This is the second article in a series on heartburn and GERD. If you haven’t read the first one, I’d suggest doing that first.
The idea that heartburn is caused by too much stomach acid is still popular in the media and the public. But as Daniel pointed out in the comments section of the last post, anyone familiar with the scientific literature could tell you that heartburn and GERD are not considered to be diseases of excess stomach acid.
Instead, the prevailing scientific theory is that GERD is caused by a dysfunction of the muscular valve (sphincter) that separates the lower end of the esophagus and the stomach. This is known as the lower esophageal valve, or LES.
The LES normally opens wide to permit swallowed food and liquids to pass easily into the stomach. Except for belching, this is the only time the LES should open.
If the LES is working properly, it doesn’t matter how much acid we have in our stomachs. It’s not going to make it back up into the esophagus. But if the LES is malfunctioning, as it is in GERD, acid from the stomach gets back into the esophagus and damages its delicate lining.
Here’s the key point. It doesn’t matter how much acid there is in the stomach. Even a small amount can cause serious damage. Unlike the stomach, the lining of the esophagus has no protection against acid.
We’ve been asking the wrong question
In a recent editorial published in the journal Gastroenterology, the author remarked:
Treating gastroesophageal reflux disease with profound acid inhibition will never be ideal because acid secretion is not the primary underlying defect.
I couldn’t agree more. For decades the medical establishment has been directing its attention at how to reduce stomach acid secretion in people suffering from heartburn and GERD, even though it’s well-known that these conditions are not caused by excess stomach acid.
Instead, the question researchers should have been asking is, “what is causing the LES to malfunction?” Since it is universally agreed upon that this is the underlying mechanism producing the symptoms of GERD, wouldn’t it make sense to focus our efforts here?
That’s exactly what we’re going to do in this article.
GERD is caused by increased intra-abdominal pressure
It is well accepted in the literature that GERD is caused by an increase in intra-abdominal pressure (IAP). Acid reflux occurs when pressure causes gastric distention (stomach bloating) that pushes the stomach contents, including acid, through the LES into the esophagus.
According to current thought, factors contributing to this include overeating, obesity, bending over after eating, lying down after eating, and consuming spicy or fatty foods.
For example, several studies have indicated an association between obesity and GERD, and this recent paper in Gastroenterology concluded that increased intra-abdominal pressure was the causative mechanism.
But while I agree that all of the currently accepted factors play a role, I do not think they are the primary causes of the increased IAP seen in GERD.
The two primary causes of increased intra-abdominal pressure
Instead, I believe the primary causes of IAP (and thus heartburn and GERD) are bacterial overgrowth and maldigestion of carbohydrates – both of which are caused at least in part by low stomach acid.
In a nutshell, the process looks like this:
Let’s look at each step in turn.
Low stomach acid causes bacterial overgrowth
As I will explain in the next article, one of the chief roles of stomach acid is to inhibit bacterial overgrowth. At a pH of 3 or less (the normal pH of the stomach), most bacteria can’t survive for more than 15 minutes. But when stomach acid is insufficient and the pH of the stomach rises above 5, bacteria begin to thrive.
The gastrin knockout mouse, which is incapable of producing stomach acid, suffers from bacterial overgrowth – as well as inflammation, damage and precancerous polyps in its intestines. It is also well documented that acid-suppressing drugs promote bacterial overgrowth. Long-term use of Prilosec, one of the most potent acid suppressing drugs, reduces the secretion of hydrochloric acid (HCL) in the stomach to near zero. In one trial, 30 people with GERD were treated with a high dose of Prilosec (40g/day) for at least 3 months. 11 of the 30 Prilosec-treated people had developed significant bacterial overgrowth, compared with only one of the ten people in the control group.
Low stomach acid causes maldigestion of carbohydrates
Stomach acid (HCL) supports the digestion and absorption of carbohydrates by stimulating the release of pancreatic enzymes into the small intestine. If the pH of the stomach is too high (due to insufficient stomach acid), the pancreatic enzymes will not be secreted and the carbohydrates will not be broken down properly.
Bacterial overgrowth + maldigested carbohydrates = GAS!
Though microbes are able to metabolize proteins and even fats, their preferred energy source is carbohydrate. The fermentation of carbohydrates that haven’t been digested properly produces gas. The resulting gas increases intra-abdominal pressure, which is the driving force behind acid reflux and GERD.
When stomach acid is sufficient and carbohydrates are consumed in moderation, they are properly broken down into glucose and rapidly absorbed in the small intestine before they can be fermented by microbes. However, if stomach acid is insufficient and/or carbohydrates are consumed in excess, some of the carbs will escape absorption and become available for intestinal microbes to ferment.
A nasty vicious cycle: the role of hydrogen gas
Hydrogen (H2) is one of the gases produced by bacterial fermentation of carbohydrates. In fact, there have been explosions during intestinal surgery due to the high amounts of hydrogen gas production in the gut. This is significant because a recent landmark study demonstrated that pathogenic bacteria feed on hydrogen gas.
So, the more undigested carbohydrate you have in your gut, the more hydrogen gas bacteria will produce. The more hydrogen gas is produced, the more bacterial overgrowth will occur. And the more bacteria you have in your gut, the more gas will be produced by fermentation of undigested carbohydrate. This becomes a nasty vicious cycle.
There is significant evidence that the carbohydrates consumed in the “standard American diet” contribute to this phenomenon. Fructose is a particular problem. In one study researchers fed fructose to 15 normal adults. They found that more than half of the 15 adults showed evidence of fructose malabsorption after just 25g of fructose, and greater than two-thirds showed malabsorption after 50g of fructose. To put this in perspective, one 12 oz. can of Coca-Cola contains 30g of fructose.
One of the measures of malabsorption used in the study was a hydrogen breath test. Both the 25g and the 50g doses caused a large increase in H2, especially the 50g dose (a 5-fold increase). Bacterial fermentation of carbohydrate is the only source of hydrogen in the human body. This means that the hydrogen measured in the study indeed came from the undigested fructose in the gut.
Certain type of fiber and starch also promote hydrogen production. Almost all of the fiber and approximately 15-20% of the starch we consume escape absorption. The amount of gas that can be produced by undigested carbohydrates is almost hard to believe. According to Suarez and Levitt, just 30g of carbohydrate (equivalent to 1/2 of a small muffin) that escapes absorption in a day could produce more than 10,000 mL of hydrogen gas. That’s equivalent to ten large one-liter water bottles full of intestinal gas!
Finally, a recent study showed that ingestion of lactose (the carbohydrate found in milk) results in an increased number of transient lower esophageal sphincter relaxations (TSELRs), increased reflux episodes, higher esophageal acid exposures, and more severe GERD symptoms. Another study showed that oral administration of fructo-oligosaccharides (FOS) produces similar findings. Together these studies suggest that colonic fermentation of malabsorbed carbohydrates contributes to the pathogenesis of GERD.
Other supporting evidence
If gas produced by microbial fermentation of carbohydrates causes acid reflux, we might expect that reflux could be treated by either 1) reducing bacterial overgrowth or 2) reducing carbohydrate intake.
In fact, that’s exactly what we see. In a study by Pehl, administration of erythromycin (an antibiotic) significantly decreased esophageal reflux. In another study by Pennathur, erythromycin strengthened the defective lower esophageal sphincter in patients with acid reflux.
To my knowledge there have only been two small trials performed to test the effects of carbohydrate restriction on GERD. Both had positive results. A small case series showed a significant, almost immediate resolution of GERD symptoms in obese individuals initiating a very low-carb diet. A more recent study found that a very low-carb diet decreased distal esophagus acid exposure and improved the symptoms of GERD. Perhaps most importantly, the magnitude of the improvement was similar to what has been reported with treatment with proton-pump inhibitors (acid suppressing drugs).
Many researchers now believe that Irritable Bowel Syndrome (IBS) is caused by bacterial overgrowth in the small intestine (SIBO). A study performed at the GI Motility Center in Los Angeles in 2002 found that 71% of GERD patients tested positive for IBS – double the percentage seen in non-GERD patients being examined.
The high prevalence of IBS in GERD patients combined with the recognition that bacterial overgrowth causes IBS is yet another line of evidence suggesting that bacterial overgrowth is also a causative factor in GERD.
A unified theory
To summarize, GERD is caused by increased pressure in the stomach resulting in a malfunction of the lower esophageal sphincter (LES). The increase in pressure is caused by bacterial overgrowth and malabsorption of carbohydrates, both of which are precipitated by low stomach acid. Reducing bacteria loads and limiting carbohydrate intake have both been shown to greatly improve, and in some cases completely cure, acid reflux and GERD.
In the Part III of the series I discuss the connection between GERD and H. pylori, and further evidence supporting the theory that GERD is caused by bacterial overgrowth. Read on!