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===Genetics=== {{Further|Genetics of aging}} The [[heritability]] of lifespan is estimated to be less than 10%, meaning the majority of [[Coefficient of variation|variation]] in lifespan is attributable due to differences in environment rather than [[genetic variation]].<ref name="lifespan_heritability">{{cite journal|vauthors=Ruby JG, Wright KM, Rand KA, Kermany A, Noto K, Curtis D, Varner N, Garrigan D, Slinkov D, Dorfman I, Granka JM, Byrnes J, Myres N, Ball C|title=Estimates of the Heritability of Human Longevity Are Substantially Inflated due to Assortative Mating|journal=Genetics|volume=210|issue=3|pages=1109β1124|date=November 2018|pmid=30401766|pmc=6218226|doi=10.1534/genetics.118.301613}}</ref> However, researchers have identified regions of the [[genome]] which can influence the length of life and the number of years lived in good health. For example, a [[genome-wide association study]] of 1 million lifespans found 12 [[genetic loci]] which influenced lifespan by modifying susceptibility to [[Cardiovascular disease|cardiovascular]] and [[Smoking#Health effects|smoking-related disease]].<ref name="timmers_elife">{{cite journal|vauthors=Timmers PR, Mounier N, Lall K, Fischer K, Ning Z, Feng X, Bretherick AD, Clark DW, Shen X, Esko T, Kutalik Z, Wilson JF, Joshi PK|title=Genomics of 1 million parent lifespans implicates novel pathways and common diseases and distinguishes survival chances|journal=eLife|volume=8|issue=e39856|date=January 2019|pmid=30642433|pmc=6333444|doi=10.7554/eLife.39856|doi-access=free}}</ref> The locus with the largest effect is [[Apolipoprotein E|APOE]]. Carriers of the APOE Ξ΅4 [[allele]] live approximately one year less than average (per copy of the Ξ΅4 allele), mainly due to increased risk of [[Alzheimer's disease]].<ref name="timmers_elife" /> [[File:Healthspan, parental lifespan, and longevity are highly genetically correlated.webp|thumb|right|500px|"Healthspan, parental lifespan, and longevity are highly genetically correlated."<ref name="Multivariate"/>]] In July 2020, scientists identified 10 genomic loci with consistent effects across multiple lifespan-related traits, including [[healthspan]], lifespan, and [[longevity]].<ref name="Multivariate">{{cite journal|vauthors=Timmers PR, Wilson JF, Joshi PK, Deelen J|title=Multivariate genomic scan implicates novel loci and haem metabolism in human ageing|journal=Nature Communications|volume=11|issue=1|pages=3570|date=July 2020|pmid=32678081|pmc=7366647|doi=10.1038/s41467-020-17312-3|bibcode=2020NatCo..11.3570T|doi-access=free}}</ref> The genes affected by variation in these loci highlighted [[Human iron metabolism|haem metabolism]] as a promising candidate for further research within the field. This study suggests that high levels of iron in the blood likely reduce, and genes involved in metabolising iron likely increase healthy years of life in humans.<ref name="ironmeta">{{cite news|author=University of Edinburgh|date=20 July 2020|title=Blood iron levels could be key to slowing ageing, gene study shows|url=https://phys.org/news/2020-07-blood-iron-key-ageing-gene.html|access-date=18 August 2020|work=phys.org}}</ref> A follow-up study which investigated the genetics of [[Frailty syndrome|frailty]] and self-rated health in addition to healthspan, lifespan, and longevity also highlighted haem metabolism as an important pathway, and found genetic variants which lower blood protein levels of [[Lipoprotein(a)|LPA]] and [[VCAM1]] were associated with increased healthy lifespan.<ref name="timmers_nataging">{{cite journal|vauthors=Timmers PR, Tiys ES, Sakaue S, Akiyama M, Kiiskinen TT, Zhou W, Hwang SJ, Yao C, Deelen J, Levy D, Ganna A, Kamatani Y, Okada Y, Joshi PK, Wilson JF, Tsepilov YA|title=Mendelian randomization of genetically independent aging phenotypes identifies LPA and VCAM1 as biological targets for human aging|journal=Nature Aging|volume=2|issue=1|pages=19β30|date=January 2022|pmid=37118362|doi=10.1038/s43587-021-00159-8|hdl-access=free|s2cid=246093885|doi-access=free|hdl=20.500.11820/1bac547c-2eb9-47e1-b4b8-e80d741941c7}}</ref>
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