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Gastro-oesophageal reflux disease (GERD), associated by the unpleasant feeling of acid in your throat and a burning sensation, is a very common problem. The prevalence of acid reflux is on the rise and most of us have experienced it at some point in our life. Whether it is triggered by a glass of red wine or spicy food, it causes a great deal of discomfort to sufferers. Unfortunately, most people don’t take it seriously and put it down to having too much food or the wrong types. Popping a pill available over the counter, is easy, and can alleviate symptoms quite effectively. However, in reality chronic reflux is often more complex and can lead to ulceration and increases the risk of oesophageal cancer.[i]
The common misconception about reflux is that it is caused by excessive production of stomach acid. While the symptoms of reflux certainly involve acid and the stomach contents regurgitating into the oesophagus, this theory doesn’t explain why it happens. Let’s explore the most current research on the causes of GERD, why suppressing stomach acid production isn’t ideal and what you can do to relieve your symptoms.
Stomach acid is responsible for:
In about 30% of GERD patients, stomach acidity is actually normal, suggesting other mechanisms.[iii][iv] Insufficient stomach acid production can be caused by certain medications (e.g. anti-histamines, Proton Pump Inhibitors - PPIs), excessive snacking, eating in a rush or mindless eating and deficiencies in nutrients needed for stomach acid production – zinc and B6. Stomach acid production also significantly reduces with age and therefore digestive complaints and indigestion are much more common in the elderly.
Long term, insufficient stomach acid can lead to different complications and further digestive symptoms. These include small intestinal bacterial overgrowth (SIBO),[v] IBS[vi], Clostridium difficile-associated diarrhoea[vii] or higher risk of H.pylori infection – the bacteria that is associated with ulcers and gastric cancer. Long term use of acid blocking medication (e.g. omeprazole) can lead to reduced nutrient absorption, in particular iron, [viii] B12[ix] [x] and vitamin C[xi], consequently contributing to the risk of developing anaemia, cardiovascular disease[xii],[xiii] dementia[xiv],[xv] or osteoporosis.[xvi],[xvii]
Another cause of reflux may be the weakening of the lower esophageal sphincter (LES), which separates the stomach from the oesophagus. In between meals, it is supposed to be closed to prevent the backflow of food into the oesophagus. However, when there isn’t enough stomach acid, the food isn’t digested properly, often leading to an overgrowth of bacteria in the small intestine (SIBO). These bacteria feed on and ferment undigested carbohydrates resulting in the feeling of fullness, discomfort, bloating and distension. This causes an increase in intra-abdominal pressure (IAP), which relaxes the LES and pushes the stomach contents and acid into the oesophagus. Other factors such as obesity, inflammation (poor diet, smoking, high alcohol intake), high intake of caffeinated drinks, spices, mint and chocolate can all relax LES and make symptoms worse.[xviii],[xix]
-Slippery elm mucilage soothes the throat and lining of the stomach and stimulates mucus secretion.[xxi]
-Marshmallow soothes irritated mucous membranes and has been used as a remedy for ulcers.[xxiv]
-Aloe vera has a long tradition of use for its wound healing and anti-inflammatory properties.[xxviii]
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[ii] Scott Merrell et al. pH-Regulated Gene Expression of the Gastric Pathogen Helicobacter pylori. Infect Immun. 2003; 71 (6): 3529-39.
[iii] Schlesinger PK et al. Limitations of 24-hour intraesophageal pH monitoring in the hospital setting. Gastroenterology. 1985; 89(4): 797-804.
[iv] Barlow WJ, Orlando RC. The pathogenesis of heartburn in nonerosive reflux disease: a unifying hypothesis. Gastroenterology. 2005; 128(3):771-8.
[v] Ardatskaia MD, Loginov VA, Minushkin ON. [Syndrome of bacterial overgrowth in
patients with the reduced stomach acid secretion: some aspects of the diagnosis].
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[vii] Aseeri M et al. Gastric acid suppression by proton pump inhibitors as a risk factor for clostridium difficile-associated diarrhea in hospitalized patients. Am J Gastroenterol. 2008;103(9):2308-13
[viii] Shikata T et al. Use of proton pump inhibitors is associated with anaemia in cardiovascular outpatients. Circ J. 2015;79(1):193-200
[ix] Lam JR et al. Proton pump inhibitor and histamine 2 receptor antagonist use and vitamin B12 deficiency. JAMA. 2013; 310(22):2435-42
[x] Hirschowitz BI, Worthington J and Mohnen J. Vitamin B12 deficiency in hypersecretors during long-term acid suppression with proton pump inhibitors. Aliment Pharmacol Ther. 2008;27(11):1110-21
[xi] Henry EB et al. Proton pump inhibitors reduce the bioavailability of dietary vitamin C. Aliment Pharmacol Ther. 2005;22(6):539-45
[xii] Ghebremariam YT et al. Unexpected effect of proton pump inhibitors: elevation of the cardiovascular risk factor asymmetric dimethylarginine. Circulation. 2013;128(8):845-53
[xiii] Charlot M et al. Proton-pump inhibitors are associated with increased cardiovascular risk independent of clopidogrel use: a nationwide cohort study. Ann Intern Med. 2010;153(6):378-86
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[xv] Wijarnpreecha K et al. Proton pump inhibitors and risk of dementia. Ann Transl Med. 2016;4(12):240
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[xvii] Anderson BN, Johansen PB and Abrahamsen B. Proton pump inhibitors and osteoporosis. Curr Opin Rheumatol. 2016;28(4):420-5
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[xx] Austin GL, et al. A very low-carbohydrate diet improves gastroesophageal reflux and its symptoms. Dig Dis
[xxi] The Review of Natural Products by Facts and Comparisons. 1999. St Louis: Wolters Kluwer Co.
[xxii] Mizuta et al. Effects of gamma oryzanol on gastric secretions in rats. Folia Farmacol Japon. 1978; 74: 285-95.
[xxiii] Ichimaru et al. Effects of gamma-oryzanol on gastric lesions and small intestinal propulsive activity. Nihon Yakurigaku Zasshi. 1984; 84 (6): 537-42.
[xxiv] The Review of Natural Products by Facts and Comparisons. 1999. St Louis: Wolters Kluwer Co.
[xxv] Khayyal. Antiulcerogenic effect of some gastrointestinally acting plant extracts and their combination. Arzneimittelforschung. 2001; 51 (7): 545-53.
[xxvi] Fukai et al. Anti-Helicobacter pylori flavonoids from licorice extract. Life Sci.2002; 71 (12): 1449-63.
[xxvii] Wittschier et al. Aqueous extracts and polysaccharides from liquorice roots (Glycyrrhiza glabra L.) inhibit adhesion of Helicobacter pylori to human gastric mucosa. J Ethnopharmacol. 2009; 125 (2): 218-23.
[xxviii] Langmead et al. Randomized, double-blind, placebo-controlled trial of oral aloe vera gel for active ulcerative colitis. Aliment Pharmacol Ther.2004; 19 (7): 739-47.
[xxix] Chen et al. Antagonistic activities of lactobacilli against Helicobacter pylori growth and infection in human gastric epithelial cells. J Food Sci. 2012; 77 (1): M9-14.
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[xxxi] Tabak M et al. Cinnamon extracts' inhibitory effect on Helicobacter pylori. J Ethnopharmacol. 1999; 67 (3): 269-77.