Gastroesophageal Reflux Disease (GERD) is a highly prevalent digestive disorder where the stomach’s contents repeatedly flow back into the esophagus. This backward flow, called reflux, causes uncomfortable symptoms such as heartburn and regurgitation. Public understanding of GERD is complicated by a debate over the role of stomach acid, with some sources claiming the problem is too much acid and others proposing it is too little. This article scientifically evaluates the hypothesis that GERD is caused by low stomach acid.
The Conventional Cause of GERD
The standard medical understanding of GERD identifies the problem as a structural and mechanical failure, not a primary issue with acid production quantity. The Lower Esophageal Sphincter (LES) is a ring of muscle at the junction between the esophagus and the stomach. Its role is to act as a one-way valve, relaxing momentarily to allow food into the stomach and then quickly contracting to prevent contents from returning upward.
In most GERD cases, this muscular barrier fails to maintain a proper seal against the stomach’s internal pressure. The most frequent cause is transient lower esophageal sphincter relaxations (TLESRs). These are spontaneous, brief relaxations of the LES that happen independent of swallowing and allow stomach contents to escape into the esophagus.
Another mechanical factor is a hiatal hernia, where a portion of the stomach slides up through the diaphragm’s opening into the chest cavity. This anatomical displacement compromises the LES’s effectiveness and disrupts the surrounding diaphragm muscle, which normally reinforces the sphincter’s function. The combination of a weakened LES and a hiatal hernia severely impairs the body’s natural anti-reflux mechanism.
This mechanical breakdown means the primary issue is where the stomach contents are, not the amount of acid produced. LES failure allows the refluxate—the liquid mixture of stomach contents—to move into the sensitive esophageal lining. Regardless of whether the stomach acid is high, normal, or low, its presence in the esophagus causes the burning symptoms and tissue damage characteristic of GERD.
The Low Acid Hypothesis
The low acid hypothesis proposes that insufficient stomach acid, or hypochlorhydria, causes GERD symptoms. The core premise is that low acid prevents the stomach from properly breaking down food, particularly carbohydrates. Stomach acid is also responsible for sterilizing ingested food and triggering subsequent digestive processes.
When acid levels are low, undigested food lingers longer and passes into the small intestine poorly prepared. This environment is conducive to Small Intestinal Bacterial Overgrowth (SIBO). These excessive bacteria ferment the undigested carbohydrates, producing large volumes of gas.
The accumulation of this gas leads to abdominal bloating and a significant increase in intra-abdominal pressure (IAP). According to this model, this physical pressure buildup forces the stomach contents upward. This mechanical force overcomes the resistance of the LES, pushing contents and associated acid back into the esophagus.
Proponents note that GERD incidence increases with age, correlating with a natural decline in stomach acid production. They argue that pressure from fermentation triggers the reflux event. This proposed mechanism directly challenges the conventional view that the root cause lies solely in the mechanical failure of the LES.
Scientific Evaluation of the Low Acid Claim
While hypochlorhydria is a genuine medical condition, the scientific consensus does not support it as the primary cause of GERD. GERD is fundamentally a disease of mechanical incompetence at the gastroesophageal junction. Symptoms are caused by the corrosive exposure of the esophageal lining to the stomach’s contents, which is allowed by LES failure.
Diagnostic procedures like 24-hour esophageal pH monitoring, considered the gold standard, measure acid exposure time in the esophagus. These studies frequently show that GERD patients exhibit abnormal acid exposure, often indicating normal or high acid production in the stomach. The problem diagnosed is the presence of acid in the wrong location, not its absence in the stomach.
In cases where reflux is non-acidic or weakly acidic, specialized testing like multichannel intraluminal impedance-pH monitoring (MII-pH) identifies the nature of the refluxate. Non-acidic reflux is often found in patients whose symptoms are resistant to standard acid-suppressing medications. This still suggests a mechanical event allowing non-acidic liquid or gas to escape, and does not validate the low acid hypothesis.
The pressure-based mechanism proposed by the low acid hypothesis is secondary to observed LES dysfunction. The conventional model highlights that a mechanical defect, such as TLESRs or a hiatal hernia, is the established enabler of reflux. The primary driver of reflux episodes is the inappropriate, spontaneous relaxation of the LES, which is a neurological and muscular event, not a constant pressure overflow.
There is a correlation between SIBO and GERD, as SIBO can exacerbate symptoms by increasing intra-abdominal pressure. However, SIBO is frequently identified as a consequence of reduced stomach acid, not the original cause of GERD. A reduction in acid from any source can set the stage for SIBO, which may then secondarily contribute to reflux symptoms.
The Relationship Between Treatment and Acid Levels
The widespread use of acid-reducing medications, such as Proton Pump Inhibitors (PPIs) and H2 blockers, might suggest that too much acid causes GERD. However, these treatments address the consequence of the mechanical failure, not the root cause. PPIs, for example, work by irreversibly blocking the hydrogen-potassium ATPase pump responsible for secreting acid in the stomach lining.
By reducing the overall production of hydrochloric acid, these medications decrease the corrosive nature of the liquid that refluxes into the esophagus. This reduction in acidity alleviates burning symptoms and allows damage to the esophageal lining to heal. Critically, these drugs do not repair the malfunctioning LES or correct a hiatal hernia; they simply make the refluxate less harmful.
While effective for symptom relief, long-term or high-dose acid suppression can lead to the state of hypochlorhydria that the alternative hypothesis describes. The sustained reduction in stomach acid can impair the sterilization of food and the absorption of certain nutrients, such as Vitamin B12 and magnesium. It can also increase the risk of secondary issues, including the development of SIBO, which itself can cause bloating and pressure. This medically induced state of low acid is a consequence of treating GERD, rather than the original cause of the disease.