Eating disorders consist of three diseases: anorexia nervosa (AN), bulimia nervosa (BN), and binge eating disorder (BED). All are multisystem diseases that affect multiple organs including the eyes.
The lifetime prevalence in the United States is 0.80% for AN, 0.28% for BN, and 0.85% for BED, with the majority being women. A cohort study of approximately 80,000 people in the Netherlands showed that patients with eating disorders have a 1.64 times higher risk of dry eye compared to the general population1).
The main ophthalmic signs are as follows.
Lagophthalmos: Corneal exposure due to incomplete eyelid closure
Dry eye: Decreased tear volume and tear film instability
Nystagmus and ophthalmoplegia: Due to Wernicke encephalopathy (thiamine deficiency)
Papilledema: Due to idiopathic intracranial hypertension (IIH)
Importantly, ocular signs can appear not only during the active phase of the disease but also during the refeeding stage (refeeding syndrome) in AN treatment.
QCan eye symptoms occur during treatment for eating disorders?
A
Yes. Rapid weight gain or rapid loss of essential nutrients during AN treatment can cause refeeding syndrome, which may lead to IIH. Even during treatment, attention should be paid to symptoms such as headache and transient visual obscurations.
The ocular symptoms that appear differ depending on the type of eating disorder.
AN (anorexia nervosa): Dryness and foreign body sensation due to lagophthalmos, subacute painless vision loss. In Wernicke encephalopathy, the triad of ataxia, confusion, and nystagmus/ophthalmoplegia appears.
BN (bulimia nervosa): Painless punctate subconjunctival hemorrhage. Caused by a sudden increase in intraocular pressure due to self-induced vomiting. Often noticed in a mirror or pointed out by others.
BED (binge eating disorder): Headache, transient visual obscurations (amaurosis), cranial nerve palsy (typically abducens nerve palsy). Symptoms due to IIH.
Clinical Findings (Findings Confirmed by Physician Examination)
The main clinical findings by disease are shown below.
AN (Anorexia Nervosa)
Enophthalmos and lagophthalmos: Atrophy of orbital fat causes enophthalmos and lagophthalmos (rabbit eye). Gaudiani et al. (2012) reported ptosis, enophthalmos, and lagophthalmos in 5 cases of severe AN. 2)
Dry keratoconjunctivitis (dry eye): Schirmer score significantly lower than controls (approximately 11 mm/5 min decrease). 4)
Reduced retinal nerve fiber layer thickness: Thinning of the retinal nerve fiber layer confirmed by OCT.
Soft exudates and retinal hemorrhages: Observed on fundus examination in severe cases.
Eyelid petechiae: Reported in purging-type AN. 3)
BN/BED
Subconjunctival hemorrhage (BN): Punctate to patchy bleeding occurs due to increased venous pressure from self-induced vomiting.
Papilledema (BED/refeeding): Swelling of the optic disc associated with IIH. If left untreated, it can progress to optic atrophy.
QDo eye symptoms differ depending on the type of eating disorder?
A
They are clearly different. In AN, the main ophthalmic issues are lagophthalmos and dry eye due to orbital fat atrophy, and nutritional deficiency visual impairment; in BN, subconjunctival hemorrhage; in BED, IIH symptoms (headache, papilledema, abducens nerve palsy) mediated by obesity due to overeating.
The mechanism of ocular signs differs by type of eating disorder.
AN → Lagophthalmos: Extreme weight loss → orbital fat atrophy → enophthalmos → incomplete eyelid closure
AN → Dry eye: Decreased tear production due to vitamin C deficiency. Concentrations of immunoglobulin A (IgA) and secretory IgA in tears also decrease1)
AN → Wernicke encephalopathy: Thiamine (vitamin B1) deficiency due to dietary restriction → nystagmus and ophthalmoplegia
BED → idiopathic intracranial hypertension: rapid weight gain from overeating → increased intracranial pressure
Refeeding syndrome → idiopathic intracranial hypertension: rapid weight gain and rapid intracellular electrolyte shifts during AN treatment
Risk factors for idiopathic intracranial hypertension are young women (18–44 years), obesity (high BMI), and endocrine disorders6). Eating disorders themselves increase the risk of dry eye by 1.64 times1).
Vitamin B1 measurement: Direct blood measurement or transketolase activity assay. Stimulation of 25% or more after TPP addition indicates B1 deficiency.
Vitamin levels: A (night blindness), C (dry eye), B9/B12 (central vision impairment).
Serum homocysteine and methylmalonic acid: Indicators of long-term B9/B12 deficiency
Electrolytes and CBC: Anemia, electrolyte abnormalities, liver enzymes, lipid profile
Refeeding syndrome monitoring: Serum phosphate level. Phosphate <0.8 mmol/L is the threshold for active management
QWhen should a patient with an eating disorder see an ophthalmologist?
A
If ocular symptoms such as decreased vision, headache, diplopia, eye pain, or dryness appear, prompt ophthalmologic consultation is recommended. Additionally, during AN treatment (refeeding phase), if rapid weight changes occur, an ophthalmologic examination is recommended to check for papilledema.
Controlling the underlying eating disorder is the top priority. Vitamin supplementation and restoration of normal diet are the first steps in treating neuro-ophthalmic signs.
Acetazolamide: First-line treatment. Start at 500 mg twice daily, and increase up to 1000 mg twice daily5)
Additionally, topiramate or furosemide may be used in some cases6)
In patients with eating disorders, weight loss recommendations may not be appropriate, but even a 5–15% weight reduction has been reported to be effective in resolving papilledema5)
Surgery for Lagophthalmos and Eyelid Incomplete Closure
Tarsorrhaphy: Narrows the excessive eyelid opening to prevent corneal exposure
Gold/Platinum Weight Implantation into the Upper Eyelid: Uses gravity to assist eyelid closure
Surgery for refractory IIH
Optic nerve sheath fenestration (ONSF): Indicated when maximal medical therapy has failed or when drug tolerance is poor
CSF diversion (shunt surgery): Considered when visual function is progressively deteriorating
QCan the ocular symptoms of Wernicke encephalopathy recover with treatment?
A
Intravenous administration of thiamine often rapidly improves eye movement disorders. However, complete recovery may take several weeks, and nystagmus may persist in chronic cases. Early treatment initiation as soon as suspected determines the prognosis.
Severe weight loss due to anorexia nervosa causes atrophy of orbital fat tissue. Loss of supporting tissue in the orbit leads to enophthalmos, preventing anatomical closure of the eyelids (lagophthalmos). This is notably reported in severe AN with multi-organ failure2).
Thiamine (vitamin B1) is an essential coenzyme in glucose metabolism. Deficiency selectively damages brain regions with high glucose metabolism.
The sites that are susceptible to damage are as follows.
Oculomotor nuclei and vestibular nuclei
Paraventricular region of the thalamus and hypothalamus
Periaqueductal gray matter and cerebellar vermis
Ocular motor abnormalities include abduction limitation, lateral gaze nystagmus, vertical nystagmus in primary position, internuclear ophthalmoplegia, and one-and-a-half syndrome. In some cases, limitation of horizontal and vertical eye movements progresses to complete ophthalmoplegia. Extraocular muscle palsy is almost always bilateral, but many cases show asymmetry. Downbeat nystagmus is particularly strongly associated with thiamine deficiency and is an important finding that should raise suspicion for Wernicke encephalopathy in malnourished patients.
IIH results from a combination of CSF dynamics dysregulation and metabolic/hormonal factors. Its association with obesity is strongest, and in BED, rapid weight gain due to overeating acts as a trigger. Genetic factors (familial occurrence, candidate regions on chromosomes 5, 13, and 14) are also involved, but no Mendelian inheritance pattern has been established6). IIH is increasingly recognized as a systemic metabolic disease with distinct metabolic features separate from obesity5).
Malnutrition reduces IgA and secretory IgA concentrations in tears and decreases the number of IgA-containing cells in lacrimal gland tissue. The secretory IgA antibody response to infectious stimuli is also blunted1). This is thought to contribute not only to dry eye but also to an increased risk of ocular surface infection.
Mechanism of Nutritional Deficiency Optic Neuropathy
Deficiencies of vitamin B9 (folate) and B12 (cobalamin) cause central visual impairment (central scotoma and centrocecal scotoma), which progresses to bilateral optic atrophy if left untreated. Serum homocysteine and methylmalonic acid are useful indicators of long-term deficiency.
7. Latest Research and Future Prospects (Research Stage Reports)
A systematic review by Markoulli et al. (2023) concluded that most studies on eating disorders and the ocular surface are low-quality cross-sectional studies, and there are no adequately powered comparative cohort studies 1). Comprehensive future research is needed on how AN-induced malnutrition manifests in the eye, which signs appear at each disease severity, the visual prognosis associated with each sign, and the optimal management of ocular complications of AN.
Novel Targeted Therapy for Idiopathic Intracranial Hypertension
Bonelli et al. (2024) demonstrated that idiopathic intracranial hypertension is a systemic metabolic disease with unique metabolic features distinct from obesity, and discussed the potential for targeted therapy 5). Results from the IIH Weight Trial showed that a 24% weight reduction is not necessarily required for resolution of papilledema, and that even a 5–15% weight loss can provide beneficial effects.
Markoulli M, et al. TFOS Lifestyle: Impact of nutrition on the ocular surface. Ocul Surf. 2023;29:226-271.
Gaudiani JL, Braverman JM, Mascolo M, Mehler PS. Lagophthalmos in severe anorexia nervosa: a case series. Arch Ophthalmol. 2012;130:928-930.
Agrawal M, Yadav P, Kumari R, Chander R. Eyelid petechiae as a window to relapse in a case of purging-type anorexia nervosa. Indian J Psychiatry. 2019;61:101-102.
Gilbert JM, Weiss JS, Sattler AL, Koch JM. Ocular manifestations and impression cytology of anorexia nervosa. Ophthalmology. 1990;97:1001-1007.
Bonelli L, et al. How to manage idiopathic intracranial hypertension in the ophthalmology clinic. Eye. 2024;38:2472-2481.
Toshniwal SS, Kinkar J, Chadha Y, et al. Navigating the Enigma: A Comprehensive Review of Idiopathic Intracranial Hypertension. Cureus. 2024;16(3):e56256. PMID:38623134. doi:10.7759/cureus.56256.
Abraham SF, Banks CN, Beaumont PJ. Eye signs in patients with anorexia nervosa. Aust J Ophthalmol. 1980;8:55-57.
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