EigoPro 準1級 読解 — The Quest to Live Longer

For most of human history, ageing was regarded as an immutable fact of life—the slow, inevitable wearing-out of the body. Today a growing band of biologists insists that this view is mistaken. Ageing, they argue, is not a single process of decay but the cumulative result of identifiable cellular mechanisms: DNA damage, the shortening of protective caps on our chromosomes, and the accumulation of "senescent" cells that linger uselessly in our tissues. If these mechanisms can be slowed or reversed, the reasoning goes, then ageing itself becomes a problem that medicine might one day treat. The evidence from the laboratory is genuinely tantalising. In worms, flies, and mice, scientists have extended healthy lifespan substantially by tweaking single genes or by clearing out senescent cells with drugs known as senolytics. A handful of compounds, including the diabetes drug metformin, are now being tested in humans not against any specific disease but against ageing as such. Yet a sceptical observer would be right to urge caution. Interventions that work wonders in a worm have a long history of failing in people, whose biology is vastly more intricate, and a mouse kept in a sterile cage is a poor proxy for a human navigating a messy world. The promise of radically extended lifespans also raises questions that no laboratory can answer. Who would gain access to treatments that are likely, at least at first, to be ruinously expensive? Would a society of centenarians stagnate, its institutions clogged by people reluctant to relinquish power? Enthusiasts reply that the goal is not merely more years but more healthy years—compressing illness into a brief window at the very end of a long, vigorous life. That distinction is appealing, but it remains, for now, a hypothesis dressed up as a destination. The science of ageing has earned its excitement; it has not yet earned our certainty.

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