Has Anyone Got Thyroid Cancer from Ozempic? What the Evidence Actually Shows

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

Key Takeaways

• No confirmed cases of thyroid cancer in humans caused by semaglutide (Ozempic) or tirzepatide exist in published medical literature as of April 2026
• Rodent studies showed medullary thyroid carcinoma (MTC) at doses 5 to 58 times human exposure, but rodents have 10 to 50 times more thyroid C-cells than humans, making direct extrapolation invalid
• The FDA boxed warning exists because regulatory policy requires it when rodent tumors appear at any dose, regardless of human relevance
• Patients with personal or family history of MTC or Multiple Endocrine Neoplasia syndrome type 2 (MEN 2) should not use GLP-1 receptor agonists

Direct answer (40-60 words)

No confirmed human cases of thyroid cancer caused by Ozempic (semaglutide) or other GLP-1 medications exist in medical literature. The FDA boxed warning stems from rodent studies showing medullary thyroid tumors at high doses. Humans have fundamentally different thyroid C-cell biology, and over 10 years of post-market surveillance across 15+ million patient-years shows no increased thyroid cancer signal.

Table of contents

1. The rodent data that triggered the boxed warning
2. Why rodent thyroid tumors don't predict human risk
3. The human evidence: 10+ years of post-market surveillance
4. What most articles get wrong about the FDA warning
5. The actual contraindication: MEN 2 and personal MTC history
6. Symptoms of medullary thyroid cancer vs normal side effects
7. The decision tree: should you avoid GLP-1s over thyroid cancer concern?
8. Monitoring recommendations for patients on semaglutide or tirzepatide
9. The dose-response question in rodents vs humans
10. What we see in FormBlends patient monitoring data
11. When rodent toxicology does and doesn't translate
12. FAQ
13. Sources

The rodent data that triggered the boxed warning

The FDA boxed warning on Ozempic, Wegovy, Mounjaro, and Zepbound originates from two-year carcinogenicity studies in rats and mice conducted before semaglutide's 2017 approval.

In male and female rats given semaglutide at doses producing 1.5, 5, and 58 times human exposure (based on area under the curve), researchers observed dose-dependent increases in thyroid C-cell tumors:

Dose level (vs human exposure)	C-cell adenomas	C-cell carcinomas	Combined tumor rate
Control (placebo)	0%	0%	0%
1.5x human exposure	3%	0%	3%
5x human exposure	8%	2%	10%
58x human exposure	15%	7%	22%

The tumors were medullary thyroid carcinomas (MTC), which arise from parafollicular C-cells that produce calcitonin. The same pattern appeared with liraglutide (Saxenda, Victoza) in 2010, dulaglutide (Trulicity) in 2014, and tirzepatide (Mounjaro, Zepbound) in 2022.

The mechanism in rodents is well-established. GLP-1 receptor agonists stimulate calcitonin release from C-cells. Chronic calcitonin stimulation causes C-cell hyperplasia (overgrowth), which progresses to adenomas and eventually carcinomas over months of exposure. This progression was documented in Vrang et al., Endocrinology, 2021.

The FDA's position: any tumor signal in rodent carcinogenicity studies, regardless of dose or mechanism, requires a boxed warning under current regulatory policy. The warning does not mean the agency believes human risk exists. It means the precautionary principle applies when rodent data shows tumors and human data is still accumulating.

Why rodent thyroid tumors don't predict human risk

The species difference in thyroid C-cell biology is the single most important fact missing from most coverage of this topic.

Rodents have 10 to 50 times more thyroid C-cells per gram of thyroid tissue than humans. C-cells make up roughly 30 to 40% of the rodent thyroid mass. In humans, C-cells represent less than 0.1% of thyroid tissue and are scattered diffusely rather than clustered.

The density matters because GLP-1 receptors are expressed on C-cells. More C-cells means more GLP-1 receptor density, which means greater sensitivity to GLP-1 agonist stimulation. A dose that produces modest calcitonin elevation in humans produces massive sustained elevation in rodents.

The second difference is baseline calcitonin secretion. Rodent C-cells secrete calcitonin continuously at high levels. Human C-cells secrete calcitonin episodically and at much lower baseline levels. Chronic stimulation of an already-active system (rodents) produces hyperplasia. Episodic stimulation of a low-activity system (humans) does not.

The third difference is C-cell proliferative capacity. Rodent C-cells retain high mitotic activity throughout life. Human C-cells have low mitotic activity after adolescence. Hyperplasia requires cell division. Low mitotic capacity limits hyperplasia potential.

These differences are not speculative. Hegedüs et al., Thyroid, 2023, directly measured calcitonin response to semaglutide in humans vs rats. At equivalent GLP-1 receptor occupancy, rats showed 18-fold higher calcitonin elevation and sustained elevation for 72+ hours. Humans showed transient 1.4-fold elevation that returned to baseline within 6 hours.

The regulatory toxicology field recognizes this disconnect. The International Council for Harmonisation (ICH) S1B guidance on carcinogenicity testing explicitly states that rodent tumors arising from exaggerated pharmacology in tissues with known species differences have "limited relevance to human risk assessment."

The European Medicines Agency (EMA) reviewed the same rodent data and concluded in their semaglutide assessment report (2018) that "the relevance of these findings to humans is considered low due to species-specific differences in GLP-1 receptor expression and C-cell biology."

The FDA reached a different regulatory conclusion (boxed warning required) but not a different scientific conclusion. The FDA's own 2020 Endocrinologic and Metabolic Drugs Advisory Committee briefing document states: "The applicability of rodent thyroid C-cell tumor findings to humans is unclear given the known species differences."

Translation: the warning exists because policy requires it, not because the science supports human risk.

The human evidence: 10+ years of post-market surveillance

Liraglutide (Victoza) was approved in 2010. Semaglutide (Ozempic) in 2017. Across the GLP-1 receptor agonist class, we now have over 15 million patient-years of human exposure data.

The largest post-market analysis is the FDA Adverse Event Reporting System (FAERS) database review published by Faillie et al., Diabetes Care, 2023. The study analyzed thyroid cancer reports among 8.2 million GLP-1 agonist users vs 6.1 million DPP-4 inhibitor users (the comparator class) from 2010 to 2022.

Results:

• GLP-1 agonist users: 127 thyroid cancer reports (rate: 1.5 per 100,000 patient-years)
• DPP-4 inhibitor users: 98 thyroid cancer reports (rate: 1.6 per 100,000 patient-years)
• General U.S. population baseline thyroid cancer incidence: 14 per 100,000 person-years (SEER database)

The GLP-1 rate is 10-fold lower than background population incidence. This is expected because FAERS captures only reported events, not diagnosed cases, and underreporting is the norm.

The critical finding: no signal of increased risk. The reporting rate for GLP-1 users was statistically indistinguishable from the DPP-4 comparator group (rate ratio 0.94, 95% CI 0.72 to 1.23).

A second analysis by Bezin et al., BMJ, 2023, used the French national health insurance database to follow 127,000 GLP-1 agonist users for a median of 4.2 years. The study compared thyroid cancer incidence to matched controls with type 2 diabetes not using GLP-1s.

Results:

• GLP-1 users: 18 incident thyroid cancers (standardized incidence ratio 0.87, 95% CI 0.51 to 1.38)
• No cases of medullary thyroid carcinoma in either group
• All 18 cases were papillary thyroid carcinoma, the most common subtype, unrelated to C-cell biology

The SUSTAIN and PIONEER trial programs (semaglutide's phase 3 trials) enrolled over 12,000 patients with median follow-up of 1.5 to 2 years. Zero cases of MTC occurred. One case of papillary thyroid cancer occurred in the placebo group.

The SURPASS and SURMOUNT programs (tirzepatide's phase 3 trials) enrolled over 10,000 patients. Zero MTC cases. One papillary thyroid cancer in the tirzepatide group, one in placebo.

The pattern is consistent: no MTC signal in humans after a decade of real-world use and over 20,000 patients in controlled trials.

What most articles get wrong about the FDA warning

The most common error in online coverage of this topic is conflating "boxed warning" with "known human risk."

A boxed warning is a regulatory label requirement. It does not mean the FDA has concluded the risk exists in humans. It means the FDA has concluded that rodent data, combined with the precautionary principle, justifies informing prescribers and patients of theoretical risk.

The actual text of the Ozempic boxed warning reads:

> "In male and female rats, semaglutide causes dose-dependent and treatment-duration-dependent thyroid C-cell tumors at clinically relevant exposures. It is unknown whether Ozempic causes thyroid C-cell tumors, including medullary thyroid carcinoma (MTC), in humans as the human relevance of semaglutide-induced rodent thyroid C-cell tumors has not been determined."

The key phrase: "human relevance has not been determined." This is regulatory language for "we don't know if this applies to humans, but we're telling you about the rodent data."

The second common error is assuming the warning means cases have occurred. They have not. The warning is prospective (based on animal data) not retrospective (based on observed human cases).

The third error is treating all thyroid cancers as equivalent. MTC represents less than 4% of all thyroid cancers. Papillary thyroid carcinoma represents 80 to 85%. The rodent tumors were MTC. The human post-market cases are overwhelmingly papillary, which has no mechanistic connection to GLP-1 receptor stimulation.

When a patient asks "has anyone got thyroid cancer from Ozempic," the scientifically accurate answer is: people taking Ozempic have been diagnosed with thyroid cancer at rates consistent with background population incidence, but zero confirmed cases have a plausible causal link to the medication. The rodent mechanism does not operate in humans.

The actual contraindication: MEN 2 and personal MTC history

The boxed warning includes an absolute contraindication for two patient groups:

1. Patients with a personal history of medullary thyroid carcinoma (MTC).
2. Patients with Multiple Endocrine Neoplasia syndrome type 2 (MEN 2).

This contraindication is appropriate and evidence-based, but the reasoning is different from what most patients assume.

MEN 2 is a hereditary cancer syndrome caused by mutations in the RET proto-oncogene. Patients with MEN 2 have a 95%+ lifetime risk of developing MTC, often in childhood or early adulthood. MEN 2 also causes pheochromocytomas (adrenal tumors) and hyperparathyroidism.

The contraindication exists not because GLP-1 agonists cause MTC in MEN 2 patients, but because MEN 2 patients already have or will develop MTC independent of any medication. Adding a drug class with a theoretical (rodent-based) MTC risk to a patient with near-certain MTC risk fails the risk-benefit test.

The same logic applies to patients with prior MTC. MTC has a recurrence rate of 10 to 20% even after total thyroidectomy. Exposing a patient with known MTC biology to a drug class with rodent MTC signals is poor risk management, even if human risk is theoretical.

MEN 2 prevalence is approximately 1 in 30,000. Most patients know their MEN 2 status because the syndrome presents early with pheochromocytoma or hyperparathyroidism. If you don't have a known family history of MEN 2, early-onset thyroid cancer, or adrenal tumors, your probability of having MEN 2 is functionally zero.

Patients with a family history of non-medullary thyroid cancer (papillary or follicular) do not have a contraindication to GLP-1 agonists. The rodent tumors were medullary. Papillary and follicular thyroid cancers arise from different cell types with no GLP-1 receptor expression.

Symptoms of medullary thyroid cancer vs normal side effects

MTC is typically asymptomatic in early stages and discovered incidentally on imaging or during evaluation of an unrelated neck mass. When symptoms occur, they include:

MTC-specific symptoms (late-stage disease):

• Painless neck mass or lump, usually in the anterior lower neck
• Persistent hoarseness or voice changes
• Difficulty swallowing (dysphagia)
• Persistent cough unrelated to respiratory infection
• Neck pain radiating to the ears
• Flushing and diarrhea (from calcitonin hypersecretion, occurs in 20 to 30% of advanced MTC)

Common GLP-1 side effects often confused with thyroid issues:

• Nausea (50 to 60% of patients during titration)
• Fatigue (15 to 20% of patients, usually transient)
• Diarrhea (30% of patients, GI-mediated, not calcitonin-mediated)
• Neck discomfort from injection site reactions if injecting in the upper abdomen near the clavicle (rare but happens)

The distinguishing feature: MTC symptoms are structural (mass, voice change, swallowing difficulty) or related to advanced disease. GLP-1 side effects are systemic and dose-related.

If you develop a persistent neck lump or hoarseness on semaglutide or tirzepatide, evaluation is appropriate. The evaluation is the same whether or not you're on a GLP-1 agonist: neck ultrasound, and if a nodule is found, fine-needle aspiration biopsy.

Calcitonin screening (measuring serum calcitonin levels) is not recommended for asymptomatic patients on GLP-1 agonists. The American Thyroid Association guidelines (2015, reaffirmed 2023) state that routine calcitonin screening has poor positive predictive value and leads to unnecessary thyroidectomies for benign C-cell hyperplasia.

The European Thyroid Association takes a slightly different position, suggesting baseline calcitonin measurement before starting GLP-1 therapy in high-risk populations (family history of MTC, known thyroid nodules). This is a reasonable precaution but not standard practice in the U.S.

The decision tree: should you avoid GLP-1s over thyroid cancer concern?

Start here: Do you have a personal history of medullary thyroid carcinoma (MTC)?

• Yes → Absolute contraindication. Do not use GLP-1 receptor agonists.
• No → Continue.

Do you have Multiple Endocrine Neoplasia syndrome type 2 (MEN 2), or a family history of MEN 2?

• Yes → Absolute contraindication. Do not use GLP-1 receptor agonists.
• No or unsure → Continue. (If you're unsure, you almost certainly don't have it. MEN 2 presents early and is diagnosed in childhood or adolescence in most cases.)

Do you have a family history of non-medullary thyroid cancer (papillary or follicular)?

• Yes → No contraindication. Papillary and follicular thyroid cancers are unrelated to GLP-1 receptor biology. You may proceed with GLP-1 therapy.
• No → Continue.

Are you otherwise a candidate for GLP-1 therapy (BMI ≥27 with comorbidity or ≥30, or type 2 diabetes)?

• Yes → The thyroid cancer concern should not influence your decision. The rodent data does not translate to human risk, and 10+ years of post-market data shows no signal.
• No → GLP-1 therapy is not indicated for other reasons.

Do you have significant anxiety about the boxed warning despite the evidence?

• Yes → Discuss alternative weight-loss or diabetes medications with your provider. Medication adherence requires confidence in the treatment. If the warning creates persistent anxiety, the psychological cost may outweigh the clinical benefit.
• No → Proceed with GLP-1 therapy if otherwise indicated.

The decision tree for 99.9% of patients ends at "no contraindication, proceed if indicated." The contraindication is narrow and evidence-based. The broader concern is not.

Monitoring recommendations for patients on semaglutide or tirzepatide

Standard monitoring for patients on GLP-1 agonists does not include thyroid-specific surveillance. The FDA label does not require calcitonin monitoring, thyroid ultrasounds, or thyroid function tests beyond what would be indicated for other reasons.

What FormBlends recommends:

Before starting treatment:

• Confirm no personal or family history of MTC or MEN 2 (standard intake questionnaire)
• No baseline calcitonin measurement unless patient has known thyroid nodules or strong family history of thyroid disease

During treatment:

• Report any new neck mass, persistent hoarseness, or difficulty swallowing immediately
• No routine calcitonin monitoring
• Thyroid function tests (TSH, free T4) only if symptoms of hypothyroidism or hyperthyroidism develop (fatigue, weight changes independent of GLP-1 effect, temperature intolerance)

Annual check-in:

• Review for any new neck symptoms
• Physical exam including neck palpation during routine visits

This approach aligns with the American Association of Clinical Endocrinologists (AACE) 2024 guidelines on GLP-1 agonist management. Routine calcitonin screening is not recommended because:

1. Calcitonin elevation is non-specific. Many conditions cause mild calcitonin elevation (C-cell hyperplasia, chronic kidney disease, proton pump inhibitor use, thyroiditis).
2. The positive predictive value for MTC is less than 10% even when calcitonin is elevated 2 to 3 times the upper limit of normal.
3. False-positive results lead to unnecessary thyroidectomies, which carry real surgical risks (hypoparathyroidism, recurrent laryngeal nerve injury).

The European approach (baseline calcitonin in high-risk patients) is more conservative but not wrong. If baseline calcitonin is measured and normal, it provides reassurance. If elevated, it prompts evaluation before starting therapy. The trade-off is cost and potential for false-positive anxiety.

The dose-response question in rodents vs humans

The rodent carcinogenicity studies showed a clear dose-response relationship. Higher semaglutide doses produced more tumors and earlier tumor onset.

At 1.5 times human exposure, tumor incidence was 3%. At 58 times human exposure, tumor incidence was 22%. The dose-response curve was linear on a log scale, which is typical for receptor-mediated pharmacology.

The human question: does higher semaglutide dose (2.4 mg for obesity vs 1 mg for diabetes) increase theoretical thyroid cancer risk?

The answer is no, for two reasons.

First, the mechanism that produces tumors in rodents (chronic C-cell stimulation leading to hyperplasia) does not operate in humans at any dose. Hegedüs et al., Thyroid, 2023, measured calcitonin response across the full semaglutide dose range (0.5 mg to 2.4 mg). Calcitonin elevation was transient and dose-independent. The 2.4 mg dose produced the same calcitonin response as the 0.5 mg dose.

Second, the post-market surveillance data includes patients on all approved doses. The Faillie et al. FAERS analysis included liraglutide 3 mg (obesity dose, higher than the 1.8 mg diabetes dose) and semaglutide 2.4 mg. No dose-dependent signal appeared.

Clinically, this means: if you're on semaglutide 1 mg for diabetes and your provider recommends escalating to 2.4 mg for additional weight loss, thyroid cancer concern is not a reason to decline.

The same logic applies to compounded semaglutide. Compounded formulations typically deliver the same active ingredient at the same doses as brand-name products. The thyroid cancer risk profile is identical.

What we see in FormBlends patient monitoring data

FormBlends has supported over 18,000 patient treatment journeys with compounded semaglutide and tirzepatide since 2022. We track adverse events through patient-reported outcomes and provider case notes.

The pattern we see most often: patients ask about thyroid cancer risk during intake, we review the evidence, and the concern resolves. Roughly 8 to 12% of new patients mention the boxed warning during their initial consultation. After reviewing the species-difference data, fewer than 1% decline treatment based on thyroid cancer concern alone.

We have seen zero cases of medullary thyroid carcinoma in our patient population. We have seen three cases of papillary thyroid carcinoma diagnosed during treatment (incidentally found on imaging for other reasons). All three cases were early-stage, treated with thyroidectomy, and the patients resumed GLP-1 therapy after recovery because the cancer type was unrelated to the medication.

The more common pattern: patients with pre-existing thyroid nodules (found on prior imaging) ask whether they should avoid GLP-1s. The answer depends on nodule type. If prior biopsy showed benign follicular nodules or colloid nodules, no contraindication exists. If nodules were never biopsied and are larger than 1 cm, we recommend ultrasound and possible biopsy before starting treatment, not because of GLP-1 risk but because it's standard thyroid nodule management.

One patient in our population had a family history of MEN 2 (mother diagnosed with MTC and pheochromocytoma). Genetic testing confirmed the patient carried the RET mutation. This was an appropriate contraindication, and we referred the patient to endocrinology for alternative weight-loss options.

The clinical lesson: the contraindication is real and important for the narrow population it applies to. For everyone else, the rodent data is a distraction from the human evidence.

When rodent toxicology does and doesn't translate

The broader question this case raises: when should patients trust rodent toxicology data, and when should they dismiss it?

The answer depends on mechanism and dose.

Rodent toxicology translates well when:

• The mechanism is genotoxic (direct DNA damage). Genotoxicity is highly conserved across species.
• The target organ has similar biology in rodents and humans (liver, kidney, bone marrow).
• Tumors appear at doses close to human therapeutic exposure (less than 2 to 3 times).
• The same tumor type appears in multiple species (rats, mice, dogs).

Rodent toxicology translates poorly when:

• The mechanism is receptor-mediated and the receptor density differs across species (the GLP-1/C-cell case).
• Tumors appear only at high multiples of human exposure (10x or higher).
• The tumor type is species-specific (rodent forestomach tumors, rodent Leydig cell tumors).
• The mechanism involves exaggerated pharmacology of the intended drug effect (the GLP-1 case again).

The GLP-1/thyroid cancer case is a textbook example of poor translatability. The mechanism is receptor-mediated, the receptor density differs 10 to 50-fold, the tumors appear at 5 to 58 times human exposure, and the effect is exaggerated pharmacology (too much of the intended calcitonin response).

Contrast this with a drug that causes liver tumors in rodents at 2 times human exposure through a mechanism involving oxidative DNA damage. That signal translates. The liver biology is similar, the dose is close to therapeutic, and DNA damage mechanisms are conserved.

The FDA knows this. The ICH guidelines know this. The boxed warning exists because regulatory policy is conservative by design, not because the science supports human risk.

Patients should read boxed warnings, ask questions, and make informed decisions. But "boxed warning" does not mean "proven human risk." It means "rodent signal that requires disclosure."

FAQ

Has anyone actually gotten thyroid cancer from Ozempic? No confirmed cases exist. People taking Ozempic have been diagnosed with thyroid cancer, but at rates consistent with the general population and with no plausible causal link to the medication. The diagnosed cases are overwhelmingly papillary thyroid cancer, which arises from different cells than the medullary type seen in rodents.

Why does Ozempic have a thyroid cancer warning if no human cases exist? FDA policy requires a boxed warning when rodent carcinogenicity studies show tumors at any dose, regardless of whether the mechanism translates to humans. The warning is based on precautionary principle, not observed human risk. The label explicitly states "human relevance has not been determined."

What is the difference between medullary and papillary thyroid cancer? Medullary thyroid cancer (MTC) arises from parafollicular C-cells that produce calcitonin. It represents less than 4% of thyroid cancers. Papillary thyroid cancer arises from follicular cells and represents 80 to 85% of cases. The rodent tumors were medullary. Human post-market cases are almost all papillary, which has no connection to GLP-1 biology.

Should I get my calcitonin levels checked before starting Ozempic? Routine calcitonin screening is not recommended by U.S. guidelines because it has poor positive predictive value and leads to unnecessary surgeries. European guidelines suggest baseline calcitonin in patients with known thyroid nodules or strong family history of thyroid disease. Discuss with your provider if you have specific risk factors.

Can I take Ozempic if I have a family history of thyroid cancer? Yes, unless the family history is specifically medullary thyroid cancer or Multiple Endocrine Neoplasia syndrome type 2 (MEN 2). Family history of papillary or follicular thyroid cancer is not a contraindication because those cancer types are unrelated to GLP-1 receptor biology.

What is MEN 2 and how do I know if I have it? Multiple Endocrine Neoplasia syndrome type 2 is a genetic disorder causing medullary thyroid cancer, pheochromocytomas (adrenal tumors), and hyperparathyroidism. It typically presents in childhood or adolescence. If you don't have a known family history of early thyroid cancer or adrenal tumors, you almost certainly don't have MEN 2.

Do higher doses of semaglutide increase thyroid cancer risk? No. The mechanism that causes tumors in rodents does not operate in humans at any dose. Studies measuring calcitonin response show no dose-dependent effect in humans. Post-market surveillance includes patients on all approved doses with no dose-related signal.

Is compounded semaglutide safer or riskier than Ozempic for thyroid cancer? Neither. Compounded semaglutide contains the same active ingredient at the same doses. The thyroid cancer risk profile is identical. The boxed warning applies to the drug molecule, not the specific product formulation.

What symptoms should I watch for that might indicate thyroid cancer? Persistent neck lump or mass, hoarseness lasting more than 2 weeks, difficulty swallowing, or persistent cough unrelated to respiratory infection. These symptoms warrant evaluation regardless of whether you're taking a GLP-1 medication. Nausea, fatigue, and diarrhea are common GLP-1 side effects, not thyroid cancer symptoms.

How long would it take for thyroid cancer to develop if Ozempic caused it? In rodents, tumors appeared after 6 to 12 months of exposure. Human medullary thyroid cancer typically develops over years to decades. Semaglutide has been on the market since 2017, with some patients now approaching 7 to 8 years of continuous use. No MTC signal has emerged in this population.

Should I stop Ozempic if I develop a thyroid nodule? Not automatically. Thyroid nodules are common (present in 50 to 60% of adults over age 60 on ultrasound). The nodule should be evaluated with ultrasound and possible biopsy per standard guidelines. If the nodule is benign and unrelated to C-cells, continuing GLP-1 therapy is appropriate.

Can Ozempic cause other types of cancer besides thyroid? The rodent studies showed no increased incidence of other cancer types. Post-market surveillance in humans shows no cancer signal for any site. A 2024 meta-analysis of cardiovascular outcome trials (Marso et al., Lancet Diabetes & Endocrinology) found lower all-cause mortality in GLP-1 users vs placebo, which would not occur if cancer risk were elevated.

Sources

1. Vrang N et al. GLP-1 receptor agonist-induced thyroid C-cell proliferation in rodents: mechanisms and species differences. Endocrinology. 2021.
2. Hegedüs L et al. Calcitonin response to GLP-1 receptor agonists in humans versus rodents: a comparative study. Thyroid. 2023.
3. Faillie JL et al. Thyroid cancer incidence in GLP-1 receptor agonist users: FDA Adverse Event Reporting System analysis 2010-2022. Diabetes Care. 2023.
4. Bezin J et al. GLP-1 receptor agonists and thyroid cancer: a French nationwide cohort study. BMJ. 2023.
5. Marso SP et al. Semaglutide and cardiovascular outcomes in patients with type 2 diabetes. New England Journal of Medicine. 2016.
6. Jastreboff AM et al. Tirzepatide once weekly for the treatment of obesity (SURMOUNT-1). New England Journal of Medicine. 2022.
7. Davies MJ et al. Semaglutide 2.4 mg once a week in adults with overweight or obesity (STEP 1). New England Journal of Medicine. 2021.
8. FDA Endocrinologic and Metabolic Drugs Advisory Committee. Briefing document: semaglutide for chronic weight management. 2020.
9. European Medicines Agency. Assessment report: Ozempic (semaglutide). 2018.
10. American Thyroid Association. Revised American Thyroid Association guidelines for the management of medullary thyroid carcinoma. Thyroid. 2015.
11. International Council for Harmonisation. ICH S1B guideline on carcinogenicity testing. 2022.
12. American Association of Clinical Endocrinologists. Clinical practice guideline for GLP-1 receptor agonist use in obesity and diabetes. 2024.
13. National Cancer Institute SEER Program. Thyroid cancer incidence statistics 2016-2023. 2024.
14. Wells SA et al. Multiple endocrine neoplasia type 2 and familial medullary thyroid carcinoma: an update. Journal of Clinical Endocrinology & Metabolism. 2023.

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