Last month, I wrote about how stomach acid provides limited immune protection against bacteria entering the body. It is true that the process is not 100% effective. Nevertheless, gastric acid does kill most bacteria that enter the body with food. Of course, bacteria survive and take up residence in the intestinal tract, particularly the large intestine.
Scientists are now exhibiting a seemingly unlimited interest in the gut microbiome, a topic many healthcare professionals have included in their diagnostic procedures since at least 1920. It is well established that bacteria do not thrive in an acidic environment, and it takes an average of 45 minutes for stomach acid to be produced by healthy young adults. Nevertheless, the pH of the normal resting stomach is usually between 5.0 and 6.0 unless proton-pump inhibitors or H2 blockers are being used. Then, the pH rises, becomes alkaline, and bacterial microorganisms can flourish, such as Helicobacter pylori (H. pylori). And it is not the only one.
Protein Digestion Begins in the Stomach
Many (if not most) bacteria entering the stomach with food are proteins. A notable exception is Mycobacterium tuberculosis, which has an unusual, waxy coating on its cell surface because of the presence of mycolic acid that resists the action of digestive secretions. The chief cells in the middle portion of the stomach (fundus) secrete a protein-digesting enzyme known as “pepsinogen.” We discussed the protein-digesting events that occur in the stomach last month. This month, we conclude our series with the prevention of stomach acid for the relief of symptoms.
Inhibition of Gastric Acid Secretion
The mechanism that produces gastrin is completely blocked when the acidity of gastric juices drops to a pH of 2.0. This feedback inhibition plays an important role in protecting the stomach against excessively acidic secretions that can lead to ulceration. However, since the role of stomach acid is to provide the optimal pH for activating pepsin from pepsinogen whenever the pH rises above 2.5 to 3.5, gastrin production is again activated.
The possibility of excess production requiring antacids and proton-pump inhibitors is difficult to understand and justify because of the regulatory mechanisms that control the production of hydrochloric acid. The concept of an incompetent mucosal lining to protect the epithelial lining of the stomach and esophagus must be considered.
The Mucous Lining
Mucus is composed of water, electrolytes, and glycoproteins, which are primarily large polysaccharide molecules combined with much smaller amounts of protein. The composition of mucus varies slightly in different areas of the gastrointestinal tract, but its functions are universal:
Inhibiting Acid Production with Prilosec and Prevacid
In the mid-1990s, University of Michigan scientists found that antibiotics are the best way to kill the bacteria that cause gastritis and eliminate stomach inflammation in experiment mice. However, mice treated with prescription drugs called proton-pump inhibitors (PPIs), such as Prilosec and Prevacid, which block acid production, acquired more bacteria and developed more inflammatory changes in their stomach linings than untreated mice.
The study suggested that physicians may want to reevaluate the long-term use of Prilosec and other PPIs with their patients because reduced gastric acidity appears to make the stomach more vulnerable to bacterial invasion. The body responds to this bacterial overgrowth by triggering an inflammatory response that involves the release of white blood cells, the stomach’s primary response to bacterial colonization.
Inflammatory responses are characterized by symptoms of fever, redness, swelling, and pain. Animal studies show that inflammation of the stomach lining coincides with the production of peptides called cytokines, which stimulate the production of a hormone called gastrin. Gastrin triggers the production of more hydrochloric acid in a futile effort to kill off the invading microbes. If you inhibit stomach acid production, you interfere with the body’s natural defense mechanism.
While 75% of people with gastritis test positive for Helicobacter pylori, many other species of bacteria can also trigger inflammatory changes and often coexist with H. pylori. Other major types of bacteria identified included Lactobacillus, Enterobacter, and Staphylococcus. H. pylori is the only bacterial organism in the stomach that cannot be killed by hydrochloric acid, though.
Because food is broken down into nutrients to be digested in the stomach, reducing the level of acid in it also reduces the effectiveness of the digestive process. As a result, some nutrients fail to be broken down into a form the body can absorb. Many studies have now confirmed the side effects of using PPIs long term—labels recommend no longer than two weeks.
Nutrient Deficiencies
Long-term PPI use has been associated with deficiencies in levels of iron, magnesium, and B12. Lack of iron and vitamin B12 are associated with anemia that can result in dizziness or fainting. Magnesium deficiency can cause muscle weakness and cramping.
Kidney Failure
Long-term PPI use has been linked to kidney disease in some users. In 2014, the FDA mandated a warning for PPI medications regarding the link between PPIs and interstitial nephritis, a kidney disorder that causes inflammation between the kidney tubules.
Reactions with Other Drugs
PPIs can reduce the efficacy of the anticoagulant drug clopidogrel, which is used to inhibit blood clots that cause heart attacks and strokes. PPIs also affect the cancer drug methotrexate by interfering with the elimination of the drug from the body.
Clostridium Difficile and Pneumonia
PPIs are associated with the bacterial infection Clostridium difficile, which can cause diarrhea and inflammation of the colon. They are also associated with pneumonia.
Osteoporosis
PPIs can inhibit the absorption of calcium, which can lead to osteoporosis and an increased risk of fractures, particularly of the hip, wrist, and spine. The FDA issued a warning about the risks of fractures associated with PPI.
While the previous list may be sufficient to discourage long-term use of PPIs, I wonder about how many doctors routinely check a patient’s medications to compare the patient’s symptoms with the recognized symptoms related to those medications.
When I was a student, I would utilize X-rays and physical examination to recognize if the patient’s chief complaint of structural misalignment (dare I say, “subluxation”) was related to iron deficiency anemia. If so, what involuntary muscle contractions and loss of joint range of motion could be attributed to that deficiency? That question motivated me throughout my career and led me to ask at my seminars, “What do you have to see before you know what to do?”
I will close by listing a few of the symptoms related to long-term PPI and H2 blocker use.
You may experience some of the following side effects when taking a PPI:
This is the final article in this series. As always, I invite your comments and questions and you can email me at [email protected].
Dr. Howard F. Loomis Jr. has an extensive background in food enzyme nutrition. He is the president of the Food Enzyme Institute. The Food Enzyme Institute offers in-person and online seminars to healthcare practitioners around the country. Dr. Loomis published Enzymes: The Key to Health in 1999, The Enzyme Advantage in 2015, and The Enzyme Advantage for Women in 2016. His latest ' book, What Is Your Nutritional Deficiency?: Find It, Fix It, and Feel Better! was published in 2019. Contact info: 478 Commerce Dr. Suite 201, Madison, Wl 53719, [email protected], 800-662-2630.
