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The Myth of GERD: It’s Not the Acid, Stupid!

The Myth of GERD: It’s Not the Acid, Stupid!

by | Jun 16, 2018 | Chronic Disease, Health

There is a myth that GERD, popularly known as heartburn, is due to having too much stomach acid, a condition known as hyperchlorhydria. But there is ample research (1,2,3,4) demonstrating the opposite is true, that is, that GERD is most likely due to not having enough stomach acid.

How It Works

Lower esophageal sphincter (LES) tone is reduced and so the LES relaxes when there is not enough acid in the stomach, a condition known as hypochlorhydria. Hence, the sphincter does not close properly and acidic contents are much more likely to reflux upward from the upper GI into the esophagus. Interestingly, the hypochlorhydria theory of GERD, proponents of which include Jonathan Wright, M.D., author of Why Stomach Acid is Good for You (2001), has been called an alternative medicine theory, when it’s actually grounded in basic med school physiology.

Turn Off the Symptom Rather than Treat the Cause

To treat GERD, modern medicine prescribes drugs first-line in the on-average 7-minute visit: antacids like Tums which neutralize stomach acid; and H2 blockers like Tagamet and proton pump inhibitors (PPI’s) like Prilosec, that temporarily turn off our stomach’s ability to produce stomach acid. But turning off stomach acid in response to gastric reflux is the equivalent of an auto mechanic pulling the automotive fuse for your sudden dashboard engine warning light, or worse yet, simply cutting the wiring which carries the signal, because it is bothersome and annoying, rather than troubleshooting to find the underlying cause.

Common sense tells us there will be downstream consequences for the life of any car (in medicine, these are known as sequelae) if any engine light warning goes unheeded for long enough. Stomach pH varies from roughly 1.5 (more acidic: normal fasting) to 3.5 (less acidic: with food), and proper pH is essential to breaking down proteins as well as a healthy microbiome (5).

Our Addiction to GERD Drugs Causing More Chronic Disease

Our use of drugs to treat GERD is supposed to be short-lived (for example, an initial course of PPI’s is supposed to last no more than 8 weeks), but millions of people end up dependent on these drugs for years, and even decades. And weaning off these drugs, particularly PPI’s, can be challenging. There is an ample body of research now linking chronic PPI use to osteoporosis, increased infection risk, magnesium deficiency, and depression and dementia. But PPI’s are blockbuster drugs, as the market is projected to generate $4.34 billion by 2025.

On a yearly basis:

  • More than 80 million experience GERD symptoms in the U.S. alone.
  • 25 million suffer from heartburn daily in the U.S. alone.
  • 60 million suffer from heartburn monthly in the U.S. alone.

Also, there is evidence that the body upregulates stomach acid production when it is blocked, because the body is smart enough to know that without proper stomach acid it will essentially starve.

Too Much Stomach Acid Actually A Rare Condition

Having too much stomach acid, a condition known as hyperchlorhydria, is actually rare, seen in cases such as Zollinger-Ellison Syndrome (ZES), where tumors in your pancreas produce excessive amounts of gastrin, which leads to excessive stomach acid and thereby causes stomach ulcers. HCl production declines significantly with age, and GERD onset presents on average at age 50, another fact suggesting that GERD is due to hypochlohydria. Though GERD can be due to a number of causes, such as stress, hiatal hernia, or ZES, it is most likely that it is due to not having enough stomach acid.

Treat the Whole Person, Treat the Underlying Cause, and Stimulate the Vital Force, to Help Improve GERD

In naturopathic medicine, we treat the whole person and usually that begins with diet and lifestyle, but people need to be met where they are at. The innate healing mechanism of the body needs to be stimulated and obstacles to cure need to be eliminated for symptoms to improve.

For people who have symptoms of GERD, it is important to determine if they are hypochlorhydric and if so, then to stimulate the production of stomach acid, so that not only can the lower esophageal sphincter maintain proper tone so that it remains closed when it’s supposed to, but so that healthy flora are maintained in the gut and digestion and absorption is optimized. Of course  a person must consult their doctor before engaging in any medical treatment.

Four natural ways to stimulate the production of stomach acid include:

  • Apple cider vinegar (ACV)
  • Digestive bitters
  • Betaine HCl
  • Deglycerrhizinated licorice (DGL).

What do you think? I’d love to hear your thoughts!

Also, here are three excellent articles I greatly appreciated on GERD and hypochlorhydria:

Sources:

  1. Ayazi S, Leers, JM, Oezcelik A, Abate E, et al. Measurement of gastric pH in ambulatory esophageal pH monitoring. Surg Endosc. 2009 Sep;23(9):1968-73.
  2. Giles GR, Humphries C, Mason C, Clark G, et al. Effect of pH changes on the cardiac sphincter. Gut 1969;10:852-856.
  3. Kaye MD. On the relationship between gastric pH and pressure in the normal human lower oesophageal sphincter. Gut 1979;20:59-63.
  4. Giles GR, Mason MC, Humphries C, and Clark CG. Action of gastrin on the lower oesophageal sphincter in man. Gut 1969;10:730-734.
  5.     Shreiner AB, Kao JY, and Young BV. The gut microbiome in health and disease. Curr Opin Gastroenterol. 2015 Jan;31(1):69-75.
Is Food Allergy Testing Really the Answer?

Is Food Allergy Testing Really the Answer?

by | Jun 12, 2018 | Diet, Food Allergy, Lab Testing

In alternative healthcare, food allergy panels are routinely ordered. An estimated 20% of the world believes it reacts adversely to specific foods (1), while as many as 15 million Americans suffer from food allergies (2).

Food reaction can be non-immune mediated, as in food intolerance or sensitivity, or immune mediated, as in food allergy, but there is confusion even among the medical establishment. Alternative food allergy tests usually measure serum IgG antibodies, while conventional allergy tests measure serum IgE antibodies.

Do IgG Antibodies Really Identify Food Intolerance or Sensitivity?

IgG antibodies represent a delayed as opposed to an immediate, immune-mediated food reaction (IgE), and are purported by some, though scientific evidence is scant (3), to identify food intolerance or sensitivity.

How can an immune-mediated food allergy test measure something that is non-immune mediated, such as an enzyme deficiency? And is the $300 to $700 of an IgG food intolerance panel worth the cost?

While Cyrex is the most well-known food allergy lab, Great Plains Laboratory and US Biotek are also reputable. While many alternative practitioners pay lip service to root-cause medicine, food allergy panels may reveal food reactivities which are more symptom than etiology.

Are Dietary Restrictions Revealed by Food Intolerance Testing Possible to Follow?

Routinely revealing long lists of common foods to which a person is producing high serum antibody loads (titers), patients are often placed on ultra-restrictive diets, such as low-FODMAPS (4), which can be difficult to follow, induce stress, and produce low compliance.

The question is: Why are IgG levels high for these specific foods? The answer seems to lie in increased intestinal permeability.

Increased Intestinal Permeability

The immune system, merely doing its job, generates antibody labels to all foods consumed, and because these now-offending foods are crossing the gut barrier into the bloodstream, it’s working overtime. Trained to attack any invader, the immune system begins to recognize the offending foods as antigens. Later on, overwhelmed by constant vigilance and hyperactivity, the body is triggered to begin attacking its own tissues (autoimmunity), as seen in Celiac disease where gliadin antibodies attack the intestinal lining. (5)

Antibody titers will be highest, naturally, to foods consumed most often and in the greatest quantities. When these foods are dietarily removed, antibody titers to said foods gradually lower and disappear. This is why testing for tissue transglutaminase auto-antibodies (tTG-IgA) in Celiac disease, e.g., must be done before going gluten-free. (6)

Leaky Gut, Gliadin Fractions in Gluten, and Zonulin

Increased intestinal permeability, aka leaky gut, will naturally increase food reactivity, and recent research indicates that gluten plays a key role. Gliadin fractions in gluten upregulate the protein zonulin which modulates gut mucosal barrier activity, thereby causing intercellular epithelial gap junctions to expand and produce leaky gut in the intestinal lining. (7) Bad gut bacteria or SIBO can also cause leaky gut, which can lead to metabolic endotoxemia. (8) Higher systemic inflammation results, measured by biomarkers, such as hs-CRP. (9)

The Physiology of the Intestinal Lining in the Small Intestine

The epithelial lining of the small intestine is like a cheesecloth one cell layer thick, just beneath which lies connective tissue called lamina propria. (10) When this cheesecloth stretches out, undigested food particles move from the lumen (tubular inside) of the small intestine into the bloodstream. (11)

When this cheesecloth tears, it takes 3 to 7 days for it to heal, during which many food stuffs supposed to be digesting end up permeating through the intestinal lining and ending up in the blood. (12) A slight degree of intestinal permeability is supposed to be happening, as this is the immune system’s way of sampling what is being eaten, to be on the lookout for infectious organisms. But when too much occurs, autoimmune disease can develop.

Attached to the GI tract’s epithelial cells are microvilli, finger-like projections that increase the surface area of the intestines and absorb vital nutrients, fatty acids, and glycerol from food. Interestingly, tiny arteries (arterioles) go to the top of each microvilli, and tiny veins (venules) go down. (An artery carries blood to something, whereas a vein carries blood away from something.) (13)

In the middle of these arterioles and venules are lymphatic capillaries (lacteals) which absorb dietary fats taken in through the microvilli. So, basically the microvilli and epithelial intestinal lining have a blood supply their own, which nourishes and regenerates them. These microvilli are also sloughed off every 7 days, but only pieces at a time. This is why a large portion of our fecal matter is made of dead skin-like tissue, such as sloughed microvilli. (14)

The Role of Stress in the Absorption of Nutrients in the Small Intestine

At the microvilli base is an A-V shunt or connection, that’s supposed to stay closed. But when it opens, blood naturally shunts across. If this is occurring, then the microvilli will not have the required blood supply and so they will be sloughed off, inducing temporary malabsorption syndrome. Without properly functioning microvilli, zero nutrient absorption will occur, and this can last up to a few days, or be chronic. (15)

Two hormones in particular will naturally open the A-V shunt. These are epinephrine (adrenaline) and norepinephrine, which are released during fight or flight. Chronic stress will cause the adrenal medullae to release these stress hormones into the blood, inducing malabsorption and causing energy levels to plummet. (16)

The Real Cause(s) of Food Intolerance/Sensitivity and Allergy

While following the restrictive recommendations gleaned from food allergy panels may lower or resolve some chronic symptoms initially or temporarily, the jury is still out as to whether they are financially feasible or lifestyle-amenable. There is growing evidence that increased intestinal permeability (17,18,19) and subsequent low-level, systemic inflammation, due to a compromised microbiome, the consumption of excess amounts of wheat, and chronic stress, needs to be addressed in order to resolve food allergies, particularly of the delayed IgG variety. Of course, ultimately it’s up to the patient and to their healthcare practitioner.

  1. Lomer, M. (2018). Review article: the aetiology, diagnosis, mechanisms and clinical evidence for food intolerance.
  2. “Facts and Statistics.” Food Allergy Research & Education, www.foodallergy.org/life-with-food-allergies/food-allergy-101/facts-and-statistics.
  3. Lavine, E. (2012). Blood testing for sensitivity, allergy or intolerance to food. CMAJ : Canadian Medical Association Journal, 184(6), 666–668. http://doi.org/10.1503/cmaj.110026
  4. Magge, S., & Lembo, A. (2012). Low-FODMAP Diet for Treatment of Irritable Bowel Syndrome. Gastroenterology & Hepatology, 8(11), 739–745.
  5. Meresse, B., Malamut, G., & Cerf-Bensussan, N. (2012). Celiac Disease: An Immunological Jigsaw. Immunity,36(6), 907-919. doi:10.1016/j.immuni.2012.06.006
  6. Screening. (n.d.). Retrieved from https://celiac.org/celiac-disease/understanding-celiac-disease-2/diagnosing-celiac-disease/screening/
  7. Fasano, A. (2012). Zonulin, regulation of tight junctions, and autoimmune diseases. Annals of the New York Academy of Sciences, 1258(1), 25–33. http://doi.org/10.1111/j.1749-6632.2012.06538.x
  8. Ferolla, S. M., Armiliato, G. N. A., Couto, C. A., & Ferrari, T. C. A. (2014). The Role of Intestinal Bacteria Overgrowth in Obesity-Related Nonalcoholic Fatty Liver Disease. Nutrients, 6(12), 5583–5599. http://doi.org/10.3390/nu6125583
  9. Tetzlaff, W. F., Meroño, T., Menafra, M., Martin, M., Botta, E., Matoso, M. D., … Brites, F. (2017). Markers of inflammation and cardiovascular disease in recently diagnosed celiac disease patients. World Journal of Cardiology, 9(5), 448–456. http://doi.org/10.4330/wjc.v9.i5.448
  10. Sollid, L. M., & Jabri, B. (2013). Triggers and drivers of autoimmunity: lessons from coeliac disease. Nature Reviews. Immunology, 13(4), 10.1038/nri3407. http://doi.org/10.1038/nri3407
  11. Kumar, V., Abbas, A. K., & Aster, J. C. (2015). Robbins and Cotran pathologic basis of disease(Ninth edition.). Philadelphia, PA: Elsevier/Saunders.
  12. O’Bryan, T. (2016). The Autoimmune Fix: How to Stop the Hidden Autoimmune Damage that Keeps you Sick, Fat, and Tired Before it Turns into Disease. Emmaus, PA: Rodale Books.
  13. Sauvanet, C., Wayt, J., Pelaseyed, T., & Bretscher, A. (2015). Structure, Regulation, and Functional Diversity of Microvilli on the Apical Domain of Epithelial Cells. Annual Review of Cell and Developmental Biology, 31(1), 593-621. doi:10.1146/annurev-cellbio-100814-125234
  14. Anatomy Of The Small Intestine. (n.d.). Retrieved from https://jonbarron.org/article/anatomy-small-intestine
  15. Tritz, G. J., & KCOM. (n.d.). Gastrointestinal Manifestations of Disease. Retrieved from https://www.atsu.edu/faculty/chamberlain/website/tritzid/gastro.htm
  16. Hasibeder, W. (2010). Gastrointestinal microcirculation: Still a mystery? British Journal of Anaesthesia, 105(4), 393-396. doi:10.1093/bja/aeq236
  17. Perrier, C., & Corthésy, B. (2010). Gut permeability and food allergies. Clinical & Experimental Allergy, 41(1), 20-28. doi:10.1111/j.1365-2222.2010.03639.x
  18. Järvinen, K. M., Konstantinou, G. N., Pilapil, M., Arrieta, M., Noone, S., Sampson, H. A., . . . Nowak-Węgrzyn, A. (2013). Intestinal permeability in children with food allergy on specific elimination diets. Pediatric Allergy and Immunology, 24(6), 589-595. doi:10.1111/pai.12106
    De Punder, K., & Pruimboom, L. (2015). Stress Induces Endotoxemia and Low-Grade Inflammation by Increasing Barrier Permeability. Frontiers in Immunology, 6, 223. http://doi.org/10.3389/fimmu.2015.00223