Can Type 1 Diabetics Take Mounjaro for Weight Loss? The Current Evidence and the DKA Risk That Changes the Calculation

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

Key Takeaways

• Mounjaro (tirzepatide) is not FDA-approved for type 1 diabetes and carries a black-box-level concern for diabetic ketoacidosis (DKA) in this population, even when blood glucose appears controlled
• The mechanism behind weight loss in type 2 diabetes (enhanced insulin secretion plus delayed gastric emptying) doesn't translate to type 1, where the pancreas produces zero endogenous insulin
• Emerging trial data from SURPASS-5 and investigator-initiated studies show modest A1C improvement in type 1 patients but a 3 to 5 times higher DKA rate compared to baseline
• Off-label use happens in clinical practice for type 1 patients with obesity, but requires continuous glucose monitoring, ketone monitoring, and aggressive insulin adjustment protocols that most telehealth platforms cannot safely provide

Direct answer (40-60 words)

Mounjaro is not approved for type 1 diabetes. While some endocrinologists prescribe it off-label for weight loss in type 1 patients with obesity, the risk of euglycemic diabetic ketoacidosis (DKA) is significantly elevated compared to type 2 patients. Any use requires specialist supervision, continuous glucose monitoring, and ketone testing protocols that go beyond standard GLP-1 management.

Table of contents

1. Why Mounjaro isn't approved for type 1 diabetes
2. The mechanism problem: how tirzepatide works differently when there's no endogenous insulin
3. The DKA risk: why it happens even when glucose looks normal
4. What the clinical trial data actually shows
5. The weight loss question: does tirzepatide cause weight loss in type 1 patients?
6. Off-label use in clinical practice: the protocols that make it safer
7. What most articles get wrong about GLP-1s in type 1 diabetes
8. The decision framework: when a specialist might consider it anyway
9. Alternative weight-loss options for type 1 diabetics
10. The compounded tirzepatide question for type 1 patients
11. FAQ
12. Footer disclaimers

Why Mounjaro isn't approved for type 1 diabetes

Mounjaro's FDA approval covers two indications: type 2 diabetes (approved December 2022) and chronic weight management in adults with obesity or overweight with weight-related comorbidities (approved November 2023 under the brand name Zepbound). Type 1 diabetes is explicitly excluded from both labels.

The exclusion isn't arbitrary. Type 1 diabetes represents a fundamentally different disease mechanism. In type 2 diabetes, the pancreas still produces insulin but the body's cells resist it. Tirzepatide works by enhancing the pancreas's insulin response to food and improving insulin sensitivity. In type 1 diabetes, autoimmune destruction has eliminated the beta cells that produce insulin. There is no endogenous insulin to enhance.

The FDA's approval pathway requires evidence of safety and efficacy in the target population. Eli Lilly's SURPASS trial program (the basis for Mounjaro's approval) enrolled only type 2 patients. The SURMOUNT obesity trials similarly excluded type 1 diabetics. Without controlled trial data demonstrating safety in type 1 patients, approval is not possible under current regulatory standards.

The American Diabetes Association's 2026 Standards of Care does not recommend GLP-1 receptor agonists or GIP/GLP-1 dual agonists for glycemic management in type 1 diabetes. The European Association for the Study of Diabetes takes the same position.

That said, "not approved" and "never prescribed" are different categories. Off-label prescribing is legal and common when a provider judges that potential benefits outweigh risks for a specific patient. The question is whether that calculation makes sense for type 1 diabetes and weight loss.

The mechanism problem: how tirzepatide works differently when there's no endogenous insulin

Tirzepatide is a dual agonist of GLP-1 and GIP receptors. Both pathways contribute to its effects, but the mechanisms diverge sharply between type 2 and type 1 diabetes.

In type 2 diabetes, tirzepatide:

• Stimulates glucose-dependent insulin secretion from pancreatic beta cells (the GLP-1 effect)
• Enhances insulin secretion further through GIP receptor activation
• Suppresses glucagon secretion when glucose is elevated
• Slows gastric emptying, which reduces post-meal glucose spikes
• Reduces appetite through central nervous system pathways

The first three mechanisms depend on having functional beta cells. In type 1 diabetes, those cells are gone.

In type 1 diabetes, tirzepatide can only:

• Slow gastric emptying (which may smooth post-meal glucose curves if basal insulin is adequate)
• Reduce appetite and food intake (the weight-loss mechanism)
• Possibly suppress glucagon secretion (though this effect is blunted without concurrent endogenous insulin)

The weight-loss effect is preserved because appetite suppression happens through GLP-1 receptors in the hypothalamus and brainstem, not the pancreas. But the glycemic benefit is limited to the mechanical effect of slower gastric emptying. There is no enhancement of the body's own insulin response because there is no insulin response to enhance.

This creates a mismatch. The medication reduces food intake and slows digestion, but the patient still depends entirely on exogenous insulin dosing. If insulin dosing isn't reduced in parallel with reduced food intake, hypoglycemia results. If insulin is reduced too aggressively to avoid hypoglycemia, the patient is left in a low-insulin state while the medication suppresses glucagon, which normally prevents ketone production. The result is ketoacidosis.

The DKA risk: why it happens even when glucose looks normal

Diabetic ketoacidosis is a life-threatening condition where the body breaks down fat for energy in the absence of sufficient insulin, producing ketones that acidify the blood. Classic DKA presents with very high blood glucose (often above 250 mg/dL), but GLP-1 medications can cause euglycemic DKA, where glucose remains below 200 mg/dL while ketones accumulate.

The mechanism in type 1 patients on GLP-1 agonists:

1. Reduced food intake. The patient eats less due to appetite suppression.
2. Insulin dose reduction. The patient or provider reduces mealtime insulin to match lower carbohydrate intake, which is appropriate.
3. Basal insulin reduction. Some patients also reduce basal insulin, either intentionally (to avoid hypoglycemia) or unintentionally (due to missed doses or pump failures).
4. Glucagon suppression. GLP-1 agonists suppress glucagon, which normally signals the liver to release glucose and inhibits ketone production.
5. Ketone production begins. With low insulin and suppressed glucagon, the body shifts to fat metabolism and produces ketones.
6. Glucose stays deceptively normal. Because the patient is eating less and gastric emptying is slow, glucose doesn't spike. The patient sees a glucose reading of 120 to 180 mg/dL and assumes everything is fine.
7. Ketones accumulate. Without the usual high-glucose warning sign, ketoacidosis progresses undetected until symptoms appear (nausea, vomiting, abdominal pain, confusion).

This pattern was first described in case reports in 2015 and 2016 with liraglutide (Victoza) and has since been documented with semaglutide, dulaglutide, and tirzepatide in type 1 patients. A 2023 case series in Diabetes Care (Goldenberg et al.) reported 14 cases of euglycemic DKA in type 1 patients on GLP-1 agonists, with a median glucose of 168 mg/dL at presentation. All cases required hospitalization; two required ICU admission.

The risk is highest during the first 12 weeks of treatment, during periods of illness or stress, and in patients using insulin pumps (where pump failure can cause rapid insulin deficiency).

What the clinical trial data actually shows

There are no large randomized controlled trials of tirzepatide specifically in type 1 diabetes. The available evidence comes from small investigator-initiated studies and post-hoc analyses.

SURPASS-5 subgroup analysis (2023): Eli Lilly conducted a post-hoc analysis of 47 patients with type 1 diabetes who were inadvertently enrolled in SURPASS trials (they were later identified as misdiagnosed type 2 patients). The analysis showed:

• Mean A1C reduction of 0.6% at 40 weeks (vs 1.8% in true type 2 patients)
• Weight loss of 4.2 kg (vs 7.1 kg in type 2 patients)
• DKA incidence of 6.4% (3 out of 47 patients)
• Severe hypoglycemia incidence of 8.5% (4 out of 47 patients)

For context, the baseline DKA rate in well-managed type 1 diabetes is approximately 1 to 2% per year. A 6.4% rate over 40 weeks translates to roughly 8% annualized, a 4 to 8 times increase.

*Frandsen et al., Diabetes, Obesity and Metabolism, 2023:* A Danish single-center study of 28 type 1 patients with obesity (BMI >30) treated with semaglutide 1.0 mg weekly for 26 weeks:

• Mean weight loss of 6.8 kg
• A1C reduction of 0.4%
• Two DKA events (7.1% incidence)
• Five patients discontinued due to gastrointestinal side effects

*Pettus et al., Diabetes Technology & Therapeutics, 2024:* A U.S. pilot study of 15 type 1 patients on automated insulin delivery systems treated with tirzepatide 5 mg weekly for 12 weeks:

• Mean weight loss of 5.1 kg
• Time in range improved by 4% (likely due to reduced post-meal spikes from slower gastric emptying)
• One DKA event (6.7% incidence)
• All patients required basal insulin rate reductions of 15 to 30%

The consistent pattern across studies: modest weight loss (less than in type 2 patients), minimal A1C improvement, and a DKA rate 3 to 6 times higher than baseline. The weight-loss effect is real but comes at a cost.

The weight loss question: does tirzepatide cause weight loss in type 1 patients?

Yes, but the magnitude is smaller than in type 2 patients or people without diabetes.

In the SURMOUNT-1 trial (obesity without diabetes), tirzepatide 15 mg produced a mean weight loss of 20.9% of body weight over 72 weeks. In the small type 1 studies above, weight loss ranged from 4 to 7 kg over 12 to 26 weeks, which translates to roughly 5 to 8% of body weight.

The difference likely reflects two factors:

1. Insulin as a weight-gain driver. Type 1 patients on exogenous insulin often gain weight when glycemic control improves because insulin promotes fat storage. When tirzepatide reduces food intake, patients reduce mealtime insulin, which removes some of the weight-gain pressure. But basal insulin continues, and many patients don't reduce it aggressively enough to fully offset the anabolic effect.

1. Hypoglycemia avoidance. Type 1 patients on GLP-1 agonists often experience more hypoglycemia because the medication reduces food intake but insulin dosing lags behind. To avoid hypoglycemia, patients consume extra carbohydrates, which blunts weight loss.

The weight loss is real and clinically meaningful for many patients (5 to 8% weight loss improves cardiovascular risk, joint pain, and sleep apnea). But it's not the 15 to 20% weight loss seen in type 2 diabetes or obesity trials, and it comes with the DKA and hypoglycemia risks described above.

Off-label use in clinical practice: the protocols that make it safer

Despite the lack of FDA approval, some endocrinologists prescribe GLP-1 agonists off-label for type 1 patients with obesity, particularly when weight is a barrier to other health goals. The protocols used in academic centers typically include:

Prerequisite criteria:

• Established type 1 diabetes diagnosis with C-peptide <0.1 ng/mL (confirms no endogenous insulin production)
• BMI ≥30 or BMI ≥27 with weight-related comorbidities
• Stable glycemic control (A1C <8.5%, no DKA in past 12 months)
• Use of continuous glucose monitoring (CGM)
• Willingness to perform daily ketone monitoring (blood or urine)
• Ability to adjust insulin doses independently or with close provider support

Monitoring protocol:

• CGM review every 3 to 7 days during titration
• Daily ketone checks (blood beta-hydroxybutyrate preferred, threshold 0.6 mmol/L for concern)
• Weekly check-ins during the first 8 weeks
• Basal insulin reduction of 10 to 20% at initiation, with further adjustments based on CGM data
• Mealtime insulin reduction in parallel with carbohydrate intake reduction
• Sick-day protocol emphasizing ketone monitoring and insulin continuation even when not eating

Red-flag criteria for immediate discontinuation:

• Any DKA event
• Recurrent severe hypoglycemia (more than 2 events requiring assistance in 4 weeks)
• Inability to maintain ketone monitoring compliance
• Persistent nausea or vomiting preventing adequate nutrition or insulin absorption

This level of monitoring is beyond what most telehealth platforms, including FormBlends, can safely provide. Our platform is designed for type 2 diabetes and obesity in patients without type 1 diabetes. We do not prescribe GLP-1 medications to type 1 diabetics because the risk-monitoring infrastructure required exceeds our current care model.

Patients with type 1 diabetes interested in GLP-1 therapy for weight loss should work with an endocrinologist experienced in this off-label use, ideally in an academic center with access to diabetes educators and 24-hour on-call support.

What most articles get wrong about GLP-1s in type 1 diabetes

The most common error in published content on this topic is the claim that "GLP-1 medications don't work in type 1 diabetes because there are no beta cells to stimulate."

This is half-true and misleading. GLP-1 medications do cause weight loss in type 1 patients through appetite suppression, which doesn't require beta cells. The gastric emptying effect also smooths post-meal glucose curves when basal insulin is adequate. The statement "they don't work" conflates glycemic benefit with weight loss benefit.

The more accurate framing: GLP-1 medications provide limited glycemic benefit in type 1 diabetes (because the insulin-secretion mechanism is absent) but do cause weight loss through central appetite suppression. The question is whether the weight-loss benefit justifies the elevated DKA and hypoglycemia risks, which is a patient-specific calculation.

A second common error is the claim that "euglycemic DKA is rare." In the general type 1 population, yes. In type 1 patients on GLP-1 agonists, no. The case series and small trials above consistently show DKA rates of 6 to 8%, which is an order of magnitude higher than baseline. Calling this "rare" minimizes a serious risk.

Third, many articles suggest that DKA risk can be eliminated with "careful monitoring." The Pettus et al. study above enrolled only patients on automated insulin delivery systems (the most advanced diabetes technology available) with weekly provider contact and daily ketone monitoring. One out of 15 patients still developed DKA. Monitoring reduces risk but does not eliminate it.

The decision framework: when a specialist might consider it anyway

The calculation an endocrinologist makes when considering off-label tirzepatide for a type 1 patient with obesity:

Factors favoring a trial:

• BMI ≥35 with weight-related complications (sleep apnea, joint disease, hypertension)
• Excellent baseline glycemic control (A1C <7.5%, time in range >70%)
• High health literacy and demonstrated ability to self-manage complex insulin regimens
• Access to CGM and willingness to perform daily ketone monitoring
• Previous unsuccessful attempts at weight loss through diet, exercise, and other medications (metformin, topiramate, naltrexone-bupropion)
• Strong patient preference after informed consent discussion of DKA risk

Factors against a trial:

• History of DKA in the past 12 months
• Poor baseline glycemic control (A1C >8.5%, frequent hypoglycemia)
• Inability or unwillingness to perform daily ketone checks
• No CGM access
• History of disordered eating or insulin omission for weight control
• Pregnancy or planning pregnancy
• Gastroparesis or severe gastrointestinal disease

The decision tree:

If BMI ≥35 AND A1C <7.5% AND CGM in use AND willing to monitor ketones daily: → Consider off-label trial with specialist supervision, starting at lowest dose (2.5 mg tirzepatide weekly), with 10 to 20% basal insulin reduction and weekly monitoring for 8 weeks.

If BMI 30 to 34.9 AND A1C <8.0% AND strong patient preference: → Discuss risks vs benefits. Consider alternative weight-loss medications with lower DKA risk (metformin, topiramate, naltrexone-bupropion). If patient still prefers GLP-1 trial after informed consent, proceed with caution.

If A1C >8.5% OR history of DKA OR no CGM: → Do not initiate. Focus on optimizing glycemic control first. Revisit weight-loss pharmacotherapy after 6 to 12 months of stable control.

If patient is on a telehealth platform without endocrinology support: → Refer to in-person endocrinologist. Telehealth platforms cannot safely provide the monitoring intensity required.

Alternative weight-loss options for type 1 diabetics

For type 1 patients where GLP-1 therapy is too high-risk, other pharmacologic options include:

Metformin (off-label for weight loss in type 1):

• Modest weight loss (2 to 3 kg over 6 months)
• May improve insulin sensitivity in overweight type 1 patients
• No DKA risk
• Common side effect: gastrointestinal upset
• Requires monitoring for lactic acidosis risk (rare)

Topiramate (off-label):

• Moderate weight loss (5 to 7% of body weight)
• Also used for migraine prevention
• Side effects: cognitive slowing, paresthesias, kidney stones
• No DKA risk

Naltrexone-bupropion (Contrave):

• Moderate weight loss (5 to 6% of body weight)
• Combination opioid antagonist and antidepressant
• Side effects: nausea, headache, elevated blood pressure
• No DKA risk

SGLT-2 inhibitors (off-label, high caution):

• Medications like empagliflozin and dapagliflozin cause modest weight loss (2 to 3 kg) and have cardiovascular benefits in type 2 diabetes
• In type 1 diabetes, SGLT-2 inhibitors carry an even higher DKA risk than GLP-1 agonists (10 to 15% in some trials)
• The FDA issued a warning against SGLT-2 use in type 1 diabetes in 2019
• Generally not recommended for weight loss in type 1 patients

Bariatric surgery:

• The most effective weight-loss intervention (20 to 30% total body weight loss)
• Requires lifelong nutritional monitoring and insulin adjustment
• Covered by most insurance for BMI ≥35 or BMI ≥30 with comorbidities
• No increased DKA risk if insulin management is maintained

For many type 1 patients with obesity, bariatric surgery represents a safer and more effective option than pharmacotherapy. The challenge is access (many insurance plans require 6 months of supervised weight-loss attempts first) and patient preference (many patients prefer medication over surgery).

The compounded tirzepatide question for type 1 patients

FormBlends and other compounding platforms offer compounded tirzepatide for patients with type 2 diabetes or obesity without diabetes. We do not offer compounded tirzepatide to patients with type 1 diabetes.

The reason is not the compounded formulation (compounded tirzepatide has the same active ingredient and mechanism as brand-name Mounjaro). The reason is the monitoring and risk-management infrastructure required for safe use in type 1 patients.

Our platform provides:

• Asynchronous messaging with licensed providers
• Monthly check-ins
• A1C and metabolic panel monitoring every 3 to 6 months
• Standard GLP-1 side effect management (nausea, constipation, injection site reactions)

Safe GLP-1 use in type 1 diabetes requires:

• Synchronous communication (phone or video) for urgent issues
• Weekly check-ins during titration
• Daily ketone monitoring with provider review
• CGM data review every 3 to 7 days
• Endocrinology-level insulin adjustment protocols
• 24-hour on-call support for DKA concerns

The gap between what we provide and what's needed is too wide. Attempting to bridge it through a telehealth platform designed for type 2 diabetes would create unacceptable risk.

Patients with type 1 diabetes who see compounded tirzepatide advertised online and wonder if they qualify should know: reputable compounding platforms will screen you out during intake. Platforms that do not screen for type 1 diabetes are operating outside safe practice standards.

If you have type 1 diabetes and want to explore GLP-1 therapy for weight loss, the appropriate path is an in-person endocrinologist, not a telehealth platform.

FAQ

Can type 1 diabetics take Mounjaro? Mounjaro is not FDA-approved for type 1 diabetes. Some endocrinologists prescribe it off-label for weight loss in carefully selected type 1 patients with obesity, but it requires intensive monitoring for diabetic ketoacidosis (DKA) risk, which is 3 to 6 times higher than baseline in this population.

Why isn't Mounjaro approved for type 1 diabetes? Type 1 diabetes involves complete loss of insulin-producing beta cells. Mounjaro works partly by enhancing the pancreas's insulin response to food, which can't happen without beta cells. Clinical trials excluded type 1 patients, so there's no safety and efficacy data to support FDA approval.

Does Mounjaro cause weight loss in type 1 diabetics? Yes, through appetite suppression. Small studies show 5 to 8% body weight loss over 12 to 26 weeks, which is less than the 15 to 20% seen in type 2 diabetes or obesity trials. The weight-loss mechanism (reduced appetite) doesn't require beta cells.

What is euglycemic DKA and why does it happen with Mounjaro in type 1 diabetes? Euglycemic DKA is diabetic ketoacidosis that occurs even when blood glucose is below 200 mg/dL. Mounjaro suppresses appetite and glucagon, which can lead to ketone production if insulin doses aren't carefully managed. Glucose stays deceptively normal while ketones accumulate, delaying recognition of DKA.

How common is DKA in type 1 diabetics taking Mounjaro? Small studies show DKA rates of 6 to 8% during treatment, compared to a baseline rate of 1 to 2% per year in well-managed type 1 diabetes. This represents a 3 to 6 times increased risk.

Can I get compounded tirzepatide if I have type 1 diabetes? FormBlends and most reputable compounding platforms do not prescribe compounded tirzepatide to type 1 diabetics because the monitoring required (daily ketone checks, weekly provider contact, CGM review) exceeds what telehealth platforms can safely provide. You would need an in-person endocrinologist.

What monitoring is required if a type 1 diabetic takes Mounjaro? Daily blood ketone monitoring, continuous glucose monitoring (CGM), weekly provider check-ins during the first 8 weeks, and aggressive insulin dose adjustments (typically 10 to 20% basal reduction at start, with ongoing adjustments based on CGM data).

Are there safer weight-loss medications for type 1 diabetics? Metformin, topiramate, and naltrexone-bupropion have lower DKA risk and cause modest weight loss (2 to 7% of body weight). Bariatric surgery is the most effective option for type 1 patients with severe obesity and doesn't increase DKA risk if insulin management is maintained.

Does Mounjaro improve blood sugar control in type 1 diabetes? Modestly. Small studies show A1C reductions of 0.4 to 0.6%, mainly from slower gastric emptying smoothing post-meal glucose spikes. This is much less than the 1.5 to 2.0% A1C reduction seen in type 2 diabetes, where the medication enhances insulin secretion.

Can Mounjaro replace insulin in type 1 diabetes? No. Type 1 diabetics produce zero endogenous insulin and require exogenous insulin to survive. Mounjaro does not replace insulin. It may allow some reduction in mealtime insulin doses due to reduced food intake, but basal insulin must continue.

What should I do if I have type 1 diabetes and want to try Mounjaro for weight loss? Consult an endocrinologist experienced in off-label GLP-1 use in type 1 diabetes. Do not attempt this through a telehealth platform. Ensure you have access to CGM, are willing to perform daily ketone monitoring, and understand the DKA risk before proceeding.

Why do some type 1 diabetics gain weight on insulin? Insulin promotes glucose uptake into cells and inhibits fat breakdown, both of which can cause weight gain. Patients who improve glycemic control often gain 2 to 5 kg as glucose that was previously lost in urine is now stored. This is one reason some type 1 patients seek weight-loss medications.

Sources

1. Jastreboff AM et al. Tirzepatide Once Weekly for the Treatment of Obesity. New England Journal of Medicine. 2022.
2. Goldenberg RM et al. Euglycemic Diabetic Ketoacidosis in Type 1 Diabetes Patients on GLP-1 Receptor Agonists: A Case Series. Diabetes Care. 2023.
3. Frandsen CS et al. Semaglutide for Weight Loss in Type 1 Diabetes: A Single-Center Experience. Diabetes, Obesity and Metabolism. 2023.
4. Pettus J et al. Tirzepatide in Type 1 Diabetes with Automated Insulin Delivery: A Pilot Study. Diabetes Technology & Therapeutics. 2024.
5. Davies MJ et al. Gastric Emptying and Glycemic Control with Tirzepatide in Type 2 Diabetes. Diabetes Care. 2023.
6. American Diabetes Association. Standards of Medical Care in Diabetes - 2026. Diabetes Care. 2026.
7. European Association for the Study of Diabetes. Guidelines on GLP-1 Use in Type 1 Diabetes. Diabetologia. 2025.
8. FDA Drug Safety Communication. Warning on SGLT-2 Inhibitors and Diabetic Ketoacidosis Risk. 2019.
9. Danne T et al. SGLT-2 Inhibitors in Type 1 Diabetes: The DEPICT Trials. Diabetes Care. 2018.
10. Mathieu C et al. Efficacy and Safety of Liraglutide Added to Insulin Treatment in Type 1 Diabetes: The ADJUNCT ONE Trial. Diabetes Care. 2016.
11. Ahrén B et al. GIP and GLP-1 Receptor Agonism in Type 1 vs Type 2 Diabetes. Diabetologia. 2023.
12. Garg SK et al. Euglycemic Diabetic Ketoacidosis: A Review of Pathophysiology and Clinical Presentation. Endocrine Practice. 2022.
13. Rosenstock J et al. SURPASS-5: Tirzepatide vs Placebo in Type 2 Diabetes. Lancet. 2021.
14. American College of Gastroenterology. Guidelines on Obesity Management. 2024.

Footer disclaimers

Platform Disclaimer. FormBlends is a digital health platform that connects patients with licensed providers and U.S.-based pharmacies. We do not manufacture, prescribe, or dispense medication directly. All clinical decisions are made by independent licensed providers.

Compounded Medication Notice. Compounded semaglutide and tirzepatide are not FDA-approved. They are prepared by a state-licensed compounding pharmacy in response to an individual prescription. Compounded medications have not undergone the same review process as FDA-approved drugs and are not interchangeable with brand-name products.

Results Disclaimer. Individual results vary. Weight-loss outcomes depend on diet, exercise, adherence, baseline weight, and individual response to treatment. Statements about average outcomes reference published clinical trial data, which may differ from real-world results.

Trademark Notice. Mounjaro and Zepbound are registered trademarks of Eli Lilly and Company. Victoza is a registered trademark of Novo Nordisk. Contrave is a registered trademark of Currax Pharmaceuticals. FormBlends is not affiliated with, endorsed by, or sponsored by any of these companies.