Within a few years, Mounjaro has become a major treatment for type 2 diabetes and obesity. Its active substance, tirzepatide, often brings about a marked fall in blood glucose and substantial weight loss. Like Ozempic, it acts on the incretin system. But the two drugs are not identical, and that difference matters when it comes to the eyes.
For several years, GLP-1 receptor agonists have been monitored for two very different ophthalmic questions: a possible early worsening of diabetic retinopathy when blood glucose falls rapidly and, more recently, a possible risk of non-arteritic anterior ischaemic optic neuropathy, or NAION. For semaglutide, the NAION signal became strong enough for the European Medicines Agency to recognise it in 2025 as a very rare adverse effect. Can we conclude that Mounjaro carries the same risk? To date, no: the data on tirzepatide are different and far more nuanced.
Ozempic contains semaglutide, an agonist of the GLP-1 receptor alone. Tirzepatide, on the other hand, acts simultaneously on two receptors, those for GIP and GLP-1. This dual action partly explains its considerable effect on blood glucose and weight.
It also means that not every effect observed with semaglutide can automatically be extrapolated to tirzepatide. This is particularly true of the risk to the eyes.
The European summary of product characteristics (SmPC) for Mounjaro carries a warning about diabetic retinopathy, but NAION is not listed as an adverse effect. The regulatory situation is therefore different from that of semaglutide, although this does not mean the NAION question is definitively settled.
Two receptors instead of one: what holds for Ozempic does not necessarily hold for Mounjaro.
Patients treated with Mounjaro often combine several risk factors for NAION. That is what makes the signal so hard to read.
Non-arteritic anterior ischaemic optic neuropathy is caused by insufficient blood supply to the front part of the optic nerve, the optic disc. It usually causes a sudden, painless and most often one-sided loss of vision, frequently accompanied by the loss of part of the visual field.
Diabetes, high blood pressure, dyslipidaemia, obstructive sleep apnoea and certain anatomical configurations of the optic disc are known risk factors.
Yet these factors are precisely very common in patients treated with Mounjaro or other drugs in the same family. In an observational study, it is therefore difficult to separate any effect of the drug from that of the patient's underlying risk profile.
A study published in 2025 in JAMA Network Open nonetheless reopened the question.
The researchers analysed more than 1.5 million patients with type 2 diabetes and compared those receiving semaglutide or tirzepatide with those receiving other glucose-lowering drugs.
After statistical matching, NAION had been diagnosed within the following two years in 35 of 79,699 patients (0.04%) in the semaglutide or tirzepatide group, compared with 19 of 79,699 (0.02%) in the control group. The hazard ratio was 1.76, with a confidence interval ranging from 1.01 to 3.07: significant, but only just.
Taken in isolation, this result might suggest that Mounjaro shares the risk observed with Ozempic. But there is a major problem. Of the 82,972 patients initially exposed, 63,926 had received semaglutide and only 3,815 tirzepatide, while 15,231 had received both drugs. The signal therefore cannot be attributed specifically to tirzepatide.
The authors also attempted a direct comparison between the two molecules. After matching, 3,806 patients remained in each group, with two cases of NAION on semaglutide and only one on tirzepatide. That is far too few to establish any reliable difference.
Fewer than 5% of the patients in this study had received tirzepatide alone. It raises a question; it proves nothing about Mounjaro.
If all GLP-1 activity carried the same NAION risk, we would not expect to see fewer cases on tirzepatide.
A study published in 2026 in Ophthalmology Retina compared patients with diabetes starting tirzepatide with patients starting a GLP-1 receptor agonist without GIP activity, such as semaglutide or dulaglutide. After matching, each group comprised 102,590 patients, followed for up to three years.
Tirzepatide was associated with fewer eye complications: a hazard ratio of 0.79 for diabetic retinopathy, 0.82 for diabetic macular oedema, 0.66 for vitreous haemorrhage or retinal detachment and 0.65 for the need for sight-preserving treatment. More surprisingly, the risk of NAION was also lower on tirzepatide, with a hazard ratio of 0.45 (confidence interval 0.27 to 0.86).
This does not mean that Mounjaro protects the optic nerve. It is a retrospective study, not a randomised trial designed to answer this question, and differences between populations may persist despite careful matching. But this result is hard to reconcile with the idea that all drugs with GLP-1 activity necessarily carry the same risk of NAION.
In 2026, the situation can be summed up fairly simply. For semaglutide, several large studies have found a NAION signal, meta-analyses have reinforced it, and the EMA has added this complication to the drug's official product information. We covered this in detail in our article Ozempic et la vision : quel est le risque réel de NOIA ? (in French), published on the website of La Sauvagère medical centre.
For tirzepatide, a few data points raise the question, but no comparable evidence exists. One large recent study even suggests a lower incidence of NAION than with conventional GLP-1 receptor agonists.
The consensus statement published in 2026 by the North American Neuro-Ophthalmology Society and the American Academy of Ophthalmology points out that the data on GLP-1 receptor agonists come mainly from observational studies and that the absolute risk of NAION remains low. It advocates shared, individualised decision-making rather than a blanket contraindication for this class of drugs.
It cannot be claimed today that Mounjaro carries the same risk of NAION as Ozempic.
Improving long-standing poorly controlled diabetes too quickly can, paradoxically, make the retina worse first.
The best-established eye problem with tirzepatide actually concerns diabetic retinopathy. The phenomenon has been known for several decades: when diabetes that has long been poorly controlled is corrected very rapidly, pre-existing retinopathy can worsen temporarily. This is known as early worsening of diabetic retinopathy.
It was observed with insulin long before semaglutide or tirzepatide arrived. Mounjaro raises the question particularly because it can lower HbA1c substantially.
The European SmPC for Mounjaro states it explicitly: "Rapid improvement in glucose control has been associated with a temporary worsening of diabetic retinopathy." It adds: "Patients with diabetic retinopathy should be monitored closely and treated according to clinical guidelines."
This mechanism is worth understanding properly: it does not mean that tirzepatide is toxic to the retina. The problem appears to lie mainly in the speed of the metabolic improvement.
The large trials that led to the approval of tirzepatide were broadly reassuring as far as the retina is concerned. No cases of treatment-emergent retinopathy were reported in SURPASS-1 or SURPASS-5. In SURPASS-2, SURPASS-3 and SURPASS-4, such events were rare, in the order of 1% at most.
These figures should nevertheless be read with caution. All the SURPASS trials excluded patients with the most worrying forms of retinopathy: proliferative retinopathy, diabetic maculopathy, or non-proliferative retinopathy requiring urgent treatment.
In other words, the very patients in whom rapid worsening was most to be feared were absent. The lack of a signal in these trials therefore does not allow us to conclude that the risk does not exist in a person with diabetes whose retinopathy is already advanced.
The trials excluded the most fragile retinas: their silence says nothing about them.
More proliferative retinopathy in retinas already affected, less new retinopathy in the others: the paradox of early worsening.
A study published in Diabetologia in 2025 followed 3,435 patients treated with tirzepatide, matched with 3,434 unexposed patients. New proliferative retinopathy developed in 1.1% of patients on tirzepatide compared with 0.5% of controls.
After adjustment for risk factors, tirzepatide was associated with a more than twofold risk of proliferative retinopathy (odds ratio 2.15). The phenomenon mainly affected patients who already had mild non-proliferative retinopathy with maculopathy, or moderate to severe retinopathy.
Yet the same study found an apparently contradictory result. In patients without retinopathy at the outset, tirzepatide was associated with a lower risk of developing retinopathy (odds ratio 0.73). Nor was it associated with significant progression in those who had only mild retinopathy.
This paradox is exactly what early worsening would lead us to expect: rapid metabolic correction can temporarily destabilise retinopathy that is already vulnerable, whereas better diabetes control remains beneficial for the retina in the long term.
Since then, several studies in much larger populations have produced favourable results. A study published in Ophthalmology in 2026 compared 86,923 patients on tirzepatide with the same number of matched patients managed with lifestyle measures alone. At twelve months, the tirzepatide group had less new mild retinopathy, less proliferative retinopathy, less macular oedema, fewer vitreous haemorrhages and fewer tractional retinal detachments. Intravitreal anti-VEGF injections and panretinal photocoagulation were also less frequent.
The Ophthalmology Retina study mentioned above, which compared tirzepatide directly with other GLP-1 receptor agonists, likewise found less retinopathy, less macular oedema and fewer retinal procedures on tirzepatide.
Finally, an international study published in September 2026 found, at one year, no increase in eye complications on tirzepatide compared with other GLP-1 receptor agonists in people with diabetes: 3.5% in both groups. It did, however, exclude patients with pre-existing eye disease, that is, precisely those whom early worsening concerns.
Not a drug that is toxic to the retina, but a period of vigilance for patients whose retina is already affected.
Known retinopathy and a large expected fall in HbA1c: this is the time to check that ophthalmic follow-up is in place.
No guideline requires a specific eye examination for everyone who starts Mounjaro. In a person with obesity but no diabetes, no visual symptoms and no known eye disease, nothing currently justifies particular screening because of tirzepatide alone.
For patients with diabetes, the situation is different. They should in any case undergo the recommended screening for diabetic retinopathy.
When retinopathy is already known, particularly if it is moderate or severe, proliferative, or associated with macular oedema, it is reasonable to check that appropriate ophthalmic follow-up is arranged before or shortly after starting a treatment capable of lowering HbA1c substantially.
This is all the more relevant when diabetes is very poorly controlled at the outset and rapid metabolic correction is expected. A fundus examination, supplemented if needed by OCT of the macula, makes it possible to stage the retinopathy and adjust the frequency of monitoring.
This question is harder. For semaglutide, caution is now clearly justified by the available data and by the EMA's position. For tirzepatide, there is currently no signal strong enough to make a history of NAION a formal contraindication.
In a patient who has lost a significant part of the vision in one eye following NAION, the decision nonetheless deserves to be individualised. The spontaneous risk of the second eye being affected, vascular risk factors, any sleep apnoea, the configuration of the optic nerves and above all the expected metabolic and cardiovascular benefits must all be weighed up.
On the basis of current data, it would be excessive to refuse Mounjaro to these patients as a matter of course. The decision is made together with the prescribing doctor and the ophthalmologist.
A history of NAION is not a formal contraindication to tirzepatide, but it calls for a case-by-case decision.
Sudden loss of vision in one eye or an area suddenly missing from the visual field: seek urgent care.
A sudden, painless loss of vision in one eye, the sudden appearance of a missing area in the visual field or any rapid, unexplained drop in vision should lead to an urgent ophthalmic consultation.
These symptoms may point to NAION, but also to a retinal vascular occlusion, a retinal detachment, a vitreous haemorrhage or another condition requiring prompt treatment. They do not mean that Mounjaro is to blame.
In a patient with diabetes and known retinopathy, the appearance of a sudden shower of new floaters, a drop in vision or straight lines that look wavy or distorted should also prompt a check-up.
The practical message therefore differs from the one for Ozempic: in a patient with known diabetic retinopathy, especially if it is advanced, appropriate ophthalmic monitoring must be ensured while glucose control is improving rapidly. And, as for any patient, a sudden or rapidly progressive loss of vision warrants an urgent ophthalmic consultation.
