BCMO1 rs750133: Genetics and Beta-Carotene Conversion
The rs750133 variant is a missense single-nucleotide polymorphism located in the BCMO1 gene, which encodes the primary enzyme responsible for converting dietary provitamin A carotenoids into active vitamin A. Inheriting the alternative allele has been associated with reduced enzymatic activity, leading to lower efficiency in turning plant carotenoids like beta-carotene into retinal. This variant helps explain why some healthy individuals display a 'poor converter' profile during dietary carotenoid metabolism.
What each genotype means
Typical beta-carotene conversion
You carry two copies of the common reference allele for the BCMO1 variant rs750133 (also cited as rs7501331 or A379V). Research indicates typical enzymatic activity for converting dietary provitamin A carotenoids, like beta-carotene, into active vitamin A (retinol). Current nutritional evidence does not indicate a genetically reduced conversion capacity from this specific site.
Carried by approximately 50% to 60% of individuals of European ancestry and roughly 55% of individuals in East and Southeast Asian populations.
Moderately reduced beta-carotene conversion
You carry one copy of the T variant allele for rs750133. Clinical and biochemical studies indicate that carriers of the T allele can experience a moderate reduction (around 32% lower in initial volunteer studies) in their ability to convert dietary beta-carotene into active vitamin A. Because evidence for clinical hypovitaminosis A remains limited and depends heavily on overall diet, nutritional impact is modest.
Carried by approximately 35% to 45% of individuals across European and Asian populations, but it is rare or absent in certain West African ancestries.
Significantly reduced beta-carotene conversion
You carry two copies of the T variant allele for rs750133, which encodes the A379V substitution in the BCMO1 enzyme. Observational and intervention studies associate this genotype with significantly reduced conversion efficiency of plant-based beta-carotene into retinal and lower baseline plasma retinol levels when relying primarily on provitamin A. Evidence is limited regarding long-term health outcomes, as preformed dietary vitamin A sources easily bypass this enzymatic pathway.
Carried by approximately 5% to 10% of individuals of European and East Asian descent, while being virtually absent in some indigenous African lineages.
Molecular Profile: The rs750133 Variant
The single-nucleotide polymorphism rs750133 (commonly evaluated in literature alongside its neighboring coding variant record rs7501331) represents a coding missense change situated within the BCO1 (historically known as BCMO1) gene on human chromosome 16. In standard dbSNP annotations, the genomic variation corresponds to a nucleotide substitution that results in an amino acid alteration, commonly characterized as an alanine-to-valine shift at codon position 379 (A379V). Because it changes the primary sequence of the polypeptide chain, researchers have evaluated this variant as a functional contributor to differences in carotenoid metabolism. Human BCMO1 acts as a monomeric cytosolic cleavage enzyme located largely in the small intestine mucosa and liver, where it facilitates symmetrical central cleavage of ingested carotenoid rings. Consequently, structural alterations in this region can alter enzymatic dynamics, protein folding, or substrate affinity.
Biological Role: Carotenoid Cleavage and Vitamin A
Dietary vitamin A enters the human system in two forms: preformed vitamin A (retinol and retinyl esters) derived from animal products, and provitamin A carotenoids (predominantly beta-carotene, alpha-carotene, and beta-cryptoxanthin) obtained from plant foods. Before provitamin A carotenoids can participate in retinoid signaling, vision pathways, or immune defense, they must be cleaved into active retinoids. The enzyme beta-carotene 15,15'-monooxygenase (BCMO1) carries out symmetrical oxidative cleavage at the central 15,15'-double bond of beta-carotene, yielding two molecules of all-trans retinal. This retinal is then enzymatically converted to retinol for transport or further oxidized into retinoic acid. Although a secondary carotenoid cleavage enzyme exists (BCO2), animal knock-out models demonstrate that BCO2 alone cannot sustain retinoid homeostasis, establishing BCMO1 as the rate-limiting gatekeeper for converting plant provitamin A into biologically usable vitamin A.
Research Findings and Quality of Evidence
Early nutritional intervention trials identified substantial inter-individual variability in conversion rates, identifying up to 45 percent of people as 'poor converters.' Seminal investigations by Leung and colleagues linked this trait to nonsynonymous BCMO1 polymorphisms, demonstrating that the 379V-encoding allele was associated with a 32 percent reduction in conversion efficiency in female volunteers in vivo. When paired in double-mutant haplotypes with the R267S coding variant (rs12934922), catalytic activity dropped by approximately 57 percent in vitro and 69 percent in vivo. Despite these notable functional findings, the overall evidence strength for rs750133 remains categorized as limited. Most clinical evidence originates from small candidate-gene cohorts, specific female trial panels, and isolated observational populations, meaning large-scale multi-ancestry validation across broad randomized nutrition trials is still needed to establish definitive clinical effect sizes.
Population Distribution and Ancestry Differences
The allele frequencies of BCMO1 coding polymorphisms demonstrate marked diversity across global populations, which researchers speculate may reflect historical dietary exposure and local selection pressures. In populations of European ancestry, the minor allele frequency of rs750133 typically ranges between 0.25 and 0.35, with roughly 40 to 45 percent of individuals carrying at least one copy of the variant allele. By comparison, studies in East Asian populations, including Han Chinese and Japanese cohorts, observe variant allele frequencies between 24 and 31 percent. In Filipino cohorts, carrier frequencies of at least one variant allele have been observed at nearly 45 percent. In contrast, the variant allele is substantially rarer or absent in certain indigenous African populations, such as the Yoruba in Nigeria, highlighting that carotenoid-cleaving genetic traits cannot be generalized across ancestries.
Nutrigenomic Context: Interpreting the Data
A genetic variation in rs750133 does not diagnose a medical condition or guarantee clinical hypovitaminosis A. While individuals carrying the variant may convert plant-derived beta-carotene into retinal with reduced efficiency, dietary provitamin A continues to provide antioxidant and cellular benefits. Furthermore, individuals consuming omnivorous diets readily absorb preformed vitamin A from animal sources such as eggs, dairy, and fish, which bypasses the BCMO1 enzymatic pathway entirely. The biological effect of reduced conversion capacity becomes most relevant for strict vegetarians or vegans who depend entirely on carotenoids for their retinoid status. Rather than attempting self-treatment with high-dose vitamin A supplements—which carry documented toxicity risks—individuals curious about their nutritional status should discuss serum retinol testing and balanced meal composition with a registered dietitian or physician.
How common is this variant?
The minor allele frequency for rs750133 is approximately 0.25 to 0.35 in European ancestries, with roughly 44% carrying at least one variant allele. Frequencies vary globally, remaining prevalent across East Asian populations (24% to 31%) but dropping significantly in certain Sub-Saharan African populations.
Frequently asked questions
Does having the rs750133 variant mean I am vitamin A deficient?
No, carrying this variant does not mean you have a vitamin deficiency. The SNP is associated with a statistical reduction in how efficiently your body converts carotenoids from plants into retinal, but overall vitamin A status depends on total diet, gut absorption, and preformed retinol consumption.
Can I overcome reduced BCMO1 conversion by eating more carrots?
Consuming higher amounts of beta-carotene rich vegetables can supply additional carotenoid substrates, but enzymatic cleavage remains rate-limited by your BCMO1 capacity. Pairing vegetables with healthy dietary fats also helps improve fat-soluble carotenoid absorption from the digestive tract.
Should people with this variant take vitamin A supplements?
Routine genetic results are not a reason to start high-dose vitamin A supplements, which can accumulate in tissues and cause toxicity. If you have concerns about your retinoid levels, a doctor or registered dietitian can order a serum retinol blood test and evaluate your nutritional needs safely.
Why does the rs750133 variant affect vegans and vegetarians more?
Strict plant-based diets contain no preformed vitamin A, meaning all systemic retinoids must be synthesized internally from plant carotenoids via BCMO1. If that conversion enzyme functions at a lower efficiency, individuals relying solely on plant sources may be more susceptible to low retinoid reserves.
Sources & further reading
Educational information only, last refreshed 9/10/2026. Not medical advice — these associations describe population statistics, not individual predictions.
Curious what your genotype is for rs750133?
Upload a raw DNA file from 23andMe, AncestryDNA, MyHeritage, or FamilyTreeDNA and see this variant — plus thousands more — interpreted in your full report.
Get my report — $29