Prevalence of Low Stomach Acid
A large variance in the reported prevalence of hypochlorhydria is noted in the literature. While aging is regularly associated with decreased gastric acid production, fasting hypochlorhydria is reported to be less common (~10% or less) in elderly American subjects, while it is reported to be more common (>60%) in elderly Japanese subjects, and as high as 80% in a small cohort of Norwegian subjects in their eighth and ninth decades of life (average age: 84 years, range: 80-91).8-11 These studies illustrate the lack of consensus in the literature for the prevalence of fasting hypochlorhydria and achlorhydria in the aging population as many factors are likely to affect fasting gastric pH (e.g., gender, testing method and cutoff values, number of parietal cells to produce HCl, coincident disease states such as H. pylori infection and overall health, etc.).12
Nevertheless, while fasting gastric pH is likely an important marker for achlorhydria, especially when this condition is related to chronic atrophic gastritis, the gradual “functional” decline in gastric acid secretion during and after consuming a meal (a biomarker rarely reported in the literature) may be a much more important measure of acid-related digestive issues. Interestingly, studies performed by researchers at the University of Michigan nearly two decades ago give us some clues to investigate this phenomenon. They reported on the fasting, mealtime and postprandial stomach pH levels in healthy young and elderly subjects.13,14 Gastric pH levels were measured using a tethered radio-telemetric capsule (Heidelberg) in 15-second intervals. After 12 hours of fasting, gastric pH was measured for one hour before a “standard meal”i and continuously for another four hours once subjects commenced eating the meal. In the fasted state, the average gastric pH was similar in both the younger (mean age 25 years) and the older (mean age 71 years) subjects, with a slight statistical trend toward lower pH (more acid) in the elderly subjects (See Figure 1). However, it should be noted that while none of the younger subjects had a fasting pH > 5.0 (the study’s definition of achlorhydria), 11% of the elderly subjects had a fasting gastric pH >5.0, similar to the prevalence noted above in US elderly subjects. Using this fasting data alone, one might conclude that ~90% of elderly subjects have similar gastric acid production compared to younger subjects. However, while both groups saw an expected rise in stomach pH upon consumption of the meal, the time required to re-acidify the gastric contents was much slower in the older subjects. For instance, while the average pH after consuming the meal was similar in young and old subjects (5.0 and 4.9, respectively), the time it took to re-acidify the stomach to a pH of 3.0 was 42 minutes in the younger subjects and 89 minutes in the older subjects, averaging nearly an hour longer to reach a pH of 2.0 (16.4% of the elderly subjects did not return to pH of 2.0 within four hours).
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These data suggest that a diminution of gastric acid secretion may gradually worsen with aging, which cannot be readily detected in the fasted state (i.e., independent of atrophic gastritis/achlorhydria). This extended mealtime/postprandial hypochlorhydria may contribute to poor protein digestion, reduced micronutrient absorption, increased risk of dysbiosis, SIBO, or other symptoms associated with functional dyspepsia. Therefore, based upon this progressive “functional” hypochlorhydria in older subjects, it is not unreasonable for integrative and functional medicine clinicians to consider oral supplementation of “gastric acid” in the form of betaine HCl (often with pepsin) to help reduce meal-time stomach pH; but what is the evidence for this approach?
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