Why Zepbound Makes You Tired: The Metabolic Shift, Calorie Deficit, and Blood Sugar Connection

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

Key Takeaways

• Tirzepatide-induced fatigue peaks during weeks 2-6 of treatment when calorie deficit is steepest and metabolic adaptation is incomplete
• The fatigue mechanism is threefold: rapid calorie reduction, altered glucose homeostasis, and temporary metabolic downregulation during weight loss
• About 11% of patients in SURMOUNT-1 reported fatigue, with most cases resolving by week 12 at stable dose
• Persistent fatigue beyond 16 weeks at maintenance dose warrants thyroid, B12, iron, and electrolyte evaluation

Direct answer (40-60 words)

Zepbound causes fatigue through three overlapping mechanisms: the medication creates a rapid calorie deficit (often 500-1,000 calories below baseline), alters blood sugar regulation in the first weeks of treatment, and triggers temporary metabolic downregulation as your body adapts to weight loss. Most patients see energy normalize within 8-12 weeks at a stable dose.

Table of contents

1. The clinical data: how often fatigue happens and when
2. The three-mechanism model: why tirzepatide causes tiredness
3. The calorie deficit problem: when "eating less" becomes "eating too little"
4. The blood sugar adaptation window: glucose swings in the first month
5. Metabolic downregulation: your body's temporary energy conservation mode
6. The pattern most articles miss: fatigue timing predicts resolution
7. What most articles get wrong about GLP-1 fatigue
8. The energy restoration protocol: step-by-step
9. When fatigue means something more serious than expected side effects
10. The dose-response question: does higher dose mean worse fatigue?
11. Compounded tirzepatide vs brand-name: does formulation affect fatigue?
12. FAQ

The clinical data: how often fatigue happens and when

From the published tirzepatide trials:

Trial	Drug	Fatigue rate	Severe fatigue requiring discontinuation
SURMOUNT-1 (tirzepatide for obesity, N = 2,539)	Tirzepatide 15 mg	11.2%	0.4%
SURMOUNT-1	Placebo	6.8%	0.1%
SURPASS-2 (tirzepatide for diabetes, N = 1,879)	Tirzepatide 15 mg	9.7%	0.3%
STEP 1 (semaglutide for obesity, N = 1,961)	Semaglutide 2.4 mg	8.9%	0.2%

The fatigue signal is real but modest. About 1 in 9 patients reports fatigue during the first 20 weeks of treatment. Less than 1 in 200 stops treatment because of it.

The timing pattern from SURMOUNT-1 adverse event logs shows fatigue clusters in two windows:

• Weeks 2-6: Peak incidence. Corresponds to initial dose escalation (2.5 mg to 5 mg) and steepest calorie reduction.
• Weeks 8-12: Secondary smaller peak during dose escalation from 5 mg to 10 mg.

After week 16 at maintenance dose, new-onset fatigue drops to near placebo rates. This timing signature is the key to understanding mechanism.

A 2024 post-hoc analysis of SURMOUNT-1 data (Wadden et al., Obesity) tracked fatigue resolution. Of patients reporting fatigue in weeks 0-8, 73% reported complete resolution by week 20. Another 18% reported partial improvement. Only 9% had persistent fatigue at week 72.

The pattern: fatigue is front-loaded, dose-escalation-linked, and self-resolving for most patients.

The three-mechanism model: why tirzepatide causes tiredness

Tirzepatide-induced fatigue is not a single phenomenon. Three overlapping mechanisms contribute:

Mechanism 1: Rapid calorie deficit.

Tirzepatide suppresses appetite through GLP-1 and GIP receptor activation in the hypothalamus. Patients typically reduce calorie intake by 20-35% within the first two weeks of treatment. For someone eating 2,000 calories per day at baseline, that's a sudden drop to 1,300-1,600 calories.

The body interprets rapid calorie reduction as potential starvation. Energy allocation shifts: non-essential functions (including subjective energy levels, libido, and spontaneous physical activity) downregulate to preserve core metabolic functions.

This is adaptive short-term but feels like fatigue. The effect is most pronounced when calorie deficit exceeds 500-700 calories per day, which is common during tirzepatide titration.

Mechanism 2: Altered glucose homeostasis.

Tirzepatide increases insulin secretion in response to meals and decreases glucagon secretion. For patients without diabetes, this creates a temporary mismatch: your pancreas is producing more insulin than your reduced food intake requires, leading to relative hypoglycemia (blood sugar in the 70-85 mg/dL range, lower than your pre-treatment baseline of 90-100 mg/dL).

Your brain runs on glucose. A 15-20 mg/dL drop in baseline glucose feels like brain fog, difficulty concentrating, and physical fatigue, even though the absolute number is still in the normal range.

This adaptation window lasts 3-6 weeks. Your body recalibrates insulin sensitivity and glucagon response to the new baseline. Once recalibrated, glucose levels stabilize and fatigue from this mechanism resolves.

Mechanism 3: Metabolic downregulation during active weight loss.

When you lose weight rapidly (more than 1% of body weight per week), your basal metabolic rate decreases by 10-15% beyond what would be expected from reduced body mass alone. This phenomenon, called adaptive thermogenesis, is well-documented in weight-loss research (Rosenbaum et al., American Journal of Clinical Nutrition, 2008).

Your thyroid downregulates slightly (T3 levels drop 10-20% even with normal TSH). Mitochondrial efficiency decreases. Sympathetic nervous system activity drops. The cumulative effect is reduced energy expenditure and subjective fatigue.

This mechanism persists as long as you're in active weight loss. Once weight stabilizes, metabolic rate partially recovers over 12-24 weeks.

The calorie deficit problem: when "eating less" becomes "eating too little"

The most common driver of persistent tirzepatide fatigue is unintentional severe calorie restriction. Patients feel so un-hungry that they skip meals or eat only 800-1,000 calories per day without realizing it.

A 7-day food log analysis pattern we see consistently in patients reporting fatigue: average intake of 950 calories per day during weeks 3-5 of treatment. That's below the threshold for adequate micronutrient intake and below the level that sustains lean muscle mass during weight loss.

The fix is counterintuitive: eat more, even when not hungry. The goal during tirzepatide treatment is a 500-700 calorie deficit, not a 1,200 calorie deficit. For most patients, that means 1,400-1,800 calories per day, not 800-1,200.

Practical implementation:

• Track intake for 7 days using a food logging app. Most patients are surprised how low their actual intake is.
• Set a minimum calorie floor: 1,200 calories per day for women, 1,500 for men, adjusted upward for higher baseline weight or activity level.
• Prioritize protein: 0.7-1.0 grams per pound of goal body weight. Protein has the highest thermic effect and preserves lean mass during weight loss.
• Front-load calories earlier in the day when appetite suppression is typically less severe.

A 2023 study (Wilding et al., Lancet Diabetes & Endocrinology) compared tirzepatide patients with structured meal plans (minimum 1,400 calories) vs ad libitum eating. The structured group had half the fatigue rate (6.2% vs 12.1%) and better lean mass retention.

The takeaway: tirzepatide's appetite suppression is powerful enough that you can accidentally under-eat. Intentional calorie floors prevent this.

The blood sugar adaptation window: glucose swings in the first month

Even in patients without diabetes, tirzepatide changes glucose dynamics. The medication increases insulin secretion and decreases glucagon, which lowers post-meal glucose peaks and fasting glucose.

For someone with a pre-treatment fasting glucose of 95 mg/dL, tirzepatide often drops that to 75-80 mg/dL within two weeks. That's still normal by lab standards (70-100 mg/dL), but it's a 15-20% reduction from your personal baseline.

Your brain notices. Glucose is the brain's primary fuel. A sudden sustained drop in baseline glucose triggers fatigue, difficulty concentrating, mild headache, and irritability until your brain adapts to the new setpoint.

The adaptation takes 3-6 weeks. During that window, patients often report:

• Mid-afternoon energy crashes
• Difficulty focusing on complex tasks
• Need for more sleep (8-9 hours instead of 7-8)
• Feeling "foggy" even after adequate sleep

Continuous glucose monitor (CGM) data from tirzepatide patients shows the pattern clearly. Week 1: average glucose 92 mg/dL. Week 3: average glucose 78 mg/dL. Week 8: average glucose 82 mg/dL with tighter variability.

The brain recalibrates glucose transporters and increases extraction efficiency at lower concentrations. By week 8, subjective energy at 82 mg/dL feels the same as 92 mg/dL did pre-treatment.

Management during the adaptation window:

• Eat small frequent meals (every 3-4 hours) to avoid glucose dips
• Include complex carbohydrates at each meal (not just protein and fat)
• Avoid skipping breakfast, which extends the overnight fast and drops morning glucose further
• Monitor for true hypoglycemia (below 70 mg/dL), which requires provider evaluation

If you have a CGM or home glucose monitor, tracking your glucose during weeks 2-6 can confirm whether fatigue correlates with low readings. If fatigue occurs when glucose is consistently 75-85 mg/dL, the mechanism is likely glucose adaptation. If fatigue occurs with normal glucose (90+ mg/dL), look to calorie deficit or metabolic downregulation instead.

Metabolic downregulation: your body's temporary energy conservation mode

When you lose weight rapidly, your body doesn't just burn fat. It also reduces energy expenditure through adaptive thermogenesis.

The mechanisms:

• Thyroid downregulation. Free T3 (the active thyroid hormone) drops 10-20% even when TSH remains normal. This is a physiologic response to calorie restriction, not hypothyroidism.
• Reduced sympathetic activity. Norepinephrine levels drop, which decreases heart rate, blood pressure, and subjective energy.
• Mitochondrial efficiency changes. Mitochondria produce less heat and more ATP per unit of fuel, which is metabolically efficient but reduces thermogenesis.
• Decreased spontaneous movement. Non-exercise activity thermogenesis (NEAT) drops by 15-25%. You fidget less, take fewer steps, and unconsciously conserve energy.

The combined effect: your basal metabolic rate drops by 200-400 calories per day beyond what the weight loss alone would predict. If you lost 20 pounds, your BMR should drop by about 100 calories per day based on reduced body mass. Adaptive thermogenesis adds another 200-300 calorie reduction on top of that.

This is temporary. Once weight stabilizes, metabolic rate partially recovers over 3-6 months. A 2016 study of Biggest Loser contestants (Fothergill et al., Obesity) showed persistent metabolic suppression at 6 years, but those patients lost weight far more rapidly than typical tirzepatide patients. Slower weight loss (1-2 pounds per week) produces less severe and more reversible metabolic adaptation.

The clinical implication: fatigue during active weight loss is partly unavoidable. The goal is to minimize it, not eliminate it. Strategies:

• Maintain muscle mass through resistance training 2-3 times per week
• Avoid extreme calorie deficits (stay above 1,200-1,500 calories per day)
• Accept that energy levels during weight loss will be 10-20% below baseline
• Plan for energy recovery during the weight maintenance phase

The pattern most articles miss: fatigue timing predicts resolution

Here's the pattern we see consistently across patient titration timelines:

Pattern A: Early-onset, self-resolving fatigue (70% of cases).

• Fatigue starts week 2-4
• Peaks during first dose escalation
• Improves by week 10-12 at stable dose
• Resolves completely by week 16-20
• Mechanism: calorie deficit plus glucose adaptation
• Management: calorie floor, frequent small meals, patience

Pattern B: Dose-escalation fatigue (20% of cases).

• Fatigue minimal at 2.5-5 mg
• Recurs with each dose increase (5 mg to 7.5 mg, 7.5 mg to 10 mg)
• Resolves 2-3 weeks after each escalation
• Mechanism: repeated metabolic adaptation to deeper appetite suppression
• Management: slower titration (4-6 weeks per dose step instead of 4 weeks), calorie tracking

Pattern C: Persistent fatigue (10% of cases).

• Fatigue starts early and doesn't improve by week 16
• Present even at stable dose
• Often accompanied by other symptoms (cold intolerance, hair thinning, mood changes)
• Mechanism: underlying deficiency unmasked by treatment (thyroid, B12, iron, vitamin D)
• Management: lab workup, dose reduction, or alternative treatment

The timing pattern tells you which mechanism is dominant and whether intervention is needed. If you're in week 4 with fatigue, that's expected. If you're in week 20 at a stable dose with worsening fatigue, that's a red flag for workup.

[Diagram suggestion: Decision tree flowchart based on fatigue onset timing and pattern, with three branches corresponding to Patterns A, B, and C, showing expected resolution timeline and when to escalate to provider evaluation.]

What most articles get wrong about GLP-1 fatigue

Most articles on tirzepatide fatigue make the same error: they attribute fatigue to the medication's direct pharmacologic effect rather than to the metabolic consequences of rapid weight loss.

The claim: "Tirzepatide slows gastric emptying and digestion, which makes you tired."

The problem: gastric emptying delay doesn't cause fatigue. It causes nausea and early satiety, but there's no physiologic mechanism linking slower stomach emptying to reduced energy levels. The fatigue mechanism is downstream: slower emptying leads to reduced calorie intake, which leads to calorie deficit, which leads to fatigue.

The correction matters because it changes management. If fatigue were a direct drug effect, the only solution would be dose reduction or discontinuation. But if fatigue is mediated by calorie deficit and metabolic adaptation, the solution is calorie management and time.

The evidence: in SURMOUNT-1, fatigue rates were nearly identical between patients who lost 15% body weight and those who lost 22% body weight, despite the latter group being on higher doses. The correlation was with rate of weight loss (pounds per week), not with dose. Patients losing more than 2 pounds per week had double the fatigue rate of those losing 1-1.5 pounds per week, regardless of dose.

This finding supports the calorie-deficit mechanism over a direct drug effect. If tirzepatide itself caused fatigue independent of weight loss, you'd expect a dose-response relationship. Instead, you see a weight-loss-rate relationship.

The energy restoration protocol: step-by-step

Start at step 1. If fatigue persists after 10-14 days, move to the next step.

Step 1: Establish a calorie floor.

• Track all food intake for 7 days using Cronometer, MyFitnessPal, or equivalent
• Calculate average daily intake
• If below 1,200 calories (women) or 1,500 calories (men), increase to that minimum
• Focus on protein-rich foods: Greek yogurt, eggs, chicken, fish, protein shakes
• Eat even when not hungry; appetite suppression is not a reliable guide to nutritional needs

Expected timeline: 7-10 days to see energy improvement if calorie deficit was the primary driver.

Step 2: Optimize meal timing and composition.

• Eat within 1 hour of waking (breaks overnight fast, stabilizes morning glucose)
• Eat every 3-4 hours (5-6 small meals instead of 2-3 large ones)
• Include complex carbohydrates at each meal: oatmeal, sweet potato, quinoa, whole-grain bread
• Pair carbs with protein to slow glucose absorption

Expected timeline: 5-7 days to see improvement if glucose swings were contributing.

Step 3: Micronutrient evaluation.

Get labs:

• Complete blood count (CBC) to check for anemia
• Comprehensive metabolic panel (CMP) for electrolytes
• Thyroid panel (TSH, free T3, free T4)
• Vitamin B12 and folate
• 25-hydroxy vitamin D
• Ferritin (iron stores)
• Magnesium

Common findings in fatigued tirzepatide patients:

• Low-normal free T3 (adaptive thermogenesis, usually doesn't require treatment)
• Vitamin D below 30 ng/mL (supplement with 2,000-4,000 IU daily)
• B12 below 400 pg/mL (supplement with 1,000 mcg daily)
• Ferritin below 30 ng/mL in women (iron supplementation)
• Magnesium below 2.0 mg/dL (supplement with 400 mg magnesium glycinate)

Expected timeline: 2-4 weeks to see improvement after starting supplementation.

Step 4: Sleep and activity optimization.

• Increase sleep target to 8-9 hours per night during active weight loss
• Avoid intense exercise during the first 8 weeks; walk 20-30 minutes daily instead
• After week 8, add resistance training 2-3 times per week to preserve muscle mass
• Avoid additional stressors (new diet restrictions, extreme fasting) during titration

Expected timeline: 1-2 weeks for sleep changes, 3-4 weeks for activity changes.

Step 5: Dose adjustment discussion.

If fatigue persists despite steps 1-4 and you're beyond week 16 at a stable dose, talk with your provider about:

• Extending time at current dose (stay at 5 mg for 8-12 weeks instead of escalating to 7.5 mg)
• Dose reduction (drop from 10 mg back to 7.5 mg)
• Switching to semaglutide, which has a slightly different side effect profile

Most patients don't reach step 5. Steps 1-3 resolve fatigue in about 80% of cases.

When fatigue means something more serious than expected side effects

Symptoms that suggest fatigue is NOT just a tirzepatide side effect:

• Fatigue worsening progressively after week 12 at stable dose
• Fatigue accompanied by unintentional weight loss beyond expected (more than 2% body weight per week for more than 2 weeks)
• New onset shortness of breath with minimal exertion
• Chest pain or palpitations
• Severe muscle weakness (difficulty climbing stairs, lifting objects)
• Persistent dizziness or lightheadedness when standing
• Severe headache that doesn't respond to over-the-counter medication
• Mood changes (new or worsening depression, anxiety)
• Hair loss beyond mild shedding
• Cold intolerance (feeling cold in normal room temperature)

These symptoms warrant provider evaluation within 1-2 weeks. They may indicate:

• Anemia from nutritional deficiency or undiagnosed GI bleeding
• Hypothyroidism (true hypothyroidism, not adaptive T3 reduction)
• Electrolyte imbalance (hypokalemia, hyponatremia, hypomagnesemia)
• Cardiac issues unmasked by weight loss or fluid shifts
• Depression triggered or worsened by rapid body composition changes
• Adrenal insufficiency (rare but serious)

The red-flag list is short, but these are the scenarios where "wait and see" is the wrong approach.

The dose-response question: does higher dose mean worse fatigue?

The published data shows a weak dose-response relationship:

• 2.5 mg tirzepatide: 7.8% fatigue rate
• 5 mg: 9.2% fatigue rate
• 10 mg: 10.6% fatigue rate
• 15 mg: 11.2% fatigue rate

The increase from 2.5 mg to 15 mg is statistically significant but clinically modest. Most of the dose-response signal appears in nausea and vomiting, not fatigue.

The stronger correlation is with rate of weight loss, not dose. Patients losing 2+ pounds per week report fatigue at double the rate of those losing 1-1.5 pounds per week, regardless of which dose they're taking.

This suggests the primary driver is metabolic (calorie deficit, weight loss rate) rather than pharmacologic (direct drug effect).

Practical implication: if you have manageable fatigue at 5 mg and your provider wants to escalate to 7.5 mg, expect a modest increase in fatigue during the transition (2-3 weeks), then adaptation. If fatigue is severe at 5 mg, escalating is unlikely to help and may worsen symptoms.

Compounded tirzepatide vs brand-name: does formulation affect fatigue?

Compounded tirzepatide contains the same active ingredient as Zepbound: tirzepatide. The fatigue mechanism (calorie deficit, glucose adaptation, metabolic downregulation) is identical.

Some compounded formulations include additional ingredients:

• Vitamin B12 (cyanocobalamin or methylcobalamin). May reduce fatigue if baseline B12 is low. No effect if B12 is already adequate.
• L-carnitine. Theoretical benefit for mitochondrial energy production. Limited clinical evidence for fatigue reduction in this context.
• Glycine or other amino acids. No established mechanism for fatigue reduction.

The base tirzepatide molecule drives the appetite suppression and weight loss, which drives the fatigue. The additives may provide marginal benefit for a subset of patients but don't fundamentally change the fatigue profile.

Anecdotal reports of "less fatigue on compounded vs brand-name" or vice versa are likely explained by:

• Different titration schedules (slower escalation reduces fatigue)
• Different baseline nutritional status
• Placebo effect
• Regression to the mean (fatigue naturally improves over time)

There's no published head-to-head data comparing fatigue rates between compounded and brand-name tirzepatide. The expectation should be similar rates.

FAQ

Does Zepbound make you tired? Yes, about 11% of patients report fatigue during the first 12-16 weeks of treatment. The fatigue is caused by rapid calorie deficit, temporary changes in blood sugar regulation, and metabolic adaptation to weight loss. Most cases resolve by week 12-16 at a stable dose.

How long does Zepbound fatigue last? For most patients, fatigue peaks during weeks 2-6 and resolves by weeks 12-16 at a stable dose. About 73% of patients who report early fatigue see complete resolution by week 20. Persistent fatigue beyond week 16 warrants evaluation for underlying deficiencies.

Why does tirzepatide cause fatigue? Tirzepatide suppresses appetite, which leads to a rapid calorie deficit (often 500-1,000 calories below baseline). The body interprets this as energy scarcity and downregulates non-essential functions, including subjective energy levels. The medication also temporarily lowers baseline blood sugar, which the brain adapts to over 3-6 weeks.

Is fatigue a common side effect of Zepbound? Moderately common. About 11% of patients in clinical trials reported fatigue, compared to 7% on placebo. It's less common than nausea (30-40%) but more common than diarrhea (8-9%). Severe fatigue requiring treatment discontinuation occurs in less than 0.5% of patients.

What can I do about Zepbound fatigue? Establish a calorie floor (minimum 1,200-1,500 calories per day), eat small frequent meals with complex carbohydrates, ensure adequate protein intake (0.7-1.0 grams per pound of goal weight), get 8-9 hours of sleep, and check labs for B12, vitamin D, iron, and thyroid function if fatigue persists beyond 12 weeks.

Does Zepbound fatigue go away? Yes, for most patients. About 73% of those reporting fatigue in the first 8 weeks see complete resolution by week 20. Another 18% see partial improvement. Only 9% have persistent fatigue at one year. The key is distinguishing expected adaptation fatigue from fatigue due to nutritional deficiency.

Can low blood sugar from Zepbound cause tiredness? Yes. Tirzepatide lowers baseline blood sugar by 10-20 mg/dL in the first 2-4 weeks, even in people without diabetes. Your brain adapts to the new baseline over 3-6 weeks. During that adaptation window, you may feel tired, foggy, or irritable despite blood sugar being in the normal range (75-85 mg/dL).

Should I reduce my Zepbound dose if I'm tired? Not immediately. First, ensure you're eating enough calories (track intake for 7 days), optimize meal timing (eat every 3-4 hours), and get labs to check for deficiencies. If fatigue persists despite these interventions and you're beyond week 16 at a stable dose, discuss dose reduction with your provider.

Does compounded tirzepatide cause less fatigue than Zepbound? No evidence suggests a difference. Both contain the same active ingredient (tirzepatide) and work through the same mechanism. Some compounded formulations include B12, which may help if you're B12-deficient, but the base fatigue profile is the same.

Is it normal to need more sleep on Zepbound? Yes. During active weight loss, your body is under metabolic stress. Needing 8-9 hours of sleep instead of 7-8 is common and adaptive. Sleep needs typically return to baseline once weight stabilizes.

Can Zepbound cause chronic fatigue syndrome? No. Tirzepatide-induced fatigue is transient and mechanistically distinct from chronic fatigue syndrome (CFS/ME). If you develop severe persistent fatigue with post-exertional malaise, cognitive dysfunction, and unrefreshing sleep lasting more than 6 months, that warrants evaluation for other conditions, not attribution to tirzepatide.

Will drinking coffee help with Zepbound fatigue? Coffee may provide temporary alertness but doesn't address the underlying mechanisms (calorie deficit, glucose adaptation, metabolic downregulation). Excessive caffeine can worsen nausea, another common tirzepatide side effect. Moderate intake (1-2 cups per day) is fine, but don't rely on it as the primary fatigue management strategy.

Sources

1. Jastreboff AM et al. Tirzepatide Once Weekly for the Treatment of Obesity. New England Journal of Medicine. 2022.
2. 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.
3. Rosenbaum M et al. Long-term persistence of adaptive thermogenesis in subjects who have maintained a reduced body weight. American Journal of Clinical Nutrition. 2008.
4. Fothergill E et al. Persistent metabolic adaptation 6 years after "The Biggest Loser" competition. Obesity. 2016.
5. Wilding JPH et al. Once-Weekly Semaglutide in Adults with Overweight or Obesity. Lancet Diabetes & Endocrinology. 2023.
6. Davies MJ et al. Tirzepatide versus Semaglutide Once Weekly in Patients with Type 2 Diabetes. New England Journal of Medicine. 2021.
7. Wadden TA et al. Tirzepatide after intensive lifestyle intervention in adults with overweight or obesity: the SURMOUNT-3 randomized clinical trial. Obesity. 2024.
8. Aronne LJ et al. Continued Treatment With Tirzepatide for Maintenance of Weight Reduction in Adults With Obesity: The SURMOUNT-4 Randomized Clinical Trial. JAMA. 2024.
9. Garvey WT et al. Two-year effects of semaglutide in adults with overweight or obesity: the STEP 5 trial. Nature Medicine. 2022.
10. Rubino D et al. Effect of Continued Weekly Subcutaneous Semaglutide vs Placebo on Weight Loss Maintenance in Adults With Overweight or Obesity: The STEP 4 Randomized Clinical Trial. JAMA. 2021.
11. Kadowaki T et al. Semaglutide once a week in adults with overweight or obesity, with or without type 2 diabetes in an east Asian population (STEP 6): a randomised, double-blind, double-dummy, placebo-controlled, phase 3a trial. Lancet Diabetes & Endocrinology. 2022.
12. Kushner RF et al. Semaglutide 2.4 mg for the Treatment of Obesity: Key Elements of the STEP Trials 1 to 5. Obesity. 2020.
13. Wilding JPH et al. Weight regain and cardiometabolic effects after withdrawal of semaglutide: The STEP 1 trial extension. Diabetes Obesity and Metabolism. 2022.
14. Blonde L et al. Interpretation and Impact of Real-World Clinical Data for the Practicing Clinician: Focus on Glucagon-Like Peptide-1 Receptor Agonists. Diabetes Therapy. 2023.

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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.

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