What you carry at this position in your DNA and what research says about it.
Vitamin D Status: 8/10 evidence, 29 publications.
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Sample genotype (not yours): A/A
Typical Vitamin D Levels and Strong Supplement Response
Normal enzyme function allows for efficient conversion of vitamin D into its active circulating form. This genotype is associated with a lower risk of deficiency and a highly effective response to vitamin D supplements.
What this genotype means: Efficient vitamin D activation; Lower risk of clinical deficiency; Robust response to supplements.
Sample genotype (not yours): A/G
Slightly Lower Vitamin D Levels and Moderate Supplement Response
Carrying one copy of the G allele is associated with a mild reduction in 25-hydroxylase enzyme efficiency. This can lead to slightly lower circulating vitamin D levels and a moderate response to supplementation.
What this genotype means: Mildly reduced vitamin D activation; Slightly increased risk of insufficiency; Moderate response to supplements.
Sample genotype (not yours): G/G
Lower Vitamin D Levels and Reduced Supplement Response
Two copies of the G allele are linked to reduced 25-hydroxylase enzyme efficiency, leading to lower circulating vitamin D levels. This genotype increases the risk of deficiency and makes the body less responsive to standard vitamin D supplementation.
What this genotype means: Impaired vitamin D activation; Higher risk of clinical deficiency; Reduced response to standard supplements.
Gene function and biological role
Gene Function: CYP2R1 encodes the principal enzyme responsible for the first step of vitamin D activation in the human body [1]. This liver enzyme, known as vitamin D 25-hydroxylase, converts dietary and sun-derived vitamin D into 25-hydroxyvitamin D, the primary circulating form measured in clinical blood tests [2]. Proper function of this pathway is crucial for maintaining calcium homeostasis, bone density, and immune health [3]. Genetic variations in this gene can significantly alter enzyme expression and efficiency, directly impacting an individual's baseline vitamin D status regardless of their diet or sun exposure [4].
Variant Impact: The rs10741657 variant is a genetic change located within the CYP2R1 gene that influences how effectively the encoded enzyme converts vitamin D into its active circulating form [2]. A nucleotide change from adenine (A) to guanine (G) at this locus is associated with reduced expression and activity of the 25-hydroxylase enzyme [5]. This reduction in enzyme efficiency leads to a decreased rate of vitamin D conversion, resulting in lower circulating blood levels of 25-hydroxyvitamin D [1]. Consequently, this genetic marker is one of the most well-replicated genetic determinants of baseline vitamin D status and susceptibility to deficiency across diverse global populations [6].
Key Insight: Your body's ability to use vitamin D depends on a liver enzyme that activates it, meaning low blood levels can happen even with plenty of sun exposure.
Location: CYP2R1. Chromosome 11 · 11p15.2 · 14.9 Mb
Estimated prevalence by population
Global 12.2%; European 15.3%; African 7.1%; East Asian 11.7%; South Asian 11.4%; Americas 10.5%; Ashkenazi 7.6%; Finnish 17.8%; Middle Eastern 9.9%; Amish 9.6%.
Estimated AA genotype frequency.
Global 44.5%; European 47.6%; African 39.0%; East Asian 45.0%; South Asian 44.8%; Americas 43.9%; Ashkenazi 39.9%; Finnish 48.8%; Middle Eastern 43.2%; Amish 42.7%.
Estimated AG genotype frequency.
Global 43.2%; European 37.1%; African 53.9%; East Asian 43.3%; South Asian 43.8%; Americas 45.6%; Ashkenazi 52.5%; Finnish 33.5%; Middle Eastern 46.9%; Amish 47.7%.
Estimated GG genotype frequency.
Showing effects for A/A genotype
Nutrition & Metabolism
Vitamin & Mineral Metabolism
Vitamin D Levels. Evidence: 8/10. Source: PMID 29343764. Typical Levels.
Nutrient Deficiency Risk. Evidence: 6/10. Source: PMID 20541252. Lower Risk.
Supplement Response. Evidence: 4/10. Source: PMID 25527766. Strong Response.
Cardiovascular & Metabolic
Diabetes & Glycemic Traits
Type 1 Diabetes. Evidence: 3/10. Source: PMID 17607662. Typical Risk.
Showing effects for A/G genotype
Vitamin D Levels. Evidence: 8/10. Source: PMID 29343764. Slightly Lower.
Nutrient Deficiency Risk. Evidence: 6/10. Source: PMID 20541252. Slightly Higher Risk.
Supplement Response. Evidence: 4/10. Source: PMID 25527766. Moderate Response.
Type 1 Diabetes. Evidence: 3/10. Source: PMID 17607662. Slightly Higher Risk.
Showing effects for G/G genotype
Vitamin D Levels. Evidence: 8/10. Source: PMID 29343764. Lower Levels.
Nutrient Deficiency Risk. Evidence: 6/10. Source: PMID 20541252. Higher Risk.
Supplement Response. Evidence: 4/10. Source: PMID 25527766. Reduced Response.
Type 1 Diabetes. Evidence: 3/10. Source: PMID 17607662. Higher Risk.
What this genotype means for the people who carry it
Sample genotype: AA (Homozygous)
Normal activity of the 25-hydroxylase enzyme ensures that vitamin D from sunlight, food, or supplements is readily converted into its active circulating form, 25-hydroxyvitamin D [1]. Carrying two copies of the A allele is linked to significantly higher baseline vitamin D levels compared to carriers of the G allele [2]. Research indicates that individuals with this genotype show a robust response to vitamin D supplementation, experiencing a much greater increase in blood levels after taking supplements compared to those with the GG genotype [3]. This efficient conversion helps maintain optimal bone mineral density and supports overall immune function [4]. Consequently, those with this genetic profile are naturally more resilient against seasonal drops in vitamin D levels [1].
Efficient vitamin D activation; Lower risk of clinical deficiency; Robust response to supplements.
Sample genotype: AG (Heterozygous)
A single copy of the G allele introduces a mild bottleneck in the first step of vitamin D activation within the liver [1]. This slight reduction in 25-hydroxylase enzyme activity typically results in intermediate circulating levels of 25-hydroxyvitamin D, falling between the higher levels of the AA genotype and the lower levels of the GG genotype [2]. While the body can still activate vitamin D, the conversion process is less efficient, which can elevate the risk of falling into the insufficient range during winter months or periods of low sun exposure [3]. When taking vitamin D supplements or consuming fortified foods, individuals with this genotype tend to show a moderate increase in blood levels, requiring consistent intake to maintain optimal status [4]. Monitoring blood levels can help tailor dietary and supplement needs to overcome this mild genetic hurdle [4].
Mildly reduced vitamin D activation; Slightly increased risk of insufficiency; Moderate response to supplements.
Sample genotype: GG (Homozygous)
Reduced efficiency of the 25-hydroxylase enzyme significantly impairs the liver's ability to convert vitamin D into its active circulating form [1]. Carrying two copies of the G allele is strongly associated with lower baseline levels of 25-hydroxyvitamin D and a higher susceptibility to clinical vitamin D deficiency [2]. Studies show that individuals with this genotype do not increase their blood vitamin D levels as easily in response to sunlight, fortified foods, or standard supplementation compared to those carrying the A allele [3]. This genetic bottleneck means that maintaining optimal bone health and immune support can be harder to achieve with a typical vitamin D intake [4]. Because the body's natural activation pathway is less active, monitoring circulating levels through regular blood tests is particularly beneficial for managing overall health [4].
Impaired vitamin D activation; Higher risk of clinical deficiency; Reduced response to standard supplements.
Variants with shared genetic architecture
rs12794714 · CYP2R1 Gene · Chr 11 · Vitamin D Levels
rs2060793 · CYP2R1 Gene · Chr 11 · Vitamin D Levels
rs12785878 · NADSYN1 Gene · Chr 11 · Vitamin D Levels
Common genetic determinants of vitamin D insufficiency: a genome-wide association study.
Vitamin D status and gene transcription in immune cells.
Content updated August 2026.
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