Free Genetic Interpretation Tool

Longevity Gene
Variant Lookup

Look up 11 longevity-related variants from your 23andMe, AncestryDNA or other raw data file. Genotypes are listed the way raw files print them, with what published studies found, sourced, and where the evidence is weak or conflicting.

How to Find Your SNP Data
  1. 1
    Log in to your 23andMe, AncestryDNA, or other genetic testing account
  2. 2
    Download your raw data file (usually .txt or .zip)
  3. 3
    Open in a text editor and search for the rsID (e.g., rs429358) — or use Promethease, Genetic Genie, or SNPedia
  4. 4
    Find your two letters (e.g., CT) and look them up below. This tool lists genotypes exactly as raw files print them, which for some genes differs from the letters used in research papers.
🧠
APOE: Alzheimer's risk and cholesterol Two SNPs that together give your APOE type (e2, e3 or e4)
rs429358 APOE Alzheimer's risk (e4)
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APOE Chr 19 Alzheimer's risk (e4)
This SNP and rs7412 together define your APOE type. A C here marks the e4 form, a major genetic risk factor for late-onset Alzheimer's disease in every ethnic group studied.[1,2] Across a 2007 meta-analysis, LDL cholesterol and coronary risk rose step by step from e2/e2 to e4/e4, though e4 carriers' coronary risk was only slightly higher than e3/e3 (odds ratio 1.06, with a confidence interval that included no effect).[3] e4 is also linked with lower odds of reaching extreme old age.[4]
Raw files print this SNP as T or C, the same letters research papers use.
Your raw fileSummaryWhat studies found
TT Typical No e4 copy. Check rs7412 to tell e3/e3 apart from the e2 combinations.
CT Higher risk One e4 copy (usually e3/e4). In data pooled from 40 research teams, e3/e4 carried about 3 times the odds of Alzheimer's of e3/e3 among white participants in clinic and autopsy studies (odds ratio 3.2). The link was stronger in Japanese participants (5.6) and weaker in African American and Hispanic participants.[2] An odds ratio is relative risk, not a forecast for one person.
CC Higher risk Two e4 copies (e4/e4). The same pooled analysis found 14.9 times the odds of Alzheimer's among white participants.[2] In a 2024 study, almost all e4/e4 carriers showed Alzheimer's brain changes, nearly all had abnormal amyloid in spinal fluid by age 65, and symptoms began at about 65 on average; the authors proposed treating e4/e4 as a genetic form of the disease.[5]
How common: the e4-defining C allele is found on 16% of chromosomes in European samples, 27% in African, 9% in East Asian and 10% in admixed American samples (1000 Genomes), so the same genotype can be common in one ancestry and rare in another.[6]
What to do with it
Joint guidelines from the American College of Medical Genetics and the National Society of Genetic Counselors set out how to assess risk and counsel people around Alzheimer's genetic testing, which matters because an APOE result also says something about your relatives.[7] In the FINGER trial, two years of diet, exercise, cognitive training and vascular risk management helped cognition in older at-risk adults, and the benefit was no smaller in e4 carriers than in non-carriers.[8]
rs7412 APOE Alzheimer's risk (e2)
▾
APOE Chr 19 Alzheimer's risk (e2)
Read together with rs429358. A T here marks the e2 form, which is linked with lower Alzheimer's risk.[9]
Raw files print this SNP as C or T, the same letters research papers use.
Your raw fileSummaryWhat studies found
CC Typical No e2 copy. Check rs429358 to tell e3/e3 apart from e3/e4 and e4/e4.
CT Lower risk One e2 copy (usually e2/e3). e2/e3 carried about 0.6 times the odds of Alzheimer's of e3/e3, and the protection looked the same across ethnic groups.[2] e2 carriers had about 20% lower coronary risk (odds ratio 0.80)[3], and e2/e3 or e2/e2 was linked with higher odds of reaching extreme old age.[4]
TT Mixed Two e2 copies (e2/e2). The Alzheimer's estimate was lower but uncertain (odds ratio 0.6 with a wide confidence interval).[2] Triglyceride differences between APOE types were largely confined to e2/e2[3], and e2/e2 is the usual genetic basis of familial dysbetalipoproteinemia, a cholesterol disorder that typically appears only after an added metabolic hit.[10]
How common: the e2-defining T allele is found on 6% of chromosomes in European samples, 10% in African, 10% in East Asian and 5% in admixed American samples (1000 Genomes), so the same genotype can be common in one ancestry and rare in another.[6]
What to do with it
A standard lipid panel shows whether triglycerides or cholesterol are actually raised. If they are and you know you are e2/e2, tell your clinician.
🧬
FOXO3: a replicated longevity gene One of only two genes linked with longevity in multiple independent studies
rs2802292 FOXO3 Longevity association
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FOXO3 Chr 6 Longevity association
Only two genes, APOE and FOXO3, have shown an association with longevity in multiple independent studies.[11] For this FOXO3 SNP, the G allele was first linked with reaching very old age in long-lived Japanese-American men[12], then in German centenarians, where the link was stronger in centenarians than in people in their nineties and applied to women as well as men.[13] A 2014 meta-analysis of seven studies estimated an odds ratio of 1.36 for the G allele.[14] In cell experiments, the G allele creates a binding site for the stress-response protein HSF1, which switches FOXO3 on under stress.[15] These are associations in groups of very old people; the variant does not predict any one person's lifespan.
Raw files print this SNP as T or G, the same letters research papers use.
Your raw fileSummaryWhat studies found
TT Typical No G copy.
GT Longevity-associated One G copy.
GG Longevity-associated Two G copies. Among Japanese-American men, two copies of the minor FOXO3A allele carried 2.75 times the odds of being in the long-lived group compared with two copies of the major allele, and the GG genotype went with markers of better insulin sensitivity.[12]
How common: the G allele is found on 43% of chromosomes in European samples, 83% in African, 31% in East Asian and 39% in admixed American samples (1000 Genomes), so the same genotype can be common in one ancestry and rare in another.[6]
What to do with it
Nothing specific. No trial has tested whether any diet, supplement or drug changes outcomes through this variant.
🔄
MTHFR: folate metabolism and homocysteine Two common variants that slow an enzyme in folate processing
rs1801133 MTHFR Homocysteine (C677T)
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MTHFR Chr 1 Homocysteine (C677T)
Research papers call this variant C677T. It produces a heat-sensitive MTHFR enzyme with reduced activity, and people with two copies have higher blood homocysteine.[16]
Check your letters. MTHFR is read from the reverse strand, so raw files print G where papers write C, and A where papers write T. AA in your file is 677TT.
Your raw fileSummaryWhat studies found
GG677CC Typical No copies of 677T.
AG677CT Mild One copy of 677T. In the original study, enzyme activity was reduced with one or two copies, and the rise in homocysteine was reported in people with two.[16]
AA677TT Higher homocysteine Two copies of 677T. In a randomized trial, TT volunteers on a low-folate diet had homocysteine of 14.5 µmol/L versus 8.9 in CC; they responded to more folate, from fortified foods or a 400 µg folic acid supplement, but needed higher intakes than CC to reach the same level.[17] In 40 studies of coronary heart disease, TT carried 16% higher odds than CC (odds ratio 1.16), with no excess in the North American studies; the authors put the difference down largely to folate status.[18]
How common: the allele papers call 677T is found on 36% of chromosomes in European samples, 9% in African, 30% in East Asian and 47% in admixed American samples (1000 Genomes), so the same genotype can be common in one ancestry and rare in another.[6]
What to do with it
Folic acid works with this variant: in the trial above, folate from fortified foods or a standard 400 µg folic acid supplement both lowered homocysteine in TT carriers.[17] That evidence runs against the common claim that people with MTHFR variants must avoid folic acid. The American College of Medical Genetics advises against MTHFR testing in routine evaluations for clotting risk, because it has minimal clinical use.[19] If you want a direct measure, a homocysteine blood test shows the thing this variant affects.
rs1801131 MTHFR Folate enzyme (A1298C)
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MTHFR Chr 1 Folate enzyme (A1298C)
Research papers call this variant A1298C. It lowers MTHFR activity, more so with two copies, but on its own it was not linked with higher homocysteine or lower folate.[20]
Check your letters. Raw files print T where papers write A, and G where papers write C. GG in your file is 1298CC.
Your raw fileSummaryWhat studies found
TT1298AA Typical No copies of 1298C.
GT1298AC Typical One copy. On its own, no change in homocysteine was found.[20] If you also carry one copy of 677T (AG at rs1801133), the combination looked like two copies of 677T in studies: lower enzyme activity, higher homocysteine and lower folate[20], with 50 to 60% of normal enzyme activity in lymphocytes.[21]
GG1298CC Mild Two copies. Enzyme activity was about 60% of normal in lymphocytes[21], without the homocysteine rise seen with two copies of 677T.[20]
How common: the allele papers call 1298C is found on 31% of chromosomes in European samples, 15% in African, 22% in East Asian and 15% in admixed American samples (1000 Genomes), so the same genotype can be common in one ancestry and rare in another.[6]
What to do with it
The same as for C677T: ordinary folate intake, and a homocysteine test if you want a direct measure. Routine MTHFR testing is not recommended.[19]
🛡️
SOD2: mitochondrial antioxidant enzyme A variant that changes how the enzyme enters mitochondria
rs4880 SOD2 Antioxidant enzyme (Ala16Val)
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SOD2 Chr 6 Antioxidant enzyme (Ala16Val)
Research papers call this variant Ala16Val or Val16Ala. In lab experiments, the alanine (Ala) form produced 30 to 40% more active enzyme inside mitochondria than the valine (Val) form.[22] In a Danish cohort enrolled at age 92 to 93, people with at least one Ala copy had slightly lower mortality over the following decade (hazard ratio 0.91).[23]
Check your letters. SOD2 is read from the reverse strand. Raw files print A or G: A is the Val form and G is the Ala form. Papers often write the same alleles as T (Val) and C (Ala), and some studies use A to mean alanine, which is not the A in your file.
Your raw fileSummaryWhat studies found
AAVal/Val No established effect Two Val copies.
AGVal/Ala No established effect One copy of each.
GGAla/Ala Mixed Two Ala copies: the more active form in the lab[22] and part of the group with slightly lower mortality in the Danish cohort.[23] In one US case-control study, premenopausal women with two Ala copies had about 4 times the odds of breast cancer (odds ratio 4.3), mostly among women who ate fewer fruits and vegetables.[24]
How common: the Ala-coding G allele is found on 47% of chromosomes in European samples, 42% in African, 12% in East Asian and 58% in admixed American samples (1000 Genomes), so the same genotype can be common in one ancestry and rare in another.[6]
What to do with it
Nothing genotype-specific. These are modest associations from single studies, and no trial has tested antioxidant supplements by SOD2 genotype.
🔥
IL-6: inflammation signaling A promoter variant that affects how much IL-6 is made
rs1800795 IL-6 IL-6 level (-174G/C)
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IL-6 Chr 7 IL-6 level (-174G/C)
Research papers call this variant -174G>C. In lab tests the C version drove less IL-6 production, and among healthy adults in North London the C allele went with lower blood IL-6.[25] For longevity, a meta-analysis of eight European studies found no overall difference between the oldest old and younger controls (odds ratio 0.96). Fewer GG genotypes were seen among male Italian centenarians, but that was not replicated in other European groups.[26]
Raw files print this SNP as G or C, the same letters research papers use.
Your raw fileSummaryWhat studies found
GG No consistent effect Two G copies. Nearly everyone of East Asian or African ancestry has this genotype, because the C allele is rare in those groups.
GC No consistent effect One copy of each.
CC No consistent effect Two C copies, the version linked with lower IL-6 levels.[25]
How common: the C allele is found on 42% of chromosomes in European samples, 1.8% in African, 0.1% in East Asian and 18% in admixed American samples (1000 Genomes), so the same genotype can be common in one ancestry and rare in another.[6]
What to do with it
Nothing genotype-specific. No study has shown that this variant should change diet, supplements or testing.
❤️
CETP: HDL cholesterol transfer Linked with longevity in one population, with conflicting results since
rs5882 CETP Lipids (I405V)
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CETP Chr 16 Lipids (I405V)
Research papers call this variant I405V. Among Ashkenazi Jewish people with exceptional longevity (average age 98), the valine/valine (VV) genotype was 2.7 to 2.9 times as common as in controls, and VV carriers had larger lipoprotein particles and lower blood CETP.[27] The finding was not confirmed in Italian centenarians.[28] In Chinese studies and a meta-analysis, the V allele was linked with lower odds of longevity in East Asian groups, with no association in European or white American groups.[29]
Check your letters. Raw files print G or A: G is the valine (V) form and A is the isoleucine (I) form. GG in your file is VV.
Your raw fileSummaryWhat studies found
GGVV Conflicting evidence Two V copies: the genotype enriched among the Ashkenazi centenarians[27], but linked with lower odds of longevity in East Asian studies.[29]
AGIV No consistent effect One copy of each.
AAII No consistent effect Two I copies.
How common: the valine-coding G allele is found on 33% of chromosomes in European samples, 64% in African, 44% in East Asian and 40% in admixed American samples (1000 Genomes), so the same genotype can be common in one ancestry and rare in another.[6]
What to do with it
No action follows from this genotype. A standard lipid panel measures your actual cholesterol levels.
⏳
SIRT1: sirtuin pathway A popular longevity gene with no established human variant effect
rs2273773 SIRT1 Sirtuin gene variant
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SIRT1 Chr 10 Sirtuin gene variant
Altering the SIRT1 gene changes lifespan in yeast, worms and rodents, which made it a candidate human longevity gene. But a study of common SIRT1 variants in German centenarians found no association with exceptional longevity at the allele, genotype or haplotype level[30], and in a Chinese longevity region this particular SNP was not associated either.[31]
Raw files print this SNP as T or C.
Your raw fileSummaryWhat studies found
TT No established effect Two T copies, the usual genotype in European and African samples.
CT No established effect One copy of each.
CC No established effect Two C copies, uncommon outside East Asian samples.
How common: the C allele is found on 8% of chromosomes in European samples, 2% in African, 31% in East Asian and 13% in admixed American samples (1000 Genomes), so the same genotype can be common in one ancestry and rare in another.[6]
What to do with it
Nothing. No human study has linked this variant to how people respond to fasting, NAD+ precursors or resveratrol.
🔁
TERT: telomerase Linked with telomere length and some cancers, not with lifespan
rs2736100 TERT Telomerase gene
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TERT Chr 5 Telomerase gene
TERT makes the catalytic part of telomerase. Genome-wide studies link the TERT region to telomere length[32], and this SNP to risk of lung adenocarcinoma[33] and glioma (odds ratio 1.28 in a meta-analysis).[34] No study we reviewed links it to lifespan.
Check your letters. TERT is read from the reverse strand, so the allele papers call G appears as C in raw files, and T appears as A.
Your raw fileSummaryWhat studies found
AATT No established lifespan effect No copies of the allele papers call G.
ACGT No established lifespan effect One copy.
CCGG No established lifespan effect Two copies of the allele papers call G, which in a cohort of Chinese women went with longer telomeres and higher lung cancer risk.[33]
How common: the allele papers call G is found on 50% of chromosomes in European samples, 47% in African, 41% in East Asian and 43% in admixed American samples (1000 Genomes), so the same genotype can be common in one ancestry and rare in another.[6]
What to do with it
Nothing genotype-specific. Telomere-length tests and this genotype are not used for medical decisions.
💉
PCSK9: LDL cholesterol A loss-of-function variant that lowers LDL for life
rs11591147 PCSK9 LDL cholesterol (R46L)
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PCSK9 Chr 1 LDL cholesterol (R46L)
Research papers call this variant R46L. PCSK9 controls how many LDL receptors the liver keeps; mutations that strengthen it cause inherited high cholesterol[35], while the 46L form weakens it and lowers LDL.[36]
Raw files print this SNP as G or T: T is the 46L allele.
Your raw fileSummaryWhat studies found
GGRR Typical No copy of 46L.
GTRL Lower LDL One copy of 46L. In the Atherosclerosis Risk in Communities study, the 3.2% of white participants with an LDL-lowering PCSK9 variant had 15% lower LDL cholesterol and 47% lower risk of coronary heart disease over 15 years.[37] Pooled across studies, 46L carriers had 12% lower LDL and 28% lower risk of ischemic heart disease.[36]
TTLL Lower LDL Two copies of 46L, which is rare. In a Danish study, median LDL was 97 mg/dL in homozygotes, 104 in heterozygotes and 124 in non-carriers.[38]
How common: the 46L-coding T allele is found on 2% of chromosomes in European samples, none in African, none in East Asian and 1.6% in admixed American samples (1000 Genomes), so the same genotype can be common in one ancestry and rare in another.[6]
What to do with it
This genotype does not replace an LDL or ApoB test; your measured level is what guides treatment.
Try:
Enter an rsID above to look up a longevity-related gene variant
Genetic Information Disclaimer
This tool summarizes published research on 11 genetic variants for education. It is not a diagnostic test and should not be used for medical decisions. Associations seen in groups of people do not predict what will happen to any one person. Discuss genetic results, especially APOE, with a genetic counselor or physician.

Understanding Your Longevity Genes

Consumer genetic tests report hundreds of thousands of SNPs. This tool covers 11 that are often searched in connection with aging and longevity, and says plainly where the evidence is solid, conflicting or absent.

Two replicated longevity genes

Only two genes, APOE and FOXO3, have shown an association with longevity in multiple independent studies.[11] APOE e4 is a major genetic risk factor for late-onset Alzheimer's disease.[2] The FOXO3 rs2802292 G allele has been linked with reaching very old age in Japanese-American and German studies and in a meta-analysis.[12,13,14]

How much of lifespan is genetic?

Estimates range widely. A study of Danish twins put the heritability of lifespan at about 25%.[39] An analysis of hundreds of millions of people in Ancestry family trees put it well below 10% once it accounted for partners sharing lifespan-related traits.[40] A 2026 analysis that set aside deaths from external causes such as accidents and infections estimated the heritability of intrinsic lifespan at above 50%.[41] None of the variants on this page predicts any one person's lifespan.

MTHFR and folic acid

The MTHFR C677T variant (rs1801133) is widely discussed online. People with two copies have higher homocysteine, and in a randomized trial they responded to ordinary folate, from fortified foods or a 400 µg folic acid supplement, though they needed more of it than others to reach the same homocysteine level.[17] The American College of Medical Genetics recommends against MTHFR testing in routine evaluations for clotting risk.[19]

Method, limits and how to read your result

How it works

Look up a gene or variant to see what published research says about it, with each finding linked to its source. Only two genes, APOE and FOXO3, have been linked to longevity in multiple independent studies (reference 11); most other variants have small or unconfirmed effects.

Limits

A variant changes probabilities, not destiny, and most findings come from people of European ancestry. Professional guidelines describe who may benefit from testing for Alzheimer's risk genes and recommend genetic counseling around it (reference 7). The tool does not interpret raw consumer test files.

How to read your result

Read each entry as population-level evidence. A higher-risk variant is a reason to focus on the modifiable risk factors that matter for everyone. An analysis of the FINGER trial concluded that lifestyle changes may benefit cognition even in people with APOE-related genetic susceptibility (reference 8). Discuss significant results with a doctor or genetic counselor.

References

  1. 1Corder EH, et al. "Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer's disease in late onset families." Science. 1993;261(5123):921-3. PubMed · DOI
  2. 2Farrer LA, et al. "Effects of age, sex, and ethnicity on the association between apolipoprotein E genotype and Alzheimer disease. A meta-analysis. APOE and Alzheimer Disease Meta Analysis Consortium." JAMA. 1997;278(16):1349-56. PubMed
  3. 3Bennet AM, et al. "Association of apolipoprotein E genotypes with lipid levels and coronary risk." JAMA. 2007;298(11):1300-11. PubMed · DOI
  4. 4Sebastiani P, et al. "APOE Alleles and Extreme Human Longevity." J Gerontol A Biol Sci Med Sci. 2019;74(1):44-51. PubMed · DOI
  5. 5Fortea J, et al. "APOE4 homozygozity represents a distinct genetic form of Alzheimer's disease." Nat Med. 2024;30(5):1284-1291. PubMed · DOI
  6. 6Auton A, et al. "A global reference for human genetic variation." Nature. 2015;526(7571):68-74. PubMed · DOI
  7. 7Goldman JS, et al. "Genetic counseling and testing for Alzheimer disease: joint practice guidelines of the American College of Medical Genetics and the National Society of Genetic Counselors." Genet Med. 2011;13(6):597-605. PubMed · DOI
  8. 8Solomon A, et al. "Effect of the Apolipoprotein E Genotype on Cognitive Change During a Multidomain Lifestyle Intervention: A Subgroup Analysis of a Randomized Clinical Trial." JAMA Neurol. 2018;75(4):462-470. PubMed · DOI
  9. 9Corder EH, et al. "Protective effect of apolipoprotein E type 2 allele for late onset Alzheimer disease." Nat Genet. 1994;7(2):180-4. PubMed · DOI
  10. 10Heidemann BE, et al. "Establishing the relationship between familial dysbetalipoproteinemia and genetic variants in the APOE gene." Clin Genet. 2022;102(4):253-261. PubMed · DOI
  11. 11Broer L, et al. "GWAS of longevity in CHARGE consortium confirms APOE and FOXO3 candidacy." J Gerontol A Biol Sci Med Sci. 2015;70(1):110-8. PubMed · DOI
  12. 12Willcox BJ, et al. "FOXO3A genotype is strongly associated with human longevity." Proc Natl Acad Sci U S A. 2008;105(37):13987-92. PubMed · DOI
  13. 13Flachsbart F, et al. "Association of FOXO3A variation with human longevity confirmed in German centenarians." Proc Natl Acad Sci U S A. 2009;106(8):2700-5. PubMed · DOI
  14. 14Bao JM, et al. "Association between FOXO3A gene polymorphisms and human longevity: a meta-analysis." Asian J Androl. 2014;16(3):446-52. PubMed · DOI
  15. 15Grossi V, et al. "The longevity SNP rs2802292 uncovered: HSF1 activates stress-dependent expression of FOXO3 through an intronic enhancer." Nucleic Acids Res. 2018;46(11):5587-5600. PubMed · DOI
  16. 16Frosst P, et al. "A candidate genetic risk factor for vascular disease: a common mutation in methylenetetrahydrofolate reductase." Nat Genet. 1995;10(1):111-3. PubMed · DOI
  17. 17Ashfield-Watt PA, et al. "Methylenetetrahydrofolate reductase 677C-->T genotype modulates homocysteine responses to a folate-rich diet or a low-dose folic acid supplement: a randomized controlled trial." Am J Clin Nutr. 2002;76(1):180-6. PubMed · DOI
  18. 18Klerk M, et al. "MTHFR 677C-->T polymorphism and risk of coronary heart disease: a meta-analysis." JAMA. 2002;288(16):2023-31. PubMed · DOI
  19. 19Hickey SE, et al. "ACMG Practice Guideline: lack of evidence for MTHFR polymorphism testing." Genet Med. 2013;15(2):153-6. PubMed · DOI
  20. 20van der Put NM, et al. "A second common mutation in the methylenetetrahydrofolate reductase gene: an additional risk factor for neural-tube defects?" Am J Hum Genet. 1998;62(5):1044-51. PubMed · DOI
  21. 21Weisberg I, et al. "A second genetic polymorphism in methylenetetrahydrofolate reductase (MTHFR) associated with decreased enzyme activity." Mol Genet Metab. 1998;64(3):169-72. PubMed · DOI
  22. 22Sutton A, et al. "The Ala16Val genetic dimorphism modulates the import of human manganese superoxide dismutase into rat liver mitochondria." Pharmacogenetics. 2003;13(3):145-57. PubMed · DOI
  23. 23Soerensen M, et al. "The Mn-superoxide dismutase single nucleotide polymorphism rs4880 and the glutathione peroxidase 1 single nucleotide polymorphism rs1050450 are associated with aging and longevity in the oldest old." Mech Ageing Dev. 2009;130(5):308-14. PubMed · DOI
  24. 24Ambrosone CB, et al. "Manganese superoxide dismutase (MnSOD) genetic polymorphisms, dietary antioxidants, and risk of breast cancer." Cancer Res. 1999;59(3):602-6. PubMed
  25. 25Fishman D, et al. "The effect of novel polymorphisms in the interleukin-6 (IL-6) gene on IL-6 transcription and plasma IL-6 levels, and an association with systemic-onset juvenile chronic arthritis." J Clin Invest. 1998;102(7):1369-76. PubMed · DOI
  26. 26Di Bona D, et al. "Effect of interleukin-6 polymorphisms on human longevity: a systematic review and meta-analysis." Ageing Res Rev. 2009;8(1):36-42. PubMed · DOI
  27. 27Barzilai N, et al. "Unique lipoprotein phenotype and genotype associated with exceptional longevity." JAMA. 2003;290(15):2030-40. PubMed · DOI
  28. 28Cellini E, et al. "Cholesteryl ester transfer protein (CETP) I405V polymorphism and longevity in Italian centenarians." Mech Ageing Dev. 2005;126(6-7):826-8. PubMed · DOI
  29. 29Sun L, et al. "Trans-ethnical shift of the risk genotype in the CETP I405V with longevity: a Chinese case-control study and meta-analysis." PLoS One. 2013;8(8):e72537. PubMed · DOI
  30. 30Flachsbart F, et al. "Sirtuin 1 (SIRT1) sequence variation is not associated with exceptional human longevity." Exp Gerontol. 2006;41(1):98-102. PubMed · DOI
  31. 31Huang J, et al. "[Association between SIRT1 gene polymorphisms and longevity of populations from Yongfu region of Guangxi]." Zhonghua Yi Xue Yi Chuan Xue Za Zhi. 2013;30(1):55-9. PubMed · DOI
  32. 32Codd V, et al. "Identification of seven loci affecting mean telomere length and their association with disease." Nat Genet. 2013;45(4):422-7, 427e1-2. PubMed · DOI
  33. 33Lan Q, et al. "Longer telomere length in peripheral white blood cells is associated with risk of lung cancer and the rs2736100 (CLPTM1L-TERT) polymorphism in a prospective cohort study among women in China." PLoS One. 2013;8(3):e59230. PubMed · DOI
  34. 34Wu Q, et al. "An Updated and Comprehensive Meta-Analysis of Association Between Seven Hot Loci Polymorphisms from Eight GWAS and Glioma Risk." Mol Neurobiol. 2016;53(7):4397-405. PubMed · DOI
  35. 35Abifadel M, et al. "Mutations in PCSK9 cause autosomal dominant hypercholesterolemia." Nat Genet. 2003;34(2):154-6. PubMed · DOI
  36. 36Benn M, et al. "PCSK9 R46L, low-density lipoprotein cholesterol levels, and risk of ischemic heart disease: 3 independent studies and meta-analyses." J Am Coll Cardiol. 2010;55(25):2833-42. PubMed · DOI
  37. 37Cohen JC, et al. "Sequence variations in PCSK9, low LDL, and protection against coronary heart disease." N Engl J Med. 2006;354(12):1264-72. PubMed · DOI
  38. 38Langsted A, et al. "PCSK9 R46L Loss-of-Function Mutation Reduces Lipoprotein(a), LDL Cholesterol, and Risk of Aortic Valve Stenosis." J Clin Endocrinol Metab. 2016;101(9):3281-7. PubMed · DOI
  39. 39Herskind AM, et al. "The heritability of human longevity: a population-based study of 2872 Danish twin pairs born 1870-1900." Hum Genet. 1996;97(3):319-23. PubMed · DOI
  40. 40Ruby JG, et al. "Estimates of the Heritability of Human Longevity Are Substantially Inflated due to Assortative Mating." Genetics. 2018;210(3):1109-1124. PubMed · DOI
  41. 41Shenhar B, et al. "Heritability of intrinsic human life span is about 50% when confounding factors are addressed." Science. 2026;391(6784):504-510. PubMed · DOI
Related Reading
Longevity Genomics: What Your Genes Determine → Lp(a): The Genetic Cardiovascular Risk Factor → MTHFR: Folate vs Folic Acid → APOE4 and Alzheimer's Prevention →