Anti-obesity medications impacting the eye: An emerging concern - a narrative review

Abstract

Obesity has reached epidemic proportions globally, with projections indicating that by 2050, nearly 3.8 billion adults will be overweight or obese. Despite the critical need for effective interventions, current obesity treatments ranging from lifestyle changes to bariatric surgery are often limited in efficacy or suitability. Pharmacotherapy is increasingly utilized for individuals with significant obesity or related comorbidities. However, some anti-obesity medications have been linked to ocular complications such as non-arteritic anterior ischemic optic neuropathy and diabetic retinopathy progression. This review analyzes currently approved anti-obesity medications, emphasizing their potential ocular adverse effects and the underlying mechanisms by which these occur. A comprehensive literature search identified the historical evolution, classification, and spectrum of ocular effects associated with these agents. The findings underscore the importance of evaluating both the risks and benefits of anti-obesity pharmacotherapy and highlight the need for vigilant clinical assessment of ocular health in patients undergoing such treatments.

Key Words: Anti-obesity drugs; Ocular side effects; Optic neuropathy; Diabetic retinopathy; Glaucoma

Core Tip: Anti-obesity medicines are being used more than ever, especially glucagon-like peptide-1 receptor agonists and newer incretin-based therapies. Along with clear metabolic benefits, emerging reports suggest potential eye-related complications such as non-arteritic anterior ischemic optic neuropathy, early worsening of diabetic retinopathy, acute angle closure from uveal effusion, and vitamin A-related visual dysfunction. These risks appear biologically plausible through vascular, metabolic, and neuro-ophthalmic pathways, particularly during rapid weight loss or quick glycaemic change. Clinicians should stratify risk, counsel patients on warning symptoms, and ensure timely ophthalmic evaluation.

INTRODUCTION

Obesity represents one of the most significant global health crises, with its prevalence rising dramatically across all demographics and regions worldwide. The scope of this epidemic is staggering. Current global estimates suggest that 19% of women and 14% of men are classified as obese[1]. A forecasting study was conducted utilizing historical data patterns, and it projects that by the year 2050, approximately 3.80 billion individuals aged 25 years and older will be classified as overweight or obese. The countries anticipated to contribute the largest numbers to this statistic are China, with an estimated 627 million individuals, followed by India at 450 million and the United States at 214 million[2]. The burden of obesity extends beyond cardiometabolic disease, with increasing recognition of its impact on ocular health, including diabetic retinopathy (DR), age-related macular degeneration, and optic neuropathies.

The multifaceted nature of obesity necessitates a comprehensive approach to treatment that encompasses lifestyle modifications, pharmacotherapy, and behavioural interventions. Nevertheless, available treatment options for obesity are constrained, and lifestyle changes, such as dietary adjustments and physical activity, often fail to yield significant or sustainable weight loss outcomes. Bariatric surgery demonstrates efficacy; however, it is typically reserved for individuals classified as morbidly obese due to concerns regarding perioperative mortality and potential surgical complications[3,4]. Anti-obesity pharmacotherapy, in conjunction with lifestyle modifications, when body mass index is ≥ 30 kg/m² or ≥ 27 kg/m² in the presence of comorbidities, has been endorsed by numerous obesity treatment guidelines[5-9].

As the use of these agents increases, reports of ocular adverse events temporally associated with anti-obesity medications, particularly glucagon-like peptide-1 (GLP-1) receptor agonists, have raised concern among ophthalmologists and prescribing clinicians. Contemporary pharmacovigilance studies and large observational cohorts have reported associations with non-arteritic ischemic optic neuropathy (NAION), early worsening of DR, and other retinal or neuro-ophthalmic conditions. Although causality has not been definitively established, the potential severity of these complications underscores the need for critical appraisal of the evidence and proactive ocular monitoring.

This review aims to systematically classify currently approved anti-obesity medications by pharmacological group and mechanism of action, summarize reported ocular adverse effects and their strength of evidence, examine proposed vascular, metabolic, and neuro-ophthalmic mechanisms underlying these effects, and provide practical, practice-oriented recommendations for ocular screening and follow-up in patients receiving anti-obesity pharmacotherapy.

LITERATURE REVIEW

A comprehensive literature review was conducted to assess the ocular effects of anti-obesity medications. PubMed, Scopus, and Web of Science were searched from database inception to July 2025 for English-language, peer-reviewed articles. Search terms were used in combinations with Boolean operators (“AND/OR”) and included: “anti-obesity drugs”, “weight loss medications”, “GLP-1 receptor agonist”, “semaglutide”, “liraglutide”, “tirzepatide”, “orlistat”, “phentermine”, “topiramate”, “naltrexone/bupropion”, “setmelanotide”, “ocular adverse effects”, “eye complications”, “optic neuropathy”, “diabetic retinopathy”, and “angle-closure glaucoma. Eligible publications included case reports, case series, observational studies, randomized or non-randomized clinical trials, pharmacovigilance analyses, and narrative/systematic reviews that reported ocular outcomes related to anti-obesity medications. Titles and abstracts were screened for relevance, followed by full-text review when appropriate. Extracted variables included/class and mechanism of action, type of ocular adverse event, timing in relation to drug initiation or dose escalation, reversibility/outcomes, proposed pathophysiology, patient risk factors (e.g., diabetes, pre-existing retinopathy, optic disc crowding), and level of evidence (case report, observational study, trial, or pharmacovigilance analysis). Studies were excluded if they did not report specific ocular outcomes, focused solely on bariatric surgery or lifestyle interventions, were written in a language other than English, were conference abstracts lacking sufficient clinical detail, or duplicated previously reported datasets. A narrative review methodology was selected because of the heterogeneity of the available evidence, which includes case reports, pharmacovigilance analyses, observational studies, and mechanistic literature, thereby precluding meaningful quantitative synthesis or meta-analysis.

EVOLUTION, CLASSIFICATION, AND OCULAR EFFECTS OF SEVERAL ANTI-OBESITY MEDICATIONS

The review identified the evolution, classification, and ocular effects of several anti-obesity medications.

Evolution of anti-obesity drugs

The history of anti-obesity pharmacotherapy can be traced back to the 1950s and 1960s, when centrally acting sympathomimetics, including amphetamine derivatives, were used for weight management[10]. Notable among these early agents were desoxyephedrine, phentermine, and diethylpropion. However, growing concerns regarding cardiovascular risks and the potential for abuse contributed to a decline in their use. During the 1970s and 1980s, serotonin-releasing agents such as fenfluramine and dexfenfluramine became increasingly popular[11]. This trend was followed in the 1990s by the combination therapy of phentermine and fenfluramine[12]. However, the association of these agents with serious adverse effects, including cardiac valvulopathy and primary pulmonary hypertension, ultimately resulted in their withdrawal from the market[13]. Rimonabant, a type-1 cannabinoid receptor antagonist/inverse agonist introduced in the mid-1990s[14], showed promise in clinical trials, but reports of serious psychiatric adverse effects led to the suspension of its marketing authorizations[15]. Sibutramine, a dual monoamine reuptake inhibitor, was introduced in the late 1990s, but concerns about cardiovascular risks led to its suspension by the European Medicines Agency in 2010[16,17]. Lorcaserin, a serotonin 2C receptor agonist, was approved by the United States Food and Drug Administration (FDA) in 2012 and initially demonstrated favorable tolerability and significant weight loss[18]. However, it was subsequently withdrawn from the market because of an increased risk of cancer associated with its use[19]. Orlistat, a pancreatic lipase inhibitor, received regulatory approval in 1998 for the treatment of obesity[20]. It has been shown to produce modest weight loss[21] and to yield beneficial effects on cardiovascular risk factors[22]. In recent years, GLP-1 receptor agonists have emerged as a promising class of pharmacological interventions for the treatment of obesity. GLP-1 is a hormone that plays a critical role in the regulation of appetite, satiety, and glucose metabolism. Medications such as semaglutide (marketed under the brand names Wegovy and Ozempic) and liraglutide have demonstrated significant efficacy in promoting weight loss and improving cardiovascular risk factors[23]. The development of anti-obesity medications reflects the ongoing pursuit of effective and safe treatments, alongside a deeper understanding of the complex biological mechanisms that regulate appetite and energy homeostasis.

Classification of anti-obesity medications

The currently approved anti-obesity medications are classified based on their mechanism of action[24]. Broadly, they can be classified as under.

Centrally acting appetite suppressants: These agents primarily act on hypothalamic and mesolimbic pathways to reduce appetite, increase satiety, or modify reward-related eating behaviour. This group includes sympathomimetic agents and centrally acting combination therapies: (1) Phentermine-topiramate: Combines a sympathomimetic amine (phentermine) that suppresses appetite via noradrenergic pathways with topiramate, which enhances satiety through gamma-aminobutyric acid modulation and glutamate inhibition; and (2) Naltrexone-bupropion: Acts on hypothalamic appetite regulatory centres and the mesolimbic dopamine reward system to reduce food cravings. Reported ocular adverse events associated with topiramate, phentermine, and naltrexone-bupropion are derived predominantly from isolated case reports and small case series, limiting the generalizability and strength of causal inference.

Nutrient-stimulated hormone-based medications: These drugs mimic or enhance endogenous entero-pancreatic hormones involved in appetite regulation, glucose homeostasis, and energy balance. The elucidation of the gut-brain axis function in appetite regulation has introduced new biological targets for drug development, specifically in the realm of nutrient-stimulated hormone-based therapeutics that replicate the metabolic effects of naturally occurring entero-pancreatic hormones[25]. These hormones encompass GLP-1[26], glucose-dependent insulinotropic polypeptide[27], glucagon[28], and amylin[29]. Among these agents, GLP-1 receptor agonists have received the most extensive research attention due to their incretin effect, which amplifies insulin secretion in response to oral glucose ingestion, and also exhibit various pleiotropic cardiometabolic effects, such as the reduction of blood pressure and inflammation, which are mediated by the extensive distribution of GLP-1 receptors throughout the body: (1) GLP-1 receptor agonists: Liraglutide and semaglutide reduce appetite, delay gastric emptying, and improve glycemic control through GLP-1 receptor stimulation; and (2) Dual incretin agonists: Tirzepatide acts on both GLP-1 and glucose-dependent insulinotropic polypeptide receptors, producing potent metabolic and weight-reducing effects.

Intragastrointestinal agents: Function by either forming covalent bonds with intestinal lipases, thereby inhibiting digestion[30], or by expanding to occupy gastric space, which simulates the sensation of fullness and satiety[31,32]: (1) Lipase inhibitors: Orlistat reduces dietary fat absorption by inhibiting gastric and pancreatic lipases; and (2) Gastric space-occupying agents: Oral cellulose-citric acid hydrogel expands in the stomach to induce early satiety.

Drugs approved for syndromic obesity[33]: These agents target specific genetic or molecular pathways implicated in rare forms of obesity. Setmelanotide: A melanocortin-4 receptor (MC4R) agonist approved for obesity due to pathogenic variants in the MC4R signalling pathway. A comparative overview of drug classes, reported ocular adverse effects, incidence, and proposed mechanisms is summarized in Table 1, while major pathogenic pathways are outlined in Table 2.

Table 1 Various anti-obesity drugs and ocular side effects.

Drug/class	Ocular adverse effects	Incidence	Mechanism	Ref.
Semaglutide (GLP-1 RA)	NAION, DR progression, possible neovascular age-related macular degeneration	Very rare (approximately 1:10000)	Microvascular compromise, rapid glycemic shifts	[39,42-45,47,50]
Tirzepatide	NAION, bilateral papillitis, paracentral acute middle maculopathy, lower cataract risk		Rapid glycemic shift	[39,48-50,81]
Topiramate	Acute angle closure	3 per 100000	Ciliochoroidal effusion	[61-65,73]
Phentermine	Angle closure glaucoma, visual hallucinations, retinal vasoconstriction, and anterior ischaemic optic neuropathy	-	Sympathomimetic effect	[66,67,69-71]
Naltrexone-bupropion	Blurred vision, rare glaucoma	Unclear	CNS/anticholinergic	[50,72,73]
Orlistat	Indirect icterus	Unclear	Secondary to hepatotoxicity	[74]
Setmelanotide	Scleral, periocular discoloration	Not mentioned	Metabolic or hepatic effect	[80]

GLP-1 RA: Glucagon-like peptide-1 receptor agonist; NAAION: Non-arteritic anterior ischemic optic neuropathy; DR: Diabetic retinopathy; CNS: Central nervous system.

Table 2 Mechanisms of anti-obesity drug-induced visual impairment.

Mechanism	Description	Examples
Vascular	Ischemia due to altered ocular blood flow or microvascular injury	GLP-1 receptor agonists (NAION)
Metabolic	Indirect effects, such as rapid glycemic improvement or hepatic dysfunction	GLP-1 receptor agonists (DR)
Direct drug toxicity	Physical or chemical injury to ocular structures	Topiramate (anatomic shift, effusion)

GLP-1 RA: Glucagon-like peptide-1 receptor agonist; NAAION: Non-arteritic anterior ischemic optic neuropathy; DR: Diabetic retinopathy.

Various anti-obesity drugs and their ocular side effects

Anti-obesity drugs can have ocular side effects that are often underestimated. Understanding these effects is crucial for assessing the ocular safety profile of these medications. Ocular adverse effects associated with anti-obesity medications can be broadly categorised into vision-threatening events, including non-arteritic anterior ischemic optic neuropathy (NAAION), progressive DR, and angle-closure glaucoma, and transient or reversible symptoms such as dry eye, blurred vision, and accommodative disturbances, which typically resolve with dose adjustment or drug discontinuation. The potential ocular effects, their incidences, and the underlying pathogenic mechanisms associated with various anti-obesity medications are outlined below (Figure 1).

Figure 1 Shows three vertical pathways labelled “vascular”, “metabolic”, and “direct drug toxicity”, each leading to its respective mechanisms and anti-obesity drugs. GLP-1 RAs: Glucagon-like peptide-1 receptor agonists; NAAION: Non-arteritic anterior ischemic optic neuropathy.

GLP-1 receptor agonists: Drugs such as semaglutide and liraglutide engage glucagon-like peptide-1 receptors to manage diabetes mellitus and obesity. However, several studies have suggested a potential association between these medications and the development of NAION, progression of DR, and an increased incidence of neovascular age-related macular degeneration[34-38].

NAION risk: Recent cohort studies indicate an elevated risk of papillitis-like features due to rapid reduction of blood sugar[39], which may result in a compartment-like syndrome, especially in eyes with a small cup-to-disc ratio because of the restricted space available for tissue expansion in and around the lamina cribrosa[40,41]. This condition can subsequently lead to NAAION associated with the administration of semaglutide, liraglutide, and tirzepatide[35,42-45]. A comprehensive analysis of a Danish national cohort comprising more than 400000 individuals with type 2 diabetes mellitus who were monitored for five years demonstrated that the use of semaglutide more than doubled the risk of developing NAAION, yielding a hazard ratio of 2.19 (95% confidence interval: 1.54-3.12). The majority of cases occurred within the initial 22 months of drug administration[35]. Additionally, findings from a matched institutional study indicated an even higher hazard ratio of 7.64 (95% confidence interval: 2.21-26.36; P < 0.001) for NAAION in patients treated with semaglutide, with an incidence of 6.7% at 36 months compared with 0.8% among non-users[42]. The risk of NAAION in individuals using GLP-1 receptor agonists is estimated at approximately 1 in 10000[35]. Clinical presentations may include bilateral sequential NAAION, visual field deficits, or atypical symptoms.

Proposed mechanisms for this heightened risk may involve GLP-1-mediated microvascular compromise, rapid fluctuations in glycemic control impairing vascular autoregulation, as well as direct impacts on optic nerve circulation and vascular endothelium, resulting in ischemic injury[35,42,43]. Although the causal relationship is still under investigation, healthcare professionals need to remain vigilant, particularly in patients with predisposing factors such as hypertension, sleep apnea, or a reduced cup-to-disc ratio[35]. Physicians should monitor patients for sudden visual loss or significant vision decline and promptly discontinue medication upon confirmation of diagnosis[43].

DR progression: There are concerns that GLP-1 receptor agonists may temporarily exacerbate DR and increase macular edema, particularly in cases of rapid glycemic control. However, long-term studies indicate that there is no additional risk when glycemic levels are decreased gradually[36,37].

The SUSTAIN-6 trial demonstrated that the administration of semaglutide in patients with type 2 diabetes mellitus was associated with a 76% increase in retinal complications. These complications encompass vitreous hemorrhage, diabetic blindness, including proliferative retinopathy, and macular edema, which may necessitate intravitreal injections or photocoagulation therapy[46]. However, a direct causal relationship has yet to be firmly established, and some of these complications may be transient. Paradoxically, a case report has indicated potential regression of proliferative DR associated with semaglutide, prompting inquiries into its possible protective effects on retinal health, potentially through anti-inflammatory mechanisms and vascular endothelial growth factor protection[47].

It is noteworthy that while managing blood glucose levels, tirzepatide may paradoxically exacerbate early non-proliferative DR[48]. In a study, new-onset proliferative DR was observed in 1.1% of individuals using tirzepatide who had pre-existing non-proliferative DR, with an odds ratio of 2.15 determined through multivariate analysis (95% confidence interval: 1.24, 3.74; P < 0.01)[49]. The implication is that the rapid correction of glycemia, rather than any direct toxicity of the medication, is a contributing factor to this phenomenon. Conversely, tirzepatide may offer a protective effect against the onset of DR in individuals without any existing retinal pathology. Among GLP-1 receptor agonists, research has indicated that tirzepatide exhibits a significantly reduced risk of developing age-related cataract in diabetic patients compared to those treated with alternative medications[50].

Neovascular age-related macular degeneration: In a cohort of patients with diabetes undergoing treatment with semaglutide, the incidence of neovascular age-related macular degeneration was observed to be twice that of patients receiving non-GLP-1 medications. Specifically, the incidence was approximately 1 in 500 in the semaglutide group compared to 1 in 1000 in the non-GLP-1 cohort, following more than 30 months of therapy[51]. The proposed mechanism is attributed to the exacerbation of hypoxic processes resulting from a rapid systemic reduction of glucose, given that the retina is equipped with GLP-1 receptors. GLP-1 receptor agonists elevate the levels of a chemokine, C-X-C motif chemokine 12, which is known to increase under hypoxic conditions and enhance the expression of vascular endothelial growth factor. This interplay promotes choroidal neovascularization through the hypoxia-induced expression of C-X-C motif chemokine 12 in retinal pigment epithelial cells[52-54].

Paracentral acute middle maculopathy: Paracentral acute middle maculopathy has been observed in cases of arteritic anterior ischemic optic neuropathy[55], due to compromised blood flow to the deep capillary plexus that supplies the inner nuclear layer[56]. Even in the absence of giant cell arteritis, a case report has documented paracentral acute middle maculopathy in a patient receiving treatment with semaglutide[39]. Research has indicated that GLP-1 receptors are located on a fraction of neurons of the ganglion cell layer in the retina; however, the effects of GLP-1 receptor agonists are yet to be thoroughly investigated[57].

Topiramate (Topamax, Eprontia, Qudexy XR)

Topiramate is predominantly utilized as an anticonvulsant medication; however, it is also employed in the management of obesity when used in conjunction with phentermine as a fixed drug combination (Qsymia, Vivus, Inc., CA, United States)[58].

Topiramate-associated acute angle-closure: This is a recognized clinical phenomenon that typically occurs within days to two weeks following the initiation of therapy. The estimated incidence rate is approximately three cases per 100000 patients, with a higher prevalence observed in females[59].

The underlying mechanism involves topiramate-induced myopic shift, ciliochoroidal effusion and edema of the ciliary body, which leads to anterior rotation of the ciliary body and forward displacement of the iris-lens diaphragm, ultimately resulting in angle closure[60]. Effective management necessitates the immediate discontinuation of topiramate, along with the initiation of antiglaucoma medications, cycloplegics, and corticosteroids as indicated. It is important to note that laser iridotomy is not indicated in these cases. The condition typically resolves with conservative management and cessation of the medication[61].

Topiramate-induced ocular inflammatory reactions like conjunctivitis, uveitis, areflexic mydriasis and vitritis have been reported in various case reports[62-64]. Other ocular effects include retinal striae, rhegmatogenous retinal detachment, visual field defects, diplopia, nystagmus, palinopsia and scleritis[65].

Phentermine (Adipex-P, Lomaira)

This compound is classified as a sympathomimetic amine that is pharmacologically similar to amphetamine. It acts primarily through noradrenergic pathways within the central nervous system. The substance received approval from the FDA in 1959 for its application in the short-term management of obesity[66]. Ischemic retinopathy and optic neuropathy: Excessive sympathomimetic effects associated with misuse of this drug can lead to severe complications, including mydriasis, angle-closure glaucoma, diminished accommodation and convergence, visual hallucinations, and even NAAION[67]. Branch retinal artery occlusion and central retinal vein occlusion have also been documented as potential complications associated with the use of phentermine for weight reduction[68]. The proposed mechanism underlying these occurrences involves significant vasospasm and vasoconstriction of the retinal vasculature secondary to the sympathomimetic effect of the drug[69-71].

Naltrexone-bupropion (Contrave, Orexigen Therapeutics, Inc., CA, United States)

This combination received approval from the FDA in September 2014 as a therapeutic intervention for obesity. It operates by centrally targeting the hypothalamus and the mesolimbic dopamine circuit to promote the sensation of satiety[72].

Angle-closure glaucoma: The potential mechanism underlying angle closure may be attributed to pharmacologic dilation of the pupils. Additionally, choroidal effusion may occur, as noted in cases involving topiramate. A two-fold increase in the risk of angle-closure glaucoma has been reported with the use of bupropion, while a five-fold increase in risk has been observed with topiramate[73].

Orlistat (Alli, Xenical)

Orlistat functions as a gastric and pancreatic lipase inhibitor, thereby reducing the absorption of dietary fat[74].

Acquired xerophthalmia and night blindness: Current literature does not provide consistent evidence of direct ocular toxicity associated with orlistat. However, there have been documented cases of severe hepatotoxicity, which may have implications for the absorption of fat-soluble vitamins, including vitamin A, thereby potentially increasing the theoretical risk of acquired night blindness; severe hepatotoxicity may also present with icterus[75]. Most studies indicate that the absorption of vitamin E is notably affected[76,77]. However, concurrent supplementation with multivitamins can help prevent these adverse effects.

Setmelanotide (Imcivree)

The compound operates by targeting the MC4R and is indicated for the management of severe obesity resulting from specific genetic syndromes associated with deficiencies in the MC4R signalling pathway, as evidenced by the VENTURE trial[78].

Ocular hyperemia and scleral pigmentation: Skin hyperpigmentation is a potential adverse effect that arises from the activation of melanocortin receptors, which results in increased melanin production. There exists a possibility of developing periocular pigmentary alterations as well as ocular hyperemia; however, these changes may revert upon cessation of the medication[79,80].

Mechanisms of ocular adverse effects

The proposed mechanisms underlying ocular complications of anti-obesity medications can be broadly grouped into vascular, metabolic, and neuro-ophthalmic pathways. Rapid improvement in glycemic control may transiently impair retinal autoregulation, contributing to early worsening of DR. Microvascular compromise and endothelial dysfunction may predispose susceptible individuals to ischemic optic neuropathy, particularly in the presence of structural risk factors such as a small cup-to-disc ratio. In addition, GLP-1 receptors expressed in retinal and optic nerve tissues raise the possibility of direct or indirect neurovascular effects, although definitive causal mechanisms remain under investigation (Table 2).

DISCUSSION

This mini-review highlights that while most anti-obesity medications are safe from an ophthalmologic perspective, there are important exceptions and precautionary considerations. Fat absorption inhibitors such as orlistat may induce fat-soluble vitamin deficiency, potentially leading to night blindness. Evidence linking GLP-1 receptor agonists with NAION and DR progression is derived primarily from large observational cohorts and pharmacovigilance data, whereas reports involving topiramate, phentermine, and bupropion are largely based on case reports and small series. From a clinical perspective, the potential for irreversible vision loss, even if rare, necessitates a precautionary approach. Baseline ophthalmic evaluation is particularly important in patients with diabetes, pre-existing optic nerve vulnerability, narrow anterior chamber angles, or advanced retinal disease. Gradual glycemic improvement, patient education regarding visual symptoms, and interdisciplinary communication between prescribing physicians and ophthalmologists are essential components of safe care. It is important to emphasize that reported associations between GLP-1 receptor agonists and ocular conditions such as NAAION and DR progression are correlational, as causality has not been established in randomized controlled trials.

The following points should be considered: (1) Ophthalmic history: A comprehensive assessment of patients’ ocular health is essential, particularly for identifying any preexisting conditions such as disc at risk, angle closure glaucoma, DR, or macular degeneration that the anti-obesity medications may exacerbate[81]; and (2) Systemic conditions: It is also crucial to assess patients for systemic diseases that may compromise ocular health, such as diabetes and hypertension[82]. It is necessary to review current medications to detect any potential interactions that may influence ocular health or the efficacy of the anti-obesity drugs[83]. It is prudent to identify specific contraindications related to the anti-obesity medication including pregnancy, certain psychiatric conditions, or hypersensitivity to the drug components[84].

Proposed screening protocols before initiating anti-obesity drugs

Comprehensive eye examination: It is imperative to conduct a thorough eye examination. This comprehensive assessment is essential for establishing a baseline prior to the initiation of any treatment regimen.

Visual field assessment: It is advisable to perform visual field testing to identify any pre-existing deficits, allowing for continuous monitoring for potential changes during treatment. Notably, medications such as topiramate have the potential to cause visual field loss[85-87]. Visual field assessments are strongly recommended at three-month intervals if topiramate is prescribed.

Retinal imaging: The utilization of optical coherence tomography and fundus photography is recommended to document the condition of the retina and macula at baseline. Pharmacological agents such as semaglutide, topiramate, and orlistat may lead to disc edema and maculopathy.

Follow-up evaluation: It is critical to schedule regular follow-up examinations to monitor for any changes in visual acuity or the development of new ocular symptoms during treatment. The frequency of follow-up evaluations should be adjusted according to the pretreatment risk stratification of the patient.

Patient education: It is essential to educate patients regarding symptoms that may indicate urgent issues, including sudden vision loss, eye pain, halos, redness in the eyes, double vision, visual field defects, persistent headaches accompanied by blurred vision, night blindness, or difficulties with visual adaptation, which may suggest vitamin A deficiency.

It is recommended that a multidisciplinary task force of specialists from ophthalmology, endocrinology, and internal medicine formulate guidelines to identify the most suitable patients for a specific anti-obesity drug and that the schedule for ophthalmic follow-up in these patients be clearly specified. Clinical recommendations for ocular screening and follow-up are best implemented using a risk-stratified approach, with intensified monitoring reserved for patients with diabetes, pre-existing retinal disease, or optic nerve vulnerability, while routine surveillance may not be necessary in low-risk individuals.

Proposed practice-oriented recommendations: If summarized, before initiating anti-obesity pharmacotherapy, clinicians should consider a baseline comprehensive eye examination, including visual acuity, intraocular pressure measurement, slit-lamp examination, and fundus evaluation. Optical coherence tomography and fundus photography are recommended for patients with diabetes or known retinal disease. High-risk individuals may benefit from scheduled follow-up examinations within the first 3-6 months of therapy, with frequency tailored to individual risk profiles.

Future research directions

Future research in anti-obesity pharmacotherapy and its ocular effects should focus on a deeper understanding of the underlying mechanisms, improvement of drug safety, and advancement of patient care through personalized and multidisciplinary approaches. By emphasizing these areas, researchers can help develop safer and more effective obesity treatments that also safeguard ocular health. There is an urgent need for further studies to clarify how anti-obesity medications may influence eye health, including effects on intraocular pressure, retinal structure, and optic nerve function. Future research should prioritize prospective ophthalmic monitoring within obesity pharmacotherapy trials, standardized reporting of ocular adverse events, and mechanistic studies to clarify causal pathways and identify high-risk subgroups.

It is essential to conduct longitudinal studies to assess the long-term effects of anti-obesity medications on ocular health, particularly regarding their potential cumulative influence on visual acuity. Moreover, experimental, cellular, and molecular research may further illuminate the relationship between anti-obesity medications and ocular health. Additional clinical trials are necessary to validate the potential benefits of weight loss with respect to ocular health. Should weight loss be established as an effective intervention, either as a primary or adjunctive treatment, for delaying the onset or mitigating the progression of ocular diseases in obese populations, both clinicians and patients are likely to gain further motivation to confront this pressing public health issue[88].

CONCLUSION

In summary, incorporating routine ophthalmic monitoring and patient education into the management of individuals on anti-obesity pharmacotherapy is crucial for reducing ocular risks and improving patient outcomes. Collaboration among ophthalmologists, endocrinologists, and internal medicine specialists is vital to ensure proper patient selection and to develop clear, evidence-based guidelines for ocular follow-up. As the field of anti-obesity medications advances, ongoing vigilance is necessary to promptly identify and address adverse ocular effects.

Ongoing research is vital to elucidate the mechanisms by which these medications may impact eye health and to inform the development of safer, more targeted therapies. Longitudinal and experimental studies will play a key role in determining the long-term effects of these interventions on the retina, optic nerve, and overall visual function, while also assessing the potential benefits of weight loss in preventing or mitigating ocular diseases in obese populations. Ultimately, a personalised, multidisciplinary approach remains the cornerstone of safe and effective obesity management, with the dual aims of improving both systemic and ocular health. Continued collaboration in clinical care and research will advance our understanding and support the development of innovative strategies to address this urgent public health issue.

ACKNOWLEDGEMENTS

My teachers, family and friends.