What you carry at this position in your DNA and what research says about it.
Vitamin D Levels: 8/10 evidence, 17 publications.
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Sample genotype (not yours): G/G
Lower Vitamin D and Higher Deficiency Risk
This genotype is associated with lower baseline vitamin D levels and an increased risk of vitamin D insufficiency. It may also slightly influence susceptibility to certain autoimmune conditions and liver health.
What this genotype means: Lower baseline vitamin D; Increased risk of deficiency; Slightly higher multiple sclerosis risk.
Sample genotype (not yours): G/T
Typical Vitamin D Levels
Having one copy of each allele typically results in intermediate vitamin D levels. This is a very common genetic profile that generally aligns with average baseline risks.
What this genotype means: Average baseline vitamin D; Typical risk of deficiency; Standard response to sunlight.
Sample genotype (not yours): T/T
Higher Vitamin D and Lower Deficiency Risk
This genotype is linked to naturally higher baseline levels of vitamin D and a lower risk of deficiency. It provides a protective genetic buffer against low vitamin D status.
What this genotype means: Higher baseline vitamin D; Reduced risk of deficiency; Slightly lower multiple sclerosis risk.
Gene function and biological role
Gene Function: NADSYN1 encodes nicotinamide adenine dinucleotide (NAD) synthetase 1, an enzyme crucial for the final step of NAD biosynthesis. This gene is located in close physical proximity to DHCR7, which encodes 7-dehydrocholesterol reductase [1]. DHCR7 is responsible for converting 7-dehydrocholesterol into cholesterol, thereby regulating the availability of the precursor needed for vitamin D synthesis in the skin [2]. Because of this tight genetic linkage, variations in this region are strongly associated with circulating vitamin D levels [3].
Variant Impact: The rs12785878 variant is an intronic change located within the NADSYN1 gene, very close to the DHCR7 gene. This genetic variation influences the activity of the DHCR7 enzyme, which acts as a metabolic gatekeeper [2]. By altering how much precursor is directed toward cholesterol versus vitamin D synthesis, this variant directly impacts baseline vitamin D levels [1]. Large-scale genomic studies have established this locus as one of the most significant genetic determinants of vitamin D status in human populations [3].
Key Insight: This variant acts as a metabolic gatekeeper, deciding whether your body uses raw materials to make cholesterol or vitamin D.
Location: NADSYN1. Chromosome 11 · 11q13.4 · 71.5 Mb
Origin Story: The T allele, which promotes higher vitamin D synthesis, underwent a rapid selective sweep in ancient northern European and East Asian populations as they migrated away from the equator, helping them survive in regions with low sunlight.
Estimated prevalence by population
Global 26.3%; European 6.6%; African 56.7%; East Asian 38.0%; South Asian 62.3%; Americas 26.5%; Ashkenazi 14.8%; Finnish 16.9%; Middle Eastern 28.5%; Amish 9.7%.
Estimated GG genotype frequency.
Global 40.3%; European 38.2%; African 37.2%; East Asian 47.3%; South Asian 33.3%; Americas 50.0%; Ashkenazi 47.4%; Finnish 48.4%; Middle Eastern 49.8%; Amish 42.9%.
Estimated GT genotype frequency.
Global 33.4%; European 55.2%; African 6.1%; East Asian 14.7%; South Asian 4.5%; Americas 23.5%; Ashkenazi 37.8%; Finnish 34.7%; Middle Eastern 21.7%; Amish 47.3%.
Estimated TT genotype frequency.
Showing effects for G/G genotype
Nutrition & Metabolism
Vitamin & Mineral Metabolism
Vitamin D Levels. Evidence: 8/10. Source: PMID 29343764. Lower Levels.
Vitamin D Deficiency. Evidence: 8/10. Source: PMID 20541252. Higher Risk.
Immunity & Inflammation
Autoimmune Diseases
Multiple Sclerosis. Evidence: 3/10. Source: PMID 22130326. Slightly Higher Risk.
Organ Systems
Liver Function & Disease
Liver Health in Hepatitis C. Evidence: 3/10. Source: PMID 23734184. Higher Cancer Risk.
Showing effects for G/T genotype
Vitamin D Levels. Evidence: 8/10. Source: PMID 29343764. Typical Levels.
Vitamin D Deficiency. Evidence: 8/10. Source: PMID 20541252. Typical Risk.
Multiple Sclerosis. Evidence: 3/10. Source: PMID 22130326. Typical Risk.
Liver Health in Hepatitis C. Evidence: 3/10. Source: PMID 23734184. Typical Risk.
Showing effects for T/T genotype
Vitamin D Levels. Evidence: 8/10. Source: PMID 29343764. Higher Levels.
Vitamin D Deficiency. Evidence: 8/10. Source: PMID 20541252. Lower Risk.
Multiple Sclerosis. Evidence: 3/10. Source: PMID 22130326. Slightly Lower Risk.
Liver Health in Hepatitis C. Evidence: 3/10. Source: PMID 23734184. Lower Cancer Risk.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
Baseline vitamin D levels tend to be lowest with this genetic profile [1]. The G allele reduces the availability of the precursor molecule needed for skin-based vitamin D synthesis [2]. Consequently, there is a significantly higher risk of experiencing vitamin D insufficiency or deficiency, especially during winter months [3]. This genetic tendency has also been linked to a slightly higher susceptibility to certain autoimmune conditions like multiple sclerosis [4].
Lower baseline vitamin D; Increased risk of deficiency; Slightly higher multiple sclerosis risk.
Sample genotype: GT (Heterozygous)
Intermediate baseline levels of vitamin D are typical for this heterozygous profile [1]. The presence of one G allele and one T allele creates a balanced genetic influence on the DHCR7 enzyme pathway [2]. While the risk of severe deficiency is lower than in those with two G alleles, seasonal drops in vitamin D can still occur [3]. Some studies suggest a moderate, intermediate risk level for vitamin D-related health outcomes [4]. General wellness guidelines for vitamin D intake and sun exposure are usually sufficient to maintain healthy levels [5]. No extreme genetic risks are associated with this highly common profile [6].
Average baseline vitamin D; Typical risk of deficiency; Standard response to sunlight.
Sample genotype: TT (Homozygous)
Naturally higher baseline levels of vitamin D are characteristic of this genetic profile [1]. The T allele optimizes the pathway that allows the skin to synthesize vitamin D from sunlight [2]. As a result, there is a significantly lower risk of developing vitamin D deficiency or insufficiency [3]. This robust genetic buffer helps maintain stable vitamin D levels even with limited sun exposure [4]. Some research also links this protective profile to a lower risk of autoimmune conditions like multiple sclerosis [5]. While supplementation is rarely needed under normal conditions, standard dietary intake remains beneficial [6].
Higher baseline vitamin D; Reduced risk of deficiency; Slightly lower multiple sclerosis risk.
Variants with shared genetic architecture
rs3829251 · NADSYN1 Gene · Chr 11 · Vitamin D Levels
rs10741657 · CYP2R1 Gene · Chr 11 · Vitamin D Status
rs12794714 · CYP2R1 Gene · Chr 11 · Vitamin D Levels
Common genetic determinants of vitamin D insufficiency: a genome-wide association study.
ANKRD55 and DHCR7 are novel multiple sclerosis risk loci.
Content updated August 2026.
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