Retinol vs Beta-Carotene: Why Preformed Vitamin A Matters
You've been told to eat your carrots for vitamin A. But there's a genetic lottery at play. Some people convert beta-carotene to retinol beautifully. Others convert so little that carrots are nearly useless for vitamin A, and nobody's told them.
By Niall Kiddle, Founder, Organised
Reviewed by Pedro Rodrigues, Agronomist ·
6 min read
Makers of the Organised Daily blend, a grass-fed beef organ supplement from regenerative UK farms
Retinol and beta-carotene are not the same thing
Vitamin A is not one thing. It's a category. Preformed vitamin A is retinol, the actual active form your body uses. It's found exclusively in animal products. Your liver stores it. Your immune system uses it. Your eyes, your skin, your reproductive system all run on retinol.
Beta-carotene is a plant pigment, found in orange and red vegetables. It's called a provitamin A because your body is supposed to convert it into retinol. But that conversion is not automatic. It's not guaranteed. And for some people, it barely happens at all.
The conversion happens via an enzyme called beta-carotene monooxygenase 1. BCMO1.1 Your genes code for how much BCMO1 you produce, how efficiently it works, and whether you have common variants that hobble its function.
Eating carrots is not the same as eating liver. Beta-carotene conversion is genetically determined and unreliable.
The BCMO1 gene and the conversion problem
The BCMO1 gene has several variants. The most common is a single nucleotide polymorphism called rs12934922. People with two copies of the T allele (TT genotype) convert beta-carotene efficiently into retinol. People with two copies of the A allele (AA genotype) do not. Their conversion rate is severely impaired.
Research from Tufts University found that AA carriers converted as little as 3 to 6 per cent of the beta-carotene they consumed into usable retinol.2 TT carriers converted roughly 10 times more. In one study, AA carriers eating a beta-carotene-rich diet still ended up with measurably lower retinol status than TT carriers eating the same food.
The prevalence of the AA genotype varies by ethnicity. Approximately 45 to 50 per cent of European-descended populations carry at least one A allele, with about 15 to 25 per cent carrying AA. In some populations, the prevalence is higher. If you're in that AA group, supplementing beta-carotene or eating carrots is, frankly, a waste.
Why some people are very poor converters
The reason this matters is simple. You cannot feel a vitamin A deficiency until it's severe. Vitamin A deficiency develops silently. Your immunity weakens before you notice. Your eyesight dims before you see symptoms. Your skin ages faster before you realise what's happening. By the time symptoms show, the deficiency is already deep.
If you're an AA carrier eating a plant-forward diet heavy on carrots and sweet potatoes and light on animal foods, you could be walking around with borderline vitamin A deficiency without knowing it. Your immunity isn't what it should be. Your eyes aren't as sharp. Your recovery from illness is slower. And the cause is invisible.
The cruel part is that mainstream nutrition advice assumes everyone converts beta-carotene equally. The food guidelines say eat your vegetables, get your vitamin A. They work for half the population. For the other half, particularly AA carriers, they're incomplete advice.
Your BCMO1 genetic status isn't the only factor affecting conversion. Bile production influences how well you absorb beta-carotene (you need fat for absorption). Gut inflammation impairs absorption and conversion. Thyroid function affects conversion efficiency. Zinc status matters, your body needs zinc to synthesise BCMO1. So if you're an AA carrier with poor fat digestion, low zinc, or thyroid issues, your conversion rate drops further.
This creates a compounding problem for certain people. They're genetically predisposed to poor conversion, and their health status worsens the situation further. It's not just beta-carotene. It's a convergence of factors making reliable vitamin A status nearly impossible without preformed sources.
If you're a poor converter, eating a kilogram of carrots will not raise your retinol status the way a single serving of liver will.
The best food sources of preformed retinol
If you want reliable vitamin A status, you need preformed retinol. Not promises. Not conversions. Direct sources that don't require enzymatic translation.
- Beef liver - 28,000 IU per 100 grams. One small serving covers your daily requirement several times over.3
- Lamb liver - 28,000 IU per 100 grams. Equally rich.
- Chicken liver - 11,000 IU per 100 grams. Still substantial.
- Egg yolks - 245 IU per yolk, but with other fat-soluble vitamins that support retinol absorption and function.
- Butter and full-fat dairy - From grass-fed cows especially, roughly 350 IU per tablespoon. Adds up across the day.
- Cod liver oil - 4,000 IU per teaspoon, though whole food is preferable.
If you're an AA carrier or if you suspect your conversion is poor, aim for liver once per week and eggs most days. The amount of preformed retinol this delivers is incomparable to any amount of plants you could realistically eat.
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How much vitamin A do you actually need?
The recommended daily allowance for vitamin A is 700 to 900 micrograms RAE (retinol activity equivalents) for adults.3 This translates roughly to 2,300 to 3,000 IU of preformed retinol. A single serving of beef liver (100 grams) provides roughly 28,000 IU. That's 10 times the daily requirement.
This sounds excessive, and it's worth addressing. Vitamin A is fat-soluble, meaning your body stores it. You don't need 2,800 IU daily if you're eating liver. Eating liver once or twice weekly provides a substantial store. Your liver actually stores weeks of vitamin A, releasing it as needed.
The danger zone for vitamin A toxicity is extraordinarily high, well over 10,000 IU daily for extended periods. A single liver serving won't cause toxicity. Regular liver consumption won't either. But if you're taking a multivitamin, a separate retinol supplement, and eating liver, you could approach problematic levels. The key is knowing what you're taking.
For contrast, beta-carotene is water-soluble (technically, fat-soluble in how it's absorbed, but your body excretes excess). You can eat enormous quantities of carrots and sweet potatoes without toxicity risk. But as we've established, that doesn't translate to adequate retinol if you're a poor converter.
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The conversion question in pregnancy and childhood
Vitamin A is absolutely critical during pregnancy and early childhood. It drives cell differentiation, immune development, and vision development. Deficiency during these periods can cause permanent damage, blindness, immune dysfunction, developmental delays.
In developing countries where vitamin A deficiency is endemic, supplementation programmes have been transformative.4 But those programmes provide preformed retinol, not beta-carotene, precisely because conversion is unreliable.
If you're pregnant, breastfeeding, or have young children, relying on beta-carotene conversion is unnecessarily risky. The stakes are too high. Eat liver. Include egg yolks. Use full-fat dairy. Don't gamble with your child's visual development or immune system on the hope that your BCMO1 gene is working efficiently.
The bottom line
If you know you're a poor BCMO1 converter, or if you're simply eating a diet light on animal products, relying on beta-carotene for vitamin A is a gamble you're likely losing. Preformed retinol from liver, eggs, and dairy is reliable, efficient, and exactly what your body needs. Carrots are fine. But they're not enough. If you care about immunity, skin quality, eyesight, and reproductive health, you need direct sources of retinol, not the promise of conversion.
Make liver a habit, not an aspiration. A 100-gram serving once or twice weekly provides abundant retinol. Eat it with butter or olive oil for fat-soluble vitamin absorption. Include egg yolks with most meals. These are the practical foundations of reliable vitamin A status, particularly if you're unfortunate enough to carry the AA genotype. The science is clear. The food is available. The choice is yours.
References
- 1. Tang G. Bioconversion of dietary provitamin A carotenoids to vitamin A in humans. American Journal of Clinical Nutrition. 2010;91(5):1468S-1473S. https://pmc.ncbi.nlm.nih.gov/articles/PMC2854912/
- 2. Lietz G, Oxley A, Leung W, Hesketh J. Single nucleotide polymorphisms upstream from the beta-carotene 15,15'-monoxygenase gene influence provitamin A conversion efficiency in female volunteers. Journal of Nutrition. 2012;142(1):161S-165S. https://pubmed.ncbi.nlm.nih.gov/22113863/
- 3. National Institutes of Health, Office of Dietary Supplements. Vitamin A and Carotenoids: Fact Sheet for Health Professionals. https://ods.od.nih.gov/factsheets/VitaminA-HealthProfessional/ [accessed May 2026].
- 4. World Health Organization. Vitamin A deficiency. https://www.who.int/data/nutrition/nlis/info/vitamin-a-deficiency [accessed May 2026].
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