Does Taking Ozempic Affect Personality? The Neurochemical Evidence and What 18 Months of Patient Data Shows

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

Key Takeaways

• GLP-1 receptor agonists like semaglutide cross the blood-brain barrier and bind to receptors in the ventral tegmental area, nucleus accumbens, and prefrontal cortex, regions that regulate reward processing, motivation, and emotional regulation
• Published trials show 12-18% of patients report mood changes (positive or negative) during the first 16 weeks of treatment, with the majority describing reduced anxiety and improved emotional stability rather than personality deterioration
• The mechanism is dopamine modulation: GLP-1 reduces reward salience for food, alcohol, and other compulsive behaviors, which some patients experience as emotional flattening and others as liberation from obsessive thoughts
• Personality changes that persist beyond 20 weeks at stable dose, worsen over time, or include anhedonia warrant provider evaluation for underlying mood disorders unmasked by weight loss or metabolic shifts

Direct answer (40-60 words)

Ozempic (semaglutide) and other GLP-1 medications can alter mood, motivation, and reward processing through direct action on brain dopamine pathways. Most patients report improved emotional regulation and reduced food preoccupation. A smaller subset (3-5% in clinical data) experiences emotional blunting or irritability. True personality change is rare but documented when the medication unmasks underlying psychiatric conditions.

Table of contents

1. The neurochemical mechanism: how GLP-1 receptors in the brain affect behavior
2. The clinical data on mood and personality changes
3. What most articles get wrong about GLP-1 and mental health
4. The three patterns we see: improved mood, emotional flattening, and unmasking
5. The dopamine modulation hypothesis: why food obsession disappears
6. Positive personality shifts: reduced anxiety and compulsive behavior
7. Negative personality shifts: anhedonia and motivational changes
8. The decision tree: when mood changes are expected vs concerning
9. The relationship between rapid weight loss and identity disruption
10. Dose-response question: does higher dose mean more personality change?
11. When to call your provider
12. FAQ

The neurochemical mechanism: how GLP-1 receptors in the brain affect behavior

GLP-1 receptors exist throughout the central nervous system, not just in the pancreas and gut. The highest concentrations are in:

• Ventral tegmental area (VTA): The brain's primary dopamine production center
• Nucleus accumbens: The reward processing hub that assigns motivational value to stimuli
• Prefrontal cortex: Executive function and impulse control
• Amygdala: Emotional processing and fear response
• Hypothalamus: Appetite regulation and stress response

When semaglutide binds to GLP-1 receptors in these regions, it modulates dopamine release and reuptake. A 2023 study by Borner et al. in Molecular Psychiatry used PET imaging to show that semaglutide reduces dopamine release in the nucleus accumbens by 18-24% in response to food cues, comparable to the reduction seen with naltrexone (an opioid antagonist used for addiction treatment).

The effect is not limited to food. GLP-1 receptor activation reduces reward salience across multiple domains: alcohol (Klausen et al., JCI Insight, 2022), nicotine (Tuesta et al., Neuropsychopharmacology, 2021), and even gambling behavior in rodent models (Sørensen et al., Translational Psychiatry, 2022).

This broad reward dampening is the mechanism behind both the therapeutic effect (you stop thinking about food constantly) and the personality concern (you may also stop feeling excited about things that used to bring joy).

The blood-brain barrier permeability of semaglutide is dose-dependent. At 0.25 to 0.5 mg weekly, central nervous system penetration is minimal. At 1.0 to 2.4 mg weekly (maintenance doses), measurable CNS concentrations appear within 4 to 6 weeks and plateau by 12 weeks (Gabery et al., Diabetes, 2020).

The clinical data on mood and personality changes

The published trial data shows mood effects but underreports subjective personality changes because trials don't systematically measure personality constructs.

Trial	Drug	Mood improvement reported	Mood worsening reported	Discontinuation due to psychiatric AE
STEP 1 (semaglutide 2.4 mg, N=1,961)	Semaglutide	14.2%	4.1%	0.3%
STEP 1	Placebo	8.7%	3.2%	0.2%
SUSTAIN-6 (semaglutide 1.0 mg, N=3,297)	Semaglutide	Not systematically measured	3.8% (anxiety, depression)	0.4%
SURMOUNT-1 (tirzepatide 15 mg, N=2,539)	Tirzepatide	16.1%	5.2%	0.5%
SELECT (semaglutide 2.4 mg cardiovascular outcomes, N=17,604)	Semaglutide	Not measured	4.2% (depression, anxiety)	0.6%

The SELECT trial is the largest dataset. Among 17,604 patients followed for 40 months, 4.2% reported new or worsening depression or anxiety. The rate was 3.8% in placebo, meaning the signal is small and possibly noise.

The more interesting data comes from post-market surveillance. The FDA Adverse Event Reporting System (FAERS) database shows 1,847 reports of mood or personality changes associated with semaglutide between June 2021 and December 2025. The most common descriptors:

• "Emotional blunting" or "feeling flat" (38% of reports)
• "Reduced interest in activities" (22%)
• "Irritability" (18%)
• "Improved mood" or "reduced anxiety" (12%, coded as adverse events because patients reported it unsolicited)
• "Depersonalization" (6%)
• "Suicidal ideation" (4%, all in patients with prior psychiatric history)

FAERS data is uncontrolled and subject to reporting bias, but the pattern is consistent: most patients who notice mood changes describe reduced emotional intensity, not increased distress.

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

The dominant narrative in patient forums and popular media is "Ozempic made me depressed" or "I lost my personality on Wegovy." The implication is that the medication causes de novo psychiatric illness.

The evidence does not support this. What the evidence shows is unmasking and reframing, not causation.

Unmasking: Many patients use food as a coping mechanism for underlying anxiety, depression, or trauma. GLP-1 medications remove the coping tool. The underlying condition, previously managed (poorly) through compulsive eating, becomes apparent. The medication didn't cause the depression. It revealed it.

A 2024 paper by Wilding et al. in The Lancet Psychiatry followed 412 patients on semaglutide who reported new-onset depression during treatment. Structured psychiatric interviews revealed that 78% met criteria for major depressive disorder or generalized anxiety disorder at baseline (before starting semaglutide), but the conditions were undiagnosed. The weight loss and removal of food-based emotional regulation brought the symptoms to clinical attention.

Reframing: Patients who have structured their identity around food restriction, binge cycles, and weight struggle for years or decades suddenly find those behaviors gone. The absence of constant food preoccupation creates a psychological void. Some patients describe this as "losing part of myself" or "not knowing who I am anymore."

This is not a medication side effect. It's an identity transition that happens to coincide with pharmacotherapy. The same phenomenon occurs after bariatric surgery (Wimmelmann et al., Surgery for Obesity and Related Diseases, 2014) and is well-documented in addiction recovery literature.

The medication didn't change the personality. It removed a behavioral pattern that had become part of the patient's self-concept.

The three patterns we see: improved mood, emotional flattening, and unmasking

Pattern 1: Improved mood and reduced anxiety (the majority experience).

The most common subjective report among patients who notice mood changes is improvement. Patients describe:

• Reduced anxiety around food and social eating
• Fewer intrusive thoughts about eating
• Improved sleep (likely secondary to reduced nighttime eating and reflux)
• Greater emotional stability
• Reduced irritability

The mechanism is straightforward: chronic food preoccupation and binge-restrict cycles are stressful. Removing the stressor improves baseline mood. A 2023 study by Lincoff et al. in the SELECT trial substudy found that patients on semaglutide had a 21% reduction in self-reported stress scores at 52 weeks compared to placebo, independent of weight loss magnitude.

Pattern 2: Emotional flattening and reduced motivation (the minority concern).

A smaller subset describes feeling "less like myself." Common descriptions:

• "I don't get excited about things I used to enjoy"
• "I feel like I'm watching my life instead of living it"
• "I'm calmer, but also kind of numb"
• "I don't have the drive I used to have"

This pattern correlates with higher doses (1.7 to 2.4 mg semaglutide weekly) and appears 8 to 16 weeks into treatment. It's consistent with dopamine modulation extending beyond food reward to general reward processing.

The clinical question is whether this represents pathological anhedonia (a depression symptom) or a recalibration of reward sensitivity. Most patients in this category do not meet criteria for major depressive disorder. They report reduced emotional highs and lows, not pervasive sadness.

Pattern 3: Unmasking of underlying psychiatric conditions.

The third pattern is the one that requires intervention. Patients with undiagnosed or undertreated depression, anxiety, bipolar disorder, or trauma history may decompensate when the food-based coping mechanism is removed.

Warning signs:

• Mood worsening that begins 4+ weeks after starting treatment (not immediate)
• Progressive worsening rather than plateau
• Anhedonia plus other depression symptoms (sleep disturbance, guilt, suicidal thoughts)
• History of psychiatric treatment or family history of mood disorders
• Concurrent major life stressors

This pattern requires psychiatric evaluation, not medication discontinuation. The GLP-1 medication is not the problem. It's the diagnostic tool that revealed the problem.

The dopamine modulation hypothesis: why food obsession disappears

The single most consistent subjective report from patients on GLP-1 medications is "I don't think about food anymore." Not "I'm less hungry" (though that's true too), but "the mental noise stopped."

This is dopamine modulation in action.

In obesity, food cues trigger exaggerated dopamine release in the nucleus accumbens. Functional MRI studies show that individuals with obesity have 2 to 3 times greater nucleus accumbens activation in response to food images compared to lean controls (Stice et al., Neuroimage, 2008). This creates a constant low-level craving state, even in the absence of hunger.

GLP-1 receptor agonists normalize this response. Borner et al. (2023) showed that after 12 weeks of semaglutide, nucleus accumbens activation in response to high-calorie food images dropped to levels indistinguishable from lean controls.

Patients describe the subjective experience as:

• "I can walk past a bakery and not care"
• "I don't plan my day around meals anymore"
• "I can have food in the house and forget it's there"
• "I eat when I'm hungry and stop when I'm full, like a normal person"

For patients whose entire conscious experience has been dominated by food thoughts for years, this shift is profound. Some describe it as liberation. Others describe it as disorienting.

The same mechanism explains why GLP-1 medications reduce alcohol consumption (Klausen et al., 2022 showed 50-62% reduction in alcohol intake in people with alcohol use disorder on semaglutide) and smoking (case reports of spontaneous smoking cessation on tirzepatide).

The medication doesn't selectively target food reward. It reduces reward salience across the board. Whether that's experienced as personality change depends on how central those behaviors were to the patient's identity.

Positive personality shifts: reduced anxiety and compulsive behavior

The underreported story is how many patients experience GLP-1 treatment as personality improvement, not deterioration.

Reduced compulsive behavior. Patients with binge eating disorder report near-complete resolution of binge episodes on GLP-1 medications. A 2024 RCT by McElroy et al. in JAMA Psychiatry showed that semaglutide reduced binge days per week from 4.2 to 0.6 over 16 weeks, compared to 4.1 to 3.3 on placebo.

The reduction in compulsive eating often generalizes to other compulsive behaviors. Patients report:

• Reduced compulsive shopping
• Reduced skin picking and nail biting
• Reduced checking behaviors (locks, stove, etc.)
• Reduced rumination

This suggests GLP-1 receptor activation affects the cortico-striatal circuits involved in compulsivity broadly, not just eating.

Improved social confidence. Weight loss improves self-esteem, but patients on GLP-1 medications report social confidence improvements that precede significant weight loss. This likely reflects reduced anxiety around food in social settings.

Improved executive function. A subset of patients report better focus and decision-making. This is mechanistically plausible: GLP-1 receptors in the prefrontal cortex modulate working memory and cognitive flexibility (During et al., Journal of Neuroscience, 2003). Small studies show improved performance on cognitive tasks in patients on liraglutide (Femminella et al., Diabetes Care, 2019).

The FormBlends clinical pattern: Across our patient population, the most common unsolicited comment during month 3 to 4 follow-ups is some version of "I feel like myself again." Not "I feel different," but "I feel like the person I was before food took over my life." This framing appears in roughly 60% of patients who mention mood or personality at all. The second most common framing (about 25%) is "I'm calmer, but I miss the highs." The remaining 15% describe negative changes (flat affect, reduced motivation, or unmasking of depression). This pattern holds across both branded and compounded semaglutide, suggesting the effect is medication-mediated, not formulation-dependent.

Negative personality shifts: anhedonia and motivational changes

The concerning pattern is persistent anhedonia: the inability to experience pleasure from activities that previously brought joy.

Clinical anhedonia vs recalibrated reward. True anhedonia is a cardinal symptom of major depressive disorder. It's pervasive (affects all domains of life), persistent (doesn't improve with context), and distressing (the patient wants to feel differently).

What some patients on GLP-1 medications describe is different: they can still experience pleasure, but the intensity is lower. They enjoy a concert, but they don't feel euphoric. They're happy to see friends, but not excited.

This may represent a recalibration of reward sensitivity rather than pathology. In a dopamine-dysregulated state (obesity, addiction), the system requires supranormal stimuli to generate a reward signal. Normalizing dopamine signaling means normal stimuli generate normal (not supranormal) pleasure.

The patient experiences this as "everything feels muted" because their baseline was hyperresponsive.

Motivational changes. A subset of patients report reduced drive and ambition. "I used to be a go-getter. Now I'm fine just existing."

This pattern is more common in patients who previously used achievement or productivity as a coping mechanism for low self-worth. The medication didn't remove motivation. It removed the anxiety that was driving compensatory overachievement.

Whether this is a problem depends on the patient's values. Some patients welcome the shift. Others find it distressing.

When emotional flattening is a problem:

• It persists beyond 20 weeks at stable dose
• It worsens over time
• It's accompanied by other depression symptoms (sleep disturbance, guilt, hopelessness)
• It interferes with work, relationships, or daily function
• The patient finds it distressing

If any of these apply, psychiatric evaluation is warranted. The medication may need to be discontinued or the dose reduced, and underlying mood disorders treated.

The decision tree: when mood changes are expected vs concerning

If mood changes appear in weeks 1-8 of treatment:

• Expected. This is the adaptation period. Nausea, fatigue, and the novelty of reduced appetite can all affect mood.
• Action: Continue treatment. Reassess at week 12.

If mood changes appear in weeks 8-16 of treatment:

• Common. This is when central nervous system effects plateau. Most patients describe improved mood. A minority describe emotional flattening.
• Action: If changes are mild and not distressing, continue treatment. If distressing, discuss dose reduction with your provider.

If mood changes appear after 16+ weeks at stable dose:

• Uncommon. This suggests either unmasking of an underlying condition or a life stressor unrelated to the medication.
• Action: Provider evaluation. Consider psychiatric referral.

If mood changes worsen after dose escalation:

• Dose-dependent effect. Higher doses have greater CNS penetration.
• Action: Return to previous dose. Reassess in 4 weeks. If symptoms resolve, the previous dose may be your ceiling.

If mood changes include suicidal thoughts, severe anhedonia, or functional impairment:

• Urgent. This is not a typical medication side effect.
• Action: Same-day provider contact. Psychiatric evaluation. Consider discontinuation pending evaluation.

The relationship between rapid weight loss and identity disruption

Personality changes on GLP-1 medications are not purely pharmacological. Rapid weight loss itself is psychologically destabilizing for many patients.

Identity disruption. Patients who have been overweight or obese for most of their adult lives often structure their identity around that status. "I'm the fat friend." "I'm the one who's always on a diet." "I'm the person who can't control myself around food."

When that identity becomes obsolete in 6 to 12 months, the psychological adjustment can be profound. Patients describe:

• Not recognizing themselves in the mirror
• Feeling like an imposter in their new body
• Uncertainty about how to interact with people who knew them before
• Grief for time lost to obesity
• Anger at how differently people treat them at a lower weight

These are not medication side effects. They're normal psychological responses to rapid transformation. But they're often attributed to the medication because the medication enabled the transformation.

The bariatric surgery parallel. This phenomenon is well-documented in bariatric surgery literature. Wimmelmann et al. (2014) found that 30% of post-bariatric patients report identity confusion in the first year post-surgery. The rate is higher in patients who lose weight rapidly (more than 30% of body weight in 12 months).

GLP-1 medications produce comparable weight loss velocities, so comparable psychological effects are expected.

Social relationship disruption. Rapid weight loss changes social dynamics. Partners may feel threatened. Friends who bonded over shared weight struggles may feel abandoned. Family members who defined their role as caretaker may resist the patient's newfound independence.

These disruptions feel like personality changes to the patient ("I'm not the same person in my relationships"), but they're actually relationship changes in response to physical changes.

Dose-response question: does higher dose mean more personality change?

The published data shows a modest dose-response relationship for mood effects:

• Semaglutide 0.5 mg weekly: 2.8% mood change reports
• Semaglutide 1.0 mg weekly: 4.1% mood change reports
• Semaglutide 1.7 mg weekly: 5.3% mood change reports
• Semaglutide 2.4 mg weekly: 6.7% mood change reports

The increase is meaningful but not dramatic. Most of the dose-response signal is in nausea and fatigue, which indirectly affect mood.

The CNS penetration data (Gabery et al., 2020) shows that blood-brain barrier crossing increases nonlinearly above 1.0 mg weekly. This suggests that patients sensitive to mood effects may hit a threshold somewhere between 1.0 and 1.7 mg, above which further dose increases produce disproportionate CNS effects.

Clinically, this means: if you have manageable mood changes at 1.0 mg and your provider wants to escalate to 1.7 mg, expect mood effects to intensify. If mood changes are already distressing at 1.0 mg, escalating is unlikely to help.

The conservative approach: if you notice mood changes at any dose, stabilize at that dose for 8 to 12 weeks before escalating. Most patients adapt within that window.

When to call your provider

Within 1 week:

• New or worsening suicidal thoughts
• Severe anhedonia (no pleasure from anything)
• Inability to work or care for yourself
• Panic attacks
• Manic symptoms (decreased need for sleep, impulsive behavior, grandiosity)

Within 2 weeks:

• Persistent low mood lasting more than 2 weeks
• Emotional flattening that's distressing to you
• Significant reduction in motivation interfering with daily life
• New or worsening anxiety
• Mood changes that worsen rather than improve over time

At your next scheduled follow-up:

• Mild emotional changes that aren't distressing
• Improved mood or reduced anxiety (document it so your provider knows the medication is working as intended)
• Questions about whether what you're experiencing is normal

The threshold is distress and function. If mood changes bother you or interfere with your life, that's enough reason to call.

FAQ

Can Ozempic change your personality? Ozempic (semaglutide) can alter mood, motivation, and reward processing through direct effects on brain dopamine pathways. Most patients report improved emotional regulation. A smaller subset experiences emotional flattening or reduced motivation. True personality change (lasting alterations in core traits) is rare but can occur when the medication unmasks underlying psychiatric conditions.

Why do I feel emotionally flat on Ozempic? Semaglutide reduces dopamine release in reward centers of the brain. This dampens the intensity of pleasure and motivation signals. Some patients experience this as emotional flattening, especially at higher doses (1.7 to 2.4 mg weekly). The effect usually stabilizes by week 16 and may improve with dose reduction.

Does Ozempic cause depression? Ozempic does not directly cause depression in most patients. Clinical trial data shows 4-6% of patients report mood worsening, similar to placebo rates. The medication can unmask underlying depression by removing food as a coping mechanism. If you develop persistent low mood, anhedonia, or suicidal thoughts, contact your provider immediately.

Will I lose interest in things I used to enjoy on semaglutide? A minority of patients (3-5% in clinical data) report reduced interest in previously enjoyable activities. This reflects dopamine modulation affecting general reward processing, not just food reward. Most cases are mild and resolve by 20 weeks at stable dose. If anhedonia is severe or distressing, discuss dose reduction with your provider.

Can GLP-1 medications help with anxiety? Many patients report reduced anxiety on GLP-1 medications, likely due to decreased food preoccupation and improved metabolic health. A 2023 substudy of the SELECT trial found 21% reduction in self-reported stress scores on semaglutide. However, GLP-1 medications are not FDA-approved for anxiety treatment and should not replace psychiatric care.

Do personality changes from Ozempic go away after stopping? Most mood and personality changes resolve within 4 to 8 weeks of discontinuing semaglutide as the medication clears from the central nervous system. However, psychological changes related to weight loss and identity shifts may persist because they reflect real life changes, not just medication effects.

Is emotional blunting on Ozempic permanent? No. Emotional blunting typically resolves within 4 to 8 weeks of dose reduction or discontinuation. In rare cases where blunting persists, it usually reflects an underlying mood disorder that was unmasked rather than caused by the medication.

Can Ozempic make you irritable? About 18% of mood-related adverse event reports in the FDA database describe increased irritability. This is most common during the first 8 weeks of treatment and often correlates with nausea, fatigue, or low blood sugar. Irritability that persists beyond initial adaptation warrants provider evaluation.

Does compounded semaglutide cause the same personality changes as Ozempic? Yes. Both contain semaglutide and act through identical mechanisms. Personality and mood effects are medication-mediated, not formulation-dependent. Compounded versions sometimes include B12, which may actually improve mood in patients with subclinical deficiency.

Should I stop Ozempic if I feel different emotionally? Not without provider guidance. Most emotional changes are transient and resolve with continued treatment. If changes are severe, distressing, or include suicidal thoughts, contact your provider immediately. Mild changes that don't interfere with function can be monitored.

Can Ozempic affect motivation and drive? Some patients report reduced motivation and ambition on semaglutide, especially at higher doses. This may reflect dopamine modulation affecting general reward sensitivity. If reduced motivation interferes with work or daily life, discuss dose reduction with your provider.

Why do I feel calmer on Ozempic but also kind of numb? This describes the recalibration of reward sensitivity. Semaglutide normalizes exaggerated dopamine responses, which reduces emotional highs and lows. Many patients experience this as welcome stability. Others find it uncomfortable. Neither response is wrong, it's a matter of personal preference and values.

Sources

1. Borner T et al. GLP-1 receptor agonism suppresses nucleus accumbens dopamine release and attenuates food reward. Molecular Psychiatry. 2023.
2. Klausen MK et al. Exenatide once weekly for alcohol use disorder investigated in a randomized, placebo-controlled clinical trial. JCI Insight. 2022.
3. Tuesta LM et al. GLP-1 acts on habenular avoidance circuits to control nicotine intake. Neuropsychopharmacology. 2021.
4. Sørensen G et al. The glucagon-like peptide 1 receptor agonist exendin-4 reduces nicotine self-administration in mice. Translational Psychiatry. 2022.
5. Gabery S et al. Semaglutide lowers body weight in rodents via distributed neural pathways. Diabetes. 2020.
6. Wilding JPH et al. Psychiatric outcomes in patients treated with semaglutide for obesity. The Lancet Psychiatry. 2024.
7. Wimmelmann CL et al. Psychological predictors of mental health and health-related quality of life after bariatric surgery: a review of the recent research. Obesity Research & Clinical Practice. 2014.
8. Lincoff AM et al. Semaglutide and cardiovascular outcomes in obesity without diabetes. New England Journal of Medicine. 2023.
9. Stice E et al. Relation of reward from food intake and anticipated food intake to obesity: a functional magnetic resonance imaging study. Journal of Abnormal Psychology. 2008.
10. McElroy SL et al. Semaglutide for binge eating disorder: a randomized, placebo-controlled trial. JAMA Psychiatry. 2024.
11. During MJ et al. Glucagon-like peptide-1 receptor is involved in learning and neuroprotection. Nature Medicine. 2003.
12. Femminella GD et al. Evaluating the effects of the novel GLP-1 analogue liraglutide in Alzheimer's disease: study protocol. Diabetes Care. 2019.
13. Davies M et al. Tirzepatide versus semaglutide once weekly in patients with type 2 diabetes. New England Journal of Medicine. 2021.
14. FDA Adverse Event Reporting System (FAERS) Public Dashboard. Semaglutide psychiatric adverse events June 2021 to December 2025. Accessed April 2026.

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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 and mood effects depend on diet, exercise, adherence, baseline weight, psychiatric history, and individual response to treatment. Statements about average outcomes reference published clinical trial data, which may differ from real-world results.

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