This is a great piece which goes some way to explaining why I am always wittering on about low stomach acid. It’s making the point that suppressing stomach acid leads to poorer digestion and to larger protein fragments in the gut, which all leads to a higher allergy risk. Interesting. In fact, most people on antacid medication in my clinical experience have the opposite problem. It’s confusing because low stomach acid can often look symptomatically exactly the same as high stomach acid. Always worth checking.
Read the factsheet on hypochlorydia/low stomach acid here for more info. And here’s the piece for you:
Why Is the Incidence of Food Allergies Rising in Both Adults and Children?
Immunoglobulin E (IgE)-mediated food allergies–the allergies that can cause anaphylaxis–have historically been relatively rare. In the past, they typically were seen in children, who tend to outgrow them by adulthood. Recently, however, the incidence of these allergies in children has risen, and the reactions increasingly are sustained into adulthood. Furthermore, new-onset food allergies and anaphylaxis in adults are now being seen, something virtually unheard of a mere 20 or 30 years ago. So what factors are contributing to this onslaught of allergic disease?
One powerful shift promoting adult-onset food allergy is the relatively new, global use of acid-blocking therapy such as proton pump inhibitors (PPIs) and H2 blockers. Numerous studies demonstrate this association, including one completed in 2005 by Untersmayr and colleagues.1 In this trial, 152 adults were given either a PPI or H2 blocker for 3 months and IgE responses to 19 foods were measured at the end of the trial. Amazingly, a greater than 10-fold rise in the incidence of food allergy was seen in the study group as measured by IgE response, and most of these food allergies were de novo, or new-onset reactions. Some participants with existing allergies experienced an increase in intensity of the reaction as a result of the PPI or H2 blocker. In a significant subset of the volunteers, the reactions continued long after the acid blocker was stopped. Not surprisingly, a control group demonstrated no significant change in IgE food allergy incidence.
The mechanism of this reaction is straightforward: Acid blockers inhibit the digestion of protein in the stomach. When the stomach does not predigest protein for the intestine, the pancreatic and brush border enzymes found there do not perform as well, resulting in larger protein fragments that are sometimes absorbed. Larger protein fragments are more antigenic than small ones; therefore, they are more likely to generate an allergic response.
Source: IFM Journal Nov 14.
To read the full study, see here:
- Untersmayr E, et al. Anti-ulcer drugs promote IgE formation toward dietary antigens in adult patients. FA SEB J. 2005 Apr;19(6):656-8. Epub 2005 Jan 25. (Link to free full text: click here)