What you carry at this position in your DNA and what research says about it.
Vitamin D Levels: 8/10 evidence, 13 publications.
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Sample genotype (not yours): G/G
Typical Vitamin D Levels and Normal Supplement Response
Your body processes vitamin D efficiently and responds normally to sunlight, diet, and supplements. You carry the typical genetic profile associated with optimal vitamin D activation.
What this genotype means: Efficient vitamin D activation; Typical response to supplements; Typical baseline risk of deficiency.
Sample genotype (not yours): A/A
Lower Vitamin D Levels and Poorer Supplement Response
You carry two copies of the A allele, which is strongly linked to lower circulating vitamin D levels. Your liver's conversion process is less efficient, so healthy levels may be harder to maintain.
What this genotype means: Reduced vitamin D conversion efficiency; Blunted response to oral supplements; Higher risk of chronic deficiency.
Sample genotype (not yours): G/A
Slightly Lower Vitamin D Levels and Reduced Supplement Response
You carry one copy of the A allele, which is linked to slightly lower circulating vitamin D levels. Your body may be less efficient at converting vitamin D, so optimal levels may be harder to reach.
What this genotype means: Slightly reduced vitamin D conversion; Modestly reduced response to supplements; Slightly higher risk of deficiency.
Gene function and biological role
Gene Function: The CYP2R1 gene encodes the primary vitamin D 25-hydroxylase enzyme in the liver [1]. This enzyme performs the first and most critical step in activating vitamin D by converting it into 25-hydroxyvitamin D [2]. This converted form is the main circulating type of vitamin D measured in blood tests to assess overall status [3]. Variations in this gene can alter enzyme activity, directly impacting how efficiently the body processes vitamin D from sunlight, food, or supplements [4].
Variant Impact: The rs12794714 variant is a synonymous genetic change located within the CYP2R1 gene. Although it does not alter the final amino acid sequence of the 25-hydroxylase protein, it significantly influences gene expression and translation efficiency [5]. The A allele is widely associated with lower circulating levels of 25-hydroxyvitamin D [6]. This genetic variant also reduces the body's ability to raise vitamin D levels in response to oral supplementation [4]. Consequently, individuals carrying this variant have a higher baseline risk of vitamin D deficiency [7].
Key Insight: Even though this genetic variant is synonymous and does not change the protein structure, it significantly impairs how well your body processes and responds to vitamin D supplements.
Location: CYP2R1. Chromosome 11 · 11p15.2 · 14.9 Mb
Estimated prevalence by population
Global 43.3%; European 31.7%; African 73.3%; East Asian 40.3%; South Asian 29.8%; Americas 29.2%; Ashkenazi 25.8%; Finnish 36.3%; Middle Eastern 37.5%; Amish 23.3%.
Estimated GG genotype frequency.
Global 42.3%; European 49.2%; African 24.7%; East Asian 46.4%; South Asian 49.6%; Americas 49.7%; Ashkenazi 50.0%; Finnish 47.9%; Middle Eastern 47.5%; Amish 49.9%.
Estimated GA genotype frequency.
Global 14.4%; European 19.1%; African 2.1%; East Asian 13.4%; South Asian 20.6%; Americas 21.1%; Ashkenazi 24.2%; Finnish 15.8%; Middle Eastern 15.0%; Amish 26.8%.
Estimated AA genotype frequency.
Showing effects for G/G genotype
Nutrition & Metabolism
Vitamin & Mineral Metabolism
Vitamin D Levels. Evidence: 8/10. Source: PMID 32242144. Typical.
Vitamin D Deficiency. Evidence: 8/10. Source: PMID 39024449. Typical Risk.
Supplement Response. Evidence: 3/10. Source: PMID 23456391. Typical Response.
Cardiovascular & Metabolic
Diabetes & Glycemic Traits
Type 1 Diabetes. Evidence: 3/10. Source: PMID 17607662. Typical Risk.
Heart Disease
Heart Disease. Evidence: 3/10. Source: PMID 25003556. Typical Risk.
Showing effects for A/A genotype
Vitamin D Levels. Evidence: 8/10. Source: PMID 32242144. Lower.
Vitamin D Deficiency. Evidence: 8/10. Source: PMID 39024449. Increased Risk.
Supplement Response. Evidence: 3/10. Source: PMID 23456391. Poorer Response.
Type 1 Diabetes. Evidence: 3/10. Source: PMID 17607662. Increased Risk.
Heart Disease. Evidence: 3/10. Source: PMID 25003556. Increased Risk.
Showing effects for G/A genotype
Vitamin D Levels. Evidence: 8/10. Source: PMID 32242144. Slightly Lower.
Vitamin D Deficiency. Evidence: 8/10. Source: PMID 39024449. Slightly Increased.
Supplement Response. Evidence: 3/10. Source: PMID 23456391. Reduced Response.
Type 1 Diabetes. Evidence: 3/10. Source: PMID 17607662. Slightly Increased.
Heart Disease. Evidence: 3/10. Source: PMID 25003556. Slightly Increased.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
Carrying two copies of the G allele is associated with typical, healthy levels of circulating 25-hydroxyvitamin D [1]. The CYP2R1 enzyme in your liver functions at baseline capacity, smoothly converting inactive vitamin D into its active circulating form [2]. Studies show that individuals with this genotype experience a robust and predictable increase in blood vitamin D levels when taking standard oral supplements [3]. This efficient processing helps maintain bone density, supports immune function, and lowers the risk of chronic deficiency [4]. You also have a typical baseline risk for conditions linked to low vitamin D, such as type 1 diabetes and coronary artery disease [5].
Efficient vitamin D activation; Typical response to supplements; Typical baseline risk of deficiency.
Sample genotype: AA (Homozygous)
Carrying two copies of the A allele significantly reduces the efficiency of the CYP2R1 enzyme in converting vitamin D into its active circulating form [1]. Multiple large-scale genetic studies have consistently linked this genotype to lower baseline levels of 25-hydroxyvitamin D [2]. Furthermore, clinical trials show that individuals with the A/A genotype have a significantly blunted response to oral vitamin D supplementation, so sufficiency is harder to reach [3]. This genetic profile puts you at a higher risk for chronic vitamin D deficiency, which can impact bone health, muscle strength, and immune function [4]. It is also associated with an increased susceptibility to conditions linked to low vitamin D, such as type 1 diabetes and coronary artery disease [5].
Reduced vitamin D conversion efficiency; Blunted response to oral supplements; Higher risk of chronic deficiency.
Sample genotype: GA (Heterozygous)
Having one copy of the A allele is associated with a mild reduction in the liver's ability to convert vitamin D into its active circulating form [1]. Research indicates that individuals with this heterozygous genotype tend to have slightly lower baseline 25-hydroxyvitamin D levels compared to those with the G/G genotype [2]. When taking standard vitamin D supplements, your blood levels may not rise as quickly or as high as expected [3]. This reduced efficiency slightly increases your susceptibility to vitamin D deficiency, especially during winter months or periods of low sun exposure [4]. It is also associated with a modest increase in baseline risk for conditions influenced by vitamin D status, including cardiovascular health and immune regulation [5].
Slightly reduced vitamin D conversion; Modestly reduced response to supplements; Slightly higher risk of deficiency.
Variants with shared genetic architecture
rs10741657 · CYP2R1 Gene · Chr 11 · Vitamin D Status
rs2060793 · CYP2R1 Gene · Chr 11 · Vitamin D Levels
rs12785878 · NADSYN1 Gene · Chr 11 · Vitamin D Levels
Genome-Wide Association Study of Serum 25-Hydroxyvitamin D in US Women.
Genome-wide association study identifies 143 loci associated with 25 hydroxyvitamin D concentration.
Diversity and scale: Genetic architecture of 2068 traits in the VA Million Veteran Program.
Content updated August 2026.
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