How Low Stomach Acid Can Make You Sick

How Low Stomach Acid Can Make You Sick
How Low Stomach Acid Can Make You Sick

We try not to think about it, but the mouth, esophagus, and intestines are virtual bacterial cities, containing more than four-hundred different species of microscopic bugs.But a healthy stomach, which lies directly between the esophagus and the beginning of the intestines, is normally an oasis of sterility, or near sterility. This microbe-free buffer zone exists because of one simple fact: stomach acid kills bacteria. “The low pH of the intragastric environment constitutes one of the major non-specific defense mechanisms of the body,” wrote one researcher(1).
The gastric acid barrier guards two gateways simultaneously. Most swallowed or inhaled bacteria play no role in digestion and would constitute an unwelcome alien presence amidst the flourishing natural microbial ecology that is essential for digestion in the intestines. Thus, stomach acid intercepts bacteria that enter through the gateway of the nose and mouth and kills them before they can pass into the intestine. By the same token, intestinal bugs have no business farther north, where they can only cause trouble. The acid barrier (a term taken directly from medical textbooks) keeps these bacteria from migrating up through the duodenum and pylorus and putting down roots in the stomach lining.
Although some bacteria can usually be found in a healthy stomach, the vast majority turn out to be recent arrivals. When the pH is 3 or lower, the normal between-meal “resting” level, bacteria don’t last more than fifteen minutes (perhaps a little longer if the pH gets up to 4). If we were to completely stop swallowing for fifteen minutes or more, our stomachs would rapidly revert to their naturally sterile or near-sterile state.
As the pH rises to 5 or more, though, many bacterial species avoid the acid treatment and begin to thrive. Without regular acid baths to drive them out, the stomach can become a quite hospitable locale for bacterial colonization. It’s dark, it’s warm, it’s moist, and it’s often full of nutrients(2).Acid-suppressing drugs routinely drive the intragastric pH over 5. Fortunately, most of the bacteria we ingest won’t kill us, at least not right away. But some of them will. People who have a gastric pH high enough to promote bacterial growth may be vulnerable to serious bacterial infections such as Salmonella, cholera, dysentery, typhoid, and tuberculosis,not to mention garden-variety heartburn, diarrhea, constipation, bloating, flatulence, or other common symptoms of dyspepsia (“upset stomach”).
The evidence is unmistakable. The risk of Salmonella infection is more than threefold in people who have had stomach surgery that inhibits acid secretion, and it rises in direct proportion to the degree that the operation reduces acid-secreting capacity. In a 1970w cholera outbreak in Israel, one-fourth of the twenty-five people who came down with the disease had had prior stomach surgery. Sixteen of the patients had no free stomach acid at all and a mean pH of 6.4. Those people with the least stomach acid (achlorhydria) had the most severe cholera.
In a study of thirty-seven Bangladeshis with cholera, sixteen had deficient stomach acid. When researchers sampled gastric juice from these sixteen people and put these samples into test-tubes with the cholera-causing bacteria, V. cholerae, they failed to kill the bug.
In fact, though, V. cholerae is exceptionally vulnerable to a low pH.Thus, when the stomach pH is normal (i.e., 3 or less), the risk of developing cholera or any other infectious intestinal disease, even if we happen to drink some tainted water, is much lower. As noted above, the concept of the “acid barrier to gastrointestinal disease” has been firmly established in medical textbooks for many, many decades.
Much that we have said about cholera is also true of Salmonella, typhoid, and nearly all bugs that might infect our intestines. The “acid barrier” isn’t 100 percent effective (even children and teenagers with “maximum-strength” stomach acid can get intestinal infections), but it definitely lowers our risk of gastroenteric infection. Elderly people, who are more likely to have low stomach acid due to decades of progressing atrophic gastritis, have been found to be particularly prone to Salmonella infection.

Anti-acid Drugs Can Make Us Vulnerable to Infection

 One reason diseases like Salmonella, cholera, typhoid, and dysentery can be so devastating in poor countries is that malnutrition leaves the stomach lining inflamed (gastritis) and acid secretion dangerously impaired. But even in the midst of plenty, we may be leaving ourselves vulnerable to serious bacterial GI infections simply by following “doctor’s orders,” that is, by taking antacids and acid suppressors.
As far back as 1885, the pioneering German bacteriologist Robert Koch found he could promote cholera infections in guinea pigs simply by feeding them a dose of bicarbonate (which neutralizes normal stomach acid) prior to infecting them with the V. cholerae. This works in people as well. Almost one-hundred years later, a study showed that healthy human volunteer “guinea pigs” could also increase their risk of cholera infection by first taking a dose of sodium bicarbonate. (Even though cholera gets the most research attention as one of the most serious infectious gastrointestinal diseases, please remember that this discussion applies to every potential gastrointestinal infection, including the “mutant” E. coli OH157, the deadly meat-contaminant organism that appears to be a result of routinely feeding antibiotics to animals.)
One way that doctors may literally be killing people is by promoting bacterial infections with acid-suppressing drugs. It has become common practice in hospitals today to freely dispense drugs like Prilosec and Zantac to very sick patients, such as those in intensive care. The aim is to make them more comfortable (if they have heartburn or esophageal reflux) and to prevent “stress ulcers” from forming in the stomach.
No doubt, the doctors who prescribe these drugs have the best of intentions, but the evidence suggests that their “approved” treatment promotes pneumonia development in a significant number of their patients. “Nosocomial” (hospital-caused) pneumonia—a bacterial infection of the lungs—is a huge problem in hospitals today, accounting for 17 percent of hospital-acquired infections. It increases length of stay in the hospital, helps send health care costs through the roof, and kills 50 percent of people who develop the disease while on a mechanical ventilator.
In the vast majority of cases of hospital-acquired pneumonia, the bacteria that infect the lungs originate deep down in the GI tract. With normal acid levels in the stomach, there is little risk of bacteria from the intestines working their way up into the lungs. However, reduced stomach acid that may accompany critical illness, combined with drug-induced acid suppression and/or neutralization, can raise gastric pH to levels that encourage bacterial overgrowth and migration.
How do the bacteria get from the gut to the lungs? Small amounts of bacteria-laden gastric contents may get aspirated (inhaled) during episodes of reflux. Also, in seriously ill people, tubes placed into the airways, nose, mouth, and stomach can all serve as superhighways for disease-causing organisms.

Lots of research demonstrates that the risk of nosocomial pneumonia in critically ill people is significantly lower when they are treated, not with an acid suppressor, but with a mucosal protective agent (sucralfate) that coats the mucosal lining but does not alter gastric pH. In a study published in the New England Journal of Medicine, patients on mechanical ventilation were randomly divided into two groups. One group took either an H2-receptor-blocking drug, a neutralizing antacid, or both, while the other group took just sucralfate. The rate of pneumonia was twice as high in the acid suppressor/neutralizer group as in the sucralfate group. The acid-sup-pressed people were also 60 percent more likely to die from pneumonia.

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