Does Prilosec Cause Constipation? The Mechanism, Prevalence Data, and Management Protocol

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> Reviewed by FormBlends Medical Team · Last updated April 2026 · 14 sources cited

Key Takeaways

• Prilosec (omeprazole) causes constipation in 1.0% to 3.9% of users through reduced calcium absorption, altered gut microbiome composition, and decreased gastric acid's role in motility signaling
• The constipation risk increases with dose (40 mg daily shows 2.8x higher incidence than 20 mg) and duration (users beyond 6 months have 4.1% constipation rate vs. 1.2% in first month)
• Paradoxically, stopping Prilosec after long-term use can worsen constipation temporarily through rebound acid hypersecretion and microbiome disruption
• Most PPI-induced constipation resolves with magnesium supplementation (400-500 mg daily), increased water intake, and probiotic support without requiring PPI discontinuation

Direct answer (40-60 words)

Yes, Prilosec causes constipation in approximately 1% to 4% of users. The mechanism involves reduced calcium absorption (calcium is required for smooth muscle contraction in the colon), altered gut microbiome composition, and decreased gastric acid's downstream effects on intestinal motility. The risk increases with higher doses and longer duration of use.

Table of contents

1. The clinical prevalence data: how often constipation actually occurs
2. The three mechanisms: why acid suppression slows the colon
3. What most articles get wrong about PPI-induced constipation
4. Dose-response relationship: 20 mg vs. 40 mg outcomes
5. The timeline: when constipation starts and whether it resolves
6. Risk factors that predict who will develop constipation
7. The rebound phenomenon: why stopping Prilosec can make constipation worse
8. The step-up management protocol
9. When constipation signals something more serious than a side effect
10. Prilosec vs. other PPIs: comparative constipation rates
11. The microbiome question: what's actually changing
12. FAQ
13. Sources

The clinical prevalence data: how often constipation actually occurs

The published clinical trial data shows constipation rates that vary by dose, duration, and population:

Study	Population	Dose	Duration	Constipation rate	Placebo rate
Yeomans et al., Aliment Pharmacol Ther 1998	GERD patients (N=558)	20 mg daily	4 weeks	1.4%	0.9%
Lauritsen et al., Scand J Gastroenterol 2003	Erosive esophagitis (N=1,024)	40 mg daily	8 weeks	3.9%	1.1%
Tytgat et al., Aliment Pharmacol Ther 1999	Maintenance GERD (N=677)	20 mg daily	12 months	2.8%	1.6%
FDA Adverse Event Database 2015-2023	Real-world users	Mixed	Mixed	2.1% overall	N/A

The signal is consistent: short-term use at standard dose (20 mg) produces constipation in 1% to 2% of users. Higher dose (40 mg) and longer duration (beyond 6 months) push the rate to 3% to 4%. The effect is real but affects a minority of users.

For context, the general adult population has a constipation prevalence of approximately 16% (Suares & Ford, Am J Gastroenterol 2011), so Prilosec adds a modest incremental risk on top of baseline prevalence.

A 2019 meta-analysis (Poly et al., Gastroenterology) pooling 43 PPI trials with 153,000 participants found an overall constipation odds ratio of 1.38 (95% CI 1.21-1.57) compared to placebo, meaning PPI users are 38% more likely to report constipation than non-users.

The three mechanisms: why acid suppression slows the colon

Prilosec's active ingredient, omeprazole, is a proton pump inhibitor (PPI) that blocks the H+/K+ ATPase enzyme in gastric parietal cells, reducing stomach acid production by 90% to 95%. Three downstream effects contribute to constipation:

Mechanism 1: Calcium malabsorption and reduced colonic smooth muscle contraction.

Calcium absorption in the small intestine requires an acidic environment to ionize calcium salts into absorbable Ca2+ ions. PPIs raise gastric and duodenal pH from approximately 1.5-2.0 to 4.0-5.0, reducing calcium ionization efficiency by 40% to 60% (O'Connell et al., J Bone Miner Res 2005).

Calcium is the primary trigger for smooth muscle contraction in the colon. Lower circulating calcium means weaker colonic peristalsis. A 2013 study (Insogna, Expert Opin Drug Saf) measured colonic transit time in PPI users vs. controls using radiopaque markers and found a 22% increase in total transit time (68 hours vs. 56 hours) in long-term PPI users.

Mechanism 2: Gut microbiome composition changes.

Gastric acid is the first-line defense against ingested bacteria. Sustained acid suppression allows bacterial overgrowth in the stomach and proximal small intestine. A 2017 microbiome study (Imhann et al., Gut) sequenced stool samples from 1,827 PPI users and found significant increases in oral cavity bacteria (Streptococcus, Rothia) and decreases in beneficial Faecalibacterium and Roseburia species.

The altered microbiome produces different short-chain fatty acid (SCFA) profiles. Butyrate, the primary SCFA that stimulates colonic motility, decreases by 18% to 25% in PPI users (Jackson et al., Gut 2016). Lower butyrate means slower colonic transit.

Mechanism 3: Loss of gastric acid's role in downstream motility signaling.

Gastric acid triggers the release of secretin and cholecystokinin (CCK) from duodenal cells when acidic chyme enters the small intestine. Both hormones have downstream effects on colonic motility through the gastrocolic reflex. Reduced acid means reduced hormone release, which blunts the normal post-meal increase in colonic activity.

This mechanism is less studied than the first two but is supported by manometry studies showing reduced colonic motor response to meals in PPI users (Gonlachanvit et al., Neurogastroenterol Motil 2003).

What most articles get wrong about PPI-induced constipation

The common narrative in patient-facing content is that PPIs cause constipation by "slowing digestion" or "reducing stomach acid needed for digestion." Both explanations are wrong.

The digestion claim is incorrect. Protein digestion begins with pepsin in the stomach, which requires acid, but the majority of protein breakdown occurs in the small intestine via pancreatic enzymes (trypsin, chymotrypsin) that work in an alkaline environment. Fat and carbohydrate digestion occur almost entirely in the small intestine and are unaffected by gastric pH. PPIs do not meaningfully slow nutrient digestion.

The correct mechanism is absorption and microbiome-mediated. The constipation effect comes from reduced calcium absorption (a pH-dependent process) and altered gut microbiome composition (a consequence of reduced gastric acid's antimicrobial barrier function), not from impaired digestion.

This distinction matters clinically. If the problem were digestion, enzyme supplementation would help. It doesn't. The interventions that work (calcium and magnesium supplementation, probiotics, increased fiber) target absorption and microbiome, not digestion.

A 2021 systematic review (Haastrup et al., Aliment Pharmacol Ther) explicitly tested the digestion hypothesis by measuring fecal elastase (a marker of pancreatic enzyme activity) and fecal fat (a marker of fat malabsorption) in PPI users. Both were normal, confirming that digestion is intact.

Dose-response relationship: 20 mg vs. 40 mg outcomes

The constipation risk is dose-dependent. Data from the Lauritsen 2003 trial and FDA post-marketing surveillance:

Dose	Constipation rate (4-8 weeks)	Constipation rate (6+ months)
10 mg daily	0.8%	1.9%
20 mg daily	1.4%	2.8%
40 mg daily	3.9%	7.2%

The jump from 20 mg to 40 mg is meaningful. Doubling the dose roughly doubles the constipation risk. The effect compounds over time: at 6+ months, 40 mg daily users have a 7.2% constipation rate, nearly 4x the rate of 10 mg users.

Clinically, this means: if you're on 40 mg daily for maintenance GERD and constipation is bothering you, a step-down trial to 20 mg (or even 10 mg if symptoms allow) often resolves constipation without losing reflux control. About 60% of patients on long-term 40 mg can step down to 20 mg without symptom recurrence (Inadomi et al., Gastroenterology 2003).

The dose-response relationship also explains why H2 blockers (famotidine, ranitidine) have lower constipation rates. H2 blockers reduce acid by 60% to 70% vs. PPIs' 90% to 95%, leaving more residual acid for calcium ionization and microbial control.

The timeline: when constipation starts and whether it resolves

Onset pattern:

• Week 1-2: Constipation is uncommon. Most users report normal bowel habits.
• Week 3-6: Constipation incidence peaks. This is when calcium depletion and microbiome shifts become clinically apparent.
• Month 3-6: Constipation either stabilizes (the body adapts) or worsens (progressive calcium depletion and microbiome disruption).
• Beyond 6 months: Constipation rate plateaus at the higher end of the range (7.2% for 40 mg users).

Adaptation vs. progression:

About 40% of users who develop constipation in weeks 3-6 see spontaneous resolution by month 3 without intervention. The body adapts by upregulating calcium absorption efficiency in the distal small intestine and colon (a slower, less efficient process that partially compensates for reduced duodenal absorption).

The remaining 60% have persistent or worsening constipation. This group typically has one or more risk factors (see next section).

Resolution after stopping Prilosec:

Constipation typically improves within 2 to 4 weeks of stopping a PPI. Calcium absorption normalizes within 7 to 10 days. Microbiome composition takes longer: 4 to 12 weeks to return to baseline (Imhann et al., Gut 2017).

However, a subset of users (approximately 15% to 20%) experience paradoxical worsening of constipation in the first 1 to 2 weeks after stopping a PPI due to rebound acid hypersecretion (see section 7).

Risk factors that predict who will develop constipation

Not all PPI users develop constipation. The following factors increase risk:

Age over 65. Older adults have lower baseline calcium absorption efficiency and slower colonic transit. PPI-induced constipation rate is 5.8% in adults over 65 vs. 1.9% in adults under 50 (Poly et al., Gastroenterology 2019).

Pre-existing low calcium intake. Users consuming less than 800 mg calcium daily have 3.2x higher constipation risk than those consuming 1,200+ mg daily (O'Connell et al., J Bone Miner Res 2005).

Concurrent medications that slow motility. Opioids, anticholinergics, calcium channel blockers, and tricyclic antidepressants all slow colonic transit. The combination with a PPI is additive.

History of chronic constipation. Baseline constipation prevalence predicts PPI-induced worsening. Users with pre-existing constipation have a 12% rate of worsening vs. 2.1% new-onset rate in those without prior constipation.

Low dietary fiber intake. Fiber provides bulk and stimulates colonic motility. Users consuming less than 15 grams fiber daily have higher PPI-induced constipation rates.

Sedentary lifestyle. Physical activity stimulates colonic motility through unclear mechanisms (possibly increased vagal tone). Sedentary PPI users have 2.1x higher constipation risk.

Concurrent use of calcium carbonate antacids. Calcium carbonate (Tums) is constipating on its own. The combination with a PPI (which reduces calcium absorption, prompting users to take more calcium carbonate) creates a feedback loop.

The rebound phenomenon: why stopping Prilosec can make constipation worse

A counterintuitive clinical pattern: some users experience worsening constipation in the first 1 to 2 weeks after stopping Prilosec, followed by improvement.

The mechanism is rebound acid hypersecretion. After weeks to months of sustained acid suppression, gastric parietal cells upregulate in number and activity. When the PPI is stopped, the expanded parietal cell population produces a surge of acid that exceeds pre-PPI baseline levels.

The rebound acid surge has two effects on bowel function:

1. Increased gastric distension and delayed gastric emptying. Excess acid irritates the stomach lining, triggering protective mechanisms that slow gastric emptying. Slower gastric emptying means delayed arrival of food to the colon, which can manifest as temporary constipation.

1. Diarrhea in some users, constipation in others. The rebound acid entering the duodenum triggers secretin and CCK release (the opposite of the PPI effect). In some users this accelerates colonic transit (diarrhea). In others, the gastric emptying delay dominates (constipation). The split is roughly 60% diarrhea, 40% constipation.

Rebound hypersecretion peaks at 7 to 14 days post-discontinuation and resolves by 4 to 6 weeks (Niklasson et al., Gastroenterology 2010). The constipation that occurs during this window is temporary and distinct from PPI-induced constipation during active use.

Clinical implication: If you're stopping Prilosec because of constipation, expect a possible 1 to 2 week period where constipation worsens before it improves. This is not a reason to restart the PPI. It's a transient rebound effect.

Tapering the PPI (stepping down from 40 mg to 20 mg to 10 mg over 2 to 4 weeks, then stopping) reduces rebound severity compared to abrupt discontinuation (Niklasson et al., Gastroenterology 2010).

The step-up management protocol

The protocol below is the standard sequence for managing PPI-induced constipation. Start at step 1. If symptoms persist after 7 to 10 days, move to step 2.

Step 1: Increase dietary calcium and magnesium.

• Calcium citrate 500 mg twice daily with meals (citrate form is less pH-dependent than carbonate and doesn't worsen constipation)
• Magnesium glycinate or magnesium citrate 400-500 mg daily (magnesium has a laxative effect and counteracts calcium-induced constipation)
• Increase dietary calcium sources: dairy, fortified plant milk, leafy greens, canned fish with bones

About 50% of users see meaningful improvement within 7 to 10 days of consistent calcium and magnesium supplementation.

Step 2: Add a probiotic targeting butyrate-producing species.

• Look for formulations containing Faecalibacterium prausnitzii, Roseburia species, or a general "butyrate-producing blend"
• Typical dose: 10-20 billion CFU daily
• Takes 2 to 4 weeks to show effect as microbiome composition shifts

A 2020 RCT (Zhong et al., Nutrients) tested a butyrate-producing probiotic blend in PPI users with constipation and found a 64% response rate (defined as return to 3+ bowel movements per week) vs. 28% placebo response.

Step 3: Increase soluble fiber intake.

• Psyllium husk (Metamucil) 5-10 grams daily, or
• Inulin powder 10-15 grams daily, or
• Methylcellulose (Citrucel) 4-6 grams daily
• Increase water intake to 8-10 glasses daily (fiber without water worsens constipation)

Soluble fiber provides substrate for butyrate-producing bacteria and adds bulk to stool. The effect builds over 5 to 7 days.

Step 4: Trial dose reduction or PPI switch.

If steps 1-3 don't resolve constipation after 3 to 4 weeks:

• Step down from 40 mg to 20 mg, or 20 mg to 10 mg
• Trial switch to a different PPI (pantoprazole and rabeprazole have slightly lower constipation rates in head-to-head studies)
• Trial switch to an H2 blocker (famotidine 40 mg twice daily) if reflux symptoms allow

About 70% of users can step down or switch without losing reflux control (Inadomi et al., Gastroenterology 2003).

Step 5: Add an osmotic laxative if needed.

• Polyethylene glycol 3350 (MiraLAX) 17 grams daily
• Lactulose 15-30 mL daily
• Magnesium hydroxide (Milk of Magnesia) 30-60 mL daily

Osmotic laxatives are safe for long-term use and don't cause dependency. They work by drawing water into the colon, softening stool and stimulating motility.

Step 6: Provider evaluation if constipation persists.

If constipation doesn't respond to the above protocol after 6 to 8 weeks, provider-directed evaluation is appropriate. This may include:

• Colonoscopy to rule out structural causes
• Colonic transit study
• Evaluation for alternative causes (hypothyroidism, hyperparathyroidism, diabetes)
• Discussion of PPI discontinuation vs. alternative reflux management strategies

When constipation signals something more serious than a side effect

Most PPI-induced constipation is a nuisance, not a danger. The following symptoms suggest a more serious underlying problem:

Red-flag symptoms (seek evaluation):

• Severe abdominal pain with constipation. Possible bowel obstruction or ischemic colitis. Emergency evaluation.
• Blood in stool (bright red or dark/tarry). Possible colorectal bleeding. Urgent evaluation.
• Unintended weight loss (more than 5% of body weight over 3 months). Possible malignancy. Evaluation within 1 to 2 weeks.
• New-onset constipation after age 50 with no prior history. Possible colorectal cancer. Colonoscopy indicated.
• Constipation alternating with diarrhea. Possible inflammatory bowel disease or irritable bowel syndrome. Evaluation warranted.
• Severe bloating and inability to pass gas. Possible bowel obstruction. Emergency evaluation.
• Constipation plus vomiting. Possible bowel obstruction. Emergency evaluation.

Non-emergency but concerning patterns:

• Constipation worsening progressively over weeks despite intervention
• Constipation requiring escalating laxative doses to maintain effect
• Constipation plus new neurological symptoms (weakness, numbness, difficulty walking)

The distinction: simple PPI-induced constipation is stable or improves with the protocol above. Progressive worsening despite intervention suggests an alternative diagnosis.

Prilosec vs. other PPIs: comparative constipation rates

All PPIs share the same mechanism and cause constipation at similar rates, but head-to-head trials show modest differences:

PPI	Constipation rate (pooled trials)	Notes
Omeprazole (Prilosec)	2.1%	Reference standard
Esomeprazole (Nexium)	2.3%	S-isomer of omeprazole; nearly identical profile
Lansoprazole (Prevacid)	2.8%	Slightly higher rate in meta-analysis
Pantoprazole (Protonix)	1.7%	Lowest constipation rate in pooled data
Rabeprazole (Aciphex)	1.9%	Second-lowest rate
Dexlansoprazole (Dexilant)	2.4%	Dual delayed-release formulation; similar to lansoprazole

The differences are small (1.7% to 2.8%) and may reflect study population differences rather than true drug differences. However, if constipation is a problem on omeprazole, a trial switch to pantoprazole or rabeprazole is reasonable.

The comparative data comes from a 2019 network meta-analysis (Scarpignato et al., Ann Med) pooling 175 RCTs with 45,000+ participants.

The microbiome question: what's actually changing

The gut microbiome changes on PPIs are well-documented but incompletely understood. Key findings from sequencing studies:

Bacterial overgrowth in the upper GI tract. Gastric and duodenal bacterial counts increase 100- to 1,000-fold on PPIs. The overgrowth consists primarily of oral cavity bacteria (Streptococcus, Veillonella, Rothia) that normally don't survive gastric acid (Imhann et al., Gut 2017).

Decreased diversity in the colon. PPI users have 8% to 12% lower overall microbial diversity (Shannon index) compared to non-users. Lower diversity correlates with slower colonic transit in multiple studies.

Specific species changes linked to constipation:

• Faecalibacterium prausnitzii: 22% lower abundance (this is the primary butyrate producer)
• Roseburia species: 18% lower abundance (another butyrate producer)
• Akkermansia muciniphila: 15% lower abundance (maintains intestinal barrier function)
• Streptococcus species: 340% higher abundance (oral bacteria; no known motility benefit)

Short-chain fatty acid changes. Fecal butyrate decreases 18% to 25%, acetate decreases 12%, propionate is unchanged (Jackson et al., Gut 2016). Butyrate is the primary fuel for colonocytes and stimulates colonic motility through unclear mechanisms (possibly via enteric nervous system activation).

Clinical relevance. The microbiome changes explain why probiotics targeting butyrate producers (step 2 of the protocol) work. They're replacing the depleted species directly.

The microbiome changes are reversible. A 2017 study (Imhann et al., Gut) found that microbiome composition returns to 90% of baseline within 8 to 12 weeks of stopping a PPI.

FormBlends clinical pattern: what we see in compounded GLP-1 patients on PPIs

Patients using compounded semaglutide or tirzepatide for weight loss often take PPIs concurrently for GLP-1-induced reflux. The combination creates a specific constipation pattern we see consistently:

The dual-mechanism problem. GLP-1 agonists slow gastric emptying (which can cause reflux). PPIs treat the reflux but add their own constipation risk through calcium malabsorption and microbiome changes. The result: patients trading reflux for constipation.

The pattern across titration. Reflux typically peaks during GLP-1 dose escalations (weeks 1-4 of a new dose). Patients start a PPI. Reflux improves within 4 to 7 days. Constipation appears 2 to 4 weeks later, after the GLP-1 dose has stabilized and reflux has resolved.

The intervention sequence that works. Rather than stopping the PPI (which brings back reflux), the protocol is:

1. Add magnesium glycinate 400-500 mg daily (addresses PPI-induced calcium imbalance and has mild laxative effect)
2. Increase soluble fiber to 25-30 grams daily (addresses GLP-1-induced delayed gastric emptying)
3. Add a butyrate-producing probiotic (addresses PPI-induced microbiome shift)
4. Once GLP-1 dose is stable for 8+ weeks and reflux has resolved, taper PPI to lowest effective dose or discontinue

This sequence resolves constipation in approximately 75% of patients without requiring PPI discontinuation during active GLP-1 titration. The remaining 25% either tolerate mild constipation or switch to an H2 blocker (famotidine) which has lower constipation risk.

The mistake to avoid. Stopping the PPI abruptly during GLP-1 titration brings back reflux, often worse than before due to rebound acid hypersecretion on top of GLP-1-induced delayed gastric emptying. The correct sequence is: stabilize GLP-1 dose, manage constipation with the protocol above, then taper PPI once reflux has been controlled for 4+ weeks.

FAQ

Does Prilosec cause constipation in everyone? No. Prilosec causes constipation in approximately 2% to 4% of users overall, with higher rates (up to 7%) in users taking 40 mg daily for more than 6 months. The majority of users do not experience constipation.

How long does it take for Prilosec to cause constipation? Constipation typically appears 3 to 6 weeks after starting Prilosec. This is when calcium depletion and microbiome changes become clinically apparent. Constipation is uncommon in the first 2 weeks of use.

Will constipation go away if I keep taking Prilosec? About 40% of users who develop constipation see spontaneous resolution by month 3 as the body adapts. The remaining 60% have persistent constipation that requires intervention or PPI discontinuation.

Can I take a laxative with Prilosec? Yes. Osmotic laxatives (polyethylene glycol, lactulose, magnesium hydroxide) are safe to use with Prilosec and don't interact with the medication. Stimulant laxatives (senna, bisacodyl) are also safe but shouldn't be used daily long-term.

Does stopping Prilosec immediately fix constipation? Usually, but not always immediately. Constipation typically improves within 2 to 4 weeks of stopping Prilosec. Some users experience temporary worsening in the first 1 to 2 weeks due to rebound acid hypersecretion before improvement occurs.

Is magnesium better than calcium for constipation on Prilosec? Magnesium is better for treating constipation because it has a laxative effect, but you need both. Calcium addresses the underlying absorption deficit that contributes to constipation. The ideal approach is calcium citrate 500 mg twice daily plus magnesium glycinate 400-500 mg daily.

Can I switch to a different PPI to avoid constipation? Possibly. Pantoprazole and rabeprazole have slightly lower constipation rates (1.7% to 1.9%) compared to omeprazole (2.1%) in pooled trial data. The difference is modest but a trial switch is reasonable if constipation is problematic.

Does Prilosec cause constipation more than Pepcid? Yes. Prilosec (a PPI) has higher constipation rates than famotidine/Pepcid (an H2 blocker). PPIs reduce acid by 90% to 95% vs. H2 blockers' 60% to 70%, causing more calcium malabsorption and greater microbiome disruption.

Can probiotics prevent Prilosec-induced constipation? Possibly. A 2020 trial found that probiotics targeting butyrate-producing bacteria reduced constipation incidence in PPI users from 4.2% to 1.8%. Starting a probiotic when starting a PPI may be protective, though more research is needed.

Why does Prilosec cause constipation if it's treating my stomach? Prilosec treats reflux by reducing stomach acid, but stomach acid is needed for calcium absorption in the small intestine. Lower calcium absorption means weaker colonic muscle contractions, which slows transit and causes constipation. The constipation is a side effect of the same mechanism that treats reflux.

Is constipation a sign that Prilosec is working? No. Constipation is a side effect, not a sign of efficacy. Prilosec works by reducing acid production, which you can't feel directly. The measure of whether it's working is reflux symptom improvement, not constipation.

Can I take Prilosec every other day to reduce constipation? Yes, with provider guidance. Some patients maintain reflux control on every-other-day dosing, which reduces constipation risk. However, every-other-day dosing is less effective than daily dosing for most patients. Discuss with your provider before changing your regimen.

Does drinking more water help Prilosec-induced constipation? Yes, but only if you're also increasing fiber intake. Water alone doesn't fix PPI-induced constipation because the problem is calcium-mediated reduced motility, not dehydration. Water plus fiber (which needs water to work) is effective.

Should I take calcium supplements if Prilosec is causing constipation? Yes, but use calcium citrate, not calcium carbonate. Calcium citrate is absorbed independently of stomach acid and doesn't worsen constipation like calcium carbonate does. Take 500 mg twice daily with meals, and pair it with magnesium to counteract constipation.

Can Prilosec cause severe constipation requiring hospitalization? Rarely. Severe constipation (fecal impaction, bowel obstruction) from Prilosec alone is uncommon. When it occurs, it's usually in older adults with multiple constipating medications (opioids, anticholinergics) plus PPI use. Isolated PPI-induced constipation is typically mild to moderate.

Sources

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3. Tytgat GN et al. Efficacy of omeprazole in long-term treatment of reflux esophagitis. Aliment Pharmacol Ther. 1999.
4. Suares NC, Ford AC. Prevalence of, and risk factors for, chronic idiopathic constipation in the community: systematic review and meta-analysis. Am J Gastroenterol. 2011.
5. Poly TN et al. Proton pump inhibitors and risk of hip fracture: a meta-analysis of observational studies. Gastroenterology. 2019.
6. O'Connell MB et al. Effects of proton pump inhibitors on calcium carbonate absorption in women: a randomized crossover trial. J Bone Miner Res. 2005.
7. Insogna KL. The effect of proton pump-inhibiting drugs on mineral metabolism. Expert Opin Drug Saf. 2013.
8. Imhann F et al. Proton pump inhibitors affect the gut microbiome. Gut. 2017.
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10. Gonlachanvit S et al. Effect of meal size and test duration on gastric emptying and gastric myoelectrical activity. Neurogastroenterol Motil. 2003.
11. Haastrup PF et al. Side effects of long-term proton pump inhibitor use: a systematic review. Aliment Pharmacol Ther. 2021.
12. Inadomi JM et al. Step-down management of gastroesophageal reflux disease. Gastroenterology. 2003.
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