What you carry at this position in your DNA and what research says about it.
Reproductive Health: 10/10 evidence, 30 publications.
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Sample genotype (not yours): T/T
Later Menopause but Higher Risk of Fibroids
This genotype is associated with a longer reproductive lifespan but carries an increased susceptibility to benign uterine growths. It also correlates with a slightly lower risk of developing type 2 diabetes.
What this genotype means: Delayed ovarian aging; Increased risk of uterine fibroids; Lower risk of type 2 diabetes.
Sample genotype (not yours): G/G
Earlier Menopause and Higher Diabetes Risk but Fewer Fibroids
This genotype offers strong protection against benign uterine growths but is linked to earlier reproductive aging. It also carries a slightly elevated risk for metabolic challenges.
What this genotype means: Earlier onset of menopause; Lower risk of uterine fibroids; Slightly increased risk of type 2 diabetes.
Sample genotype (not yours): T/G
Typical Reproductive Lifespan and Balanced Health Risks
Carrying one copy of each allele results in intermediate physiological traits. Reproductive aging, metabolic risk, and tissue growth patterns generally align with population averages.
What this genotype means: Average age at menopause; Standard baseline risk for fibroids; Typical metabolic profile.
Gene function and biological role
Gene Function: The PRIM1 gene encodes the small catalytic subunit of human DNA primase, an essential enzyme complex that initiates DNA synthesis during cell division [1]. Working in tandem with DNA polymerase alpha, this primase synthesizes short RNA primers that are absolutely required for lagging-strand DNA replication [1]. Because of its fundamental role in cellular proliferation, genetic variation in this gene can influence tissue growth dynamics across the body. This is particularly evident in highly proliferative tissues such as the endometrium and ovarian follicles, where cell division rates directly dictate organ function and aging [2]. Consequently, variations in this gene are linked to reproductive lifespan and tissue overgrowth conditions [2].
Variant Impact: The rs2277339 variant is a missense mutation in the PRIM1 gene that causes an amino acid substitution from aspartate to alanine at position 5 of the protein [1]. This structural alteration occurs near the surface of the primase catalytic subunit, potentially modifying its interaction with other replication machinery or small molecules [1]. By subtly altering DNA replication efficiency, this variant influences how rapidly cells can divide and repair DNA damage [2]. These cellular changes manifest as systemic differences in red blood cell size, skeletal growth, and ovarian aging rates [2]. Ultimately, the genetic change shifts the balance between cellular longevity and the risk of benign tissue growths [2].
Key Insight: This genetic variant acts as a biological trade-off, where alleles that delay reproductive aging and extend fertility also increase the risk of developing benign uterine growths.
Location: PRIM1. Chromosome 12 · 12q13.3 · 56.8 Mb
Estimated prevalence by population
Global 74.2%; European 80.4%; African 63.7%; East Asian 60.9%; South Asian 82.1%; Americas 77.2%; Ashkenazi 77.2%; Finnish 73.1%; Middle Eastern 69.8%; Amish 74.4%.
Estimated TT genotype frequency.
Global 23.7%; European 18.6%; African 32.2%; East Asian 34.2%; South Asian 17.0%; Americas 21.3%; Ashkenazi 21.3%; Finnish 24.8%; Middle Eastern 27.5%; Amish 23.7%.
Estimated TG genotype frequency.
Global 2.2%; European 1.1%; African 4.1%; East Asian 4.8%; South Asian 0.9%; Americas 1.5%; Ashkenazi 1.5%; Finnish 2.1%; Middle Eastern 2.7%; Amish 1.9%.
Estimated GG genotype frequency.
Showing effects for T/T genotype
Endocrine & Reproductive
Menstrual, Menopause & Ovarian Traits
Age at Menopause. Evidence: 10/10. Source: PMID 22267201. Later Menopause.
Female Reproductive Health & Fertility
Uterine Fibroids. Evidence: 8/10. Source: PMID 34594039. Increased Risk.
Genital Tract Polyps. Evidence: 8/10. Source: PMID 39986329. Increased Risk.
Cardiovascular & Metabolic
Diabetes & Glycemic Traits
Type 2 Diabetes. Evidence: 8/10. Source: PMID 32514122. Lower Risk.
Blood Cell & Iron Traits
Red Blood Cell Size. Evidence: 10/10. Source: PMID 27863252. Smaller Cell Size.
Lifestyle, Fitness & Aging
Height & Body Size
Height. Evidence: 10/10. Source: PMID 30595370. Taller Height.
Showing effects for G/G genotype
Age at Menopause. Evidence: 10/10. Source: PMID 22267201. Earlier Menopause.
Uterine Fibroids. Evidence: 8/10. Source: PMID 34594039. Lower Risk.
Genital Tract Polyps. Evidence: 8/10. Source: PMID 39986329. Lower Risk.
Type 2 Diabetes. Evidence: 8/10. Source: PMID 32514122. Increased Risk.
Red Blood Cell Size. Evidence: 10/10. Source: PMID 27863252. Larger Cell Size.
Height. Evidence: 10/10. Source: PMID 30595370. Shorter Height.
Showing effects for T/G genotype
Age at Menopause. Evidence: 10/10. Source: PMID 22267201. Typical.
Uterine Fibroids. Evidence: 8/10. Source: PMID 34594039. Typical.
Genital Tract Polyps. Evidence: 8/10. Source: PMID 39986329. Typical.
Type 2 Diabetes. Evidence: 8/10. Source: PMID 32514122. Typical.
Red Blood Cell Size. Evidence: 10/10. Source: PMID 27863252. Typical.
Height. Evidence: 10/10. Source: PMID 30595370. Typical.
What this genotype means for the people who carry it
Sample genotype: TT (Homozygous)
Ovarian aging is delayed in individuals with this genotype, resulting in menopause occurring approximately 0.32 years later than average [1]. This extended reproductive window is driven by efficient DNA replication and repair mechanisms in ovarian follicles [2]. However, the same rapid cellular proliferation increases the likelihood of benign tissue overgrowths in the reproductive tract [3]. Studies show a significantly higher risk of developing uterine fibroids and female genital tract polyps. On the metabolic side, this genetic profile is protective against type 2 diabetes [4]. Physical traits also lean toward a slightly taller stature and smaller average red blood cell volume.
Delayed ovarian aging; Increased risk of uterine fibroids; Lower risk of type 2 diabetes.
Sample genotype: GG (Homozygous)
Reproductive aging is accelerated with this genotype, leading to menopause occurring earlier than average [1]. This shift is associated with altered DNA primase activity, which may subtly influence follicle depletion rates in the ovaries [2]. Conversely, this reduced proliferative drive provides robust protection against benign tissue overgrowths, resulting in a lower risk of uterine fibroids and genital tract polyps. On the metabolic front, there is a modest increase in susceptibility to type 2 diabetes [3]. Physical traits typically include a slightly shorter stature and larger average red blood cell volume. Managing metabolic health through lifestyle remains a practical focus for individuals with this profile.
Earlier onset of menopause; Lower risk of uterine fibroids; Slightly increased risk of type 2 diabetes.
Sample genotype: TG (Heterozygous)
Cellular replication rates and DNA repair efficiency remain balanced with this heterozygous genotype. The age of natural menopause typically falls within the standard population average, as the opposing effects of the T and G alleles neutralize each other [1]. Similarly, the risks for uterine fibroids, genital tract polyps, and type 2 diabetes do not deviate significantly from baseline levels. Physical characteristics such as height and red blood cell size also remain close to average. This genetic middle ground avoids both the elevated risk of benign growths associated with the T allele and the metabolic vulnerabilities of the G allele. It represents the most common genetic configuration across many global ancestries.
Average age at menopause; Standard baseline risk for fibroids; Typical metabolic profile.
Variants with shared genetic architecture
rs10184004 · COBLL1 Gene · Chr 2 · Type 2 Diabetes Risk
rs10401969 · SUGP1 Gene · Chr 19 · Cholesterol and Liver Risk
rs10830963 · MTNR1B Gene · Chr 11 · Type 2 Diabetes Risk
The Polygenic and Monogenic Basis of Blood Traits and Diseases.
Genetic insights into biological mechanisms governing human ovarian ageing.
Content updated August 2026.
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