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Is Acid Reflux Caused by Too Much Stomach Acid or Too Little?

Is Acid Reflux Caused by Too Much Stomach Acid or Too Little?

Affecting almost 1 in 3 of the population, the incidence of acid reflux, and the more severe gastro-oesophageal reflux disease (GORD), appears to be widespread and steadily increasing.

With symptoms of burping, bloating and general discomfort after eating – often accompanied by stomach pain and burning in the throat – it’s not something that can be ignored.

Acid Reflux and Stomach Acid

The current medical opinion is that acid reflux and GORD happen when we produce too much stomach acid; creating a swirling pit of acidity which damages the stomach and throat, resulting in compromised digestion and searing pain.

One consequence of this viewpoint is the increasing use of antacids and acid-blockers, either as self-selected, over-the-counter products or prescribed medicines. 

Yet despite their popularity, many people report only minimal or short-term relief from their symptoms when using such medications, prompting the question: Does excessive acid production really underlie acid reflux and GORD, or is it time to consider an alternative cause?

In the following article we will:

  • look at the essential role of stomach acid in a healthy digestive system
  • discuss the far-reaching health consequences of low stomach acid
  • consider how poor carbohydrate digestion and bacterial imbalance provide the perfect acid-reflux provoking combination
  • reveal how acid-blocking medications really affect your health
  • explain the simple home-test that will indicate if your stomach acid is low
  • list the seven steps to effectively manage acid-reflux and GORD, naturally
Stomach Acid and its Role in Digestion

Let’s start with a review of normal digestive function, a multi-stage process that involves the intake, break down, absorption and elimination of food and waste.

Digestion actually begins before you take your first mouthful of food, since the mere thought of eating is enough to stimulate the salivary glands in your mouth and gastric glands in your stomach – literally getting your juices flowing in anticipation of when the food arrives.

Chewing breaks the food down into smaller pieces before it’s swallowed and passes through the lower oesophageal sphincter, or LES, to reach the stomach. (It’s “esophagus” in America, hence the odd abbreviation.)

Once there, the LES closes tightly, trapping the food in the stomach where the process of macronutrient digestion really gets going.

After the large proteins, carbohydrates and fats are broken down (to smaller amino acids and peptides; sugar molecules; and fatty acids and triglycerides respectively), they exit the stomach and enter the small intestine.

This is where most nutrient absorption happens, so by  the time the remnants of your dinner reach the large intestine, they’re pretty much ready to be packaged up for elimination. To find out more about digestion, I recommend Elizabeth Lipski’s book Digestive Wellness.

The whole process of digestion requires some precise co-ordination, primarily because there are significant changes in pH throughout the digestive tract.

Whereas the mouth is more alkaline, the stomach is acidic, ideally having a low pH of between 1 and 3. Then once we get to the small intestine, the pH becomes alkaline, shooting up to around 8.

This low stomach pH is achieved by the presence of hydrochloric acid; our multifunctional stomach acid that is involved in protein digestion. It provides a potent bath that kills the majority of the pathogens that we eat, deters microbes in the small intestine from heading up into the stomach, and signals that the stomach should empty.

Fortunately, the stomach doesn’t get damaged by this acid, as it possesses cells which secrete a thick layer of phospholipid-based mucus, which coats and protects any exposed surfaces.

In cases of acid reflux and GORD, it’s obvious that there’s some dysfunction in normal digestive processes – after all, there’s discomfort and bloating after eating, and acidic matter passing up into the oesophagus.

It’s not really a case of there just being ‘too much stomach acid’.  What we really need to know is: what could be going so wrong that normal safety mechanisms are overwhelmed? What makes the LES open, allowing stomach acid to reach the oesophagus?

To find out more, we should look at the factors affecting stomach acid release – and the health consequences of an insufficiency.

Lifestyle and Diet Affect Stomach Acid Levels

Digestion is affected by many factors. There’s an obvious link between stress and poor digestion: how often have you had ‘butterflies in your stomach’ or felt ‘sick with worry’?

Rushed meals, insufficient chewing and unresolved stress can all take their toll, but did you know that our food choices can also affect how much stomach acid we produce, and hence our digestion?

For instance, activation of the proton-pump (which releases the hydrogen ions which make up our stomach acid) is magnesium-dependent, requires energy, and relies on the exchange of sodium and potassium ions.

Fats are a source of lipids – a key component in the phospholipid-based mucus which protects our stomach from acid corrosion.

So you can already see how eating magnesium-rich foods and healthy fats would be beneficial.

We’ll talk about the types of foods to eat a bit later when we consider a strategy to manage acid-reflux and GORD.

Bacterial Overgrowth + Carb Maldigestion = Acid Reflux

We also find several changes that provide the ideal acid-reflux and GORD inducing combination, elements for the perfect digestive storm in a manner of speaking.

Without a low pH, there’s less efficiency in killing microbes, giving yeasts and pathogenic bacteria the chance to thrive.

Populations of H. pylori, a common chronic human pathogen, can increase. Research indicates such infection is closely linked to ulcers, but H. pylori also appears to have a strong association with other digestive disorders such as IBS and, of course, acid reflux.

There’s also more chance of bacterial migration from the small intestine up into the stomach (a condition known as small intestinal bacterial overgrowth, or SIBO for short). This displacement encourages the type of carbohydrate fermentation which leads to gas.

Carbohydrate and fat digestion are also affected, as stomach acid stimulates the release of digestive enzymes from the pancreas.

This is an important point, especially if you have a tendency to eat carby meals – perhaps lots of bread, pasta and fruit.

Such a high intake could mean some sugars remain unabsorbed by the small intestine, and since your intestinal bacteria love to use excess sugar as a food source, you could end up feeling gassy and bloated a little while after you’ve finished eating.

In fact, there’s a growing body of evidence exposing a link between low stomach acid and the subsequent combination of carbohydrate fermentation and SIBO, which underlies acid reflux.

Together they encourage the production of gas in the abdomen, ultimately increasing intra-abdominal pressure to a degree that forces the LES to open, allowing acidic stomach contents to escape and burn the oesophagus.

So there you have it: a viable mechanism for acid reflux, and not a hint of ‘excess stomach acid’ in sight.

Dr Jonathan Wright’s book Why Stomach Acid is Good for You provides further insight into the fundamental necessity of stomach acid for our ongoing health. Also, No More Heartburn by Dr Sherry A Rogers gives an insight into the problem and solutions to help you heal.

The Health Consequences of Acid-Blocking Medicine

We see all of these symptoms in individuals with achlorhydria. (This chronic lack of stomach acid is a common consequence of atrophic gastritis, a condition where the acid-releasing cells are destroyed.)

It’s a similar story when we assess people who frequently take acid blockers – whether it’s the popular antacids like Rennies and Gaviscon, which neutralise the acid in your stomach, or the prescribed medication which inhibits its release.

H-2 agonists like Zantac (Ranitidine) and Tagamet (Cimetidine); as well as Prevacid (Lansoprazole) and Prilosec (Omeprazole), the proton-pump inhibitors (PPIs) which drastically reduce stomach acid production, sometimes by as much as 90-95%, are common culprits.

We find bacterial overgrowth is a common consequence of achlorhydria (1) and in a 2013 meta-analysis, a statistically significant association between the use of PPIs and SIBO was revealed (2).

In one trial, 1 in 3 patients taking Prilosec for at least 12 weeks had bacterial overgrowth.  Compare this to the control group who’d taken no medication for at least 2 weeks – just 1 in 10 had SIBO (3).

PPIs also appear to be worse than H2-agonists at causing SIBO, perhaps because they raise pH to a greater degree (4).

Iron-deficiency anaemia is also of great concern.

According to the Iron Disorders Institute (5), this is the second most common type of anaemia amongst the elderly, a group who may already be losing between 50-60mg of iron every month simply because they regularly take aspirin and NSAID’s which cause bleeding in the digestive tract.

Iron deficiency anaemia is well-documented amongst PPI users (6).

There’s also a slight chicken-and-egg effect with H. pylori infection causing short-term achlorhydria; and an episode of low stomach acid allowing H. pylori to flourish.

Interestingly, a one-year prospective clinical trial found atrophic lesions healed after treatment to eradicate H. pylori.

An H. Pylori diet can be effective, especially if we eat foods like broccoli, broccoli sprouts and other brassicas, since they’re naturally rich in sulfurophane, an organosulphur compound which inhibits H. pylori (7).

In a 2002 study led by J Fahey, researchers found that sulfurophane extracted from broccoli seeds was effective at inhibiting H. pylori growth, and was actually more potent than other food-derived chemicals like resveratrol from grapes and allixin from garlic.

Furthermore, it didn’t matter if the H. pylori strains were resistant to antibiotics, or located inside or outside the cells – great news since H. pylori is notoriously difficult to eradicate due to its tendency to resist antibiotics and lurk inside our cells.

As for long-term health, atrophic gastritis is associated with disorders such as bronchial asthma, depression, pernicious anaemia, IBS and osteoporosis, which you’ll no doubt recognise as some of the previously highlighted consequences of low stomach acid.

Such issues are echoed with PPIs; a 2009 prospective study, published in the British Journal of Cancer, highlighted a possible causal relationship between long-term PPI use and increased risk of gastric cancer (8).

Sobering statistics indeed.

It seems obvious that the ultimate goal would be to reduce our use of stomach acid blockers.  Meantime, let’s look at the tests and strategies that can help you support your stomach acid levels, naturally.

Testing Your Gastric Acid Production

Start by assessing your stomach acid production with a non-invasive self test. It’s a way to determine what benefits you could get from supporting stomach acid, and to find the number of tablets that works best for you.

This can be done quite simply, over a course of several days, and only requires a supplement of betaine hydrochloride with pepsin.

Please note this test is NOT ADVISABLE and HCI supplements should NOT BE TAKEN if you are taking any anti-inflammatory medicines including aspirin, ibuprofen, corticosteroids or other NSAIDs. There is an alternative test using a Heidelberg capsule, but it’s probably best if you discuss this with your GP.

Conclusion
Dr Jonathan Wright’s book "Why Stomach Acid is Good for You" provides further insight into the fundamental necessity of stomach acid for our ongoing health. Also, "No More Heartburn" by Dr Sherry A Rogers gives an insight into the problem and solutions to help you heal.

While acid reflux and GORD are common digestive complaints, their current management with antacids and acid-blockers appears to do more harm than good – especially when you consider the nutrient deficiencies and negative health consequences that stem from their long-term use.

The incidence of low stomach acid, and its resulting impact on carbohydrate digestion and microbial populations, provides an intriguing alternative mechanism for acid reflux.

More importantly, digestive enzymes, probiotics, apple cider vinegar, omega-rich oils and greens can support digestive function, giving you a safe and effective option to manage acid reflux and GORD naturally, combined of course with dietary changes.

References:

(1) J Bures, et al (2010), ‘Small intestinal bacterial overgrowth syndrome’, World Journal of Gastroenterology, 16(24): 2978–2990. [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2890937/]

(2) Lo & Chan, (2013), “ Proton Pump Inhibitor Use and the Risk of Small Intestinal Bacterial Overgrowth: A Meta-analysis”, Clinical Gastroenterology and Hepatology, 11(5):483–490 [http://www.sciencedirect.com/science/article/pii/S154235651201511X]

(3) J Theisen et al, (2000), ‘Suppression of gastric acid secretion in patients with gastroesophageal reflux disease results in gastric bacterial overgrowth and deconjugation of bile acids’, Journal of Gastrointestinal Surgery, 4(1):50-54,

(4) K Wang et al (2004), ‘The effect of H2-receptor antagonist and proton pump inhibitor on microbial proliferation in the stomach.’, Hepatogastroenterology, 51(59):1540-3. [http://www.ncbi.nlm.nih.gov/pubmed/15362796]

(5) http://www.irondisorders.org/elderly 2011

(6) E Sarzynski et al, (2011), ‘Association Between Proton Pump Inhibitor Use and Anemia: A Retrospective Cohort Study’, Digestive Diseases and Sciences,56(8):2349-2353 [http://link.springer.com/article/10.1007/s10620-011-1589-y]

(7) P Arkkila et al (2006), ‘Helicobacter pylori eradication in the healing of atrophic gastritis: a one-year prospective study.’ Scandinavian Journal of Gastroenterology, 41(7):782-90. [http://www.ncbi.nlm.nih.gov/pubmed/16785190]

(8) A H Poulsen et al. (2009), ‘Proton pump inhibitors and risk of gastric cancer: a population-based cohort study’, British Journal of Cancer, 100:1503–1507. doi:10.1038/sj.bjc.6605024 www.bjcancer.com [http://www.nature.com/bjc/journal/v100/n9/full/6605024a.html]