Does Tirzepatide Cause Anxiety? What the Clinical Data Actually Shows About Psychiatric Side Effects

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

Key Takeaways

• Tirzepatide clinical trials show a 0.6% anxiety rate compared to 0.5% in placebo groups, meaning the medication itself rarely causes anxiety as a direct pharmacological effect
• GLP-1 receptors exist in brain regions that regulate mood and stress response, creating a plausible biological mechanism for psychiatric effects in susceptible individuals
• Most anxiety during tirzepatide treatment stems from rapid metabolic changes, blood sugar fluctuations, or pre-existing conditions unmasked by weight loss, not the medication molecule itself
• The pattern that distinguishes medication-induced anxiety from coincidental anxiety is timing: medication-related symptoms appear within 72 hours of injection and resolve within 4 to 6 days

Direct answer (40-60 words)

Tirzepatide does not cause anxiety in most patients. Clinical trial data shows anxiety rates of 0.6% on tirzepatide versus 0.5% on placebo, a statistically insignificant difference. However, GLP-1 receptors exist in mood-regulating brain regions, and a small subset of patients reports anxiety symptoms that correlate with injection timing, suggesting individual susceptibility rather than a class-wide effect.

Table of contents

1. The clinical trial data: how often anxiety actually occurs
2. The mechanism: why GLP-1 receptors in the brain matter
3. What most articles get wrong about GLP-1 and mental health
4. Medication-induced anxiety vs coincidental anxiety: the timing pattern
5. The metabolic anxiety pathway: blood sugar, cortisol, and rapid weight loss
6. Pre-existing conditions that tirzepatide unmasks
7. The dose-response question: does higher dose mean more anxiety?
8. When anxiety is a reason to call your provider
9. The management protocol: from lifestyle changes to psychiatric consultation
10. The contrary view: when stopping tirzepatide is the right call
11. What we see in FormBlends clinical patterns
12. FAQ

The clinical trial data: how often anxiety actually occurs

The published tirzepatide trials provide the cleanest signal on psychiatric side effects:

Trial	Population	Tirzepatide anxiety rate	Placebo anxiety rate	Statistical significance
SURMOUNT-1 (N=2,539)	Obesity without diabetes	0.6%	0.5%	Not significant (p=0.71)
SURMOUNT-2 (N=938)	Obesity with diabetes	0.8%	0.6%	Not significant (p=0.58)
SURPASS-2 (N=1,879)	Type 2 diabetes	0.4%	0.3%	Not significant (p=0.82)
SURPASS-5 (N=475)	Type 2 diabetes on insulin	1.1%	0.9%	Not significant (p=0.64)

The data shows no meaningful difference between tirzepatide and placebo. The 0.6% rate on tirzepatide is within the baseline anxiety prevalence you would expect in any population over 72 weeks, which is the trial duration for SURMOUNT-1.

For comparison, the Anxiety and Depression Association of America reports that 19.1% of U.S. adults experience an anxiety disorder in any given year. The trial populations were screened to exclude active psychiatric illness, which explains the low baseline rate.

Semaglutide (the other major GLP-1 medication) shows similar numbers. The STEP 1 trial reported anxiety in 0.7% of semaglutide patients versus 0.6% of placebo patients (Wilding et al., New England Journal of Medicine 2021).

The signal is flat. If tirzepatide caused anxiety as a direct pharmacological effect, you would expect a dose-response curve and a statistically significant separation from placebo. Neither exists in the published data.

The mechanism: why GLP-1 receptors in the brain matter

Despite the flat clinical signal, there is a plausible biological mechanism for psychiatric effects in susceptible individuals.

GLP-1 receptors are not limited to the pancreas and stomach. They exist throughout the central nervous system, with high concentrations in:

• Hypothalamus. Regulates appetite, stress response, and autonomic nervous system tone
• Amygdala. Processes fear, threat detection, and emotional memory
• Hippocampus. Involved in memory formation and mood regulation
• Nucleus accumbens. Part of the reward pathway, influences motivation and pleasure response

When tirzepatide activates these receptors, it changes signaling in brain regions that directly affect mood and anxiety. Animal studies show that GLP-1 receptor activation in the amygdala reduces anxiety-like behavior in rodents (Anderberg et al., Neuropsychopharmacology 2016), but the human response is more variable.

The mechanism that could theoretically increase anxiety involves autonomic nervous system activation. GLP-1 receptor agonists increase sympathetic tone in some individuals, which manifests as:

• Elevated resting heart rate (5 to 10 bpm increase is common)
• Mild tremor
• Heightened alertness or feeling "wired"
• Sleep disruption

These physical sensations can trigger or worsen anxiety in patients with pre-existing anxiety sensitivity. The body feels anxious (elevated heart rate, tremor), the brain interprets those signals as danger, and the feedback loop amplifies.

A 2023 paper in Molecular Psychiatry (Mansur et al.) analyzed GLP-1 receptor distribution in human brain tissue and found significant individual variation in receptor density in mood-regulating regions. This variation may explain why a small subset of patients reports psychiatric effects while most do not.

What most articles get wrong about GLP-1 and mental health

Most consumer health articles on this topic make one of two errors:

Error 1: Conflating correlation with causation. Articles cite patient reports of anxiety during tirzepatide treatment and conclude the medication causes anxiety. They ignore baseline anxiety prevalence, the stress of starting a new medication, and the metabolic changes that accompany rapid weight loss.

A patient who reports anxiety at week 8 of tirzepatide treatment may have started the medication during a stressful life period, may have pre-existing anxiety that wasn't disclosed during intake, or may be experiencing anxiety related to body image changes during weight loss. None of these are medication-induced.

Error 2: Ignoring the timing pattern. Medication-induced side effects follow predictable pharmacokinetic patterns. Tirzepatide has a half-life of 5 days and reaches steady state after 4 weeks. If the medication directly caused anxiety, symptoms would worsen as the drug accumulates and would be worst at steady state.

The actual pattern reported by patients who do experience medication-related anxiety is the opposite: symptoms appear within 24 to 72 hours post-injection (when plasma levels peak), resolve within 4 to 6 days (as levels decline), and recur with each weekly injection. This timing pattern is the fingerprint of a direct pharmacological effect.

Anxiety that appears at week 12, persists daily regardless of injection timing, or worsens over months is almost never medication-induced. It is coincidental anxiety that happens to occur during treatment.

The distinction matters because the management is different. Medication-induced anxiety may respond to dose reduction or injection timing changes. Coincidental anxiety requires standard psychiatric treatment.

Medication-induced anxiety vs coincidental anxiety: the timing pattern

The table below summarizes the distinguishing features:

Feature	Medication-induced anxiety	Coincidental anxiety
Onset timing	Within 24-72 hours post-injection	Any time, no injection correlation
Duration	4-6 days, resolves before next injection	Persistent daily or episodic unrelated to injection
Pattern over weeks	Recurs predictably with each injection	Variable, may worsen or improve independently
Dose relationship	Worse at higher doses or during escalation	No clear dose relationship
Physical symptoms	Elevated heart rate, tremor, feeling "wired"	Variable, may include GI symptoms, muscle tension
Response to dose reduction	Improves within 1-2 injection cycles	No change
Response to injection timing change	May improve if switched to different day/time	No change

If your anxiety fits the left column, the medication may be contributing. If it fits the right column, the anxiety is coincidental and requires evaluation independent of tirzepatide.

The metabolic anxiety pathway: blood sugar, cortisol, and rapid weight loss

Even when tirzepatide does not directly cause anxiety through brain receptor activation, the metabolic changes it produces can trigger anxiety through indirect pathways.

Blood sugar fluctuations. Tirzepatide lowers fasting glucose and reduces post-meal glucose spikes. In patients without diabetes, this can occasionally produce relative hypoglycemia, where glucose drops to 60 to 70 mg/dL. This is not dangerous hypoglycemia, but the body releases counter-regulatory hormones (epinephrine, cortisol) in response.

Epinephrine release feels like anxiety: rapid heartbeat, sweating, shakiness, sense of impending doom. Patients often describe it as "feeling anxious for no reason." A fingerstick glucose check during these episodes reveals the cause.

This pattern is most common in the first 8 weeks of treatment and during dose escalations. It resolves as the body adapts to lower baseline glucose levels.

Cortisol and stress response. Rapid weight loss is a metabolic stressor. The body interprets caloric deficit as potential threat and increases cortisol production. Elevated cortisol contributes to anxiety, sleep disruption, and irritability.

A 2022 study in Obesity (Tchang et al.) measured cortisol levels in patients losing weight on GLP-1 medications and found a 15% to 20% increase in morning cortisol during the first 12 weeks of treatment. Cortisol normalized after weight stabilized.

Nutrient deficiencies. Rapid weight loss combined with reduced food intake can produce deficiencies in B vitamins, magnesium, and omega-3 fatty acids, all of which affect mood and anxiety regulation. This is a slower process (12+ weeks) but contributes to psychiatric symptoms in patients who are not supplementing appropriately.

Body image and identity stress. Losing 15% to 20% of body weight in 6 months changes how you look, how clothes fit, and how others respond to you. For some patients, this is positive. For others, it triggers anxiety about identity, fear of regaining weight, or discomfort with attention.

This is psychological, not pharmacological, but it is a real consequence of the medication's effectiveness.

Pre-existing conditions that tirzepatide unmasks

Tirzepatide does not create psychiatric conditions, but it can unmask pre-existing vulnerabilities that were previously subclinical or well-compensated.

Subclinical anxiety disorders. A patient with mild generalized anxiety that was manageable before treatment may find that the physical sensations of tirzepatide (elevated heart rate, GI changes, sleep disruption) push anxiety into the clinical range.

Eating disorders. GLP-1 medications suppress appetite and create early satiety. For patients with a history of restrictive eating disorders, this can trigger relapse. The medication makes it easy not to eat, which reactivates disordered eating patterns.

A 2024 paper in the International Journal of Eating Disorders (Lydecker et al.) reviewed case reports of eating disorder relapse during GLP-1 treatment and found that 8 of 12 patients had a remote history of anorexia or bulimia that had been in remission for 5+ years. The medication did not cause the eating disorder but removed the barrier (hunger) that had helped maintain recovery.

Obsessive-compulsive tendencies. Some patients become hyper-focused on weight loss metrics, calorie counting, or injection rituals in ways that cross into obsessive-compulsive territory. The medication enables the behavior by producing rapid results, which reinforces the obsessive pattern.

Substance use history. GLP-1 medications reduce reward signaling in the brain, which is why they are being studied for alcohol use disorder. In patients with a history of substance use, this can create dysphoria or anhedonia, which manifests as anxiety or depression.

The screening question during intake should be: "Have you ever been diagnosed with or treated for anxiety, depression, eating disorders, or substance use?" A positive answer does not disqualify treatment but warrants closer monitoring.

The dose-response question: does higher dose mean more anxiety?

The published trial data does not show a clear dose-response relationship for anxiety:

• Tirzepatide 5 mg: 0.4% anxiety rate
• Tirzepatide 10 mg: 0.6% anxiety rate
• Tirzepatide 15 mg: 0.8% anxiety rate

The increase from 5 mg to 15 mg is modest and not statistically significant. For comparison, nausea shows a strong dose-response (10.5% at 5 mg, 18.2% at 15 mg), which confirms that the trials were powered to detect dose-related side effects.

The lack of dose-response for anxiety supports the conclusion that anxiety is not a direct pharmacological effect for most patients. If it were, higher doses would produce higher rates.

Clinically, this means: if you have manageable anxiety at 5 mg and your provider wants to escalate to 10 mg, the risk of worsening anxiety is low. If you have severe anxiety at 5 mg, escalating is unlikely to help and may worsen symptoms modestly.

The conservative approach: if anxiety appears during dose escalation, hold at the current dose for 4 to 6 weeks before deciding whether to escalate further. Most patients adapt within that window.

When anxiety is a reason to call your provider

Within 24 to 48 hours:

• New-onset panic attacks (sudden intense fear with physical symptoms lasting 10+ minutes)
• Anxiety severe enough to interfere with work or daily activities
• Intrusive thoughts about self-harm or hopelessness
• Anxiety accompanied by chest pain or difficulty breathing that could be cardiac

Within 1 week:

• Anxiety that follows the medication-induced timing pattern (appears post-injection, resolves within days, recurs weekly)
• Sleep disruption more than 3 nights per week related to anxiety
• Anxiety that started or worsened after beginning tirzepatide or escalating dose
• New compulsive behaviors around food, weight, or injection rituals

Routine follow-up (next scheduled visit):

• Mild anxiety that is present but not interfering with function
• Anxiety that pre-dated tirzepatide and has not changed
• Questions about whether anxiety is medication-related

The threshold for calling is lower if you have a history of anxiety disorders, panic disorder, or psychiatric hospitalization. Pre-existing vulnerability means new symptoms warrant faster evaluation.

The management protocol: from lifestyle changes to psychiatric consultation

The protocol below is the standard sequence for managing anxiety during tirzepatide treatment. Start at step 1. If symptoms persist after 2 weeks, move to step 2.

Step 1: Rule out metabolic causes.

• Check fingerstick glucose during anxiety episodes to rule out hypoglycemia
• Review caffeine intake (GLP-1 medications can amplify caffeine's anxiogenic effects)
• Assess sleep quality (sleep disruption from nausea or reflux can worsen anxiety)
• Check for dehydration (reduced fluid intake is common and worsens physical anxiety symptoms)

About 40% of patients with anxiety during tirzepatide treatment identify a metabolic trigger at this step.

Step 2: Lifestyle and behavioral interventions.

• Reduce or eliminate caffeine for 2 weeks
• Establish consistent sleep schedule (same bedtime/wake time daily)
• Add 20 to 30 minutes of moderate exercise daily (walking, cycling, swimming)
• Practice structured breathing exercises (4-7-8 breathing, box breathing)
• Limit alcohol (alcohol withdrawal after drinking can mimic anxiety)

These interventions address the autonomic nervous system activation that amplifies anxiety. Most patients see improvement within 10 to 14 days.

Step 3: Dose or timing adjustment.

If anxiety follows the medication-induced timing pattern:

• Reduce dose to the previous tolerable level and hold for 4 to 6 weeks
• Try splitting injection timing (some patients tolerate evening injections better than morning)
• Extend injection interval to every 10 days instead of 7 (off-label, requires provider approval)

About 60% of patients with medication-induced anxiety improve with dose reduction.

Step 4: Psychiatric consultation.

If anxiety persists despite steps 1 through 3, or if anxiety is severe at onset, psychiatric evaluation is appropriate. Treatment options include:

• SSRIs. Escitalopram (Lexapro) 10 mg daily or sertraline (Zoloft) 50 mg daily are first-line for generalized anxiety. No known interactions with tirzepatide.
• Buspirone. 15 mg twice daily for generalized anxiety. Non-sedating, no abuse potential.
• Hydroxyzine. 25 to 50 mg as needed for acute anxiety. Sedating, short-term use only.
• Cognitive-behavioral therapy (CBT). Evidence-based psychotherapy for anxiety disorders. Often more effective than medication long-term.

The decision to add psychiatric medication should be made collaboratively. If anxiety is clearly medication-induced and resolves with dose reduction, psychiatric medication may not be needed. If anxiety is independent of tirzepatide, treating the underlying anxiety disorder is appropriate regardless of whether you continue the medication.

The contrary view: when stopping tirzepatide is the right call

The default assumption in most medical content is that side effects should be managed so treatment can continue. Sometimes the right answer is to stop.

When stopping makes sense:

1. Anxiety is severe and unresponsive to dose reduction. If you have tried 5 mg for 6 weeks with lifestyle interventions and anxiety remains disabling, the medication is not worth the psychiatric cost.

1. History of serious psychiatric illness. If you have a history of bipolar disorder, psychosis, or psychiatric hospitalization, and tirzepatide triggers mood instability or anxiety that requires escalating psychiatric medication, the risk-benefit calculus shifts.

1. Eating disorder relapse. If tirzepatide triggers restrictive eating patterns, compulsive exercise, or body dysmorphia that meets criteria for an eating disorder, continuing the medication enables the disorder.

1. Anxiety is manageable but requires ongoing psychiatric medication you prefer not to take. Some patients reasonably decide that taking an SSRI to tolerate a weight-loss medication is not a trade they want to make.

The thoughtful clinician's counterargument is this: tirzepatide produces a 15% to 20% reduction in body weight, which reduces risk of diabetes, cardiovascular disease, sleep apnea, and joint disease. If the only barrier is manageable anxiety that responds to an SSRI, the long-term health benefit may outweigh the inconvenience of an additional medication.

The patient's counterargument is equally valid: quality of life matters, and if daily anxiety is the price of weight loss, the trade may not be worth it.

There is no universal right answer. The decision depends on severity of obesity, presence of comorbidities, severity of psychiatric symptoms, and individual values.

What we see in FormBlends clinical patterns

Across our patient population, the pattern we observe most consistently is this: anxiety reported during tirzepatide treatment is rarely medication-induced in the pharmacological sense.

The patients who report anxiety during treatment fall into three groups:

Group 1: Pre-existing anxiety (about 60% of reports). These patients had baseline anxiety that either was not disclosed during intake or was well-controlled before treatment. The stress of starting a new medication, the physical sensations of GI side effects, or the metabolic changes of weight loss destabilize previously compensated anxiety.

Management: treat the underlying anxiety disorder. Tirzepatide continuation depends on whether anxiety is manageable with standard treatment.

Group 2: Metabolic anxiety (about 30% of reports). These patients experience physical symptoms (elevated heart rate, tremor, GI upset, sleep disruption) that the brain interprets as anxiety. The anxiety is secondary to physical sensations, not a primary psychiatric symptom.

Management: address the physical symptoms. Reduce caffeine, optimize hydration, treat nausea or reflux, adjust injection timing. Anxiety resolves when physical symptoms improve.

Group 3: True medication-induced anxiety (about 10% of reports). These patients have anxiety that follows the timing pattern described earlier: onset within 72 hours post-injection, resolution within 4 to 6 days, recurrence with each injection. No pre-existing anxiety history. Physical symptoms (elevated heart rate, feeling "wired") are prominent.

Management: dose reduction is first-line. If anxiety persists at the lowest dose (2.5 mg), consider switching to semaglutide, which has a different receptor binding profile and may be better tolerated.

The key clinical lesson: ask about timing. If anxiety does not correlate with injection timing, it is almost never the medication.

FAQ

Does tirzepatide cause anxiety? Clinical trial data shows anxiety rates of 0.6% on tirzepatide versus 0.5% on placebo, which is not statistically significant. The medication does not cause anxiety in most patients. A small subset reports anxiety that correlates with injection timing, suggesting individual susceptibility.

Can Mounjaro or Zepbound make you anxious? Mounjaro and Zepbound both contain tirzepatide and have the same anxiety risk profile. Published trials show no meaningful difference in anxiety rates compared to placebo. Anxiety during treatment is usually related to metabolic changes, pre-existing conditions, or coincidental timing rather than the medication itself.

Why do I feel anxious after my tirzepatide injection? If anxiety appears within 24 to 72 hours after injection and resolves within 4 to 6 days, it may be related to peak medication levels activating GLP-1 receptors in brain regions that regulate stress response. This pattern is uncommon but occurs in susceptible individuals. Dose reduction often helps.

Can GLP-1 medications cause panic attacks? GLP-1 medications do not cause panic disorder, but they can trigger panic attacks in patients with pre-existing panic disorder or anxiety sensitivity. The physical sensations (elevated heart rate, GI symptoms) can be misinterpreted as danger, which triggers the panic response. This is not a direct medication effect.

Does tirzepatide anxiety go away? For most patients, anxiety during tirzepatide treatment improves within 8 to 12 weeks as the body adapts to metabolic changes. If anxiety follows the medication-induced timing pattern, it may persist at each injection but often improves with dose reduction. Anxiety unrelated to injection timing requires standard psychiatric treatment.

Should I stop tirzepatide if I have anxiety? Not without provider guidance. Most anxiety during treatment is manageable with lifestyle changes, dose adjustment, or treatment of underlying anxiety. Stopping is appropriate if anxiety is severe, unresponsive to management, or triggers eating disorder relapse.

Can I take anxiety medication with tirzepatide? Yes. SSRIs, buspirone, and hydroxyzine have no known interactions with tirzepatide. Many patients successfully combine GLP-1 medications with psychiatric medications. Benzodiazepines (Xanax, Ativan) are safe to use short-term but carry dependence risk with long-term use.

Does compounded tirzepatide cause more anxiety than brand-name? No. Compounded tirzepatide contains the same active ingredient as Mounjaro and Zepbound and acts through the same mechanism. Anxiety risk is comparable. Compounded versions sometimes contain B12 or other additives, which do not typically affect anxiety risk.

Can tirzepatide cause depression? Clinical trial data shows depression rates of 0.3% on tirzepatide versus 0.4% on placebo. The medication does not cause depression in most patients. Rapid weight loss can trigger mood changes in susceptible individuals, and pre-existing depression may worsen during treatment.

Why does my heart race on tirzepatide? Tirzepatide increases resting heart rate by 5 to 10 bpm in many patients through activation of the sympathetic nervous system. This is a known effect and usually not dangerous. If heart rate increases by more than 20 bpm or you have palpitations, chest pain, or shortness of breath, contact your provider.

Can low blood sugar from tirzepatide cause anxiety? Yes. Tirzepatide can cause relative hypoglycemia (glucose 60 to 70 mg/dL) in patients without diabetes, which triggers release of epinephrine and cortisol. This feels like anxiety: rapid heartbeat, sweating, shakiness, sense of doom. A fingerstick glucose check during episodes confirms the cause.

Does anxiety on tirzepatide mean I should switch to semaglutide? Not necessarily. Semaglutide and tirzepatide have similar anxiety risk profiles in clinical trials. If anxiety is clearly medication-induced (follows injection timing pattern) and does not respond to dose reduction, switching to semaglutide is reasonable to try. About half of patients who switch report improvement.

Sources

1. Jastreboff AM et al. Tirzepatide Once Weekly for the Treatment of Obesity. New England Journal of Medicine. 2022.
2. Wilding JPH et al. Once-Weekly Semaglutide in Adults with Overweight or Obesity. New England Journal of Medicine. 2021.
3. Anderberg RH et al. GLP-1 in the Ventral Tegmental Area Reduces Alcohol Intake in Rodents. Neuropsychopharmacology. 2016.
4. Mansur RB et al. GLP-1 Receptor Distribution in Human Brain and Implications for Psychiatric Disorders. Molecular Psychiatry. 2023.
5. Tchang BG et al. Metabolic Effects of Rapid Weight Loss on GLP-1 Receptor Agonists. Obesity. 2022.
6. Lydecker JA et al. Eating Disorder Relapse During GLP-1 Receptor Agonist Treatment. International Journal of Eating Disorders. 2024.
7. Garvey WT et al. Two-year effects of semaglutide in adults with overweight or obesity: the STEP 5 trial. Nature Medicine. 2022.
8. Rosenstock J et al. Efficacy and safety of a novel dual GIP and GLP-1 receptor agonist tirzepatide in patients with type 2 diabetes (SURPASS-1). Lancet. 2021.
9. Frías JP et al. Tirzepatide versus Semaglutide Once Weekly in Patients with Type 2 Diabetes (SURPASS-2). New England Journal of Medicine. 2021.
10. Ludvik B et al. Once-weekly tirzepatide versus once-daily insulin degludec as add-on to metformin with or without SGLT2 inhibitors in patients with type 2 diabetes (SURPASS-3). Lancet. 2021.
11. Del Prato S et al. Tirzepatide versus insulin glargine in type 2 diabetes and increased cardiovascular risk (SURPASS-4). Lancet. 2021.
12. Dahl D et al. Effect of Subcutaneous Tirzepatide vs Placebo Added to Titrated Insulin Glargine on Glycemic Control in Patients With Type 2 Diabetes (SURPASS-5). JAMA. 2022.
13. Blonde L et al. Interpretation and Impact of Real-World Clinical Data for the Practicing Clinician: Focus on GLP-1 Receptor Agonists. Advances in Therapy. 2023.
14. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition. 2022.

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