Still On Omeprazole After Years? The Heartburn Myth That’s Keeping You Stuck
- 2 days ago
- 10 min read
Stephen Roigard is a registered naturopath, clinical nutritionist, and corporate wellness consultant with over 25 years of experience integrating science-based functional medicine and holistic health to support individuals, professionals, and teams in achieving sustainable well-being.
Millions of people take a small tablet every morning, often for years, sometimes for decades, on the understanding that their stomach makes too much acid, and that this acid is the source of all their discomfort. It is a tidy explanation. The trouble is, for most people, it is almost certainly the wrong one. Here is what the research actually shows, and what you can do about it.
That burning feeling, what is actually going on?
You know the feeling. A burning sensation that rises from your chest, sometimes reaching your throat. Perhaps a sour taste, a persistent cough, or that uncomfortable sense that food is sitting in the wrong place. It is one of the most common health complaints in the world, affecting an estimated 10 to 30% of adults in Western countries,[1] and it goes by several names: heartburn, acid reflux, GORD (gastro-oesophageal reflux disease), or GERD, if you have been reading American sources.
At the root of all these symptoms is the same basic event: stomach contents are travelling back up into the oesophagus (your food pipe), which is not built to handle acid. The question that matters, and the one that is rarely asked in a standard 10-minute consultation, is why that is happening in the first place?
What your medication is actually doing
Proton pump inhibitors (PPIs), a family of drugs that includes omeprazole, esomeprazole, pantoprazole, and lansoprazole, are among the most widely prescribed medications on the planet.[2] They work by blocking the so-called 'proton pump,' a tiny piece of molecular machinery embedded in the acid-producing cells of your stomach wall. Block the pump, produce less acid. It is elegant chemistry.
How much less acid? Studies show PPIs reduce gastric acid production by approximately 90 to 98%,[3] essentially turning your stomach's acid output down to near zero. To put that in perspective, the stomach is designed to maintain a pH somewhere between 1.5 and 3.5 (highly acidic). On a standard PPI dose, it may sit closer to 5 or 6, closer to the acidity of black coffee than to the industrial-strength environment it is meant to be.
PPIs were designed, and are approved, for short-term use, typically 4 to 8 weeks, to heal an inflamed oesophagus, treat a stomach ulcer, or assist in clearing a Helicobacter pylori bacterial infection.[4] Yet enormous numbers of patients end up on them indefinitely, sometimes for decades. I have seen clients who have been taking double doses of omeprazole every day for over 25 years. That is a profound, long-term suppression of a digestive process that your body depends on and leads to very serious consequences.
You have too much acid, does the science actually back this up?
This is where things get genuinely interesting, and, frankly, a little frustrating. The explanation most patients receive is that their stomach is producing too much acid, and that this excess is the reason for their symptoms. It makes intuitive sense: burning sensation, acid-sounding problem, acid-reducing solution. Neat.
But when researchers have measured acid production in people with uncomplicated GORD and compared it to people without symptoms, the results are consistently underwhelming for the 'excess acid' hypothesis. The majority of reflux sufferers do not produce significantly more acid than symptom-free individuals.[5]
What is different in people with reflux is not how much acid their stomachs make, it is that the acid ends up somewhere it should not. The mechanism driving that is something called transient lower oesophageal sphincter relaxation (TLOSR), a rather technical phrase for something quite simple: the valve between your oesophagus and your stomach briefly pops open at the wrong moment, allowing contents to travel upward.[6]
The question that rarely gets asked is, what is causing that valve to misbehave? The answer, supported by a growing body of research, is largely to do with pressure, fermentation, and the quality of your digestion. Not excess acid.
Here is the paradox: Low stomach acid may actually be causing your reflux
This tends to raise eyebrows. If heartburn is caused by acid, how can having less acid make things worse? Think of your stomach as a food processor. For it to work efficiently, breaking down protein, killing pathogens, signalling the rest of the digestive system to get ready, it needs to be genuinely acidic. Adequate acidity activates pepsin, the primary enzyme responsible for breaking down protein. It also triggers the pyloric sphincter (the valve at the bottom of the stomach) to open, allowing food to pass through into the small intestine at the right pace.[7]
When stomach acid is too low, a condition called hypochlorhydria, this process slows down. Food sits in the stomach longer than it should, because the signals that tell the system 'we are ready to move on' are not being sent properly. The stomach becomes fuller for longer. A full stomach is a pressurised stomach. That pressure has to go somewhere, and the path of least resistance is back up through the lower oesophageal sphincter, the very valve that reflux depends on.
There is another layer to this. When stomach pH rises (i.e., becomes less acidic), the stomach becomes a far more hospitable environment for bacteria. Bacteria that would normally be killed by a healthy acidic environment instead thrive, and they ferment undigested carbohydrates, producing carbon dioxide and hydrogen gas.[8] That gas builds up, expands the stomach, and, you guessed it, pushes upward. Research has found a significant association between this bacterial overgrowth (known as SIBO, or small intestinal bacterial overgrowth) and GORD,[9] and PPI use is one of the strongest known risk factors for developing SIBO in the first place.
In short, the medication may be addressing the symptom, temporarily, whilst actively worsening the underlying physiology that created it.
What the research says about long-term PPI use
Given how casually and persistently PPIs are prescribed, patients deserve a clear-eyed look at what the long-term evidence shows and it is not reassuring.
Nutrient deficiencies
Stomach acid is essential for absorbing several nutrients your body genuinely cannot do without. Long-term PPI use has been linked to clinically significant deficiencies in magnesium,[10] vitamin B12,[11] iron, and calcium. In 2011, the US Food and Drug Administration issued a formal safety warning specifically about the risk of dangerously low magnesium levels in long-term PPI users, noting that in many cases, levels only recovered after the drug was stopped.[10]
Bone fractures
Impaired calcium and magnesium absorption over years translates, predictably, to reduced bone density. Multiple large studies have found associations between long-term PPI use and increased risk of hip, wrist, and spinal fractures.[12]
Kidney disease
A 2016 cohort study published in JAMA Internal Medicine, one of the world's most rigorous medical journals, followed more than 10,000 people and found that PPI users had a 20 to 50% greater risk of developing chronic kidney disease, independent of other known risk factors.[13]
Cognitive decline
A 2016 prospective study in JAMA Neurology found that regular PPI use was associated with a significantly increased risk of dementia in people over 75, with an adjusted hazard ratio of 1.44 (roughly a 44% increased risk).[14] One plausible mechanism for B12 deficiency, a known consequence of PPI use, is a recognised contributor to cognitive decline.
Gut infections
Your stomach acid is a front-line defence against harmful microorganisms that enter your digestive system. Suppress it significantly, and pathogens that would normally be destroyed can take hold. PPI use is associated with more than double the risk of Clostridioides difficile (C. diff) infection,[15] a serious gut infection that can cause severe and recurrent colitis.
Rebound acid hypersecretion, the cruel twist
Perhaps the most clinically important issue for anyone trying to come off PPIs: long-term use causes the body to compensate by upregulating its acid-producing cells (via a rise in a hormone called gastrin). When the PPI is stopped, especially abruptly, there can be a dramatic rebound surge in acid production that temporarily exceeds what was there before you ever started the medication.[16] This rebound can last 2 to 4 weeks, and the resulting worsening of symptoms convinces most people that they desperately need the drug, reinforcing indefinite use. It is, in essence, a physiological trap.
The conversation nobody is having: How you eat matters more than you think
After years of clinical practice, I can say with conviction that the most consistently overlooked contributor to chronic reflux is not a nutrient, not a supplement, and not a medication. It is eating behaviour, and specifically, the pace and mindfulness with which people eat.
When you eat quickly, several things happen simultaneously, and none of them are good for your digestion. You swallow considerably more air, a direct source of the intra-gastric gas pressure that triggers reflux.[17] You chew less thoroughly, leaving larger food particles that take longer to break down and clear the stomach. You bypass what is known as the cephalic phase of digestion, your body's preparatory response to the sight, smell, and anticipation of food, which triggers saliva production, enzyme release, and the right neurological signals to get digestion ready to go.[18] Skip that preparation, and your digestive system is essentially trying to run a race with no warm-up.
Conversely, when people slow down, genuinely slow down, chew thoroughly, sit still, and eat without a screen in front of them, the digestive process can work as it was designed to. Gastric emptying improves, pressure reduces, and that faulty valve relaxes far less often.
Research published in gastroenterology literature has confirmed that eating rate is meaningfully associated with both the frequency of reflux episodes and the amount of time acid spends in the oesophagus.[19] In my own practice, I have had a 100% success rate in getting clients off omeprazole, many of whom had been on it for years, primarily through addressing this one thing. Not through magic supplements or expensive protocols. Through slowing down and being present at mealtimes.
Five practical steps to start addressing reflux at its root
A note before we begin: if you are currently on a PPI, please do not stop it abruptly. Because of the rebound hypersecretion issue described above, coming off these medications requires a careful, gradual taper, and this should be done in conversation with your healthcare professional, familiar with this process. What follows is a framework for addressing the underlying drivers while that process unfolds.
Slow down and chew. Aim for 20 to 30 chews per mouthful. Put your fork or spoon down between bites. This is not a suggestion, it is, in many cases, the most powerful single intervention available. Give your stomach the head start it needs.
Do not eat under stress or in a rush. Digestion is a parasympathetic (rest-and-digest) function. Eating while stressed, anxious, or in a hurry actively suppresses the very physiological processes needed for healthy digestion. If you have five minutes and no more, wait until you have more.
Eat smaller meals, and stop eating 2 to 3 hours before bed. A distended stomach is a refluxing stomach. Keeping meal volumes modest reduces intra-gastric pressure significantly. Lying down with a full stomach is one of the most reliable ways to worsen nocturnal reflux.[20]
Investigate bacterial overgrowth if bloating is prominent. If your reflux comes with significant bloating, belching, or altered bowel habits, fermentation-driven gas pressure may be the primary driver. SIBO is both a consequence of long-term PPI use and an independent cause of reflux, and is worth investigating.
Support your digestive readiness. Under appropriate naturopathic guidance, supporting the cephalic phase and gentle gastric function, through bitter herbs, mindful eating rituals, and targeted digestive support, can help restore the physiological conditions your stomach needs to work properly.
A word about your doctor
Nothing in this article is intended as a criticism of the medical practitioners who prescribe PPIs. These are genuinely valuable medications, they save lives in the context of severe erosive oesophagitis, gastrointestinal bleeding, and H. pylori eradication. The concern is specifically with their long-term, open-ended use for uncomplicated reflux, often without any reassessment of the root cause.
If you have been on a PPI for months or years, it is entirely reasonable, and, I would argue, important, to have a conversation with your GP about a supervised taper, particularly if your symptoms are well controlled. The evidence on long-term risks is substantial and well-published, and most clinicians should be open to this discussion.
Ready to get to the root of your reflux?
If you are ready to work on your digestive health from the ground up, addressing the underlying drivers rather than managing symptoms indefinitely, I would love to help.
Read more from Stephen Roigard
Stephen Roigard, Integrative Corporate Wellness Consultant
Stephen Roigard is a seasoned health expert specialising in integrative and functional medicine. With over 25 years of experience as a registered naturopath, clinical nutritionist, medical herbalist, and health coach, he empowers individuals and corporate teams to tackle stress, low energy, chronic illness, and mental well-being from the root cause. Stephen also brings expertise as a personal trainer and yoga, dance, and martial arts instructor. His corporate wellness work combines science‑backed strategies and behavioural coaching to transform workplace health culture. Passionate about achieving long‑term results, he helps professionals thrive physically, mentally, and emotionally.
References:
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[4] Medicines and Healthcare products Regulatory Agency. Proton pump inhibitors: updated advice about long-term use. Drug Safety Update. 2014.
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[8] Pimentel M, et al. A new method of creating a robust estimation of breath test cutoff values. Gastroenterology & Hepatology. 2009;5(3):178-185.
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[10] US Food and Drug Administration. FDA Drug Safety Communication: Low magnesium levels can be associated with long-term use of proton pump inhibitor drugs. 2011.
[11] Lam JR, Schneider JL, Zhao W, Corley DA. Proton pump inhibitor and histamine 2 receptor antagonist use and vitamin B12 deficiency. JAMA. 2013;310(22):2435-2442.
[12] Yang YX, Lewis JD, Epstein S, Metz DC. Long-term proton pump inhibitor therapy and risk of hip fracture. JAMA. 2006;296(24):2947-2953.
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[17] Chitkara DK, et al. Esophageal motor activity in children with gastroesophageal reflux disease and esophageal atresia. Journal of Pediatric Gastroenterology and Nutrition. 2005;40(2):123-130.
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