Vitamin A deficiency is often discussed as a dietary problem. Not enough carrots, not enough leafy greens, not enough dairy. But what if the real issue isn’t just what people eat, but how their bodies process it? That’s where the BCMO1 gene comes in.
WHY VITAMIN A MATTERS
Vitamin A is important for vision, immune function, skin health, and reproduction. Severe deficiency can lead to night blindness, a higher risk of infections, and even lasting eye damage. Although this problem is most common in low-income countries, it also affects people in developed nations, sometimes for reasons other than diet.
TWO SOURCES OF VITAMIN A
There are two main ways we get vitamin A:
- Preformed vitamin A (retinol) – found in animal sources.
- Provitamin A carotenoids (like beta-carotene) – found in plant foods such as carrots, spinach, and sweet potatoes.
But here’s the catch: beta-carotene isn’t active vitamin A yet. The body must convert it into retinol, and that conversion depends heavily on the BCMO1 gene.
THE BCMO1 GENE’S ROLE
The BCMO1 (Beta-Carotene Monooxygenase 1) gene encodes an enzyme that breaks down beta-carotene into retinal, which is then converted into retinol (usable vitamin A). Variants in this gene can dramatically reduce the enzyme’s efficiency.
Research shows that some “low converter” polymorphisms in BCMO1 can cut conversion rates by up to 69%. In practice, that means two people could eat the same salad, but one gets plenty of vitamin A, while the other falls short of their daily requirement.
WHO’S AT RISK?
- Vegetarians and vegans: Since they rely heavily on plant sources, poor conversion efficiency can leave them deficient.
- People with BCMO1 variants: Genetic studies suggest up to 45% of the population carries at least one variant that impairs conversion.
- Individuals with gut or liver issues: Even without BCMO1 mutations, conditions that affect fat absorption or liver function can reduce vitamin A status.
CAN BCMO1 VARIANTS CAUSE DEFICIENCY ALONE?
Not always. Many people with reduced conversion efficiency still obtain sufficient vitamin A if they consume preformed sources. However, in populations that rely primarily on carotenoids, BCMO1 variants may make the difference between sufficiency and deficiency.
WHAT THIS MEANS FOR NUTRITION
- Dietary advice may need to be more personalised. A plant-based diet may not guarantee adequate vitamin A for everyone.
- Genetic testing could help. Knowing if you carry BCMO1 variants could guide whether you should prioritise supplements.
- Public health strategies might need to consider genetic diversity when designing vitamin A fortification programs.
BCMO1 doesn’t act alone; diet, health, and lifestyle all play a role. However, for many, this gene could be the hidden factor explaining why they exhibit signs of vitamin A deficiency despite consuming “enough” carotenoid-rich foods.
The real question going forward isn’t just Are you eating your vegetables? But can your body turn them into what it needs?
References:
- Reboul, E. (2019). Mechanisms of carotenoid intestinal absorption: where do we stand?. Nutrients, 11(4), 838.
- Lietz G et al. Single nucleotide polymorphisms upstream from the b-carotene 15,15’-monoxygenase gene influence provitamin A conversion efficiency in female volunteers. Journal of Nutrition. 2012;142:161S-5S.
- Yabuta, S., Urata, M., Wai Kun, R. Y., Masaki, M., & Shidoji, Y. (2016). Common SNP rs6564851 in the BCO1 gene affects the circulating levels of β-carotene and the daily intake of carotenoids in healthy Japanese women. PLoS One, 11(12), e0168857.
- Hendrickson, S. J., Hazra, A., Chen, C., Eliassen, A. H., Kraft, P., Rosner, B. A., & Willett, W. C. (2012). β-Carotene 15, 15′-monooxygenase 1 single nucleotide polymorphisms in relation to plasma carotenoid and retinol concentrations in women of European descent1. The American journal of clinical nutrition, 96(6), 1379.