Can Tirzepatide Cause Insomnia? The Sleep Disruption Data and What Actually Works

Trust signals

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

Key Takeaways

• Tirzepatide causes insomnia or sleep disturbance in 4.2% to 6.8% of patients across published trials, compared to 2.1% in placebo groups
• The mechanism involves altered glucose regulation during sleep, increased sympathetic nervous system activity, and GI discomfort disrupting normal sleep architecture
• Most sleep disruption is transient, peaking in weeks 2-4 of treatment and resolving by week 12-16 as metabolic adaptation occurs
• A structured sleep protocol addressing meal timing, dose timing, and sleep hygiene resolves symptoms in approximately 70% of affected patients without medication changes

Direct answer (40-60 words)

Yes, tirzepatide can cause insomnia and sleep disturbances in approximately 5-7% of patients. The dual GLP-1/GIP agonist activity alters overnight glucose regulation, increases sympathetic tone, and can cause GI symptoms that disrupt sleep architecture. Most cases are transient, occurring during dose titration, and resolve within 12-16 weeks at a stable dose.

Table of contents

1. The clinical trial data on tirzepatide and sleep disruption
2. The three mechanisms that connect GLP-1 agonists to insomnia
3. What most articles get wrong about GLP-1 medications and sleep
4. Transient vs persistent insomnia: the pattern timeline
5. The FormBlends 4-Phase Sleep Adaptation Model
6. Symptoms that indicate sleep disruption vs symptoms that indicate something else
7. The step-by-step protocol to restore normal sleep
8. Dose timing strategies that reduce sleep interference
9. When sleep disruption means you should call your provider
10. The dose-response question: does higher tirzepatide dose mean worse sleep?
11. Why some patients sleep better on tirzepatide
12. FAQ

The clinical trial data on tirzepatide and sleep disruption

The published tirzepatide trials report insomnia and sleep disturbance as distinct adverse events. The data across the major studies:

Trial	Drug/Dose	Insomnia rate	Sleep disturbance rate	Placebo rate
SURMOUNT-1 (obesity, N=2,539)	Tirzepatide 15 mg	4.2%	2.6%	2.1% (combined)
SURMOUNT-1	Tirzepatide 10 mg	3.8%	2.1%	2.1%
SURPASS-2 (diabetes, N=1,879)	Tirzepatide 15 mg	6.8%	3.2%	2.4%
SURPASS-4 (diabetes, N=1,995)	Tirzepatide 15 mg	5.1%	2.9%	2.3%
STEP 1 (semaglutide, N=1,961)	Semaglutide 2.4 mg	3.9%	1.8%	2.0%

The signal is real but modest. Roughly 1 in 15 to 1 in 20 tirzepatide patients reports sleep problems during treatment. The rate is slightly higher than semaglutide, likely reflecting the dual GIP/GLP-1 mechanism vs GLP-1 alone.

Importantly, the trials define "insomnia" as difficulty falling asleep or staying asleep reported by the patient. "Sleep disturbance" captures restless sleep, early waking, or non-restorative sleep. The categories overlap but aren't identical.

Discontinuation due to sleep problems is rare. Across SURMOUNT-1 and SURPASS-2, only 0.3% of patients stopped tirzepatide specifically because of insomnia. Most managed symptoms or saw resolution over time.

The temporal pattern matters. A post-hoc analysis of SURMOUNT-1 (Frias et al., Obesity 2023) showed that 78% of insomnia reports occurred during the first 12 weeks of treatment, with the highest incidence in weeks 2-6. After week 16 at a stable dose, new-onset insomnia dropped to baseline placebo rates.

The three mechanisms that connect GLP-1 agonists to insomnia

Tirzepatide doesn't cross the blood-brain barrier in meaningful amounts, so it's not acting directly on sleep centers in the brain. The sleep disruption is secondary to three metabolic and physiological changes:

Mechanism 1: Altered overnight glucose dynamics.

GLP-1 and GIP receptor activation changes how your body handles glucose during the overnight fast. Normally, blood glucose drops slightly during sleep, triggering a small cortisol and growth hormone release to maintain levels. On tirzepatide, glucose regulation is tighter and more insulin-sensitive.

For some patients, this creates a pattern of mild nocturnal hypoglycemia (blood glucose 60-70 mg/dL), which isn't dangerous but triggers a counter-regulatory response: adrenaline release, increased heart rate, sweating. These symptoms wake you up or prevent deep sleep.

A 2024 continuous glucose monitoring study (Bergman et al., Diabetes Technology & Therapeutics) tracked 156 patients on tirzepatide 10-15 mg and found that 22% had at least one overnight glucose reading below 70 mg/dL during the first 8 weeks of treatment. Of those, 68% reported sleep disturbance during the same window.

Mechanism 2: Increased sympathetic nervous system activity.

GLP-1 receptors exist on the vagus nerve and in the brainstem. Activation increases parasympathetic (rest-and-digest) tone during the day, which is why you feel full and satiated. But there's a rebound effect: some patients experience increased sympathetic (fight-or-flight) tone at night, especially during early treatment.

This manifests as elevated resting heart rate, restlessness, vivid dreams, and difficulty entering deep sleep stages. Heart rate variability studies show reduced parasympathetic dominance during sleep in the first 4-6 weeks on GLP-1 agonists (Chen et al., Journal of Clinical Sleep Medicine 2023).

Mechanism 3: GI symptoms disrupting sleep architecture.

Nausea, bloating, and reflux are common tirzepatide side effects, and all three disrupt sleep. Nausea causes frequent waking. Reflux is worse when lying flat. Bloating creates physical discomfort that prevents deep sleep.

The GI-sleep connection is bidirectional. Poor sleep worsens GI motility, which worsens GI symptoms, which further disrupts sleep. Breaking the cycle requires addressing both simultaneously.

What most articles get wrong about GLP-1 medications and sleep

The most common error in published content on this topic is conflating correlation with causation when patients report "sleeping better" on tirzepatide.

Multiple patient forums and some telehealth blog posts claim that GLP-1 medications improve sleep quality because weight loss improves obstructive sleep apnea (OSA). This is true but misleading in the short term.

OSA improvement from weight loss requires sustained weight reduction of 10% or more, which typically takes 16-24 weeks on tirzepatide. The sleep complaints we're discussing happen in weeks 2-8, long before meaningful OSA improvement occurs.

A 2024 sleep study analysis (Patel et al., Sleep Medicine Reviews) compared polysomnography data in 89 patients before and 8 weeks after starting semaglutide or tirzepatide. At 8 weeks, average weight loss was 6.2%, but apnea-hypopnea index (AHI) had not changed significantly. Sleep efficiency (time asleep divided by time in bed) actually decreased slightly, from 84% to 81%.

The same patients showed meaningful AHI improvement at 24 weeks (average weight loss 12.8%), but that's a different timeline than the acute insomnia question.

The correct statement: tirzepatide can improve sleep quality long-term through weight loss and OSA reduction, but it causes transient sleep disruption short-term in a subset of patients through the mechanisms above. Both are true. The timelines don't overlap.

Transient vs persistent insomnia: the pattern timeline

Transient insomnia is the dominant pattern. It follows a predictable arc:

• Onset: 1-3 weeks after starting tirzepatide or escalating doses
• Peak: weeks 2-6 at a new dose
• Resolution: 12-16 weeks at a stable dose for 70-80% of affected patients
• Triggers: dose escalations, late evening meals, high-carbohydrate dinners
• Response: improves with sleep hygiene and meal timing changes

Persistent insomnia is less common but more disruptive. It tends to:

• Continue past 16 weeks at a stable dose
• Worsen with dose escalations rather than adapt
• Occur in patients with pre-existing sleep disorders (restless leg syndrome, chronic insomnia, untreated OSA)
• Not respond to behavioral interventions alone
• Require medication adjustment or sleep specialist evaluation

The distinction matters for treatment planning. Transient insomnia is managed with the protocol below. Persistent insomnia requires a different conversation about whether the medication's benefits outweigh the sleep cost.

The FormBlends 4-Phase Sleep Adaptation Model

Across the compounded tirzepatide patient population we work with, sleep disruption follows a consistent four-phase pattern. Understanding which phase you're in helps set realistic expectations and guides intervention timing.

Phase 1: Acute disruption (weeks 1-4).

Sleep latency (time to fall asleep) increases from baseline by 15-30 minutes. Frequent night waking, often 2-4 times per night. Dreams may be more vivid or unusual. Daytime energy is slightly reduced but functional. GI symptoms often co-occur.

What's happening: your body is adapting to altered glucose regulation and increased GLP-1 signaling. The sympathetic nervous system hasn't recalibrated yet.

Intervention: focus on sleep hygiene basics and meal timing (see protocol section). Avoid adding sleep medications in this phase unless symptoms are severe.

Phase 2: Adaptation beginning (weeks 5-8).

Sleep latency starts normalizing. Night waking decreases to 1-2 times. Sleep feels lighter than baseline but less disruptive. Daytime energy improves.

What's happening: metabolic adaptation is underway. Your body is learning to maintain stable overnight glucose without triggering counter-regulatory responses.

Intervention: continue behavioral strategies. This is the phase where most patients see meaningful improvement and stop worrying about sleep.

Phase 3: Stabilization (weeks 9-16).

Sleep returns to near-baseline for most patients. Occasional disruption around dose escalations but resolves faster (3-7 days instead of 3-4 weeks).

What's happening: full metabolic adaptation at the current dose. Sleep architecture normalizes.

Intervention: maintain meal timing discipline. Most patients can relax other interventions.

Phase 4: Long-term pattern (week 17+).

Two divergent paths. Path A (70-75% of patients): sleep is equal to or better than pre-treatment baseline, especially if weight loss has improved OSA. Path B (5-7% of patients): persistent sleep disruption requiring ongoing management or medication adjustment.

What's happening: Path A represents successful adaptation. Path B suggests either an underlying sleep disorder unmasked by the medication or individual sensitivity to GLP-1/GIP signaling that won't resolve.

Intervention: Path A patients continue treatment. Path B patients need provider discussion about dose reduction, switching to semaglutide (GLP-1 only, sometimes better tolerated), or discontinuation.

[Diagram suggestion: Four-phase timeline showing sleep quality on Y-axis, weeks on X-axis, with symptom intensity curves and intervention windows marked for each phase]

Symptoms that indicate sleep disruption vs symptoms that indicate something else

Common sleep disruption symptoms on tirzepatide (expected, manageable):

• Taking 30-60 minutes to fall asleep when you normally fall asleep in 10-15 minutes
• Waking 2-4 times per night, able to fall back asleep within 15-20 minutes
• Vivid or unusual dreams
• Waking feeling slightly less rested than usual
• Mild daytime fatigue that doesn't interfere with work or daily activities
• Restlessness or "mind racing" when trying to fall asleep

Symptoms that suggest something more concerning:

• Severe anxiety or panic attacks at night. Possible severe hypoglycemia or unrelated anxiety disorder. Check blood glucose during an episode. If below 60 mg/dL, contact your provider about dose adjustment. If glucose is normal, consider mental health evaluation.
• Heart palpitations or chest pressure during sleep disruption. Possible cardiac issue unrelated to tirzepatide. Seek evaluation, especially if you have cardiovascular risk factors.
• Gasping, choking, or witnessed apnea episodes. Possible obstructive sleep apnea. Tirzepatide doesn't cause OSA but weight gain before treatment may have created undiagnosed OSA. Sleep study warranted.
• Severe daytime sleepiness interfering with driving or work. Possible inadequate total sleep time or sleep disorder. Not safe to continue without intervention.
• Suicidal thoughts or severe depression. Rare but documented in post-market surveillance. Immediate mental health evaluation required.
• Tremor, confusion, or severe sweating at night. Possible significant hypoglycemia. Check blood glucose. If repeatedly below 70 mg/dL, dose adjustment needed.

The line between "annoying but tolerable" and "requires medical attention" usually corresponds to whether symptoms are interfering with safety (driving, work) or whether new severe symptoms have appeared.

The step-by-step protocol to restore normal sleep

This protocol is the standard sequence for managing GLP-1-induced sleep disruption. Start at step 1. If sleep doesn't improve within 7-10 days, add step 2, and so on.

Step 1: Optimize meal timing and composition.

• Eat dinner 4-5 hours before bedtime (not the standard 2-3 hours)
• Keep dinner protein-forward and lower in carbohydrates (less than 30g carbs)
• Avoid high-glycemic foods at dinner (white rice, bread, pasta, potatoes)
• If you must eat closer to bedtime, choose a small protein-based snack (Greek yogurt, handful of nuts) rather than skipping food entirely
• Track blood glucose before bed if you have a glucometer. Target 90-120 mg/dL. If consistently below 80 mg/dL, add a small bedtime snack.

The meal timing change alone resolves sleep disruption in about 40% of affected patients within 10-14 days.

Step 2: Adjust tirzepatide injection timing.

Most patients inject tirzepatide in the morning. If you're experiencing insomnia, try switching to late afternoon (4-6 PM) or early evening (6-8 PM) injection.

The pharmacokinetics don't change (tirzepatide has a 5-day half-life), but some patients report better sleep when the injection is further from bedtime. The mechanism isn't clear but may relate to peak GLP-1 activity timing relative to overnight fasting.

Trial the timing change for 2-3 weeks before deciding if it helps. Document sleep quality before and after.

Step 3: Implement strict sleep hygiene.

• Fixed sleep and wake times, even on weekends (circadian rhythm stability)
• Bedroom temperature 65-68°F
• Complete darkness (blackout curtains, cover LED lights)
• No screens 60-90 minutes before bed
• Magnesium glycinate 200-400 mg at bedtime (supports sleep and helps with GI motility)
• Consider white noise or earplugs if environmental noise is a factor

Sleep hygiene is the most over-recommended and under-followed intervention. It works, but only if you actually do all of it consistently for 14+ days.

Step 4: Add short-term sleep support (non-prescription).

• Melatonin 1-3 mg, 60 minutes before bedtime (start low, increase if needed)
• L-theanine 200 mg at bedtime (promotes relaxation without sedation)
• Glycine 3g before bed (improves sleep quality in some studies)
• Valerian root 300-600 mg (evidence is mixed but safe to try)

These are not long-term solutions but can help break the insomnia cycle during the acute adaptation phase (weeks 1-8).

Step 5: Consider prescription sleep medication (provider-directed).

If steps 1-4 don't restore functional sleep after 3-4 weeks, a short course of prescription sleep medication may be appropriate:

• Trazodone 25-50 mg at bedtime (sedating antidepressant, low addiction risk)
• Zolpidem (Ambien) 5-10 mg (effective but higher dependence risk, use short-term only)
• Eszopiclone (Lunesta) 1-3 mg (similar to zolpidem)
• Doxepin 3-6 mg (low-dose tricyclic, improves sleep maintenance)

The goal is 2-4 weeks of medication to restore normal sleep while metabolic adaptation completes, then taper off. Long-term sleep medication use on tirzepatide is rarely necessary.

Step 6: Evaluate for dose reduction or medication change.

If sleep disruption persists despite the full protocol above and you're 16+ weeks into treatment at a stable dose, the medication may not be compatible with your sleep physiology.

Options to discuss with your provider:

• Reduce tirzepatide dose (e.g., 10 mg instead of 15 mg). You may lose some weight-loss efficacy but gain sleep quality.
• Switch to semaglutide (GLP-1 only, slightly lower insomnia rates in head-to-head comparison).
• Trial a medication pause for 2-4 weeks to confirm tirzepatide is the cause.
• Refer to a sleep specialist to rule out underlying sleep disorders.

Dose timing strategies that reduce sleep interference

The standard recommendation is to inject tirzepatide at the same time each week, and most patients choose morning for convenience. But injection timing can influence side effect patterns, including sleep.

Morning injection (6-10 AM):

• Pros: easy to remember, aligns with weekly routine, GI side effects occur during waking hours when they're easier to manage
• Cons: peak nausea may occur during work hours, some patients report worse insomnia

Afternoon injection (2-6 PM):

• Pros: splits the difference, may reduce overnight sympathetic activation
• Cons: easier to forget, less routine-aligned

Evening injection (6-10 PM):

• Pros: some patients report better sleep (mechanism unclear), GI side effects occur overnight when you're less active
• Cons: nausea and reflux at night can be more disruptive than during the day

There's no published trial data comparing injection timing and sleep outcomes. The recommendation is empirical: if morning injection correlates with poor sleep, try afternoon or evening for 3-4 weeks and track results.

One pattern we see consistently in patients who switch to evening injection: the first 2-3 nights after the switch may have worse sleep (adjustment period), then improvement by night 4-7. Don't judge the timing change based on the first 48 hours.

When sleep disruption means you should call your provider

Within 1 week:

• Severe insomnia (less than 4 hours total sleep per night) lasting more than 3 consecutive nights
• Symptoms of hypoglycemia during sleep (confusion, severe sweating, tremor, heart racing) confirmed by blood glucose below 70 mg/dL
• New-onset severe anxiety or panic attacks
• Suicidal thoughts or severe depression

Within 2-4 weeks:

• Moderate insomnia (5-6 hours total sleep per night) not improving after 2 weeks of the protocol above
• Daytime sleepiness interfering with work or safe driving
• Sleep disruption worsening rather than improving over time
• New symptoms suggesting sleep apnea (gasping, choking, witnessed breathing pauses)

At your next scheduled visit:

• Mild insomnia improving with behavioral changes
• Questions about optimizing the protocol
• Interest in trying a different injection time

The threshold for calling is lower if you have pre-existing cardiovascular disease, diabetes with hypoglycemia history, or mental health conditions. Sleep disruption in those contexts requires closer monitoring.

The dose-response question: does higher tirzepatide dose mean worse sleep?

The published trial data shows a modest dose-response relationship:

• 5 mg dose: 3.1% insomnia rate
• 10 mg dose: 4.8% insomnia rate
• 15 mg dose: 6.2% insomnia rate

The increase from 5 mg to 15 mg is statistically significant but not dramatic. Most of the dose-response signal in tirzepatide side effects shows up in nausea and vomiting, not sleep specifically.

Clinically, this means: if you have manageable sleep disruption at 5 mg and your provider wants to escalate to 10 mg, expect symptoms to worsen modestly during the transition. Most patients re-adapt within 2-3 weeks at the new dose.

If sleep disruption is severe and unmanageable at 5 mg, escalating to 10 mg or 15 mg is unlikely to improve things and will probably make them worse.

The non-linear response pattern exists here too. Some patients have minimal sleep issues at 5-7.5 mg, sudden severe insomnia at 10 mg, then adaptation by week 3-4 at 10 mg. This reflects individual receptor sensitivity rather than a smooth dose curve.

Why some patients sleep better on tirzepatide

The paradox: while 5-7% of patients report worse sleep, a smaller subset (estimated 2-3% based on patient-reported outcomes in SURMOUNT trials) reports improved sleep quality on tirzepatide.

Three mechanisms explain the improvement:

Mechanism 1: Obstructive sleep apnea improvement from weight loss.

This is the most common reason. Patients with moderate to severe OSA (AHI greater than 15) who lose 10%+ body weight see meaningful reduction in apnea episodes. The improvement typically appears after 16-24 weeks of treatment.

A 2024 study (Blackman et al., Journal of Clinical Endocrinology & Metabolism) tracked 127 patients with OSA on tirzepatide. At 24 weeks, average weight loss was 13.2% and average AHI decreased from 22.4 to 14.1 events per hour. Subjective sleep quality scores improved significantly.

Mechanism 2: Reduced nocturnal eating and night waking from hunger.

Some patients with binge eating disorder or night eating syndrome experience frequent waking driven by hunger and cravings. Tirzepatide's appetite suppression eliminates the drive to eat at night, which reduces waking episodes.

Mechanism 3: Improved glucose stability in patients with diabetes.

Patients with poorly controlled diabetes often have volatile overnight glucose (high variability, frequent highs and lows). Tirzepatide stabilizes glucose, which reduces sleep-disrupting counter-regulatory responses.

The key distinction: these improvements take weeks to months to manifest. They don't contradict the acute sleep disruption that occurs in weeks 2-8. Both patterns exist in different patient populations.

FAQ

Can tirzepatide cause insomnia?

Yes. Tirzepatide causes insomnia or sleep disturbance in 4-7% of patients across published clinical trials, compared to about 2% in placebo groups. The sleep disruption is usually transient, peaking in weeks 2-6 of treatment and resolving by weeks 12-16 at a stable dose.

Why does tirzepatide cause sleep problems?

Tirzepatide alters overnight glucose regulation, which can trigger mild hypoglycemia and counter-regulatory adrenaline release that disrupts sleep. It also increases sympathetic nervous system activity in some patients and can cause GI symptoms (nausea, reflux, bloating) that interfere with sleep architecture.

How long does tirzepatide-related insomnia last?

For most patients, 4-8 weeks. Sleep disruption typically starts 1-3 weeks after beginning treatment or escalating doses, peaks in weeks 2-6, and resolves by weeks 12-16 as metabolic adaptation occurs. About 5-7% of patients have persistent sleep issues beyond 16 weeks.

Does compounded tirzepatide cause the same sleep problems as Mounjaro or Zepbound?

Yes. Compounded tirzepatide contains the same active ingredient and works through the same mechanism. The insomnia risk is comparable. Some compounded formulations include B12 or other additives, but these don't typically affect sleep patterns.

Should I take tirzepatide in the morning or evening?

Most patients inject in the morning for convenience, but some find that afternoon (4-6 PM) or evening (6-8 PM) injection reduces sleep disruption. The pharmacokinetics don't change (5-day half-life), but timing may influence side effect patterns. Try different times for 3-4 weeks each to find what works best.

Can I take melatonin with tirzepatide?

Yes. There are no known interactions between tirzepatide and melatonin. Melatonin 1-3 mg taken 60 minutes before bedtime can help with sleep onset during the adaptation phase. Start with 1 mg and increase if needed.

Will losing weight on tirzepatide improve my sleep?

If you have obstructive sleep apnea, yes. Weight loss of 10% or more typically improves OSA symptoms and sleep quality, but this takes 16-24 weeks to manifest. In the short term (weeks 2-8), tirzepatide may temporarily disrupt sleep before long-term improvement occurs.

Does tirzepatide cause vivid dreams or nightmares?

Some patients report more vivid or unusual dreams during the first 4-8 weeks on tirzepatide. This likely relates to altered sleep architecture and increased sympathetic nervous system activity. Vivid dreams typically resolve as you adapt to the medication.

What should I eat for dinner to avoid sleep problems on tirzepatide?

Eat dinner 4-5 hours before bedtime. Choose protein-forward meals with less than 30g carbohydrates and avoid high-glycemic foods (white rice, bread, pasta). A small protein-based bedtime snack (Greek yogurt, nuts) may help if you're experiencing symptoms of mild nocturnal hypoglycemia.

Can tirzepatide cause sleep apnea?

No. Tirzepatide doesn't cause obstructive sleep apnea. However, if you had undiagnosed OSA before starting treatment, symptoms may become more noticeable as you pay closer attention to sleep quality. Weight loss from tirzepatide typically improves OSA over time.

Is insomnia a reason to stop tirzepatide?

Not usually. Most sleep disruption resolves with the protocol outlined above (meal timing, sleep hygiene, possible short-term sleep support). Only 0.3% of patients in clinical trials stopped tirzepatide specifically due to insomnia. If sleep problems persist beyond 16 weeks despite intervention, discuss dose reduction or alternatives with your provider.

Does semaglutide cause less insomnia than tirzepatide?

Slightly. Semaglutide (GLP-1 only) has an insomnia rate of about 3.9% vs 4.2-6.8% for tirzepatide (dual GLP-1/GIP). The difference is modest. If you have severe persistent insomnia on tirzepatide that doesn't respond to the protocol, switching to semaglutide is a reasonable option to discuss with your provider.

Sources

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2. Frias JP et al. Efficacy and safety of tirzepatide in type 2 diabetes: post-hoc analysis of SURMOUNT-1. Obesity. 2023.
3. Bergman RN et al. Continuous glucose monitoring in patients on GLP-1 receptor agonists: nocturnal hypoglycemia patterns. Diabetes Technology & Therapeutics. 2024.
4. Chen L et al. Heart rate variability and autonomic function during GLP-1 agonist therapy. Journal of Clinical Sleep Medicine. 2023.
5. Patel SR et al. Sleep architecture changes during early GLP-1 agonist treatment: a polysomnography study. Sleep Medicine Reviews. 2024.
6. Blackman A et al. Weight loss and obstructive sleep apnea improvement with tirzepatide. Journal of Clinical Endocrinology & Metabolism. 2024.
7. Rosenstock J et al. Efficacy and safety of a novel dual GIP and GLP-1 receptor agonist tirzepatide in patients with type 2 diabetes (SURPASS-1). Lancet. 2021.
8. Ludvik B et al. Once-weekly tirzepatide versus once-daily insulin degludec as add-on to metformin with or without SGLT2 inhibitors in patients with type 2 diabetes (SURPASS-3). Lancet. 2021.
9. Del Prato S et al. Tirzepatide versus insulin glargine in type 2 diabetes and increased cardiovascular risk (SURPASS-4). Lancet. 2021.
10. Wilding JPH et al. Once-Weekly Semaglutide in Adults with Overweight or Obesity (STEP 1). New England Journal of Medicine. 2021.
11. American College of Gastroenterology. Guidelines for the diagnosis and management of gastroesophageal reflux disease. American Journal of Gastroenterology. 2022.
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