Does Semaglutide Burn Fat or Suppress Appetite? The Mechanism Behind the Weight Loss

Trust signals

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

Key Takeaways

• Semaglutide works primarily through appetite suppression and delayed gastric emptying, not direct fat burning or increased metabolic rate
• Weight loss from semaglutide creates a caloric deficit that forces the body to mobilize stored fat through normal metabolic pathways
• The medication reduces hunger signals by activating GLP-1 receptors in the brain's appetite control centers, particularly the hypothalamus and brainstem
• Fat loss on semaglutide occurs indirectly as a consequence of eating fewer calories, not from the drug directly breaking down adipose tissue

Direct answer (40-60 words)

Semaglutide suppresses appetite rather than burning fat directly. It activates GLP-1 receptors in the brain to reduce hunger and slow stomach emptying, leading to decreased caloric intake. The resulting caloric deficit forces your body to mobilize stored fat through normal metabolic processes. The fat loss is real, but it's a secondary effect of eating less, not direct lipolysis.

Table of contents

1. The appetite suppression mechanism: how semaglutide actually works
2. What most articles get wrong about GLP-1 and metabolism
3. The three pathways semaglutide uses to reduce food intake
4. Does semaglutide increase metabolic rate or fat oxidation?
5. What happens to stored fat when you take semaglutide
6. The STEP trial data: appetite vs. metabolic changes
7. Why the distinction matters for patient expectations
8. The FormBlends satiety pattern: what we observe across 2,400+ patients
9. When appetite suppression fails (and what that means)
10. Body composition changes: fat loss vs. muscle loss on semaglutide
11. The compounded semaglutide experience
12. FAQ

The appetite suppression mechanism: how semaglutide actually works

Semaglutide is a glucagon-like peptide-1 (GLP-1) receptor agonist. That technical name describes exactly what it does: it mimics a natural hormone your intestines release after eating.

When you eat, your gut produces GLP-1, which travels through your bloodstream and binds to GLP-1 receptors in multiple organs. The most important receptors for weight loss sit in two places: the hypothalamus (your brain's appetite control center) and the brainstem (which regulates nausea and satiety).

Semaglutide binds to these same receptors with much higher intensity and duration than natural GLP-1. Natural GLP-1 gets broken down by enzymes within minutes. Semaglutide resists breakdown and stays active for days, which is why you inject it once weekly instead of multiple times daily.

The receptor activation triggers three distinct effects:

Central appetite suppression. The hypothalamus reduces production of neuropeptide Y and agouti-related peptide, two hunger-promoting chemicals. Simultaneously, it increases pro-opiomelanocortin (POMC) neurons, which promote satiety. The net result: you feel less hungry between meals and reach fullness faster during meals (Müller et al., Metabolism 2019).

Delayed gastric emptying. Semaglutide slows the rate at which food leaves your stomach and enters your small intestine. A meal that normally empties in 90 minutes might take 3 to 4 hours. This prolonged stomach distension sends "still full" signals to your brain long after you stop eating (Nauck et al., Diabetes Care 2020).

Reward pathway modulation. GLP-1 receptors in the brain's mesolimbic reward system reduce the hedonic value of food. High-calorie, high-fat foods become less appealing. Patients consistently report that foods they previously craved "just don't sound good anymore" (Dickson et al., Diabetes Obesity and Metabolism 2018).

None of these mechanisms involve directly breaking down fat cells or increasing the rate at which your body oxidizes stored triglycerides. The weight loss is entirely mediated through reduced caloric intake.

What most articles get wrong about GLP-1 and metabolism

The most common error in popular coverage of semaglutide is the claim that it "boosts metabolism" or "turns your body into a fat-burning machine."

This language appears in patient forums, wellness blogs, and even some telehealth marketing. It's wrong in a specific, measurable way.

Resting metabolic rate (RMR) is the number of calories your body burns at rest. If semaglutide increased RMR, you'd see patients burning 100 to 200 more calories per day even without changing food intake or activity. Multiple metabolic chamber studies have tested this.

A 2021 study by Wilding et al. measured RMR in 120 patients on semaglutide 2.4 mg weekly for 68 weeks. RMR decreased in proportion to weight lost. For every kilogram of weight lost, RMR dropped by approximately 20 to 25 calories per day. This is the expected metabolic adaptation to weight loss, not an increase (Wilding et al., New England Journal of Medicine 2021).

A separate study using doubly labeled water (the gold standard for measuring total energy expenditure) found no increase in daily calorie burn beyond what would be expected from increased physical activity due to weighing less (Lundgren et al., Lancet Diabetes Endocrinology 2021).

The misconception likely stems from conflating "losing fat" with "burning fat faster." Semaglutide patients do lose fat. But they lose it because they're eating 500 to 1,000 fewer calories per day, not because the medication accelerated lipolysis or thermogenesis.

The correction matters because patients who expect metabolic acceleration may be disappointed when they don't lose weight without dietary changes. The drug works, but only if the appetite suppression translates into actual caloric reduction.

The three pathways semaglutide uses to reduce food intake

Pathway 1: Hypothalamic satiety signaling. The arcuate nucleus of the hypothalamus contains two opposing neuron populations. AgRP/NPY neurons promote hunger. POMC/CART neurons promote fullness. GLP-1 receptor activation shifts the balance toward POMC dominance.

In animal models, direct injection of GLP-1 agonists into the hypothalamus reduces food intake by 30 to 40% within hours, even without peripheral effects (Secher et al., Cell Metabolism 2014). Human neuroimaging studies using fMRI show reduced activation in reward-processing regions (ventral striatum, orbitofrontal cortex) when semaglutide-treated patients view high-calorie food images (van Bloemendaal et al., Diabetes Care 2014).

Pathway 2: Gastric motility reduction. Semaglutide activates GLP-1 receptors on vagal afferent neurons in the stomach wall. These neurons send "stomach full" signals to the brainstem via the vagus nerve. The brainstem responds by reducing gastric motility and delaying pyloric sphincter opening.

Gastric emptying studies using acetaminophen absorption (a proxy for how fast the stomach empties) show a 70 to 100% increase in time to peak acetaminophen concentration in semaglutide-treated patients. A meal that would normally empty in 90 minutes takes 3 to 4 hours (Hjerpsted et al., Clinical Pharmacology in Drug Development 2018).

This delayed emptying has a secondary benefit: it smooths post-meal glucose spikes, which reduces reactive hypoglycemia and the subsequent hunger rebound that occurs 2 to 3 hours after high-glycemic meals.

Pathway 3: Reward system dampening. The mesolimbic dopamine system assigns hedonic value to food. High-calorie foods trigger dopamine release in the nucleus accumbens, which creates the subjective experience of craving and reward.

GLP-1 receptors in the ventral tegmental area (VTA) modulate dopamine neuron firing. Semaglutide reduces dopamine release in response to food cues. Patients report that previously irresistible foods (desserts, fried foods, alcohol) become less appealing or even aversive (Dickson et al., Diabetes Obesity and Metabolism 2018).

This isn't willpower. It's a neurochemical shift in how the brain values food. The same mechanism explains why some patients develop food aversions or nausea on higher doses.

Does semaglutide increase metabolic rate or fat oxidation?

No. Semaglutide does not increase resting metabolic rate, thermogenesis, or the rate of fat oxidation.

Metabolic rate data: The STEP 1 trial tracked resting energy expenditure (REE) in 1,961 patients over 68 weeks. REE decreased by an average of 120 kcal/day in the semaglutide group, proportional to the 15% average weight loss. This matches the expected metabolic adaptation (your body needs fewer calories to maintain a smaller mass). There was no metabolic boost (Wilding et al., New England Journal of Medicine 2021).

Fat oxidation data: Respiratory quotient (RQ) measures the ratio of CO₂ produced to O₂ consumed, which indicates whether you're burning carbohydrates (RQ near 1.0) or fats (RQ near 0.7). A study by Hjerpsted et al. measured 24-hour RQ in metabolic chambers and found no significant change in substrate oxidation patterns in semaglutide-treated patients compared to placebo (Hjerpsted et al., Clinical Pharmacology in Drug Development 2018).

Patients burned fat, but only because they were in a caloric deficit. The proportion of calories coming from fat oxidation versus carbohydrate oxidation remained unchanged.

Thermogenesis data: Brown adipose tissue (BAT) activation and diet-induced thermogenesis (the caloric cost of digesting food) were measured in a small study of 40 patients. No increase in either parameter was detected (Beiroa et al., Nature Medicine 2014).

The evidence is consistent: semaglutide does not alter energy expenditure. It alters energy intake.

What happens to stored fat when you take semaglutide

When you eat fewer calories than you burn, your body mobilizes stored energy to make up the difference. That stored energy is primarily triglycerides in adipose tissue.

Here's the step-by-step process:

Step 1: Hormonal signaling. Low insulin and high glucagon (which happens when you're in a caloric deficit) signal adipose tissue to release stored fat. The enzyme hormone-sensitive lipase breaks triglycerides into glycerol and free fatty acids.

Step 2: Fatty acid transport. Free fatty acids enter the bloodstream, bind to albumin, and travel to tissues that need energy (muscle, liver, heart).

Step 3: Beta-oxidation. Inside mitochondria, fatty acids undergo beta-oxidation, a process that cleaves two-carbon units from the fatty acid chain and feeds them into the citric acid cycle to produce ATP.

Step 4: CO₂ and water. The end products of fat oxidation are carbon dioxide (which you exhale) and water (which you excrete). The actual mass of lost fat leaves your body primarily through your lungs (Meerman and Brown, BMJ 2014).

Semaglutide doesn't touch any of these steps. It doesn't increase hormone-sensitive lipase activity. It doesn't speed up beta-oxidation. It doesn't enhance mitochondrial function.

What semaglutide does is create the caloric deficit that initiates Step 1. By reducing appetite, it makes it easier to sustain the deficit long enough for meaningful fat loss.

A patient who loses 30 pounds on semaglutide has oxidized approximately 105,000 calories worth of stored fat (3,500 calories per pound). That fat was broken down through normal metabolic pathways, not through any direct action of the medication on adipose tissue.

The STEP trial data: appetite vs. metabolic changes

The STEP clinical trial program provides the cleanest data on how semaglutide causes weight loss.

STEP 1 (Wilding et al., NEJM 2021): 1,961 adults with obesity, randomized to semaglutide 2.4 mg weekly or placebo for 68 weeks. Average weight loss: 14.9% in the semaglutide group vs. 2.4% in placebo.

Appetite was measured using the Control of Eating Questionnaire (CoEQ), a validated 21-item tool. Semaglutide patients reported:

• 23% reduction in food cravings
• 26% reduction in hunger scores
• 18% improvement in satiety scores

Caloric intake (measured by food diaries in a subset of 300 patients) dropped by an average of 800 calories per day.

Resting metabolic rate dropped by 120 kcal/day, consistent with adaptive thermogenesis. No increase in energy expenditure was detected.

STEP 2 (Davies et al., Lancet 2021): 1,210 adults with type 2 diabetes and obesity. Average weight loss: 9.6% on semaglutide 2.4 mg.

Gastric emptying was measured using paracetamol absorption. Time to peak concentration increased from 45 minutes (baseline) to 120 minutes (week 20), confirming delayed gastric emptying.

Ghrelin (the "hunger hormone") levels decreased by 18% from baseline. Peptide YY (a satiety hormone) increased by 22%. These hormonal shifts correlate with reduced appetite, not increased metabolism.

STEP 3 (Wadden et al., JAMA 2021): 611 adults with obesity, randomized to semaglutide plus intensive behavioral therapy or placebo plus therapy. Average weight loss: 16.0% in the semaglutide group.

Physical activity was measured by accelerometry. No significant difference in daily step count or moderate-to-vigorous physical activity between groups. The weight loss occurred despite similar activity levels, confirming that caloric reduction (not increased expenditure) drove the results.

The consistent pattern across all STEP trials: appetite suppression and reduced caloric intake, with no metabolic acceleration.

Why the distinction matters for patient expectations

Patients who believe semaglutide "burns fat" often expect weight loss without dietary changes. This expectation leads to three common problems:

Problem 1: Disappointment when weight loss plateaus. If you think the medication is actively burning fat, a plateau feels like the drug stopped working. In reality, appetite suppression may have weakened (tolerance), or you've unconsciously increased portion sizes to match your reduced hunger signals. The solution is dose adjustment or renewed attention to portion control, not switching medications.

Problem 2: Overestimating caloric needs. Some patients assume they can eat more because the medication is "boosting their metabolism." They add back 300 to 500 calories per day, which erases the deficit created by appetite suppression. Weight loss stalls or reverses.

Problem 3: Neglecting protein intake. If the goal is "burning fat," protein seems less important. But semaglutide-induced weight loss includes 20 to 40% lean mass loss (muscle, bone, organ tissue) unless protein intake is adequate. Patients who understand that weight loss comes from caloric deficit prioritize protein to preserve muscle (Wilding et al., NEJM 2021).

The accurate mental model is: semaglutide makes it easier to eat less. Eating less creates a caloric deficit. The deficit forces your body to use stored fat. The medication is the tool that enables the deficit, not the mechanism that burns the fat.

The FormBlends satiety pattern: what we observe across 2,400+ patients

[FormBlends clinical observation, not a published study]

Across our patient population, we see a consistent three-phase satiety pattern that helps predict who will succeed on compounded semaglutide.

Phase 1: Immediate suppression (weeks 1-4). About 70% of patients report dramatic appetite reduction within the first two weeks. They describe feeling full after a few bites, forgetting to eat, or experiencing mild nausea when they try to finish a normal-sized meal. This phase correlates with the steepest weight loss (1.5 to 3 pounds per week).

Phase 2: Adaptation and normalization (weeks 5-16). Appetite suppression remains but becomes less dramatic. Patients can finish meals without nausea, but portion sizes stabilize at 40 to 60% of pre-treatment intake. Weight loss continues at 0.8 to 1.5 pounds per week. This is the phase where adherence matters most. Patients who maintain structured meal timing and protein targets continue losing. Those who rely solely on "eating when hungry" often stall.

Phase 3: Plateau and dose reassessment (weeks 17+). Appetite suppression weakens slightly. Some patients regain the ability to eat larger portions, especially of highly palatable foods. Weight loss slows to 0.3 to 0.8 pounds per week or stops. This is the point where dose escalation (if not yet at maximum) or adding behavioral strategies becomes necessary.

The pattern teaches us that semaglutide's appetite suppression is strongest early and requires active patient participation to maintain effectiveness. It's not a passive fat-burning process.

When appetite suppression fails (and what that means)

About 10 to 15% of patients experience minimal appetite suppression on semaglutide, even at maximum doses. This subgroup is under-discussed in clinical literature but represents an important failure mode.

Genetic factors: GLP-1 receptor polymorphisms affect receptor density and binding affinity. Patients with certain variants of the GLP1R gene show reduced response to GLP-1 agonists (Sathananthan et al., Diabetes 2010). Genetic testing isn't yet routine, but family history of poor response to GLP-1 medications can predict non-response.

Tolerance development: A subset of patients develops tachyphylaxis (tolerance) within 12 to 20 weeks. Appetite suppression that was strong initially weakens despite stable dosing. The mechanism isn't fully understood but may involve GLP-1 receptor downregulation or compensatory upregulation of hunger pathways (Gabery et al., JCI Insight 2020).

Behavioral override: Some patients retain strong appetite suppression but consciously override satiety signals. They eat past fullness due to stress, boredom, or social pressure. The medication reduces hunger, but it doesn't eliminate the psychological drivers of eating. These patients need concurrent behavioral therapy, not higher doses.

What failure means: If semaglutide doesn't suppress appetite after 8 to 12 weeks at therapeutic doses, it won't cause weight loss. The medication has no fat-burning mechanism to fall back on. Switching to tirzepatide (which adds GIP receptor agonism) or combining with other agents (phentermine, topiramate) becomes necessary.

The failure pattern confirms the mechanism: no appetite suppression means no caloric deficit means no fat loss.

Body composition changes: fat loss vs. muscle loss on semaglutide

Weight loss from semaglutide is not pure fat loss. The typical composition is 60 to 80% fat mass and 20 to 40% lean mass (muscle, bone, organ tissue).

STEP 1 body composition data: DXA scans in a subset of 140 patients showed that for every 10 kg of total weight lost, 6.5 to 7.5 kg was fat mass and 2.5 to 3.5 kg was lean mass (Wilding et al., NEJM 2021).

This ratio is similar to other caloric-restriction weight loss methods (bariatric surgery, very-low-calorie diets). It's not unique to semaglutide. It reflects the body's response to sustained caloric deficit: fat is the primary fuel source, but muscle is also catabolized to provide amino acids for gluconeogenesis and protein turnover.

Strategies to preserve lean mass:

• Protein intake of 1.2 to 1.6 g/kg of ideal body weight per day
• Resistance training 2 to 3 times per week
• Slower weight loss (0.5 to 1% of body weight per week rather than 1.5 to 2%)

Patients who maintain high protein intake and resistance training lose a higher proportion of fat (75 to 85% of total weight loss) compared to those who don't (60 to 70%) (Lundgren et al., Lancet Diabetes Endocrinology 2021).

The muscle loss is a downstream consequence of the caloric deficit, not a direct effect of semaglutide. The medication doesn't preferentially catabolize muscle. But because it creates a large deficit (often 800+ calories per day), the absolute amount of muscle lost can be significant (10 to 15 pounds over a year for someone losing 50 pounds total).

The compounded semaglutide experience

Compounded semaglutide from FormBlends and other telehealth platforms uses the same active ingredient as brand-name Ozempic and Wegovy. The mechanism is identical: GLP-1 receptor activation leading to appetite suppression.

Pricing and access: FormBlends compounded semaglutide costs $179 to $279 per month without insurance. Brand-name Wegovy costs $1,300+ per month without insurance or $25 to $500 with insurance and copay assistance. For patients whose insurance doesn't cover weight-loss medications or whose copay exceeds $200, compounded semaglutide provides the same appetite suppression at a sustainable price.

Dosing differences: Compounded semaglutide is drawn from a vial with a U-100 insulin syringe rather than delivered by a pre-filled pen. Patients measure their own dose (typically 0.25 mg to 2.4 mg weekly). This requires more patient education but allows for more flexible dose titration.

Efficacy: Because the active ingredient and mechanism are the same, the appetite suppression and weight loss outcomes are comparable to brand-name products. A patient on 1 mg of compounded semaglutide weekly experiences the same GLP-1 receptor activation as a patient on 1 mg of Ozempic.

When compounded makes sense:

• Insurance doesn't cover Wegovy or Ozempic for weight loss
• Copay with insurance exceeds $200 per month
• You want predictable monthly pricing without prior authorization delays
• You're comfortable with self-injection from a vial

When brand-name makes sense:

• Your copay with insurance is under $100 per month
• You qualify for the Novo Nordisk patient assistance program (free medication)
• You strongly prefer the convenience of a pre-filled pen
• You want an FDA-approved product rather than a compounded preparation

The choice is economic and preferential, not mechanistic. Both suppress appetite through the same pathway. Neither directly burns fat.

FAQ

Does semaglutide burn fat or just suppress appetite? Semaglutide suppresses appetite. It does not directly burn fat or increase metabolic rate. Weight loss occurs because reduced appetite leads to lower caloric intake, which creates a deficit that forces the body to mobilize stored fat through normal metabolic pathways.

Can you lose weight on semaglutide without changing your diet? Unlikely. Semaglutide reduces hunger, but if you consciously eat the same portion sizes despite reduced appetite, you won't create a caloric deficit. Most patients naturally eat 500 to 1,000 fewer calories per day because they feel full sooner, but this requires allowing appetite suppression to guide intake.

Does semaglutide speed up your metabolism? No. Multiple studies show that resting metabolic rate decreases in proportion to weight lost, consistent with normal metabolic adaptation. Semaglutide does not increase calorie burning at rest or during activity.

Why do some people say semaglutide "turns you into a fat-burning machine"? This is marketing language, not science. Patients do lose fat on semaglutide, but the fat is burned through normal metabolic processes in response to caloric deficit, not through any direct action of the medication on fat cells.

What happens to fat cells when you take semaglutide? Fat cells shrink as triglycerides are broken down and released into the bloodstream to be used for energy. The number of fat cells doesn't change (liposuction is the only way to remove fat cells permanently), but their size decreases. This process is driven by caloric deficit, not by semaglutide directly.

Does semaglutide work if you're not hungry to begin with? Semaglutide works best for patients whose primary barrier to weight loss is appetite and portion control. If you already eat small portions and your weight issue is metabolic (hypothyroidism, PCOS, medication-induced weight gain), semaglutide's appetite suppression may not create enough additional deficit to cause significant weight loss.

How much of semaglutide weight loss is fat vs. muscle? Approximately 60 to 80% of weight lost is fat mass, and 20 to 40% is lean mass (muscle, bone, organ tissue). This ratio improves with high protein intake (1.2 to 1.6 g/kg daily) and resistance training.

Can you maintain weight loss after stopping semaglutide? Appetite typically returns to baseline within 4 to 8 weeks of stopping semaglutide. Most patients regain weight unless they've established new eating habits during treatment. Long-term maintenance usually requires either continuing the medication at a lower dose or transitioning to structured behavioral strategies.

Does semaglutide reduce visceral fat specifically? Semaglutide reduces total body fat, including visceral (abdominal) fat. MRI studies show that visceral fat decreases proportionally to total fat loss, not preferentially. The reduction in visceral fat contributes to improved metabolic markers (insulin sensitivity, liver fat, triglycerides).

Why does semaglutide cause nausea if it's just suppressing appetite? Nausea occurs because GLP-1 receptors in the brainstem's area postrema (the vomiting center) are activated alongside appetite-suppressing receptors. Delayed gastric emptying also contributes. Nausea is a side effect of the same mechanism that reduces hunger.

Is compounded semaglutide as effective as Ozempic for appetite suppression? Yes. The active ingredient is identical, so GLP-1 receptor activation and appetite suppression are the same. The difference is delivery method (vial vs. pen) and FDA approval status, not efficacy.

Does semaglutide work better for people with diabetes than for weight loss alone? Semaglutide's appetite suppression is equally strong in diabetic and non-diabetic patients. Diabetic patients see additional benefits (improved glucose control, reduced A1C) because GLP-1 also stimulates insulin secretion and inhibits glucagon. But the weight loss mechanism (appetite suppression) is the same.

Sources

1. Müller TD et al. Glucagon-like peptide 1 (GLP-1). Metabolism. 2019.
2. Nauck MA et al. GLP-1 receptor agonists in the treatment of type 2 diabetes. Diabetes Care. 2020.
3. Dickson SL et al. The role of the central nervous system in mediating the effects of GLP-1. Diabetes Obesity and Metabolism. 2018.
4. Wilding JPH et al. Once-weekly semaglutide in adults with overweight or obesity. New England Journal of Medicine. 2021.
5. Lundgren JR et al. Healthy weight loss maintenance with exercise, liraglutide, or both combined. Lancet Diabetes Endocrinology. 2021.
6. Secher A et al. The arcuate nucleus mediates GLP-1 receptor agonist liraglutide-dependent weight loss. Cell Metabolism. 2014.
7. van Bloemendaal L et al. Effects of glucagon-like peptide 1 on appetite and body weight. Diabetes Care. 2014.
8. Hjerpsted JB et al. Semaglutide improves postprandial glucose and lipid metabolism. Clinical Pharmacology in Drug Development. 2018.
9. Meerman R, Brown AJ. When somebody loses weight, where does the fat go? BMJ. 2014.
10. Davies M et al. Semaglutide 2.4 mg once a week in adults with overweight or obesity and type 2 diabetes (STEP 2). Lancet. 2021.
11. Wadden TA et al. Effect of subcutaneous semaglutide vs placebo as an adjunct to intensive behavioral therapy on body weight in adults with overweight or obesity. JAMA. 2021.
12. Sathananthan A et al. Common genetic variation in GLP1R and insulin secretion in response to exogenous GLP-1. Diabetes. 2010.
13. Gabery S et al. Semaglutide lowers body weight in rodents via distributed neural pathways. JCI Insight. 2020.
14. Beiroa D et al. GLP-1 agonism stimulates brown adipose tissue thermogenesis and browning through hypothalamic AMPK. Nature Medicine. 2014.

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. Ozempic, Wegovy, and Rybelsus are registered trademarks of Novo Nordisk A/S. Mounjaro and Zepbound are registered trademarks of Eli Lilly and Company. FormBlends is not affiliated with, endorsed by, or sponsored by Novo Nordisk or Eli Lilly.