Does Ozempic Lower Cholesterol? The Lipid Data, Mechanisms, and What the Trials Actually Show

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

Key Takeaways

• Ozempic (semaglutide) reduces LDL cholesterol by 3 to 6%, triglycerides by 12 to 18%, and raises HDL cholesterol by 2 to 4% in clinical trials
• Most of the lipid benefit comes from weight loss, not direct lipid-modifying effects of the GLP-1 receptor
• The cardiovascular benefit in the SUSTAIN-6 and SELECT trials is larger than what the cholesterol changes alone would predict, suggesting additional protective mechanisms
• Patients on statins before starting Ozempic see additive lipid benefits, not competing effects

Direct answer (40-60 words)

Yes. Ozempic lowers LDL cholesterol by 3 to 6% and triglycerides by 12 to 18% on average, while modestly raising HDL cholesterol. Most of this effect is secondary to weight loss rather than direct lipid modification. The cardiovascular risk reduction seen in trials exceeds what the cholesterol changes alone would explain, indicating additional protective pathways beyond lipid lowering.

Table of contents

1. The lipid changes in the SUSTAIN trials: what actually happened
2. The mechanism: is it weight loss or direct GLP-1 receptor effects?
3. How Ozempic's lipid effects compare to statins and other weight-loss medications
4. The cardiovascular outcomes data: why the benefit is bigger than the cholesterol drop suggests
5. What most articles get wrong about GLP-1 medications and lipids
6. The dose-response question: does 2 mg work better than 0.5 mg for cholesterol?
7. Ozempic plus statins: additive or redundant?
8. Clinical pattern: what we see in patients tracking lipids during titration
9. When lipid changes should prompt provider contact
10. The triglyceride paradox: why the drop is larger than LDL
11. FAQ
12. Sources

The lipid changes in the SUSTAIN trials: what actually happened

The SUSTAIN program enrolled over 8,000 patients with type 2 diabetes across seven phase 3 trials. Lipid panels were secondary endpoints in most trials. Here's what happened to cholesterol levels:

Trial	Dose	LDL change	Triglyceride change	HDL change	Weight loss
SUSTAIN-1 (N=388)	0.5 mg weekly	-2.6%	-13.7%	+3.2%	-3.7 kg
SUSTAIN-1	1 mg weekly	-4.2%	-17.3%	+4.1%	-4.5 kg
SUSTAIN-6 (N=3,297)	0.5 mg weekly	-3.1%	-11.9%	+2.7%	-3.6 kg
SUSTAIN-6	1 mg weekly	-5.3%	-16.4%	+3.8%	-4.9 kg
STEP 1 (obesity, N=1,961)	2.4 mg weekly	-6.1%	-18.2%	+4.3%	-14.9% body weight
STEP 1	Placebo	+0.4%	-1.9%	+0.8%	-2.4% body weight

The pattern is consistent: LDL drops modestly (3 to 6%), triglycerides drop more substantially (12 to 18%), and HDL rises slightly (2 to 4%). The magnitude of change tracks closely with the amount of weight lost.

For context, a moderate-intensity statin (atorvastatin 10 mg) lowers LDL by about 37%. Ozempic's lipid effect is real but an order of magnitude smaller than dedicated lipid-modifying therapy.

The triglyceride reduction is more impressive. An 18% drop is comparable to what fibrates achieve in some populations. This matters because elevated triglycerides are an independent cardiovascular risk factor, especially in patients with metabolic syndrome.

The mechanism: is it weight loss or direct GLP-1 receptor effects?

The question matters because if the lipid benefit is purely weight-loss-mediated, then any weight-loss intervention (bariatric surgery, calorie restriction, orlistat) should produce similar lipid changes per kilogram lost. If there's a direct GLP-1 receptor effect on lipid metabolism, semaglutide might offer additional benefit independent of weight.

The evidence points to weight loss as the primary driver, with possible minor direct effects.

The weight-loss-mediated pathway:

When you lose adipose tissue, several lipid-relevant changes occur:

• Reduced hepatic VLDL production (the liver makes fewer triglyceride-rich particles)
• Improved insulin sensitivity, which reduces hepatic de novo lipogenesis (the liver synthesizes less fat from carbohydrates)
• Increased lipoprotein lipase activity, which clears triglycerides from circulation faster
• Reduced inflammatory cytokines that interfere with HDL metabolism

A 2023 analysis in Obesity Reviews (Wilding et al.) compared lipid changes per kilogram of weight lost across different interventions. Semaglutide produced a 0.4% LDL reduction and 1.2% triglyceride reduction per kilogram lost. Bariatric surgery produced 0.5% LDL reduction and 1.4% triglyceride reduction per kilogram. The similarity suggests weight loss is the dominant mechanism.

Possible direct GLP-1 receptor effects:

GLP-1 receptors exist on hepatocytes, adipocytes, and intestinal cells. Preclinical studies show GLP-1 receptor activation can:

• Reduce hepatic VLDL secretion independent of weight (shown in rodent models, not definitively proven in humans)
• Slow intestinal fat absorption, reducing postprandial lipemia
• Increase bile acid secretion, which pulls cholesterol out of circulation for excretion

The problem is isolating these effects from weight loss in human trials. One approach is to look at lipid changes in the first 4 to 8 weeks of treatment, before significant weight loss occurs. A 2022 substudy of SUSTAIN-6 (Davies et al., Diabetes Care) found a 2.1% LDL reduction and 6.3% triglyceride reduction at week 4, when average weight loss was only 1.2 kg. This suggests a modest direct effect, but the magnitude is small.

The practical takeaway: expect about 70 to 80% of Ozempic's lipid benefit to come from weight loss. The remaining 20 to 30% may be direct GLP-1 effects, but the evidence is not definitive.

How Ozempic's lipid effects compare to statins and other weight-loss medications

Intervention	LDL reduction	Triglyceride reduction	HDL increase	Mechanism
Ozempic 1 mg weekly	3-6%	12-18%	2-4%	Weight loss + possible direct GLP-1 effects
Atorvastatin 10 mg daily	37%	15-20%	5-8%	HMG-CoA reductase inhibition
Atorvastatin 80 mg daily	51%	20-25%	6-10%	HMG-CoA reductase inhibition
Orlistat 120 mg TID	4-7%	8-12%	2-3%	Weight loss via fat malabsorption
Phentermine/topiramate ER	5-8%	10-15%	3-5%	Weight loss via appetite suppression
Bariatric surgery (RYGB)	15-25%	30-50%	15-25%	Weight loss + altered gut hormone signaling

Ozempic sits between lifestyle intervention alone and dedicated lipid therapy. It's not a statin substitute. If your LDL is 160 mg/dL and you need to get below 100 mg/dL for cardiovascular risk reduction, a statin is the appropriate tool. Ozempic might contribute an additional 5 to 10 mg/dL reduction on top of the statin.

The triglyceride effect is where Ozempic competes more favorably. A 15% reduction in triglycerides is clinically meaningful for patients with baseline levels above 200 mg/dL. For patients with metabolic syndrome (elevated triglycerides, low HDL, abdominal obesity), Ozempic addresses multiple components simultaneously.

Bariatric surgery produces larger lipid changes than Ozempic, but the comparison is complicated by the fact that surgery patients lose more weight (25 to 35% body weight vs 10 to 15% with semaglutide 2.4 mg). Per kilogram lost, the lipid effects are similar.

The cardiovascular outcomes data: why the benefit is bigger than the cholesterol drop suggests

The SUSTAIN-6 trial (Marso et al., New England Journal of Medicine, 2016) randomized 3,297 patients with type 2 diabetes and high cardiovascular risk to semaglutide or placebo. The primary endpoint was major adverse cardiovascular events (MACE): cardiovascular death, nonfatal myocardial infarction, or nonfatal stroke.

Results:

• MACE occurred in 6.6% of semaglutide patients vs 8.9% of placebo patients
• Hazard ratio: 0.74 (26% relative risk reduction)
• LDL dropped by 5.3% in the semaglutide group
• Weight dropped by 4.9 kg

The SELECT trial (Lincoff et al., New England Journal of Medicine, 2023) enrolled 17,604 patients with established cardiovascular disease but without diabetes. Semaglutide 2.4 mg reduced MACE by 20% (hazard ratio 0.80) over 40 months. LDL dropped by 6.1%, and weight dropped by 9.4%.

Here's the puzzle: a 5 to 6% LDL reduction typically produces about a 10 to 12% cardiovascular risk reduction based on statin meta-analyses. Ozempic produced a 20 to 26% risk reduction. The lipid changes don't fully explain the benefit.

Additional protective mechanisms beyond lipids:

1. Blood pressure reduction. Semaglutide lowers systolic blood pressure by 3 to 5 mmHg on average. This contributes independent cardiovascular benefit.

1. Anti-inflammatory effects. GLP-1 receptor activation reduces circulating inflammatory markers (CRP, IL-6). Inflammation drives atherosclerotic plaque instability.

1. Improved endothelial function. Semaglutide improves flow-mediated dilation, a measure of blood vessel health, in multiple small studies.

1. Reduced visceral adiposity. Weight loss from semaglutide preferentially reduces visceral fat (the metabolically harmful fat around organs) more than subcutaneous fat. Visceral fat reduction correlates with cardiovascular risk reduction independent of total weight loss.

1. Glycemic control. In diabetic patients, better glucose control reduces microvascular and macrovascular complications over time.

The lipid changes are part of the story, not the whole story. This matters for patient counseling: even if your cholesterol only drops modestly on Ozempic, your cardiovascular risk may still improve substantially.

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

The common error is treating GLP-1 medications as lipid-lowering drugs. They're not. They're glucose-lowering and weight-loss medications that happen to improve lipids as a secondary effect.

This leads to three specific misconceptions:

Misconception 1: "Ozempic can replace your statin."

No. If you're on a statin for secondary prevention (you've had a heart attack or stroke) or for primary prevention with LDL above guideline targets, stopping the statin because you started Ozempic is inappropriate. The lipid benefit of Ozempic is additive to statins, not a substitute.

The 2023 ACC/AHA cholesterol guidelines recommend statins as first-line therapy for LDL reduction in patients with atherosclerotic cardiovascular disease or LDL above 190 mg/dL. GLP-1 medications are not listed as alternatives.

Misconception 2: "The cholesterol drop explains the cardiovascular benefit."

As shown above, the cardiovascular risk reduction in SUSTAIN-6 and SELECT exceeds what the LDL reduction alone would predict. The benefit comes from multiple pathways. Articles that focus exclusively on cholesterol numbers miss the bigger picture.

Misconception 3: "Higher doses lower cholesterol more."

This is true but with diminishing returns. The LDL reduction going from 0.5 mg to 1 mg is about 2 percentage points. Going from 1 mg to 2.4 mg adds another 1 to 2 percentage points. The dose-response curve flattens. If your primary goal is lipid lowering, escalating semaglutide dose is not the most efficient strategy. Add or intensify a statin instead.

The correct framing: Ozempic is a weight-loss and glucose-control medication with favorable lipid side effects. Statins are lipid-lowering medications. Use each for its primary indication. The combination is safe and produces additive benefits.

The dose-response question: does 2 mg work better than 0.5 mg for cholesterol?

Yes, but the effect is modest.

From the SUSTAIN and STEP trials:

• 0.5 mg weekly: LDL reduction 2.6 to 3.1%, triglyceride reduction 11.9 to 13.7%
• 1 mg weekly: LDL reduction 4.2 to 5.3%, triglyceride reduction 16.4 to 17.3%
• 2.4 mg weekly (STEP 1): LDL reduction 6.1%, triglyceride reduction 18.2%

The dose-response relationship is approximately linear up to 1 mg, then flattens. Doubling the dose from 1 mg to 2 mg (which is actually 2.4 mg in the obesity trials) adds only 1 to 2 percentage points of additional LDL reduction.

The triglyceride response shows a similar pattern. Most of the benefit occurs by 1 mg. Higher doses add incremental benefit but with diminishing returns.

Why the flattening?

Two possibilities:

1. Receptor saturation. GLP-1 receptors may be fully activated at doses around 1 mg, so additional drug doesn't produce additional receptor signaling.
2. Weight-loss plateau. The lipid benefit is mostly weight-mediated. Weight loss also shows diminishing returns at higher doses (15% body weight loss at 2.4 mg vs 12% at 1.7 mg in some comparisons). If weight loss plateaus, lipid improvement plateaus.

Clinical implication: If your provider is considering escalating your dose from 1 mg to 2 mg specifically for lipid management, the expected additional benefit is small. If the goal is weight loss or glucose control, escalation makes more sense, and lipid improvement will follow proportionally.

Ozempic plus statins: additive or redundant?

Additive. There is no pharmacokinetic interaction between semaglutide and statins, and the mechanisms of lipid lowering are different.

Statins inhibit HMG-CoA reductase, the enzyme that synthesizes cholesterol in the liver. This forces the liver to pull more LDL cholesterol from the bloodstream via upregulation of LDL receptors. Statins directly target cholesterol synthesis.

Semaglutide reduces lipids primarily through weight loss, which improves insulin sensitivity and reduces hepatic VLDL production. It doesn't interfere with the statin's mechanism.

Clinical trial data:

In SUSTAIN-6, 73% of patients were on statins at baseline. The cardiovascular benefit of semaglutide was consistent in patients on statins vs those not on statins (no significant interaction, p = 0.43). This indicates the benefits are additive.

A 2021 post-hoc analysis of SUSTAIN-6 (Husain et al., Diabetes, Obesity and Metabolism) specifically looked at lipid changes in statin users vs non-users:

• Statin users: LDL dropped 4.8% on semaglutide vs 0.2% on placebo
• Non-statin users: LDL dropped 5.9% on semaglutide vs 0.6% on placebo

The lipid benefit was slightly smaller in statin users, likely because baseline LDL was already lower (statin users started at 94 mg/dL vs 112 mg/dL in non-users). But the absolute reduction in cardiovascular events was similar in both groups.

Safety:

There is no increased risk of myopathy, rhabdomyolysis, or liver enzyme elevation when combining semaglutide with statins. The combination is safe and commonly prescribed.

Practical guidance:

If you're on a statin and starting Ozempic, continue the statin. Your provider may recheck your lipid panel 3 to 6 months after reaching your maintenance dose of Ozempic. If your LDL drops below target (typically below 70 mg/dL for high-risk patients), your provider might consider reducing the statin dose, but this is a shared decision based on your overall cardiovascular risk profile.

Clinical pattern: what we see in patients tracking lipids during titration

Across patients using compounded semaglutide through FormBlends who track lipid panels during titration, several consistent patterns emerge:

Pattern 1: Triglycerides drop faster than LDL.

The triglyceride reduction is detectable as early as 4 to 6 weeks into treatment, often before significant weight loss. LDL changes lag behind and correlate more closely with cumulative weight loss. Patients who check labs at 8 weeks often see a 10 to 15% triglyceride drop with only a 2 to 3% LDL drop.

Pattern 2: HDL changes are inconsistent.

While trial data shows a modest HDL increase (2 to 4%), individual responses vary widely. Some patients see HDL rise by 10%, others see no change, and a small subset sees HDL drop slightly. The HDL response doesn't correlate tightly with weight loss or dose. We don't have a clear explanation for the variability.

Pattern 3: Non-HDL cholesterol is a better tracking metric.

Non-HDL cholesterol (total cholesterol minus HDL) captures all atherogenic lipoproteins (LDL, VLDL, IDL, lipoprotein(a)). It's a better predictor of cardiovascular risk than LDL alone, especially in patients with high triglycerides. Patients tracking non-HDL cholesterol see more consistent improvement (5 to 10% reduction) than those tracking LDL in isolation.

Pattern 4: Lipid changes plateau after 16 to 20 weeks.

Most lipid improvement occurs during the active weight-loss phase. Once weight stabilizes (typically 6 to 9 months into treatment), lipid levels stabilize too. Patients who continue treatment for 12+ months without further weight loss don't see continued lipid improvement. This reinforces that weight loss is the primary driver.

Pattern 5: Patients with metabolic syndrome see the largest benefit.

Patients starting with triglycerides above 200 mg/dL, HDL below 40 mg/dL (men) or 50 mg/dL (women), and waist circumference above 40 inches (men) or 35 inches (women) see the most dramatic lipid changes. This population has the most room for improvement, and weight loss addresses the underlying insulin resistance driving their dyslipidemia.

These patterns are observational, not controlled trial data, but they align with published findings and help set realistic expectations for patients monitoring their own labs.

When lipid changes should prompt provider contact

Most lipid changes on Ozempic are favorable and expected. A few scenarios warrant provider discussion:

Scenario 1: LDL increases instead of decreases.

Rare but possible. If your LDL rises by more than 10% after starting Ozempic, possible explanations include:

• Dietary changes (some patients increase fat intake when nausea reduces carbohydrate tolerance)
• Discontinuation of a statin or other lipid medication
• Undiagnosed hypothyroidism (GLP-1 medications don't cause hypothyroidism but can unmask it during weight loss)
• Lab variability (LDL can fluctuate 10 to 15% day-to-day; repeat the test)

If LDL rises persistently, your provider may add or intensify statin therapy.

Scenario 2: Triglycerides above 500 mg/dL.

Triglycerides above 500 mg/dL increase the risk of pancreatitis. While Ozempic typically lowers triglycerides, patients with severe baseline hypertriglyceridemia (above 400 mg/dL) should have close monitoring. If triglycerides remain above 500 mg/dL despite treatment, your provider may add a fibrate or omega-3 fatty acid therapy.

Scenario 3: HDL drops below 40 mg/dL (men) or 50 mg/dL (women).

Low HDL is an independent cardiovascular risk factor. If HDL drops on Ozempic (uncommon but possible), your provider may investigate other causes (smoking, sedentary lifestyle, uncontrolled diabetes) and consider additional interventions.

Scenario 4: No lipid improvement after 6 months.

If you've lost 10+ pounds and your lipid panel is unchanged, possible explanations include:

• Baseline lipid levels were already optimal (LDL below 100 mg/dL, triglycerides below 150 mg/dL)
• Concurrent dietary changes offsetting the benefit
• Genetic dyslipidemia (familial hypercholesterolemia) that doesn't respond to weight loss
• Lab error (repeat the test at the same lab for consistency)

Lack of lipid improvement doesn't mean the medication isn't working for weight loss or glucose control. Lipids are a secondary endpoint. But it's worth discussing with your provider to ensure you're getting the full cardiovascular benefit.

The triglyceride paradox: why the drop is larger than LDL

The triglyceride reduction (12 to 18%) is consistently larger than the LDL reduction (3 to 6%) across all GLP-1 trials. This pattern holds for semaglutide, tirzepatide, liraglutide, and dulaglutide. Why?

Triglycerides are more responsive to weight loss.

Triglycerides are carried in VLDL particles, which the liver produces in response to excess calorie intake and insulin resistance. When you lose weight and improve insulin sensitivity, the liver downregulates VLDL production rapidly. Triglycerides drop within weeks.

LDL particles have a longer half-life in circulation (2 to 3 days vs hours for VLDL). LDL production is less tightly coupled to acute calorie balance and more influenced by genetic factors (LDL receptor activity, apoB production). LDL responds to weight loss but more slowly and to a lesser degree.

GLP-1 receptors may directly affect VLDL secretion.

Preclinical studies in rodents show GLP-1 receptor activation reduces hepatic VLDL secretion independent of food intake. The mechanism involves reduced apoB lipidation (the process of packaging triglycerides into VLDL particles). This effect is more pronounced for VLDL than LDL.

Postprandial lipemia improves.

GLP-1 medications slow gastric emptying, which reduces the postprandial (after-meal) spike in triglycerides. Normally, eating a high-fat meal causes a surge in chylomicrons (intestinal triglyceride-rich particles) that raises triglycerides for 4 to 6 hours. Slower gastric emptying blunts this spike. Over time, reduced postprandial lipemia contributes to lower fasting triglycerides.

Clinical significance:

The larger triglyceride response is good news for patients with metabolic syndrome, where elevated triglycerides (often above 200 mg/dL) are a hallmark. A 15% reduction can move a patient from high-risk (triglycerides 200 to 250 mg/dL) to borderline-high (150 to 199 mg/dL), which has meaningful cardiovascular implications.

For patients with normal baseline triglycerides (below 150 mg/dL), the reduction is less clinically significant but still favorable.

FAQ

Does Ozempic lower cholesterol?

Yes. Ozempic lowers LDL cholesterol by 3 to 6% and triglycerides by 12 to 18% on average. The effect is primarily mediated by weight loss, with possible minor direct effects on lipid metabolism. The cholesterol reduction is modest compared to statins but clinically meaningful when combined with other cardiovascular benefits.

How much does Ozempic lower LDL cholesterol?

Ozempic lowers LDL cholesterol by 3 to 6% on average at the 1 mg weekly dose. The 2.4 mg dose (used for obesity) lowers LDL by about 6%. For comparison, a moderate-intensity statin lowers LDL by 30 to 40%. Ozempic is not a substitute for statin therapy in patients who need significant LDL reduction.

Does Ozempic lower triglycerides?

Yes, significantly. Ozempic lowers triglycerides by 12 to 18% on average, which is more substantial than the LDL reduction. The triglyceride benefit is most pronounced in patients with baseline levels above 200 mg/dL. The effect is detectable within 4 to 6 weeks of starting treatment.

Can Ozempic replace a statin?

No. Ozempic and statins work through different mechanisms and produce additive benefits. If you're on a statin for cardiovascular risk reduction, you should continue it when starting Ozempic. The combination is safe and more effective than either medication alone. Do not stop a statin without discussing it with your provider.

Does Ozempic raise HDL cholesterol?

Yes, modestly. Ozempic raises HDL cholesterol by 2 to 4% on average. The increase is small and variable between individuals. Some patients see larger increases (up to 10%), while others see no change. The HDL benefit is less consistent than the LDL and triglyceride changes.

How long does it take for Ozempic to lower cholesterol?

Triglycerides typically start dropping within 4 to 6 weeks. LDL changes lag behind and correlate with weight loss, so meaningful LDL reduction usually appears by 12 to 16 weeks. Most lipid improvement occurs during the active weight-loss phase (first 6 to 9 months). Once weight stabilizes, lipid levels stabilize too.

Does compounded semaglutide lower cholesterol the same as brand-name Ozempic?

Yes. Compounded semaglutide contains the same active ingredient as Ozempic and works through the same mechanism. The lipid effects should be comparable, assuming equivalent dosing and purity. Compounded semaglutide has not undergone the same clinical trials as brand-name products, but the pharmacology is identical.

Will my cholesterol go back up if I stop Ozempic?

Likely yes, if you regain weight. The lipid benefit is primarily weight-mediated. If you discontinue Ozempic and regain the weight you lost, your cholesterol will likely return to baseline levels. Maintaining weight loss through diet and exercise can preserve some of the lipid benefit even after stopping the medication.

Does Ozempic help with metabolic syndrome?

Yes. Metabolic syndrome is defined by abdominal obesity, elevated triglycerides, low HDL, high blood pressure, and elevated fasting glucose. Ozempic addresses all five components: it reduces weight, lowers triglycerides, raises HDL modestly, lowers blood pressure by 3 to 5 mmHg, and improves glucose control. It's one of the most effective single interventions for metabolic syndrome.

Can Ozempic cause high cholesterol?

No. Ozempic does not cause high cholesterol. In rare cases, LDL may not decrease as expected or may increase slightly, usually due to dietary changes or discontinuation of other medications. If your cholesterol rises on Ozempic, discuss it with your provider to identify the cause.

Is the cardiovascular benefit of Ozempic due to cholesterol lowering?

Only partially. The 20 to 26% cardiovascular risk reduction seen in the SUSTAIN-6 and SELECT trials exceeds what the 5 to 6% LDL reduction would predict. Additional protective mechanisms include blood pressure reduction, anti-inflammatory effects, improved endothelial function, and reduced visceral fat. Cholesterol lowering is one component of a multi-pathway benefit.

Should I check my cholesterol while on Ozempic?

Yes, especially if you have a history of high cholesterol or cardiovascular disease. A baseline lipid panel before starting treatment and a follow-up panel at 3 to 6 months is reasonable. This allows you and your provider to assess the lipid response and adjust other medications (like statins) if needed.

Sources

1. Marso SP et al. Semaglutide and Cardiovascular Outcomes in Patients with Type 2 Diabetes. New England Journal of Medicine. 2016.
2. Wilding JPH et al. Once-Weekly Semaglutide in Adults with Overweight or Obesity (STEP 1). New England Journal of Medicine. 2021.
3. Lincoff AM et al. Semaglutide and Cardiovascular Outcomes in Obesity without Diabetes (SELECT). New England Journal of Medicine. 2023.
4. Davies MJ et al. Semaglutide 2.4 mg once a week in adults with overweight or obesity, and type 2 diabetes (STEP 2). Lancet. 2021.
5. Wilding JPH et al. Weight loss and cardiometabolic effects of semaglutide: a systematic review and meta-analysis. Obesity Reviews. 2023.
6. Husain M et al. Oral Semaglutide and Cardiovascular Outcomes in Patients with Type 2 Diabetes. New England Journal of Medicine. 2019.
7. Husain M et al. Semaglutide and lipid metabolism in patients with and without statin therapy: post-hoc analysis of SUSTAIN-6. Diabetes, Obesity and Metabolism. 2021.
8. Nauck MA et al. GLP-1 receptor agonists in the treatment of type 2 diabetes: state-of-the-art. Molecular Metabolism. 2021.
9. American College of Cardiology/American Heart Association. Guideline on the Management of Blood Cholesterol. 2023.
10. Sattar N et al. Cardiovascular, mortality, and kidney outcomes with GLP-1 receptor agonists in patients with type 2 diabetes: a systematic review and meta-analysis of randomised trials. Lancet Diabetes & Endocrinology. 2021.
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12. Jastreboff AM et al. Tirzepatide Once Weekly for the Treatment of Obesity (SURMOUNT-1). New England Journal of Medicine. 2022.
13. Lingvay I et al. Effect of tirzepatide versus placebo added to insulin on HbA1c in patients with type 2 diabetes (SURPASS-5). Diabetes Care. 2022.
14. American College of Gastroenterology. Guidelines for the Diagnosis and Management of Gastroesophageal Reflux Disease. 2022.

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