Why Vitamin A Backfires in Sensitive Kids

Vitamin A is essential. For the immune system. For the brain. For copper metabolism. And for so many of the functions we support daily in children with autism, PANS, and PANDAS.

But some children react to it – even the cleanest, gentlest forms.

Cod liver oil, retinyl palmitate, whole food supplements. What should help instead makes things worse. Parents report mood swings, rashes, gut flares, sleep disruption, and in some cases, complete regression.

The common assumption? “It must be histamine.”

But clinically, that doesn’t always hold. Reactions to vitamin A often occur even when histamine levels are low and mast cells are stable. What’s really going on?

Vitamin A Needs to Be Converted

Retinol – the form of vitamin A found in cod liver oil and many supplements – isn’t biologically active. It must convert to retinoic acid. This is the form the body uses to regulate gene expression, activate copper pathways, and support immune balance.

That conversion happens in two key steps. Both rely on specific enzymes, zinc, a healthy liver, and a steady supply of NAD+ (the same molecule needed for mitochondrial energy).

When any part of this system is sluggish, retinol builds up. The body can’t use it. But it can still store it – often in the liver or fat tissue. The result? Symptoms of both deficiency and toxicity at the same time.

-Mood swings
-Fatigue
-Light sensitivity
-Sleep disruption
-Low ceruloplasmin
-Copper stuck in tissues
-No clinical progress

We’ve seen this repeatedly in children with complex neuroimmune symptoms. More vitamin A does not fix it. It makes things worse.

What Blocks the Conversion?

-Low zinc
-Sluggish thyroid
-Liver congestion
-Inflammation
-Genetic variants in the enzymes that process vitamin A

These are all common in the children we see. But one block gets overlooked more than most: sulphite toxicity.

Sulphite Toxicity: The Hidden Block

Sulphites are by-products of sulphur metabolism – and they pile up fast when phenol load is high or when the gut microbiome is disrupted. Salicylates, amines, food additives, even certain healthy foods can increase sulphite demand.

To convert sulphites into usable sulphate, the body relies on an enzyme called sulphite oxidase. This enzyme depends on molybdenum, and it can be impaired in children with genetic variants in the SUOX gene.

When this enzyme slows down, sulphites accumulate. These reactive compounds interfere with aldehyde metabolism – including the critical step from retinal to retinoic acid.

This is why some children react not just to supplements, but even to food-based vitamin A. The system is jammed up. Retinol arrives. Retinoic acid doesn’t.

The Gut-Liver Connection

There’s more.
Fat-soluble vitamins like vitamin A rely on bile flow, gallbladder function, and proper fat digestion. If bile is sluggish – often the case in children with constipation, pale stools, or fat intolerance – then even the best vitamin A source may stall.

Add in liver congestion or a history of viral load, and the picture gets clearer. This isn’t a supplement issue. It’s a bottleneck in the system that processes it.

The Mitochondrial Link

The final step in vitamin A activation needs NAD+, a cofactor made in the mitochondria. But NAD+ gets drained under stress – infections, toxins, inflammation, or poor sleep all deplete it. Without it, the enzyme that turns retinal into retinoic acid slows down or stops altogether.

We’ve seen this in children with chronic fatigue, post-viral crashes, and neuroimmune flare-ups. Their mitochondria are under pressure. So is their vitamin A metabolism.

So What Do We Do Instead?

We don’t throw vitamin A out altogether. But we stop guessing. We assess whether the system can convert it. And if not, we pause, support the blocks, and only reintroduce when the downstream pathways are ready.

That means:

-Supporting zinc, thyroid, and bile flow
-Checking for SUOX gene variants
-Using molybdenum when appropriate
-Supporting sulphation and phenol metabolism
-Calming inflammation
-Building mitochondrial resilience
-Tracking signs of copper utilisation, not just intake

This isn’t just about vitamin A. It’s about understanding what the body is asking for – and what it’s not ready to handle.

 

Clinical Clues That Conversion May Be Blocked

-Reactions to cod liver oil
-Light sensitivity
-Strong response to liver or organ supplements
-Worsening fatigue or mood after adding retinol
-Persistently low ceruloplasmin despite copper
-Elevated vitamin A on testing without clear benefit

These are not random. They are data points – and when taken seriously, they can reshape how we intervene.

The Takeaway

Vitamin A reactions are not always histamine-driven. In many cases, they reflect a deeper metabolic traffic jam – one involving sulphites, mitochondrial stress, sluggish detox pathways, and genetic variables that stall the body’s ability to activate what it’s being given.

When we support these blocks in sequence, children improve. Sleep deepens. Mood steadies. Nutrient signalling returns. And vitamin A stops feeling like a trigger and starts working like it should.

We don’t guess. We test, track, and listen to what the body is saying.

IMPORTANT

The information provided in this article is for educational purposes only and is not a substitute for professional medical advice, diagnosis, or treatment. It is crucial to consult with medical doctors or qualified functional medicine practitioners to address specific health concerns and obtain personalised guidance tailored to individual needs. Never add any supplements to your plan until it has been assessed and approved by your medical doctor or a suitable qualified practitioner who is familiar with your health history.

Concerned about your child’s health? We’d love to have a chat with you.

References

Kedishvili, N.Y., 2016. Retinoic acid synthesis and degradation. Subcellular Biochemistry, vol. 81, pp. 127‑161.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5551983

Li, J.-T., Chen, Z.-X., Chen, X.-J., Jiang, Y.-X. et al., 2022. Mutation analysis of SUOX in isolated sulfite oxidase deficiency with ectopia lentis as the presenting feature: insights into genotype–phenotype correlation. Orphanet Journal of Rare Diseases, vol. 17, art. no. 392, published 27 October. https://ojrd.biomedcentral.com/articles/10.1186/s13023-022-02544-x

Waring, R.H. and Klovrza, L.V., 2000. Sulphur metabolism in autism. Journal of Nutritional & Environmental Medicine, 10(1), pp.25–32.  https://www.tandfonline.com/doi/pdf/10.1080/13590840050000861

Tanumihardjo, S.A., 2011. Vitamin A: biomarkers of nutrition for development. The American Journal of Clinical Nutrition, 94(2), pp.658S–665S. https://europepmc.org/articles/PMC3142734