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Centenarians escape, or at least have a delay in, age associated diseases that normally cause mortality at earlier ages. Considerable evidence supports the involvement of genetic components to longevity. Accordingly, the siblings of centenarians have a markedly increased probability of living to 100 years of age. A recent study showed that the offspring of centenarians had a markedly reduced prevalence of age associated diseases, particularly cardiovascular disease and cardiovascular risk factors. On the other hand, this is not unexpected in view of the fact that cardiovascular diseases account for about 50% of all deaths worldwide.1–3
Key points
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Centenarians escape, or at least delay, age associated diseases that normally cause mortality at earlier ages. Considerable evidence supports involvement of genetic components to longevity. Accordingly, siblings of centenarians have a marked increased probability of living to 100 years of age. The major trait of the offspring of centenarians is a significantly reduced prevalence of cardiovascular diseases.
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Patients with atherosclerosis have a proinflammatory genotype, and tight control of inflammatory reactions might decrease the incidence of atherosclerosis. Gene polymorphisms for proinflammatory cytokines seem to contribute considerably to the risk of coronary heart disease, including acute myocardial infarction, so alleles associated with susceptibility to acute myocardial infarction are expected to be less represented in genetic backgrounds that favour longevity. On the other hand, in Italian centenarian men, the frequency of the genotype associated with interleukin 10 (−1082GG) is associated with significantly increased production of the antiinflammatory cytokine interleukin 10.
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In two different populations from north and south Italy, analysis of genotype distributions showed a significantly higher frequency of the −1082GG genotype among oldest old participants than in controls and patients with acute myocardial infarction. Conversely, the frequency of the −1082AA genotype, associated with low production of interleukin 10, was significantly higher in patients …
Footnotes
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Conflicts of interest: none declared.
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Funding: The “Gruppo di Studio sull’immunosenescenza” coordinated by CC, is funded by grants from Ministry of Education, University and Research (MIUR; 40% to CC and DL and 60% to CC, DL, GC, and GCR) and from Ministry of Health Projects “Determinanti immunogenetici di Salute: un confronto interregionale”. CF was funded by MIUR (ex 40% and ex 60%), Ministry of Health projects (1998 and 2001 “Chronic diseases prevention in ageing: the model of centenarians” and “Biological and genetic markers of successful and unsuccessful ageing”).