Acidity and GERD

Acidity is the word most Indian patients use for burning behind the breastbone or high in the stomach. The medical name for its commonest cause is gastro-oesophageal reflux disease — GERD — and it describes stomach contents travelling upward into the oesophagus often enough, or with enough force, to cause symptoms or visible damage.

A little reflux happens in everyone, several times a day, and passes unnoticed. What separates ordinary physiology from disease is frequency, duration and consequence.

The gate between oesophagus and stomach is the lower oesophageal sphincter, a ring of muscle held closed at rest and reinforced from outside by the muscular hoop of the diaphragm. The commonest fault is not a weak gate. It is a gate that opens at the wrong moment — transient sphincter relaxations, brief openings unrelated to swallowing, triggered largely by stomach distension after a meal. That one mechanism explains why a large dinner produces symptoms a small one does not, and why volume often matters more than content.

Several things load the system further. A hiatus hernia, where part of the stomach slides up through the diaphragm, separates the two pressure barriers that ordinarily sit on top of each other and work as one. Delayed gastric emptying keeps the stomach distended for longer, which is common in long-standing diabetes and after very fatty meals. Raised pressure inside the abdomen — weight carried around the waist, pregnancy, chronic constipation, a tight waistband, heavy lifting — pushes contents upward against the gate. And after eating there is an unbuffered layer of acid floating on top of the meal, close to the junction, described as the acid pocket. That layer is what refluxes, which is why food does not neutralise the problem the way people assume.

Unlike the stomach lining, the oesophagus has little defence against acid and pepsin. Repeated exposure inflames it, producing oesophagitis. Healing with scarring can narrow the tube into a stricture, felt as food sticking. In a minority the lining adapts by converting to intestinal-type cells — Barrett's oesophagus — which carries a small but genuine increase in oesophageal cancer risk. That progression is uncommon and slow, and it is the honest reason long-standing symptoms are worth investigating rather than medicating indefinitely.

Indian studies put symptomatic reflux somewhere between one in twelve and one in five adults, with wide variation by region and by how the question is asked. Whatever the true figure, it is rising, and it tracks the same shifts as fatty liver and prediabetes: larger portions, more fried and refined food, more weight around the abdomen, dinner at ten and bed at eleven.

ⓘThis information is educational and not a diagnosis.

Two symptoms carry most of the diagnostic weight. Heartburn is a burning that begins behind the lower breastbone and travels upward, usually twenty to sixty minutes after eating. Regurgitation is the effortless return of sour or bitter fluid into the throat or mouth, without the retching that goes with vomiting. Together they identify reflux reasonably well.

Around that core, people describe waking at night with a sour taste or a cough, a sudden flood of saliva, chest tightness after a heavy meal, and upper abdominal fullness with frequent belching. Bloating sits alongside reflux far more often than the textbooks suggest, because the same distended stomach that triggers sphincter relaxations also produces the pressure people describe as gas.

The pattern is more informative than any single symptom. Reflux follows meals, worsens on lying flat or bending forward, eases on sitting up or walking, and responds at least partly to an antacid. Symptoms that ignore meals entirely, or that arrive with exertion, are pointing elsewhere.

If your main trouble is in the throat rather than the chest — constant throat clearing, a lump sensation, a dry cough, a voice that tires by evening — with little or no heartburn at all, that pattern has its own name and its own logic, and it is described separately as silent reflux. The treatment overlaps but the expectations differ considerably.

Chest pain deserves particular care. Oesophageal and cardiac pain share nerve pathways and can feel identical, and relief from an antacid does not reliably exclude the heart.

The features listed below are different in kind. They do not mean something serious is present, but they do mean the diagnosis is worth confirming rather than assuming.

For someone under 45 with a typical pattern and no warning features, reflux is often treated on the history alone. A defined trial of acid suppression, usually eight weeks, serves as both treatment and a rough diagnostic test. Investigating everyone at the outset would add cost and anxiety without improving outcomes.

Endoscopy answers a narrower question: is there damage. It is normal in roughly half of people with genuine reflux symptoms — a pattern called non-erosive reflux disease. A clear endoscopy means the lining has come through undamaged. It does not mean the symptoms were imagined, and that distinction matters, because many patients are told the report is normal and left without an explanation. In private centres a diagnostic endoscopy commonly costs a few thousand rupees, and it is performed at most district hospitals for considerably less.

Helicobacter pylori testing sits alongside rather than inside the reflux assessment. The organism causes gastritis and peptic ulcers and raises gastric cancer risk. Background infection rates in India are high, which is precisely why a blood antibody test is close to useless for deciding treatment; a urea breath test or stool antigen reflects current infection. Whether eradication improves reflux specifically is debated, though its value in ulcer disease is not.

A 24-hour pH-impedance study is kept for situations where the diagnosis will not resolve — normal endoscopy with persistent symptoms, a poor response to treatment, or planning for surgery. Manometry answers a different question again: whether the muscle is coordinating normally.

Testing is done to change a decision. If a result would not alter what happens next, its main effect is on the bill.

Reflux responds best to layers rather than to a single measure, and the layers that cost nothing tend to be the ones people skip.

Timing and size of meals. Dinner at ten, bed at eleven is close to a national habit, and it is the most consistently useful thing to change. Leaving around three hours between the last substantial meal and lying down allows the stomach to empty and lets the acid pocket disperse. Making lunch the largest meal and dinner the lighter one suits Indian working schedules better than most imported advice.

What is on the plate. Volume and fat content usually matter more than chilli. Deep-fried snacks, rich gravies, large quantities of liquid with the meal, and eating past comfortable fullness all distend the stomach and provoke sphincter relaxations. Triggers are genuinely individual — citrus, tomato, mint, chocolate, fizzy drinks and alcohol are common — and a two-week diary identifies yours better than a printed list of forbidden foods.

Weight carried at the waist. Abdominal fat raises intra-abdominal pressure directly. Studies of modest, sustained reduction show meaningful improvement in reflux symptoms, and this is one of the few interventions that addresses the mechanism rather than the acid.

Sleeping position. Raising the head end of the bed by fifteen to twenty centimetres on blocks uses gravity through the night. Extra pillows bend the body at the waist and raise abdominal pressure, which defeats the purpose. Lying on the left side keeps the junction above the fluid level and helps many people.

Tobacco and alcohol. Smoking reduces sphincter tone and saliva production, both of which protect the oesophagus. Chewed tobacco, gutka and betel quid deserve the same mention, being far more common in some Indian communities than cigarettes.

Antacids and alginates. Antacids neutralise acid already present and act for under an hour. Alginates work differently and more interestingly: they form a gel raft that floats on the stomach contents and physically covers the acid pocket, which is why they suit post-meal and breakthrough symptoms and why they behave unlike a simple neutraliser.

H2 blockers block the histamine receptor on the acid-producing cell. They act within an hour, which makes them useful for predictable evening symptoms, but the effect fades with continuous daily use over a few weeks as tolerance develops.

Proton pump inhibitors bind irreversibly to the acid pump itself and produce far more complete suppression. Two practical points get lost. They reach full effect only after three to five days, so judging them after two doses is unfair. And they act on pumps that are actively working, which means taking them thirty to sixty minutes before a meal matters — taken at bedtime on an empty stomach, much of the dose is wasted. Incorrect timing is one of the commonest reasons a PPI appears to fail.

The debate about long-term use is worth understanding rather than fearing. Observational studies have linked prolonged use to several harms; the associations are modest, hard to separate from the reasons people were taking the drug, and largely unsupported by randomised follow-up. Set against that, staying on acid suppression for years without establishing why is treating a symptom whose cause remains unknown. Both things can be true. Stepping down, moving to on-demand use, or stopping is a conversation for your prescriber, informed by rebound acid hypersecretion and why the first few weeks after stopping mislead.

Prokinetics have a limited role where slow emptying dominates, in short courses because of their side effects. Laparoscopic fundoplication remains an option for selected people with objectively confirmed reflux, particularly where regurgitation rather than burning is the problem.

Reflux is one of those conditions where the explanation does most of the work. Once it is clear that the difficulty is a valve opening at the wrong time rather than a stomach making too much acid, the plan stops being a list of forbidden foods and becomes a few changes around when and how much you eat, the pressure your abdomen puts below the valve, and what any medicine is genuinely for.

The Learning Session below works through this in a small group — reading your own endoscopy report, understanding what each class of medicine does, and building a routine that survives festivals, travel and late working hours.

If symptoms have run for years, or any of the features listed above are present, that is a conversation for a consultation rather than an article.