The two groups did not differ with regard to smoking behaviour, alcohol consumption, and coffee intake, but symptomatic patients were significantly less likely to drink tea than their asymptomatic peers, at Symptomatic patients also had greater scores for somatisation, depression, anxiety, and psychotism and general severity index of psychopathology compared with asymptomatic patients.
Understanding the characteristics of functional dyspepsia will provide a rationale for the clinician to explain the meaning of the symptoms and to achieve better management. Conclusion: Functional Dyspepsia FD with gastric reddish streaks exhibited increased somatisation, more stressful life events, less belief in religion, and less tea consumption as compared with asymptomatic counterparts. The findings of the study suggest the importance of adopting a more comprehensive holistic bio-psycho-socio-spiritual model when dealing with FD patients.
Comment: In natural or non allopathic medicine, some reductionists criticise the term holism and dismiss the idea that a patient is any more than the sum of a number of often disparate symptoms. This article is interesting in that the treatment strategy recognises that the complaint is also managed by a number of social and lifestyle factors that when taken in context with the patient is the optimal approach to resolution.
Low hydrochloric acid levels are very common. The older you are, the more likely you are to have low levels. There are a number of reasons for this situation, including stress and age. However, another reason is nutrient deficiencies. Low levels of the mineral zinc and vitamins B1 and B6 can also contribute to low levels of stomach acid.
Deficiencies in zinc and B vitamins are extremely common either due to lack of intake from food or due to increased needs for example, chronic stress, or due to depletion by alcohol or smoking for example.
As we have seen from the functions of hydrochloric acid, it plays vital functions in digestion and if these are not capable of working properly because your stomach acid is too low then you increase your risk for developing food intolerance.
This test is called the Gastro-Test. Your answers to the questionnaire identify whether you should do this test or not. The results of the Gastro-Test identify whether you should ultimately take supplements of hydrochloric acid. A very small minority of people actually have high stomach acid, but this is considerably lower than the number we are lead to believe. The observational questions below help you to identify if you have low HCl acid and support the further investigations discussed below.
The test consists of a weighted gelatin capsule with 70 cm of highly absorbent cotton floss attached to one end of the capsule. The test kit also includes a surface marking pH stick and a pH colour chart. Water, but not food, is allowed anytime during the fast. The patient then drinks one to two cups of water — ml and swallows the capsule.
The patient then lies on their left side for ten minutes. Lying down allows for maximal contact between the floss and the gastric pool. After ten minutes, the patient is asked to sit in a comfortable chair with their head slightly extended.
The floss is then placed on a piece of white exam paper to augment visualisation of the colour change. The pH stick is then rubbed along the moist end of the string and the resultant colour change is then compared to the pH colour chart. A pH of less than 3 on any part of the distal half of the floss indicates that the stomach is secreting hydrochloric acid properly. A pH greater than 3 indicates hypochlorhydria, whereas a pH of 5 or above indicates achlorhydria.
If you do have a low level of stomach acid, as proven by the Gastro-Test, then you should also then look to test for the presence of a bacterium called Helicobacter Pylori that can cause this, prior to commencing any hydrochloric acid supplements.
Helicobacter Pylori is the most common chronic bacterial pathogen in humans. It lowers stomach acid levels whilst damaging the mucosal protection within the stomach. It has been attributed as one of the prime causes of stomach and duodenal ulcers. Helicobacter pylori is a gram-negative, microaerophilic bacterium that can inhabit various areas of the stomach, particularly the antrum.
It causes a chronic low-level inflammation of the stomach lining and is strongly not only linked to the development of duodenal and gastric ulcers but also stomach cancer. The bacterium was initially named Campylobacter pyloridis, then renamed C. When 16S rRNA gene sequencing and other research showed in that the bacterium did not belong in the genus Campylobacter, it was placed in its own genus, Helicobacter. Infection is more prevalent in developing countries, and incidence is decreasing in Western countries.
Interest in understanding the role of bacteria in stomach diseases was rekindled in the s, with the visualization of bacteria in the stomach of gastric ulcer patients. The bacterium had also been observed in by Australian pathologist Robin Warren, who did further research on it with Australian physician Barry Marshall beginning in After numerous unsuccessful attempts at culturing the bacteria from the stomach, they finally succeeded in visualising colonies in , when they unintentionally left their Petri dishes incubating for 5 days over the Easter weekend.
In their original paper, Warren and Marshall contended that most stomach ulcers and gastritis were caused by infection by this bacterium and not by stress or spicy food, as had been assumed before. Marshall is well-known for proving that the bacterium Helicobacter pylori is the cause of most peptic ulcers, reversing decades of medical doctrine which held that ulcers were caused by stress, spicy foods, and too much acid. If you took stomach acid and had H. Pylori then this could produce unpleasant side effects, usually of a painful nature sore, burning gut lining , which is why it is so important to rule out its presence before proceeding with taking hydrochloric acid.
Ask your doctor for a breath or stool antigen test the latter is more accurate as a marker of ongoing infection because the blood test cannot tell you whether you have successfully eradicated the bacterium, except after many months the antibodies remain in the bloodstream for months.
If you do have H. Pylori then follow the Anti-H. Pylori Plan see below , which needs to be taken for 6 weeks, or more in some cases. If you do, then you should also re-test your H. Pylori to see if you are still positive. Finally, when you have eradicated the H. Pylori and you still have low levels of stomach acid you can consider HCl supplements and digestive enzymes. However, some patients will not be able to tolerate HCl for some time afterwards. An intramuscular vaccine against H.
Its clinical usefulness requires further study. A study has found that green tea can prevent Helicobacter-related inflammation. Proton pump inhibitors and potassium competitive acid blockers are widely used therapeutically to inhibit acid secretion.
In addition to their unique ability to secrete gastric acid, parietal cells also play an important role in gastric mucosal homeostasis through the secretion of multiple growth factor molecules. The gastric parietal cell therefore plays multiple roles in gastric secretion and protection as well as coordination of physiological repair. Several additional mediators have been shown to result in gastric acid secretion when infused into animals and people, including calcium, enkephalin and bombesin.
Calcium and bombesin both simulate gastrin release, while opiate receptors have been identified on parietal cells. It is unclear whether these molecules have a significant physiologic role in parietal cell function.
A variety of substances are capable of reducing gastric acid secretion when infused intravenously, including prostaglandin E 2 and several peptides hormones, including secretin , gastric inhibitory peptide , glucagon and somatostatin. PGE 2 , secretin and somatostatin may be physiologic regulators. Somatostatin inhibits secretion of gastrin and histamine, and appears to have a direct inhibitory effect on the parietal cell.
Stomach: Introduction and Index. A Bosnian translation of this page by Amina Dugalic is available at Bosnian translation. Acid is secreted by parietal cells in the proximal two thirds body of the stomach. Gastric acid aids digestion by creating the optimal pH for pepsin and gastric lipase and by stimulating pancreatic bicarbonate secretion.
Acid secretion is initiated by food: the thought, smell, or taste of food effects vagal stimulation of the gastrin-secreting G cells located in the distal one third antrum of the stomach. The arrival of protein to the stomach further stimulates gastrin output. Circulating gastrin triggers the release of histamine from enterochromaffin-like cells in the body of the stomach.
Histamine stimulates the parietal cells via their H2 receptors. The parietal cells secrete acid, and the resulting drop in pH causes the antral D cells to release somatostatin, which inhibits gastrin release negative feedback control.
Acid secretion is present at birth and reaches adult levels on a weight basis by age 2.
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