Some of these include infection , taking certain medications , and the aging process. The medical term for low stomach acid is hypochlorhydria. When this happens, the other digestive organs cannot absorb essential nutrients from the food a person eats.
This article will discuss six natural ways to increase stomach acid. It will also examine the causes of low stomach acid and some associated risk factors. Treatments for low stomach acid depend on the underlying cause. However, there are some methods a person can try at home to improve stomach acid levels.
According to a review , older adults have a higher risk of developing digestive conditions that reduce their stomach acid levels. Digestive conditions that may decrease stomach acid levels include Helicobacter pylori infection a bacterial infection of the stomach and atrophic gastritis which is characterized by chronic inflammation of the lining of the stomach. As a person ages, their stomach also produces less pepsin.
Pepsin is an enzyme that breaks down proteins and aids digestion. People with low levels of stomach acid may benefit from taking HCL supplements.
Digestive enzyme supplements that also contain pepsin may be especially beneficial for older adults. However, a person should speak with a doctor before taking any supplements. Although supplements may alleviate symptoms, the hypochlorhydria may be due to an underlying health condition that requires medical attention. People who do not get enough zinc in their diets and those with poor zinc absorption may have low stomach acid levels.
Addressing a zinc deficiency could help increase stomach acidity. People can increase their zinc intake by making dietary changes or taking zinc supplements. However, they should speak with their healthcare provider before starting any new supplements. Probiotics are microorganisms that support a healthful balance of beneficial bacteria in the gut. A review article found evidence of an association between low stomach acidity and bacterial overgrowth in the gut. Taking probiotics may inhibit the growth of harmful bacteria and help increase levels of stomach acid.
Ginger possesses anti-inflammatory properties that may help alleviate stomach inflammation due to low stomach acid. People commonly use ginger as a natural remedy for nausea, stomach pain, and indigestion. Some proponents suggest that ginger may stimulate the production and secretion of essential digestive enzymes and increase movement through the intestines.
However, there is not enough scientific evidence to fully support these claims. More high quality studies are necessary. A variety of substances have been used to produce maximal stimulation of gastric acid secretion. Two-deoxy glucose acts as a competitive antagonist of glucose receptors in the brain, which stimulates vagal-induced acid secretion in several species 25, The minimal effective dose of histamine that produced acid secretion in people was 10 times less than that required for the dog The rat is insensitive to histamine when compared to the dog, cat, pig, monkey, or rabbit Gastrin was used as a stimulant before pentagastrin was available Pentagastrin Peptavlon' Ayerst Labs contains the biologically active carboxyl terminal tetrapeptide of the gastrin molecule and is currently the preferred agent to study maximal secretory rates Cholinomimetics are relatively weak stimulants of acid secretion when compared to histamine and pentagastrin One possible reason could be that cholinergic agents may stimulate both inhibitory and stimulatory pathways.
Recently, Feldman and Schiller suggested that the weak stimulatory effect may be explained by a concomitant stimulation of nonparietal bicarbonate secretion by the surface epithelium 47, Inhibition of Acid Secretion Inhibition of acid secretion may be caused either by direct action on the parietal cell or indirectly by the release of other inhibitory agents or by changes in blood flow Atropine and H2-receptor antagonists are potent inhibitors of both pentagastrin and histamine stimulated acid secretion in the human, dog and rat As mentioned earlier, gastrin release can be inhibited by acidification of the antrum, by release of somatostatin and by vagal fibers Somatostatin cells possess cytoplasmic processes that extend to neighboring gastrin cells and parietal cells in the fundus.
Both the inhibition of gastrin release and parietal cell secretion are by paracrine and endocrine effects. Acid secretion is also inhibited in the intestinal phase by humoral agents released from the small intestine in response to duodenal acidification or hyperosmolarity or increasing lipid content 39, A variety of hormones gastric inhibitory peptide, enteroglucagon, vasoactive intestinal peptide and cholecystokinin are capable of inhibiting parietal cell response, but their physiological significance is not established Duodenal acidification causes the release of secretin from the duodenal mucosa which stimulates pancreatic bicarbonate secretion and inhibits gastric acid secretion.
Lipids cause the release of cholecystokinin from the mucosa which stimulates gall bladder contraction. Cholecystokinin is structurally related to gastrin in its carboxyl terminus and is a weak agonist of acid secretion in the cat Histamine has long been recognized as one of the most potent stimulants of acid secretion, however, its gastric secretogue effect is not blocked by conventional antihistaminic drugs, which inhibit the effects of histamine on smooth muscle of the intestinal tract and bronchi This led to the postulation that there were two separate 27 histamine receptors.
Black and co-workers discovered that a histamine analog inhibited histamine stimulated acid secretion, identified the receptor on which it acted and named it the histamine H2 receptor Since then, numerous H2 antagonists have undergone clinical trial as potent inhibitors of acid secretion The first antagonists were developed by lengthening the side chain and adding a thiourea group to the imidazole ring of histamine. Raniditine Zantac, Glaxo, Inc.
Side effects attributed to the imidazole ring of cimetidine have not been observed for ranitidine, namely: 1 antiandrogenic effect characterized by impotence and gynecomastia in men; 2 mental confusion; 3 interaction with other drugs attributed to inhibition of hepatic cytochrome P oxidase enzymes; and 4 bone marrow depression 20, Like cimetidine, ranitidine has been shown to promote significant healing in human peptic ulceration in several double-blind clinical studies It is well absorbed from the human small intestine and has a plasma half-life similar to that of cimetidine approximately 90 minutes 28 37,78,92, Ranitidine given at breakfast to people suppresses acid secretion at lunch and dinner, thus having a long duration of action.
Because of the increased potency and long duration of effect, ranitidine is prescribed twice daily and studies are underway to determine the effectiveness of once per day treatment at night when acid secretion is highest A possible cytoprotective effect of ranitidine has been described in people and rats which may be related to its ability to induce production of endogenous prostaglandins Pepsinogen Secretion Rate The term, pepsin, was introduced in by Schwann for the protease in gastric juice 39, In , almost one hundred years later, Northrup crystallized pepsin from porcine gastric mucosa.
Pepsinogen initiates the process of protein digestion which leads to the formation of peptides that serve as signals for the release of various hormones, including gastrin and cholecystokinin In turn, these hormones serve as major regulators of protein digestion. Pepsinogen is most active on collagen, which is found in greater quantity in meat than vegetable protein, implying that carnivores should have higher secretion rates Pepsinogen secretion is also thought to be important in those species where mastication of food is minimal dog Seven distinct mammalian pepsinogens have been characterized on the basis of electrophoretic mobility, pH optima and immunologic reactivity.
The five fastest migrating pepsinogens PI can be distinguished from pepsinogens 6 and 7 P2. Group 1 pepsinogens are found in the chief cells and mucous neck cells of the fundic glands, whereas group 2 pepsinogens are found in fundic, pyloric and duodenal glands.
There is a small continuous basal secretion of pepsinogen in humans 72 Additional pepsinogen secretion is stimulated by primarily muscarinic cholinergics, but is also stimulated by pentagastrin and histamine in the human and several other species 74 In the human or dog, maximal pepsinogen secretion is fold greater than basal rates The rate of pepsinogen secretion in vivo during histamine administration in dogs and cats was the subject of controversy until dose-response curves showed reduced secretion rates at high doses of histamine Initial increases, then decreases, in pepsinogen secretion may be due to release of stored pro-enzyme wash-out theory Pepsinogen secretion activated by luminal acid has also been demonstrated and probably occurs via local cholinergic reflexes Differences in species and the combined 30 possibilities of wash-out and acid activation make evaluation of pepsinogen secretory data difficult.
After secretion into the gastric lumen, pepsinogen is irreversibly converted by acid to the active enzyme, pepsin Mol. Following this loss, the protein undergoes a conformational change, apparently to expose a binding cleft that will accommodate a peptide of about 8 amino acids. The active site contains 2 aspartyl residues, which is similar to 2 other carboxyl proteases, cathepsin and rennin. The catalytic site appears similar in all species, including the horse Pepsin is an endopeptidase with a pH optimum of depending on the substrate, and is most active against peptide bonds adjacent to aromatic peptides phenylalanine and tyrosine or dicarboxylic L-amino acids 39, Some free amino acids and polypeptides are produced.
The extent of digestion is determined by the physical state of the ingested protein, the length of time it stays in the stomach and the activity of the pepsin. Gastric protein digestion is not essential in humans, since those with achlorhydria have no impairment of protein digestion and absorption The most traditional technique used to determine the concentration of pepsin in gastric fluid is by the digestion of hemoglobin substrate at pH 1. Pepsin splits off products from hemoglobin which are soluble in trichloroacetic acid.
With this technique, 1 peptic unit PU represents the activity of pepsin which releases 0. Gastric Fluid Composition The composition of gastric fluid is determined by the different secretory systems existing side-by-side in the gastric mucosa: 1 the parietal cell secretes electrolytes and acid HC1 ; 2 the chief cell synthesizes pepsinogen which is stored for rapid release but may also be made and secreted continuously; and 3 the mucous epithelial cell which constantly secretes water, mucus and bicarbonate Each secretory product has a specific role in protein digestion acid and pepsin or mucosal protection mucus and bicarbonate.
While pure parietal or nonparietal fluid has not been measured directly, several theories have been put forth to explain the composition of gastric fluid in relation to different mixtures of parietal and nonparietal components.
This active secretion results in a negative potential difference mucosa negative. This so-called non-acidic Cl- secretion manifests itself as the lumen-directed negative short circuit 33 current and PD. Gastric secretion of bicarbonate ion was postulated by Schierbeck in , and Hollander proposed that secretion of a bicarbonate-containing fluid was the main mechanism for regulating gastric acidity 52, Gastric bicarbonate has only recently been found to be an active process which can be stimulated and inhibited in the fundic, pyloric and duodenal mucosa 52, Fifty percent of perforated ulcers in one study were in the squamous mucosa.
These lesions have also been recently reported in adult horses without a history of previous medication. Diet and physical stress have been proposed as etiological factors. Ulcers in the squamous mucosa near the cardia junction of esophageal and gastric mucosa are common in swine fed high protein or pelleted diets.
Surveys of farms with equine gastroduodenal ulceration have not shown any effect of diet but additional studies are needed concerning feeding practices on these farms. The squamous mucosal ulcers in foals may be similar to "stress erosions" seen in seriously ill people following major surgery or trauma Stress erosions in people, 35 36 however, occur in the glandular mucosa.
The pathogenesis of gastric ulceration in people, in general, is less associated with excess acid and pepsin secretion and more associated with decreased mucosal resistance normally produced by secretion of mucus and bicarbonate. With restoration of normal defense mechanisms, stress ulcers heal rapidly within several days. Experimental evidence in laboratory animals also suggests that stress ulceration results from a temporary failure of gastric mucosal defense mechanisms, rather than from excessive secretion of acid and pepsin, however, mucosal lesions can not be produced without luminal acid Since the eguine sguamous epithelium does not appear on histologic sections to be covered by mucus to as great an extent as the glandular epithelium, it may be more easily damaged than the glandular epithelium when there is failure of gastric mucosal defense mechanisms.
Equine gastric ulcers of the glandular epithelium are seen less frequently than those of the squamous mucosa and have been reported in ill neonates 30 Glandular gastric ulcers have also been experimentally produced with nonsteroidal anti-inflammatory drugs NSAID ,in foals and ponies Ulceration following NSAID administration probably results partly from inhibition of endogenous prostaglandin synthesis.
Prostaglandins have been shown to inhibit acid and pepsin secretion, stimulate mucus and bicarbonate secretion and maintain mucosal blood flow ,, Additionally, 37 prostaglandins promote rapid restitution of damaged epithelium in doses which do not inhibit acid secretion , Duodenal Ulceration The eguine cranial duodenum is sigmoid-shaped with an initial ampulla separated by a slight constriction from the second ampulla into which the hepaticopancreatic duct enters Duodenal ulcers in the horse are generally located on the anti-mesenteric surface as solitary or multiple lesions in the proximal duodenum or can diffusely involve the entire duodenum 15, The hepatic duct may be secondarily obstructed due to duodenitis or stricture formation distal to its opening into the duodenum.
Duodenal ulcers are more commonly seen in month old foals and can occur as a herd outbreak Diarrhea frequently precedes other clinical signs which include teeth grinding, excessive salivation, depression, anorexia and colic. Delayed gastric emptying usually results in squamous gastritis and esophagitis.
In foals with gastric outlet obstruction from duodenal ulcer disease, gastrojejunostomy has resulted in rapid healing of gastritis and esophagitis without recurrence of duodenal ulceration Unfortunately, duodenal ulcers in foals may perforate and result in rapid life-threatening deterioration within 48 hours of the first clinical signs of ulcer disease.
Breakdown of mucosal resistance is also important in duodenal ulceration and a decreased bicarbonate secretion rate has been reported Pathophysiology The mechanisms by which the gastric and duodenal mucosa normally resists the onslaught of food and secreted acid and pepsin are not completely understood 39 It is generally thought that mucosal damage is induced by acid, pepsin and bile after the integrity of the gastroduodenal mucosa has been damaged.
Research into the etiology of human duodenal ulceration has tended to concentrate on factors that control acid and pepsin secretion, while factors that determine mucosal resistance have been investigated in gastric ulceration It is generally agreed that the presence of sufficient luminal acid and pepsin are required for both gastric and duodenal ulceration to develop.
Gastric acid is considered the primary damaging agent which also activates the proteolytic enzyme pepsin from secreted pepsinogen. Mucosal ischemia appears to compromise the ability of the gastric mucosa to dispose of intracellular acid which may 39 have diffused into the mucosa Although gastric acid and pepsin seem essential for the formation of ulcers, gastric ulcer patients frequently secrete acid at rates indistinguishable from normal patients In contrast, nearly half of the duodenal ulcer patients have increased basal and maximal acid secretion rates The mechanisms for these augmented secretory rates have been attributed to increased responsiveness of the gastric parietal cell to stimulation by neural and hormonal gastrin agents, increased parietal cell mass, hypergastrinemia and impaired duodenal mucosal bicarbonate secretion.
The pathophysiological processes underlying duodenal ulceration are not fully understood but there are indications that one of them may be an inadequate neutralization of an excessive gastric juice entering the duodenal bulb. The rate of acid and pepsin delivered to the duodenum by factors regulating gastroduodenal motility are also being investigated with regard to development of peptic ulceration.
In circumstances of normal secretory rates, acid probably plays primarily a permissive role and attention has focused on factors that may protect the mucosa from acid and pepsin. The components of the mucosal barrier include a surface layer of mucus, surface epithelial bicarbonate secretion, mucosal blood flow, epidermal growth factor concentration inhibits acid secretion and epithelial repair and regenerative processes 30,39, Agents known to "break" the barrier 40 are acids HC1, salicylic , detergents that attack the lipid portion of the plasma membrane bile acids , hyperosmolar solutions and ethanol Mucus is secreted as an insoluble gel adherent to the mucosa and as a soluble form mixed in the lumen with gastric contents It functions as a barrier for hydrogen ions with neutralization by bicarbonate secreted from the surface epithelium, as a diffusion barrier for pepsin and as a lubricant to prevent mechanical damage 14,69, Finally, the surface epithelium is capable of rapid restitution after acute superficial damage by migration of the surface epithelium.
Secretion of bicarbonate by both gastric and duodenal surface epithelium beneath the mucous layer maintains the surface pH near neutrality in spite of a luminal pH as low as 1 Bicarbonate secretion is stimulated by luminal acid and this response is mediated by endogenous prostaglandins, humoral factors and, probably, neural inputs Abnormalities of gastroduodenal motility have been investigated in people with peptic ulceration 30, In both gastric and duodenal ulceration, increased duodenogastric reflux has been reported.
Delayed gastric emptying can produce gastric ulcers by increasing the duration of mucosal contact with acid and pepsin. Delayed gastric emptying can result from gastric stasis due to gastroenteritis or can be secondary to duodenal ulceration.
In duodenal ulceration, gastric accommodation to distension is not altered nor are there changes in the rhythm or freguency of gastric peristalsis. There are reports of increased gastric emptying rates and the rapid entrance of acidified chyme into the duodenum could contribute to the inability of the duodenum to neutralize the acid, leading to ulceration. An abnormality in local motility of the duodenum might contribute to the formation of ulcers at specific sites, such as the duodenal bulb, as the proximal duodenum helps to regulate emptying of acid from the stomach.
Delayed gastric emptying has been reported in foals with duodenal ulceration and it has usually been a result of stricture formation from healed ulcers. Information is not available concerning changes in gastric secretion or motility in these foals, which could provide clues to the pathogenesis of this disease in horses.
Inhibition of endogenous prostaglandin synthesis by NSAID seems likely to be the cause of mucosal damage that can be produced by these agents , This enzyme is stimulated in the gastric parietal cell following binding of histamine as mentioned earlier.
Several experimental studies in foals and 42 ponies have shown ulcerogenic properties of phenylbutazone 30, Oral lesions were observed more frequently following oral administration than parenteral. Administration of an oral prostaglandin E2 prevented phenylbutazone-induced ulceration in ponies, although it is not known if the dose used also decreased acid secretion.
An infectious or toxic etiology has been proposed to explain the occurrence of diarrhea and clustering of affected foals on certain farms 15, Such an agent could directly damage the gastroduodenal mucosa or possibly affect gastroduodenal motility, resulting in ulceration.
An organism or toxin has not been isolated 2 Currently there is much excitement concerning the possible role of Campylobacter pyloridis in the pathogenesis of human gastric ulceration 26 Campylobacter sp. The bacteria might damage the mucosa by trapping ammonium thereby exposing the mucosa to excessive hydrogen ions. Bile salts have been implicated in causing gastric mucosal damage and have also been found to inhibit mucus and bicarbonate secretion in people With recent techniques, bile reflux has been found in normal fasting humans, dogs and pigs, and has been observed during endoscopy and experimentation in normal horses.
Bile reflux may be important if the gastric mucosa is already damaged. In foals treated for gastric outlet obstruction with 43 gastrojejunostomy, clinical signs of ulceration did not worsen after total diversion of proximal duodenal contents including bile into the stomach. Bile reflux may not be a major factor in the development of gastric ulceration in the foal.
There has been interest in pepsinogen as a contributor to the formation of peptic ulceration Pepsin constantly digests the mucous layer covering the mucosa.
Several studies have shown that the instillation of acid alone was insufficient to produce ulceration; pepsin had to be present as well. In duodenal ulcer patients, both basal and stimulated pepsin secretion, like acid secretion, are usually higher than in normal subjects. Both pepsinogens 1 and 2 can be detected in serum and Samloff et al.
Pepsinogen 1 has a mucolytic activity over a wider range of pH including that seen in the duodenal bulb. However, there is considerable overlap in serum pepsinogen concentrations between normal subjects and patients with duodenal ulcer disease and thus serum levels are not considered diagnostic.
The lack of interest in antipepsin therapy is due in part to the success of antacid therapy, since acid secretory inhibitors suppress pepsinogen secretion and lead to a higher luminal pH which reduces pepsinogen activation. Little information is therefore available on the composition and control of gastric secretion in the horse. Russian investigators described experiments in fasted young horses 1. Atropine caused regurgitation of duodenal contents and markedly decreased the volume of secretion.
The pH of equine gastric contents has been reported to range from 1. Volatile fatty acids and lactic acid were measured in gastric contents of the fed horse 8, Equine fundic and pyloric mucosa were found to absorb volatile fatty acids but only the pyloric mucosa transported significant amounts to the serosal surface The stratified epithelium did not absorb the fatty acids and had a low tissue conductance indicating it was relatively impermeable to passive ion transport.
Gastric empyting is rapid in the horse as judged from radiographic studies and from studies using liquid and particulate markers 7,12, Gastric emptying rate in foals was studied by contrast radiology and has been reported to be slower in the nursing foal than in the weaned foal in one study 7. A technique for gastric cannulation has only recently been reported and was developed by the authors for these studies 29 Equine gastric fluid was secreted continuously during basal conditions and acid output was inhibited by ranitidine given at 0.
Although several other investigators have adapted the use of this cannula technique, results of their studies have not yet been published. The gastric cannula was constructed entirely of medical grade silicone rubber tubing 1. Three flanges were made from the silastic tubing and two were permanently fixed to the tube with silicone glue, one at the inner gastric end and the other at the inner ventral body wall position. The middle flange outer gastric flange was freely movable to allow positioning after placement of the tube with the inner flange within the gastric lumen.
The cannula was also supplied with an inner tube plugged at the gastric end to occlude the cannula between experiments. The inner tube and an outer body wall flange made of soft rubber were held in place with a hose clamp.
Animal signalment. The stomach was isolated with moistened towels to prevent contamination of the abdomen with spilled gastric contents. Two stay sutures were placed about 20 cm apart on the ventral surface of the stomach between the lesser and greater curvatures and were used to elevate the stomach to the incision. Three purse-string sutures were placed around the intended gastrotomy using 2 polyglactin Vicryl, Ethicon Inc.
A stab incision was made in the center of the purse string suture pattern and the cannula was inserted into the gastric lumen. The sutures were tied allowing the serosa to invert around the tube before securing the outer gastric flange to the serosa with 2 polyglactin The cannula was brought through a stab incision in the left ventral abdomen and the abdominal incision was closed with 3 layers of suture in a routine manner. Horses were allowed to drink only water during the first 24 hours after surgery and then were gradually fed alfalfa hay.
The horses were given 2 weeks to recover from surgery and were trained to accept gentle restraint by cross-tying in a 49 stocks. Body weights were determined biweekly.
They were maintained on a diet of grain and free choice coastal hay and salt block. After several weeks, they could be turned out in a large pasture to exercise. Endoscopy was performed via the cannula to evaluate the condition of the gastric and duodenal mucosa in horses Video-Endoscope , Welch-Allyn. Each horse was euthanitized after completion of the studies and a full necropsy was performed.
Histologic sections were examined from the gastric sguamous and glandular mucosa, margo plicatus and duodenal mucosa using hematoxylin-eosin and PAS stains. Methodology Experiments were designed to address the following guestions: 1 Protocol I: What is the basal acid secretion rate in the horse? Secretory Experiments The horse was fasted for 24 hours with access to water and then placed in a room isolated from other horses and food.
A plasma sample was taken at catheter placement for determination of plasma osmolality all horses. The gastric cannula was opened for 30 minutes to allow gravity drainage of any residual chyme before beginning the 5 hour collection.
Experimental Design Protocol I Gastric fluid was collected every 15 minutes for 5 hours in 13 horses to determine basal rates of secretion. Intravenous 0. Protocol II Gastric fluid was collected as for protocol I. Two horses were given step-wise increasing doses of pentagastrin Peptavlon, Ayerst Labs at 1.
The pentagastrin was dissolved in water by increasing the pH to 9 with 0. A 51 one hour baseline collection was made and the pentagastrin infusion started at the beginning of the second hour.
These doses of pentagastrin were selected based on studies in other species. Protocol IV Gastric fluid was collected as for protocol I. At the beginning of the second hour, 4 treatments were given Table 3. A randomized block design was used where five horses received 4 treatments in random sequence and in duplicate 8 experiments per horse. The treatments were randomized to minimize effects due to the gastric cannulation fatigue and adaptation by the animal to the secretory studies learning.
As each horse served as its own control, individual variation could be evaluated and since duplicates of each treatment were performed, any missing data was accounted for by using an average of the two treatments.
The use of repeated measures also increased the confidence in the results given the small number of animals. Measured parameters The fluid was collected in a Erlenmeyer flask, and every 15 minutes the flask was emptied into a graduated cylinder.
The volume was measured to the nearest 2 ml and the sample 52 Table 3. Hour 1 2 3 4 5 Treatment 1. The intensity of surface transfers between stomach fluid and bolus particles has a significant impact on protein digestibility, whereas the variation in pepsin content in the stomach between individuals appears to have little effect on protein digestibility.
From a nutritional standpoint, the simulations show that meat protein digestibility is high under normal physiological stomach conditions. However, in a situation where masticatory capacity, hydrochloric acid secretion and gastric motor function performances are reduced, such as with advancing age, protein digestibility rapidly decreases, ultimately leading to near-zero digestibility value in the stomach in extreme cases.
Sicard, P. Mirade, S. Portanguen, S. Clerjon and A. Kondjoyan, Food Funct. To request permission to reproduce material from this article, please go to the Copyright Clearance Center request page.
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