, bronchial obstruction, acute cardiac failure, active peptic ulcer, hyper-thyroidism, gastrointestinal spasm, urinary tract obstruction, Parkinsonism, recent myocardial infarction, and, perhaps, poorly controlled blood pressure disorders are at risk for having these conditions exacerbated by cholinergic agonists.3

Management of lower GI bleeding

Resuscitation of the patient is the priority, with airway control and provision of oxygen plus large bore intravenous access. Blood should be taken for estimation of haemoglobin, urea, electrolytes, liver function and coagulation profile. Blood should be cross-matched and blood, and products given as required. Urinary and nasogastric catheters are helpful and arterial blood gas analysis will also help to guide the resuscitative effort. The history is important and evidence should be sought of previous GI bleeding, peptic ulcer or inflammatory bowel disease, liver disease, non-steroidal or warfarin usage. The abdomen and anorectum must be carefully examined and bedside examination of the anal canal and rectum are mandatory. If there is any suspicion of an upper GI source, this should be ruled out by upper GI endoscopy.

Stress and the Adrenal Gland

In 1936, a Canadian physiologist, Hans Selye, discovered that injections of a cattle ovary extract into rats (1) stimulated growth of the adrenal cortex (2) caused atrophy of the lym-phoid tissue of the spleen, lymph nodes, and thymus and (3) produced bleeding peptic ulcers. At first he attributed these effects to the action of a specific hormone in the extract. However subsequent experiments revealed that injections of a variety of substances including foreign chemicals such as formaldehyde could produce the same effects. Indeed, the same pattern occurred when Selye subjected rats to cold environments or when he dropped them into water and made them swim until they were exhausted.

Examples of Prostaglandin Actions

The stomach and intestines produce prostaglandins, which are believed to inhibit gastric secretions and influence intestinal motility and fluid absorption. Since prostaglandins inhibit gastric secretion, drugs that suppress prostaglandin production may make a patient more susceptible to peptic ulcers.

Myeloproliferative Disorders

PRV is frequently discovered incidentally when a complete blood count is performed for another reason. When symptoms are present, they are usually nonspecific. Fatigue, headache, and diaphoresis are common. Pruritis, often following a hot shower, is a frequent complaint. Up to 15 of patients may present with a thrombotic episode. Thrombotic cerebrovascular accidents, coronary artery thrombosis, Budd-Chiari syndrome, and pulmonary embolus all occur. Cavernous sinus thrombosis may also occur in untreated or poorly controlled disease. Erythromelalgia is specific to PRV and ET, and it is associated with an elevated platelet count and paradoxical vasodilation. It is characterized by redness, warmth, and a burning pain affecting the digits and responds promptly to aspirin. Gout may be a presenting manifestation of an MPD. There is an increased incidence of peptic ulcer disease in patients with PRV. Iron deficiency may occur and may initially mask the diagnosis. An elevated hematocrit with...

Test Your Knowledge ofTerms and Facts

Explain the function of bicarbonate in pancreatic juice. How may peptic ulcers in the duodenum be produced 4. Describe the mechanisms that are believed to protect the gastric mucosa from self-digestion. What factors might be responsible for the development of a peptic ulcer in the stomach

Dairy products and probiotics in childhood disease

Infection with the Gram-negative microaerophilic bacterium Helicobacter pylori is typically acquired in childhood. About 10 of patients develop symptoms of gastritis, peptic ulcer disease or MALT lymphoma, but anaemia and growth retardation is also associated with H. pylori colonisation in children (Czinn, 2005). The infection is a relevant health problem since approximately half of the world population is infected with H. pylori. In particular, high prevalence rates exist in developing countries and in populations with low socio-economic standard and poor hygienic conditions. H. pylori can be eradicated by anti-microbial therapy (typically amoxicillin plus clarithromycin

Ocular Use Of Steroids

Glucocorticoids have important effects on the nervous system, including behavior and intracranial pressure. Large doses of glucocorticoids have been associated with the development of peptic ulcer, possibly by suppressing the local immune response against Helicobactor pylori. Glucocorticoids given chronically suppress the pituitary release of adrenocorticotropic hormone, growth hormone, thyroid-stimulating hormone, and leutinizing hormone.

The pathogenesis of IBD

After the lesson of Helicobacter pylori and peptic ulcer disease, an infectious contribution to the pathogenesis of IBD is plausible. Despite intensive pursuit of a specific infectious cause for IBD, this subject remains controversial. However, an aetiological role for a single pathogenic micro-organism in the pathogenesis of IBD has not been established (Shanahan, 2004). On the other hand, compelling data from murine models of colitis as well as circumstantial evidence in patient-related studies, implicate the enteric microbiota in the pathogenesis of both Crohn's disease and ulcerative colitis (Table 5.1). The level at which the dysregulated immunity to commensal organisms occurs has not been identified. It remains unclear whether the associated inflammatory responses, both within the gut and at extra-intestinal sites, are elicited in response to a specific subset of intestinal microbes. Alternatively, sensing of commensal bacteria in general may be affected. Nevertheless, what is...

Stress And Coping

Among the symptoms of prolonged stress are persisting anxiety, depression, irritability, fatigue, loss of appetite, headache, and backache. Continuing stress can affect the course and severity of physical disorders such as peptic ulcers, migraine headaches, skin conditions, chronic backache, and bronchial asthma.


Lower incidences of urinary tract infection and now has been shown to have a capacity to decrease peptic ulcer caused by Helicobacter pylori. Isolated compounds from cranberry have been shown to reduce the risk of CVD and cancer. Functional phenolic antioxidants from cranberry such as ellagic acid have been well documented to have antimutagenic and anticarcinogenic functionality. Even though many benefits have been associated with phytochemicals from cranberry, such as ellagic acid, their mechanism of action is still not very well understood. Emerging research exploring the mechanism of action of these phyto-chemicals from cranberry usually follows a reductionist approach, and is often focused on the disease or pathological target. These approaches to understanding the mechanism of action of phytochemicals have limitations as they are unable to explain the overall preventive mode of action of phenolic phytochemicals. The current proposed mechanisms of action of these phenolic...


Small-bowel tumors are rare, but GISTs account for more than 10 of neoplasms in this location. Patients with GISTs of the small intestine often present with nonspecific abdominal complaints, such as pain or hemorrhage. These tumors may be misdiagnosed as peptic ulcer disease, gas-troesophageal reflux, or cholelithiasis. In many cases, they are initially detected by the small-bowel follow-through portion of a barium swallow larger lesions may be detected by computed tomography (CT) radiography, and bleeding lesions may be detected by angiography.

Antiulcer Activity

Based on the promising results of this study, the antiulcer activity of the individual anthocyanidins was studied. One anthocyanidin, chloride (IdB 1027, Inverni della Beffa S.p.A., Milan) showed particular promise, and so it was produced synthetically so that its effects on several animal models of acute and chronic stomach ulcers could be studied further (4). IdB 1027 administrered orally or intraperitoneally was able to inhibit acute gastric ulceration induced by pyloric ligation, stress (cold plus restraint), phenylbutazone, indometha-cin, reserpine, ethanol, and histamine, as well as duodenal ulceration induced by cysteamine and chronic gastric ulcers induced by acetic acid. Results of additional experiments suggest the mechanism of action involves stimulation of protective gastric mucosal secretions. A drawback of this study is that the severity of ulceration caused by phenylbutazone, indomethacin, ethanol, and histamine was assessed using nonvalidated ordinal scales.

Helicobacter pylori

H. pylori is a Gram-negative bacterium found in the human stomach and plays an important role in the pathogenesis of chronic gastritis and peptic ulcers (6). Additionally, both epidemiological and clinical evidence has indicated that H. pylori is associated with an increased risk of gastric carcinoma (7,8) and as such it is the first bacterium to be termed a definitive cause of cancer by the International Agency for Research into Cancer (IARC). The cag pathogenicity island appears to play an important role in the aetiology of the disease since, in developed countries, strains of H. pylori that carry it are associated with an increased risk of peptic ulcer and adenocarcinoma than strains that are negative for the cag island (9). Overexpression of cyclooxygenase 2 (COX-2) has also been observed in tissues of human gastric cancer. There are two isoforms of COX COX-1 and COX-2. These are key enzymes that convert arachidonic acid to prostaglandins. COX-1 is expressed in most human tissues,...