Jonathan E. Prousky, N.D., FRSH Editor-in-Chief
Direct correspondence to: Jonathan E. Prousky, N.D., FRSH Canadian College of Naturopathic Medicine 1255 Sheppard Ave. E., Toronto ON M2K 1E2 Canada E-mail: email@example.com
In naturopathic medicine, we sometimes use diagnoses that are not widely used by mainstream (conventional) medicine. One such diagnosis is hypochlorhydria, which refers to an increased gastric pH as a result of deficient hydrochloric acid (HCl) and pepsin secretion. Hypochlorhydria has occasionally been mentioned as a factor in certain medical conditions (e.g., pernicious anemia, alcoholism, and partial gastrectomies),1 but has received minimal recognition as a diagnostic consideration. It is now recognized that the principal reason for vitamin B12 (cobalamin) deficiency among the elderly is hypochlorhy- dria.1-3 Unfortunately, the use of hypochlorhydria as a diagnosis has been replaced with the less appropriate, food- cobalamin malabsorption syndrome (F-CMS). This syndrome refers to impairment in the cleavage of cobalamin from food proteins leading to malabsorption of the vitamin. Some of the treatments for F-CMS include crystalline cobalamin supple- mentation, food fortification, or regular parenteral injections of cobalamin. F-CMS and its treatments, however practical, cannot fully compensate for the consequences of low or absent gastric acid secretion that include an inadequate sterilizing barrier against enteric pathogens, impaired micronu- trient absorption, bacterial overgrowth of the small intestine, disruption of normal intestinal permeability, and possibly hypergastrinemia.4 The main cause of F-CMS is gastric atrophy (atrophic gastritis), which was reported to occur in some 28% of an adult Caucasian population,5 and may or may not be associated with Helicobacter pylori (H. pylori) infection.1 Although there are different types of atrophic gastritis (Types A and B), both are characterized by impairments in the secretion of HCl and differentiated on the basis of clinical and histological findings.5 Type B gastritis is associated with F- CMS and appears to result from environmental factors that irritate the gastric mucosa. All patients with a confirmed diagnosis of F-CMS should be advised to regularly supplement with HCl and pepsin at meals. With regular cobalamin administration, the patient with F-CMS will no longer be cobalamin deficient, but will continue to be at risk for more serious disease, or will persistently have other micronutrient deficiencies. The most common micronutrient deficiencies would involve fiber-bound calcium and nonheme iron, but deficiencies of other micronutrients such as folic acid, thiamin, riboflavin, pyridoxine, niacin, and vitamins A and E may develop.6
If the stomach cannot generate a sufficient gastric acid response, replenishing the stomach with HCl and pepsin during meals should facilitate the cleavage of cobalamin from food proteins. In a study of 5 patients with hypochlorhydria, all had decreased urinary excretion of protein-bound cobalamin even though they had normal absorption of unbound crystalline cobalamin.7 Four of the five patients showed improvement in protein-bound cobalamin absorption after receiving supplemental HCl, pepsin, gastric intrinsic factor, or some combination of these agents. It was concluded that the cobalamin deficiency resulted from hypochlorhydria due to acid-pepsin deficiency, and/or a relative deficiency of intrinsic factor.
Another study examined the ability of 120 ml of water, 120 ml of cranberry juice (pH 2.5-2.6), or 120 ml of a 0.1 N HCl (pH 1.2) solution upon the absorption of protein-bound cobalamin in three groups of elderly hypochlorhydric subjects.8 The study randomized healthy, elderly subjects (age > 60 years) to three groups. The first group (n=8) was comprised of healthy normal subjects, the second group (n=8) was made up subjects pre-treated with omeprazole to simulate the hypochlorhydria of atrophic gastritis, while the third group (n=3) involved subjects with a diagnosis of atrophic gastritis. The addition of dilute HCl increased the protein-bound cobalamin absorption of all three groups, reaching statistical significance in both the omeprazole- treated and normal subjects (p<0.001). The authors' noted that this improvement was the result of the acid's ability to augment the release of cobalamin from protein, or from changing the bacterial cobalamin binding activity, or by directly inhibiting/killing bacteria within the small intestine.
Supplementing with HCl (betaine or glutamic acid hydrochloride) and pepsin have been described by several investigators.4,9-11 Providing supplemental HCl (two 680 mg doses of glutamic hydrochloride given ten minutes apart) has been shown to reduce (acidify) gastric pH in fasting subjects with simulated hypochlorhydria.12 Patients usually start with one 5-10 grain (325-650 mg) capsule of HCl and pepsin with each meal. The dosage should be increased by one 5-10 grain capsule with each meal, sometimes requiring 60-80 grains to have a therapeutic effect. Patients are advised not to use supplemental HCl and pepsin if they are regularly taking nonsteroidal anti-inflammatory medications, if they have active peptic ulcer disease, if they have abdominal pain, or if they develop abdominal pain or burning from this treatment. Patients are also advised to use fewer capsules with smaller meals and more capsules at larger meals.
The subject of hypochlorhydria is not a new one. Most practitioners of conventional medicine do not use it as a diagnosis, nor do they recommend HCl and pepsin as treatment. As naturopathic physicians we should encourage our elderly patients with F-CMS to supplement with HCl and pepsin capsules with every meal. We should not lose a potentially valuable diagnosis like hypochlorhydria, even when our medical doctor colleagues have created a less useful diagnosis like F-CMS. Since hypochlorhydria is so common among the elderly population, with one of its principal manifestations being the malabsorption of protein-bound cobalamin, why not supplement with HCl and pepsin?
Jonathan E. Prousky, N.D., FRSH Editor-in-Chief
1. Andrès E, Loukili NH, Noel E, Kaltenbach G, Abdelgheni MB, Perrin AE, et al. Vitamin B12 (cobalamin) deficiency in elderly patients. CMAJ 2004;171(3):251-9.
2. Baik HW, Russell RM. Vitamin B12 deficiency in the elderly. Annu Rev Nutr 1999;19:357-77.
3. Carmel R. Cobalamin, the stomach, and aging. Am J Clin Nutr 1997;66(4):750-9.
4. Kelly GS. Hydrochloric acid: physiological functions and clinical implications. Altern Med Rev 1997;2(2):116-27.
5. Strickland RG, Mackay IR. A reappraisal of the nature and significance of chronic atrophic gastritis. Dig Dis 1973;18(5):426-40.
6. Kassarjian Z, Russell RM. Hypochlorhydria: a factor in nutrition. Amm Rev Nutr 1989;9:271-85. 7. King CE, Leibach J, Toskes PP. Clinically significant
vitamin B12 deficiency secondary to malabsorption of protein-bound vitamin B12. Dig Dis Sci 1979;24(5):397-402.
8. Saltzman JR, Kemp JA, Golner BB, Pedrosa MC, Dallal GE, Russell RM. Effect of hypochlorhydria due to omeprazole treatment or atrophic gastritis on protein-bound vitamin B12 absorption. J Am Coll Nutr 1994;13(6):544-5.
9. Wright JV. Dr. Wright’s Guide to Healing Through Nutrition. Emmaus: Rodale Press, 1984.
10. Wright JV, Lenard L. Why Stomach Acid Is Good For You. New York: M. Evans and Company, 2001.
11. Plummer N. The unseen epidemic: the linked syndromes of achlorhydria and atrophic gastritis. Towsend Lett Doctors Patients 2004;252:89-94.
12. Knapp MJ, Berardi RR, Dressman JB, Rider JM, Carver PL. Modification of gastric pH with oral glutamic acid hydrochloride. Clin Pharm 1991;10(11):866-9.