A single pea is rolled around the plate. A sandwich is pulled apart with forensic precision before being pushed aside. Pasta is rejected because the sauce “looks funny”. A spoonful of cereal is spat back into the bowl, with the unfamiliar texture triggering tears. Another meal ends in negotiation rather than nourishment, followed by parental frustration and defeat.

Selective eating is a common developmental behaviour, with the highest prevalence during the preschool years (2–6 years). Although most children gradually outgrow this phase, persistent selective eating may result in nutritional deficiencies.1

Behind a diet consisting of chips, bread, crackers, chicken nuggets, or the ‘white diet’,2 lie nutritional shortages capable of damaging the retina and the optic nerve.3 By the time visual symptoms appear, the consequences may already be difficult to correct, or impossible to reverse.

Eyes can be an early warning system, the place where a hidden nutritional crisis can surface first, sometimes providing the first visible clue.4 So what are the eyes telling us about what’s missing from the plate?

CASE VIGNETTE

Oliver’s mother first noticed something was wrong when he started bumping into things on his right side, first a doorframe, a table edge, and then difficulty negotiating steps. After one bruise too many, she took him to their local optometrist. With a finding of asymmetric optic disc pallor, Oliver was referred urgently to the ophthalmology department at a children’s hospital. The paediatric team worked methodically through the differentials. Could there be a compressive lesion? Magnetic resonance imaging (MRI) was ordered. Was this genetic? With Leber hereditary optic neuropathy (LHON) also under consideration, genetic testing was initiated. Days went by without a clear answer or cause for the vision loss. During a bedside review, a medical team member suggested breaking for lunch, and a casual comment unexpectedly brought Oliver to tears. The hospital cafeteria didn’t have chicken nuggets. His mother explained that Oliver’s diet had narrowed almost entirely to fried chicken, with the occasional plain pasta or crackers. That single detail reframed the patient’s potential diagnosis. A severely restricted ‘white diet’, low in key micronutrients, pointed toward a nutritional cause. Further investigations confirmed a significant vitamin B12 deficiency – the cause of his vision loss.

WHEN IS PICKY EATING NO LONGER ‘JUST A PHASE’?

Not all picky eating is the same. While many children go through a typical phase of refusing certain foods, persistent or severe food restriction can stem from a range of underlying factors. Understanding these differences is key to recognising when picky eating may require further attention.

Food Neophobia

Food neophobia, or reluctance to try new foods, is common among young children, particularly during the preschool years. While it can be a normal part of development, it may also affect food preferences and eating patterns.5 For most children, these behaviours fade with time as they begin eating a wider variety of foods. No harm done, no intervention needed.

Sensory Sensitivity

Sensory sensitivity is a different concern. For some children, sensory characteristics of food,

“… a child can be full, consuming enough energy to grow, while simultaneously lacking the essential nutrients that neurological and ocular development depend on”

including taste, texture, smell, and appearance may be processed differently and can strongly influence food acceptance.6 Rather than this reflecting simple food preference, these sensory aversions may make certain foods difficult to tolerate, contributing to food refusal and restricted eating patterns.7

Avoidant/Restrictive Food Intake Disorder

Avoidant/restrictive food intake disorder (ARFID) is recognised as a DSM-5(Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition) diagnosis, which is distinctly different from the typical ‘extreme fussy eating’.8 The condition is characterised by persistent disturbance in eating that results in failure to meet nutritional or energy needs, which is not driven by concerns about body, weight or shape.9

Autism Spectrum Disorder and Food Selectivity

Children with autism spectrum disorder (ASD) commonly experience food selectivity, influenced by sensory sensitivities and behavioural factors, where food refusal can result in distressing mealtimes.10

The challenge then isn’t identifying children who dislike broccoli, it’s recognising those children whose diets have become dangerously narrow. Keeping a close ‘eye’ on which children are most likely to develop preventable vision loss from the resulting nutritional deficiencies enables them to be better supported before it’s too late.

WELL FED, BUT UNDERNOURISHED?

A child who eats enough, who grows, who is never hungry, and yet is dangerously undernourished… strange, right?

The confusion lies in a simple yet overlooked assumption: calories are not the same as nutrients. A diet built entirely on carbohydrates (chips, crackers, bread) can supply enough energy while delivering inadequate essential nutrients required for a growing body.

This phenomenon, ‘hidden hunger’, is a micronutrient deficiency that exists behind a façade of adequate caloric intake.11

Micronutrients, such as vitamins and minerals, are required in small amounts but are essential for maintaining normal physiological function. They contribute towards cellular metabolism, neurotransmitter synthesis, and processes involved in brain function and cognitive health.12

So, a child can be full, consuming enough energy to grow, while simultaneously lacking the essential nutrients that neurological and ocular development depend on.

NUTRITIONAL DEFICIENCY DISGUISED AS OPHTHALMIC DISEASE

The eyes are, in many ways, a window into the nervous system. They are metabolically demanding, richly vascularised, and neurologically exposed, meaning they can be one of the first structures to show visible signs when the body is under nutritional stress.

Vitamin A plays a fundamental role in maintaining both visual function and ocular surface health. Within the retina, vitamin A is required for the production of rhodopsin, the light-sensitive pigment responsible for vision in dim lighting, making it essential for normal dark adaptation and prevention of night blindness.13 Beyond its role in vision, vitamin A is also critical for maintaining the integrity of the ocular surface. Vitamin A regulates epithelial cell differentiation, supports goblet cell function and mucin production, promotes corneal wound healing, and contributes to tear film stability.14 When vitamin A levels become inadequate, these protective mechanisms are disrupted, resulting in progressive ocular changes including conjunctival and corneal dryness, epithelial damage, and xerophthalmia.14 More severe deficiency, corneal ulceration, and keratomalacia may occur, potentially leading to irreversible blindness.13

B-group vitamins, particularly vitamin B12, play an essential role in maintaining neurological function and supporting healthy vision. Vitamin B12 is required for DNA synthesis, cellular metabolism, and the maintenance of myelin surrounding nerve fibres, meaning deficiency can disrupt normal nerve conduction and function within the visual pathway.15 When vitamin B12 levels become inadequate, damage to the optic nerve can occur, resulting in nutritional optic neuropathy, which may present as progressive, painless vision loss, reduced colour vision, and central visual field defects.16 Beyond the optic nerve, B vitamins contribute to overall ocular health by supporting retinal metabolism, cellular function, and protection against oxidative stress.15 Importantly, vitamin B12 deficiencyrelated optic neuropathy may be reversible when identified and treated early,16 highlighting the importance of exploring nutritional deficiencies in unexplained visual changes.

Each of these nutrition deficiency-related ocular presentations could be a clue, not a coincidence.

When viewed in isolation, they may be dismissed as unrelated findings. However, when considered together and in the context of a child’s diet, they point to a much more urgent concern.

BUT WHAT DOES THE DATA SHOW?

Unpublished retrospective data over a 12-year period, for children diagnosed with nutritional deficiencies at the Royal Children’s Hospital Melbourne, identified 14 children diagnosed with ophthalmic disease related to their nutritional deficiency. Children were included if they had documented nutritional deficiencies, including vitamins A, B1–B12, C and E, zinc and copper, and/or a diagnosed eating disorder, including ARFID, anorexia, and bulimia. Interestingly, more than half of the cohort had a diagnosis of ASD, and the most common presenting symptoms were blurred vision, eye pain, and nyctalopia. The most frequent examination findings included optic atrophy and xerophthalmia, most often associated with deficiencies in vitamins A and B12. Beyond these clinical features, a concerning pattern emerged. Several children had undergone extensive investigations, including genetic testing, neuroimaging, lumbar puncture, and treatment with intravenous methylprednisolone before nutritional deficiencies were explored. Five children in this cohort are now legally blind. These findings may be the most important in the entire dataset. Awareness is key; invasive investigations highlight the importance of considering nutritional deficiency within the differential diagnosis of paediatric vision loss, particularly in children with risk factors for restricted dietary intake or eating disorders.

CHANGING THE SITUATION

Certain features are worth reflecting on:

• A diet that has narrowed to fewer than 10 or 15 foods.

• A reliance on processed carbohydrates that has quietly become the child’s entire daily intake.

• A diagnosis of autism or ARFID.

• And then there are the signs in the eyes themselves: nyctalopia, a dulling of colour vision, unexplained vision loss, pallor of the optic disc.

Each finding is a small piece of a puzzle waiting to be completed.

We may view a healthy growth chart as reassurance, proof that a child is ‘growing well’, yet this cohort reminds us that growth and nutrition are not equal. Micronutrient deficiencies or ‘hidden hunger’ can be easily overlooked, particularly when a child appears otherwise well and continues to track along expected growth trajectories. A child can climb the growth curve, while the nutrients their nervous system and body depend on remain quietly and dangerously absent.

LOOKING BEYOND THE PLATE

Most children who refuse vegetables will eventually broaden their diets with time. Some, however, will quietly develop deficiencies with lifelong neurological and visual consequences. By the time those consequences become apparent, they may no longer be reversible. For eye care professionals, recognising nutritional deficiency is critical. It helps ensure children are investigated along the most appropriate diagnostic pathway and that a restricted diet is recognised as a potential cause of vision impairment rather than being overlooked. Asking about diet during history taking should become routine, not incidental; this also serves to promote awareness among caregivers and children themselves about the importance of a varied diet, healthy eyes, and that we really ‘are what we eat’. The difference between timely intervention and irreversible vision loss is not always complex. Sometimes, it is simply a few questions about what a child eats, asked early enough to matter.

Navdeep Kaur BHSci MOrth MClinEd is a senior orthoptist and clinical researcher at the Royal Children’s Hospital Melbourne and the Royal Melbourne Hospital, including coordination of Orthoptist Clinical Education. With a special interest in health professions education, Ms Kaur completed a Master of Clinical Education in 2025, with her thesis researching supervisors’ experiences in delivering feedback to allied health students in an outpatient setting.

Dr Sandra Staffieri AO is a Senior Research Fellow at the Centre for Eye Research Australia (CERA) and the Manager, Retinoblastoma Service/Senior Clinical Orthoptist, Research Lead – Department of Ophthalmology, Royal Children’s Hospital Melbourne.

Dr Staffieri completed her PhD at CERA, University of Melbourne. With the aim of reducing delayed diagnosis of retinoblastoma, her study included the development and evaluation of an information pamphlet for new parents describing important early signs of eye problems in children.

References available at mivision.com.au.