The Question Nobody Is Asking About Children’s Eyesight

Sep 23

8 min read

Vitamin A, Immune Activation Via Vaccination (MMR Specifically)

and a Myopia Epidemic That Doesn’t Have a Complete Explanation

Something is happening to children’s eyesight, and nobody can fully explain it.

In East Asia, myopia rates in young adults have gone from 20-30% a few decades ago to 80-90% today. In Europe and North America, the numbers are climbing fast. The World Health Organization has designated myopia progression a global public health concern, projecting that half the world’s population will be nearsighted by 2050 (Holden et al., 2016, Ophthalmology 123(5):1036-1042).

The standard explanations are real: more screen time, less outdoor play, less natural sunlight. Those are contributing factors, and the research behind them is solid (Rose et al., 2008, Ophthalmology 115(8):1279-1285). But the researchers studying these trends openly acknowledge that these factors alone don’t fully account for the rate of increase. Something else is contributing. It hasn’t been identified.

I want to raise a question. Not make a declaration. Not claim I’ve found the answer the field is missing. But a question that has a real mechanistic foundation underneath it, that overlaps perfectly with a developmental window that every child passes through, and that — as far as I can find — has never been formally investigated.

The question is about Vitamin A.

How Your Child’s Eyes Actually Develop

Most people think of eyesight as something you either have or don’t — good eyes or bad eyes, genetics or luck. The actual biology is more interesting than that.

During early childhood, your eyes are literally growing to the correct length. This process is called emmetropization, and it’s the eye calibrating itself to focus light precisely on the retina. If the eye grows too long, light focuses in front of the retina — that’s myopia, nearsightedness. If the eye doesn’t grow long enough, light focuses behind the retina — that’s hyperopia, farsightedness.

This growth is most active during the first three years of life and continues through early childhood. It’s not random. It’s governed by chemical signals at the sclera — the white outer shell of the eye — that tell the eye how much to grow and when to stop.

One of the most important of those signals is retinoic acid — a derivative of Vitamin A.

McFadden, Howlett, and Mertz published in Vision Research (2004, 44(7):643-653) that retinoic acid signals the direction of eye elongation. Mertz and Wallman showed in Experimental Eye Research (2000, 70(4):519-527) that choroidal retinoic acid synthesis acts as a mediator between refractive error and compensatory eye growth. This isn’t fringe science. This is decades of peer-reviewed ophthalmic research. Retinoic acid helps govern how long your child’s eye becomes during the exact window when that length determines whether they’ll need glasses for the rest of their life.

That retinoic acid comes from Vitamin A.

What Most People Don’t Know About Vitamin A

Vitamin A is fat-soluble. This is a simple fact that has significant implications most people never think about.

Water-soluble vitamins like Vitamin C wash through your system daily — what your body doesn’t use, it excretes. Fat-soluble vitamins are different. Vitamin A is stored in the liver. Your body maintains a reservoir. When demand exceeds intake, the reservoir gets drawn down. When the reservoir gets depleted, every tissue that depends on Vitamin A starts to feel it — not just the immune system, but the eyes, the skin, the developing brain, the scleral tissue that’s governing eye growth.

Rebuilding that reservoir takes time. It’s not like Vitamin C where you can drink a glass of orange juice and top off. The fat-soluble nature of Vitamin A means depletion events have longer recovery curves, and repeated depletion events can create a chronic deficit even in a child whose diet looks adequate on paper.

Now here’s where it gets more complicated.

There are two forms of dietary Vitamin A. Preformed retinol comes from animal sources — liver, eggs, dairy, fish. It enters the body ready to use. Beta-carotene comes from plant sources — carrots, sweet potatoes, leafy greens. But beta-carotene is not Vitamin A. It’s a precursor. Your body has to convert it using an enzyme called BCMO1.

And roughly 40-45% of the population carries genetic variants of BCMO1 that significantly reduce that conversion. These aren’t rare mutations. They’re common polymorphisms. A substantial portion of the population converts plant-based carotenoids to usable retinol at a fraction of the normal efficiency.

What this means practically: a child whose family relies primarily on plant-based sources for Vitamin A, and who happens to carry a BCMO1 variant, may have a Vitamin A status that looks adequate by dietary survey but is functionally marginal at the tissue level. Their liver reservoir is thinner than anyone realizes. And every time something draws on that reservoir, the deficit deepens.

What Draws Down the Reservoir

Every immune activation event costs Vitamin A.

This is basic immunology. When the immune system activates — whether fighting a natural infection or responding to a vaccine — it consumes micronutrients as raw material. Cytokine production, white blood cell multiplication, antibody manufacturing — all of these are micronutrient-dependent processes. Vitamin A, zinc, and Vitamin D are all consumed during immune response.

This is, in fact, why the World Health Organization has recommended Vitamin A supplementation alongside measles treatment since 1987 — because measles infection depletes Vitamin A so severely that the depletion itself becomes dangerous. The Cochrane Database confirmed that two doses of 200,000 IU of Vitamin A reduces measles mortality by 62-87% (Imdad et al., 2017, Cochrane CD001479). The treatment works because it replenishes what the immune response burns through.

Now consider the pediatric vaccine schedule.

A child following the CDC recommended schedule receives multiple vaccine doses at the 2-month, 4-month, 6-month, 12-month, and 15-18 month visits. Each visit involves multiple injections. Each injection is designed to trigger an immune response. Each immune response draws on Vitamin A stores.

These are not massive single-event depletions like a full measles infection. Nobody is claiming that. But they are repeated draws on the same reservoir, at regular intervals, during the same developmental window when that reservoir’s contents are also needed for scleral retinoic acid signaling during emmetropization.

Nobody measures Vitamin A levels before or after these visits. Nobody tracks whether the cumulative draw affects the reservoir in children who started with marginal stores. Nobody has asked whether the children who carry BCMO1 variants — the ones whose reservoir was already thinner — experience more significant depletion.

The Developmental Window Nobody Is Looking At

Here is where the question crystallizes.

Emmetropization — the process governing axial eye growth — is most active during the first three years of life. Retinoic acid is a key signaling molecule in that process. Retinoic acid comes from Vitamin A.

The vaccine schedule delivers its highest concentration of immune activation events during the same first three years of life. Each event draws on Vitamin A stores.

Some children enter this window with marginal Vitamin A status due to BCMO1 variants, plant-heavy diets, or both. Those children have less buffer to absorb repeated draws.

The mechanistic pathway is straightforward: repeated immune activation → repeated Vitamin A depletion → reduced retinoic acid availability at the sclera → dysregulated eye growth during the window when axial length is being calibrated.

Each individual piece of this chain is documented in peer-reviewed literature. Retinoic acid governs scleral growth. Immune activation depletes Vitamin A. BCMO1 variants reduce Vitamin A conversion. Emmetropization and the vaccine schedule occupy the same developmental window.

What has never been studied is whether the chain, taken together, is contributing to the myopia epidemic.

Not a single study has measured Vitamin A status in children before and after vaccination events and tracked refractive development outcomes. Not one. The question has simply never been asked.

What I’m Not Saying

I want to be clear about what this is and what it isn’t.

I am not claiming that vaccines cause nearsightedness. That would be overclaiming what the evidence supports. There are well-documented contributing factors to the myopia epidemic — screen time, reduced outdoor exposure, near-work intensity, genetic predisposition — and those factors are real and should not be dismissed.

What I am saying is that there is a mechanistic pathway, built entirely from documented biology, that connects repeated immune activation during the emmetropization window to potentially dysregulated scleral retinoic acid signaling in Vitamin A-marginal children — and that this pathway has never been investigated.

There are other causes of myopia. There may be many factors converging simultaneously. But when a biological question has a mechanistically plausible foundation, and the developmental timing aligns, and the population-level trends don’t have a complete explanation yet — that question deserves to be studied. Not assumed away. Studied.

The absence of investigation is not evidence that the effect is absent. It is evidence that the question has not been asked.

What Would Actually Answer This

The study that would begin to answer this question is not complicated and would not be expensive.

Measure Vitamin A levels (serum retinol and retinyl esters) in a cohort of children before and after scheduled vaccination events. Genotype them for BCMO1 variants. Track their refractive development through standard pediatric eye exams over the following years. Compare outcomes between children with adequate pre-vaccination Vitamin A stores and those with marginal stores. Compare outcomes between BCMO1 wild-type and variant carriers.

That’s it. Blood draw. Cheek swab. Standard eye exams they’re already getting. Follow-up over time. The infrastructure to do this study already exists in every pediatric research hospital in the country.

Until that study is done, we don’t have an answer. But we do have a question worth asking. And given that the world is heading toward half its population being nearsighted within twenty-five years, and given that the current explanations don’t fully account for it, and given that there is a plausible biological mechanism that nobody has tested — asking seems more responsible than not asking.

In the meantime, there are practical things any parent can consider. If your child is primarily getting Vitamin A from plant sources, be aware that BCMO1 variants are common and may mean your child isn’t converting carotenoids as efficiently as you’d expect. Preformed retinol from animal sources — egg yolks, liver, cod liver oil, full-fat dairy — doesn’t require conversion and provides Vitamin A the body can use directly. Vitamin A status can be assessed with a simple blood test. And given that Vitamin A is fat-soluble, it’s absorbed best when consumed with dietary fat.

These are reasonable nutritional steps regardless of the vaccine question. A well-nourished child with adequate Vitamin A stores is better equipped for any immune challenge — from natural infection or from vaccination — than a depleted one.

Sources referenced in this article:

1. McFadden SA, Howlett MHC, Mertz JR. “Retinoic acid signals the direction of ocular elongation in the guinea pig eye.” Vision Research 44, no. 7 (2004): 643-653.

2. Mertz JR, Wallman J. “Choroidal retinoic acid synthesis: a possible mediator between refractive error and compensatory eye growth.” Experimental Eye Research 70, no. 4 (2000): 519-527.

3. Holden BA, Fricke TR, Wilson DA, et al. “Global prevalence of myopia and high myopia and temporal trends from 2000 through 2050.” Ophthalmology 123, no. 5 (2016): 1036-1042.

4. Rose KA, Morgan IG, Ip J, et al. “Outdoor activity reduces the prevalence of myopia in children.” Ophthalmology 115, no. 8 (2008): 1279-1285.

5. Morgan IG, Ohno-Matsui K, Saw SM. “Myopia.” Lancet 379, no. 9827 (2012): 1739-1748.

6. Imdad A, et al. “Vitamin A supplementation for preventing morbidity and mortality in children.” Cochrane Database of Systematic Reviews (2017): CD001479.

7. Leung WC, Hessel S, Méplan C, et al. “Two common single nucleotide polymorphisms in the gene encoding β-carotene 15,15’-monoxygenase alter β-carotene metabolism in female volunteers.” FASEB Journal 23, no. 4 (2009): 1041-1053.

8. Troilo D, Nickla DL, Wildsoet CF. “Choroidal thickness changes during altered eye growth and refractive state in a primate.” Investigative Ophthalmology and Visual Science 41, no. 6 (2000): 1249-1258.