Antacid medications -neutralisers, suppressors and Proton Pump Inhibitors (PPIs)- are among the most prescribed and the most used medications in the world, and many of such medications are also available over the counter. The market for antacid medications is forecasted to grow at a compound annual rate of growth of 4.3% during 2019-2024, due to growing geriatric population suffering from Gastroesophageal reflux disease (GERD), poor diet and lifestyle choices and side effects of other drugs [1].
However, there is also growing awareness and evidence about the risk associated to the long-term use of PPIs [2,3] and about their inappropriate use and prescription [4,5].
Just to mention a few examples, the FDA has issued several warnings regarding unapproved uses of PPIs either from the patients themselves or as directed by healthcare professionals [6,7] and the Italian Association of Hospital Gastroenterologists (AIGO) warned that in Italy one out of two patients uses PPIs without actually needing them [8].
But what do PPIs actually do?
Just one pill of a PPI can suppress stomach acid secretions by up to 90-95% for the better part of the day, by acting on the pump mechanism inside certain cells in the stomach lining that produce and secrete hydrochloric acid [10].
In today’s blog post, we're going to continue our journey down the digestive tract and look at the reasons why we have stomach acid in the first place. In this way we can understand why making conscious lifestyle choices might be a better idea than popping in another pill to suppress symptoms!
In following articles, we'll explore more regarding the reasons some of the symptoms of gastro-esophageal reflux might occur and how to further support our digestion!
So, let’s finally get started! - Not interested in the nerdy stuff? Skip to "What does this all mean?" and the tips at the end of the post!
What are the functions of stomach acid?
1. Protection
Stomach acid is our first line of defense against food-borne pathogens and it prevents an overgrowth of bacteria and fungi in the stomach and further down the gastro-intestinal tract. Stomach acid works in this respect on 2 fronts: against common bacteria that enter the body through nose and mouth and against possible migration towards the stomach of “friendly” bacteria from the small intestine.
2. Chemical signaling
Stomach acid – or the acidity of the chyme (food substances that exit the stomach in conjunction with gastric secretions) - triggers events downstream in our gastro-intestinal tract. For example, it triggers the release of secretin and cholecystokinin (CCK) in the duodenum (upper part of the small intestine, connected to the stomach). In turn, secretin triggers the pancreas to release digestive enzymes and bicarbonate. CCK instead stimulates the release of bile from the gallbladder. These secretions are essential for digestion and consequently absorption of nutrients.
3. Chemical digestion and absorption
Stomach acid is there to support the chemical digestion of foods. It does that in different way. Let’s quickly explore them.
Role in the digestion of proteins
Proteins (one of the 3 macronutrients together with carbohydrates and fats) need to be broken down into their constituent peptides (short chains of amino acids) and amino acids (individual building blocks).
- The acidic environment in the stomach promotes unfolding of proteins which exposes the proteins’ peptide bonds,
- Stomach acidity is needed for the activation of pepsin, which is an enzyme required for breaking down those peptide bonds.
Role in the absorption of minerals and vitamins
Ample stomach acidity is directly needed for the absorption of several minerals and vitamins. Examples are iron (in particular, non-heme iron from grains and vegetables), calcium, magnesium, folates, B12 and possibly zinc. Indirectly, stomach acidity is also needed in nutrient absorption through its signaling role to organs downstream in the gastro-intestinal tract, i.e. the release of digestive enzymes from the pancreas and of bile from the gallbladder might be impaired, leading to worse digestion and absorption of both macro- and micro- nutrients.
What does this all mean?
The use of antacid medications results in insufficient acidity in the stomach. Insufficient acidity in the stomach can be caused by other factors such as an overgrowth of H-Pylori bacteria in the stomach, food allergies or sensitivities, eating a meal when in a “fight or flight state”, eating quickly without properly chewing food, autoimmune attacks to the parietal cells of the stomach or gastric-bypass surgeries.
The consequences of not having enough stomach acid might be directly inferred from an understanding of the functions of stomach acid that I just outlined:
Nutrient deficiencies such as deficiency in amino acids – which are the building block of everything in our bodies, including neurotransmitters and hormones – ever thought stomach acid might be related to depression and anxiety? Deficiencies in micronutrients such as minerals and vitamins can also occur! There seems to be an association, for instance, between long-term use of PPIs and the incidence of bone fractures, possibly linked to impaired absorption of minerals [11].
Overgrowth of bacteria in the wrong places – i.e. small intestine bacterial overgrowth (SIBO).
Problems related with inappropriate secretion of digestive juices down the gastrointestinal tract and impairment of breakdown and nutrient absorption downstream –i.e. sluggish gallbladder with consequences on fat digestion, absorption of fatty acids and fat-soluble vitamins.
Are we sure we really want to pop in an acid-blocker medication at the first sign of heartburn? Of course, as usual, it is important to check with your doctor to find where the reasons for your symptoms lay and dig deeper!
But often times following simple eating hygiene rules can go a long way in supporting our digestive health. And symptoms like heartburn might as a matter of fact be related to not having enough stomach acid, or not being in the right state for eating!
The tips I provided in the previous blogs on the cephalic phase of digestion and chewing are great for supporting stomach acidity as well.
Here some of them again, and some new tips!
Practice mindfulness strategies before eating, so that you eat in a “rest and digest” mode, rather than in “fight or flight” mode!
Experience your food through your senses before giving the first bite. This triggers the release of a neurotransmitter in the brain that signals cells in the stomach to release stomach acid!
Chew, chew, chew! The act of chewing also activates release of stomach acid in the stomach through the activation of the vagus nerve.
Avoid over-eating.
Hydrate in between meals and avoid drinking big amounts of water during meals.
Avoid eating or drinking for 2 to 3 hours before going to bed.
For people who need a little extra support, drinking some water with a small amount of raw unfiltered apple cider vinegar before meals can give an extra boost to digestion! For those who need more support, supplementation with betaine hydrochloric acid and pepsin might be of great help, but caution must be used so always discuss that with a trusted practitioner!
Do you ever experience symptoms such as indigestion, acid reflux or GERD? Do you pay attention to lifestyle factors that support digestion? Have you considered food sensitivities as a cause of your symptoms?
I’d love to hear your experiences in the comments below!
References
[2] Xie Y, Bowe B, Li T, et al, Risk of death among users of Proton Pump Inhibitors: a longitudinal observational cohort study of United States veterans, BMJ Open 2017;7:e015735. doi: 10.1136/bmjopen-2016-015735
[3] Jaynes, M., & Kumar, A. B., The risks of long-term use of proton pump inhibitors: a critical review. Therapeutic Advances in Drug Safety 2019.
[10] Wright J.W., MD and Lenard L., PhD, Why stomach acid is good for you – Natural relief from Heartburn, Indigestion, Reflux and GERD – M.Evans, 2001
[11] Nassar Y. and Richter S., Proton-pump Inhibitor Use and Fracture Risk: An Updated Systematic Review and Meta-analysis, J Bone Metab. 2018 Aug; 25(3): 141–151.
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