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How do you live to be 100?


Written by Simon Bishop

Simon Bishop com­ments on the newly-discovered longevity gene

THIS week I read a head­line that caught my eye: ‘Sci­en­tists iden­tify gene that can help you live to 100.’ Now that, I decided, sounds inter­est­ing. I wouldn’t mind a gene like that.

To many, grow­ing old is a ter­ri­fy­ing thing. To oth­ers it com­mands respect and comes with the ben­e­fits of expe­ri­ence. But to live to 100, even with mod­ern longer life spans… now that would be an achieve­ment indeed. I could travel the world, I could learn all that there is to know and wit­ness his­tory in the mak­ing, all in time for my telegram from the Queen. So tell me, what is this gene?

The gene to which the arti­cle refers is called telom­erase. But wait! This is not a newly dis­cov­ered gene! Eliz­a­beth Black­burn, Carol Grei­der and Jack Szostak won this year’s Nobel Prize in Phys­i­ol­ogy or Med­i­cine for their work on telom­erase, and their first hint at its exis­tence occurred on Christ­mas Day, 1984. Every­body has it. It is bio­log­i­cally impos­si­ble for dif­fer­ent peo­ple to have dif­fer­ent num­bers of genes, so it can­not be that some peo­ple have it and oth­ers don’t. All humans have the same com­ple­ment of genes – around 20–30,000 – because they are all needed to make you func­tion and be what you are. Take note: it is not pos­si­ble that they have a gene that you don’t. But if every­body has it, why don’t we all live to 100?

First, we need to under­stand what telom­erase is. Every time the cells in your body divide, your DNA must be dupli­cated also. But the enzymes that assem­ble new DNA can­not repli­cate your genes with 100 per cent accu­racy. A short start­ing frag­ment, which is needed to set the enzymes to work, is always lost, and with each repli­ca­tion your DNA gets ever so slightly shorter and dis­rupted. Short­en­ing of DNA ends, or telom­eres, cor­re­lates with age­ing. Telom­erase adds this short frag­ment back onto telom­eres. It keeps you bright and youth­ful and with­out it the very processes that main­tain our bod­ies would also be our undoing.

Recently, Yousin Suh and col­leagues at the Albert Ein­stein Col­lege of Med­i­cine in New York com­pared the genes of cen­te­nar­ian Ashke­nazi Jews with those of the spouses of the centenarian’s chil­dren, in doing so exam­in­ing a close-knit com­mu­nity but with­out the pos­si­bil­ity of inher­i­tance, and dis­cov­ered some­thing sub­tler than a new gene.

Every gene in your body (except those on your X or Y chro­mo­somes) comes as one of a pair. These two ver­sions of the same gene can be dif­fer­ent, some­times rad­i­cally so, and often one is dom­i­nant over the other. These gene ver­sions, or alle­les, come from a pool of many dif­fer­ent vari­eties through­out the entire pop­u­la­tion. Allele is a word you won’t often read in a news­pa­per, and I thank Red­brick for let­ting me use it, but its mean­ing is very impor­tant. Cen­te­nar­i­ans – Ashke­nazi Jews in this exam­ple – do not have a gene that you don’t: they sim­ply have an allele of telom­erase that makes the enzyme work more effi­ciently. This vari­a­tion allows bet­ter main­te­nance of telom­eres and con­fers healthy age­ing and excep­tional longevity in humans.

Am I being pedan­tic? Am I being a stick­ler for accu­racy in sci­en­tific ter­mi­nol­ogy? I would argue that we ben­e­fit from pedantry in this case. If 100 year olds have a gene that we don’t, then we can wave good­bye to that telegram. But if they have a more effi­cient ver­sion of a gene that we also have, then the key for research is to boost the effi­ciency of what we mere mor­tals already have. It’s about tweak­ing the tools at hand, not rein­vent­ing the wheel.

If they get it right, what would you do with your time?

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