Against the advances of time, many adults deny themselves even small indulgences in the belief that virtuous moderation will ensure a healthy old age. New recruits to the war against ageing receive some basic training. Body map references are used daily to target damage attributed to the enemy – a single process called “ageing.” Eventually, even keen recruits admit that they are losing the battle. The language of surrender echoes. Battle worn veterans say bluntly what younger adults avoid talking about. In late life, people fear abandonment. Everyone suspects that they will be left unwanted because they are old.
If old people feel unwanted, why is biological science taking on ageing? Outsiders assume that the aims are worthy. Vague ideas are expressed about the prevention of suffering caused by age-related diseases. Tucked away inside this easy assumption is another rather more difficult idea. For many, including some scientists, “age related” means the same as “age dependent.” By extension, the proper study of diseases that are more common with age must include careful analysis of the biology of ageing. If true, this might be a satisfactory explanation of what biological ageing research is all about. As the pace of ageing research quickened, the assumption that “age related” diseases were “age dependent” did not stand up to scrutiny. As the detritus of life was peeled away from ageing, a great deal was lost, but what remained proved crucial. Long regarded as cardinal features of ageing, the detritus could be explained by the lifelong accumulation of wear and tear, the damage caused by episodes of illness or, to more devastating effects, poverty, stress and malnutrition. Much as a house battered by winter storms will succumb to a spring tempest, so an individual’s capacity to withstand adversity in old age is diminished by recurrent illness. The typical picture of old age is now seen to result from at least two processes. One is the depletion of resources available to cope with illness. Another – loosely termed “intrinsic ageing” – concerns the properties of ageing cells. Once the precise tools of molecular biology were applied to these intrinsic processes, rapid advances were made. The problem of ageing has yielded to a better understanding of what is happening now to old people. There are more of them, they are healthier and when they have a serious illness it is often their last. In the developed world, the evidence of gradual but portentous changes in the well-being of old people is easy to find. In 1975, around one in seven US men aged 80 was disabled in some way. By 1996, this had halved. Clinical scientists began to describe sizable and growing numbers of “elite” old men (but fewer old women) who did not deteriorate as expected. Community health studies showed that not only were old people becoming healthier, their experiences of illness were “compressed” into the last year or two of life. These improvements were the direct result of improved living standards and community measures to reduce vascular disease and discourage smoking. Benefits like these are built on decades of sound progress in economic development and public health medicine. They will not be intentionally undone and are certain to continue to improve and maintain the health of old people for years to come. Biological science, too, had its successes. Researchers identified molecular targets with the potential to slow or even arrest components of intrinsic ageing processes. One example will suffice. Antioxidant damage control and repair systems help contain the harmful effects of respiration on the cell. With ageing, these systems become inefficient and their failures can trigger a cascade of damage leading to cell death. Chemists have synthesized compounds capable of mimicking the beneficial effects of some antioxidant enzymes but with up to 100 times their potency. Animal experiments tested these novel and highly potent compounds. They showed this type of agent could extend the lifespan of a laboratory animal by up to 50%. Of course, short term experiments like these do not establish such agents as safe for the decades of use that seem likely if they prove to be effective “anti-ageing” drugs. More likely they will be first evaluated as drugs to prevent the complications of acute tissue damage after, say, a heart attack or stroke. Only later will they be tested for long-term use, probably as adjuncts to other life-style interventions. Improved health of old people with added disease “compression” looks likely to stay. Medical science is confident enough to predict extensions and consolidations of these improvements and may soon introduce safe and effective anti-ageing agents. But at what cost? It is certain that old people will enjoy and benefit from an old age with fewer disabilities. Many will prefer a short final illness to a more delayed departure. But what will be the quality of a life extended by 20 or even 40 years? Will old people feel any more wanted because of these gains? Or will they, as some do, believe that it is all to sustain a cult of youth and beauty, aimed to diminish the fears of the young and to postpone the prospect of worn out old age? While the public remains fixed on the idea that old people are a burden, specialists in the care of the old must set out the broader picture. Healthy old people may not wish to leave productive work. Compulsory retirement on grounds of age is already indefensible. Instead, we should develop opportunities that retain old people as net contributors to our prosperity. Much as molecular biology drives the pharmaceutical industry and the development of novel agents, so the computer industry has revolutionized the workplace. These two powerful forces must be harnessed together to serve the common good of old people.