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Is More Life Always Better? The New Biology of Aging and the Meaning of Life by D AVID G EMS The social consequences of extending the human life span might be quite bad; perhaps the worst outcome is that power could be concentrated into ever fewer hands, as those who wield it gave way more slowly to death and disease. But the worry that more life would damage individuals’ quality of life is not persuasive. Depending on what the science of aging makes possible, and on how people plan their lives, longer life might even facilitate a richer and deeper life. He had passed that great meridian, the age of forty, nematode life were translated into human terms, this when for every man the process of spiritual evolution would represent a lifespan of around 700 years. stops, and he goes on thenceforward working out to the Common sense tells us that aging is universal, in- end a character that has become fixed and evitable, and associated with gradual physical decline. unalterable.”—G. Baker, in Tiberius Caesar But in this case, common sense is wrong. Some ani- mal species, such as tiny betentacled hydra, do not ap- he American biologist Andrzej Bartke recent- pear to age at all.3 There exist, for example, individual ly showed that a combination of genetic alter- colonies of corals that are over 20,000 years old.4 T ation and nutritional restriction can increase What is more, within the last decade biologists have the lifespan of a laboratory mouse by around 70 per- found that the rate of aging is remarkably easy to alter cent.1 While control mice withered and died, the test in laboratory animals such as nematodes, fruit flies, animals were still zestfully scurrying about, fleet of and mice. It is no longer far-fetched to think that one foot with glossy fur and unclouded eyes, and appar- day it will be possible to retard the aging process in ently as full of joie de vivre as any young rodent. Dis- humans and extend the human life span. coveries of this sort are now far from rare. I recently Do we really want this research to succeed? Some found that alteration of a gene called daf-2 can in- bioethicists have professed horror at the thought of crease the maximum life span of male nematode dramatic life extension. Many recoil at the notion of worms from 31 to 199 days—a 6.4-fold increase.2 If a extending the lives of people undergoing irreversible physical decline, like the senile and decrepit Struld- bruggs in Gulliver’s Travels. Yet recent research shows David Gems, “Is More Life Always Better? The New Biology of Aging and the Meaning of Life,” Hastings Center Report 33, no. 4 (2003): 31- it may be possible not just to extend life, but to ex- 39. tend youth. What if each of us could live a longer life, July-August 2003 HASTINGS CENTER REPORT 31 in peak physical and mental health, in the 1940s by the British geneticist is unable to purge the Huntington’s then suddenly shrivel away at the J.B.S. Haldane, working at University mutation from the general popula- end, like Dracula when he is exposed College London, who was interested tion, what about mutations that do to the sunlight? Would bioethicists in diseases caused by defective (mu- not strike until even later? Could it be still be so dour? Perhaps so, yet it tant) genes. One such disease, Hunt- that aging itself is the result of muta- would no longer be quite so clear ington’s, puzzled Haldane. Hunting- tions that strike very late in life, at an why. There may be reasons to worry, ton’s disease attacks the nervous sys- age beyond the reach of natural selec- but I want to suggest that aging re- tem, causing uncontrollable flaying tion? If this were true, then what we search raises philosophical questions spasms (chorea), insanity, and death. now think of as the process of aging is about the shape and purpose of life It is unusual in two respects: first, it a form of late-onset, invariably fatal that bioethics has thus far failed to does not strike until later in life—the genetic disease caused by genetic mu- address. mean age of onset is about thirty-five. tations that natural selection has been Second, the Huntington’s mutation is unable to purge from the population. The New Biology of Aging dominant, not recessive. This means This idea is at the heart of the evolu- that even people with only one copy tionary theory of aging. Its essence revolution has occurred in the bi- of the mutation will get the disease. can be distilled into a single phrase: Aology of aging, trans- the force of natural selec- forming a sleepy backwa- tion decreases with in- ter of research into a p until about fifteen years ago, creasing age after the onset rapidly advancing disci- U of reproduction. 5 pline. Up until about fif- research into the causes of aging was a An elaboration of the teen years ago, research evolutionary theory of into the causes of aging aging, proposed by was a somewhat disrep- somewhat disreputable activity George C. Williams, sug- utable activity occurring gests that aging may result at the fringes of biology. occurring at the fringes of biology. What from mutations that in Although the researchers early life enhance fitness, working on aging were changed everything was the but that have harmful ef- few, the number of theo- fects later in life—the ries they managed to gen- development of a theory of the trade-off theory. 8 Because erate were many—by one of the relative unimpor- estimate, over 300.6 Not evolution of aging with real explanatory tance of events later in life many of these theories to reproductive success, a have proved useful. The power and conceptual beauty. small early advantage may Russian immunologist outweigh a later catastro- Elie Metchnikoff believed phe. These two theories that aging resulted from have been tested experi- toxins released by bacteria in the in- Generally, one would expect that mentally, and the balance of evidence testinal tract. He suggested that a yo- dominant mutations causing fatal dis- favors the trade-off theory over the ghurt diet would extend human life eases would quickly disappear from simple mutation accumulation theo- span to 200 years. Another early the- the population. But as Haldane saw, ry. ory had it that aging in men resulted the awful thing about Huntington’s is While the evolutionary theory of from a reduction in the level of secre- that by the time the disease strikes, aging explains why aging occurs, it is tions from the testicles. This led to a most people have already had chil- not able to explain how it occurs— craze in the 1920s for surgically im- dren, to whom they have passed the what exactly happens when we age, planting the testicles of goats or mon- Huntington’s gene about half of the and what controls how fast it hap- keys into the scrotum of the recipient. time. Thus dominant, lethal muta- pens. To try to answer this, many bi- These crank theories have often tions can be maintained in a popula- ologists who study the genetics of found an audience among aging souls tion at a high frequency, so long as aging work with animals with very all too eager to grasp at the hope of their effects are delayed until after re- short life spans in order to save time. cheating death.7 production. Haldane’s insight solved Like a number of others in the field, I What changed everything was the the evolutionary puzzle of Hunting- work with a tiny nematode worm development of a theory of the evolu- ton’s. called Caenorhabditis elegans—C. ele- tion of aging with real explanatory But instead of stopping there, Hal- gans for short. These little creatures power and conceptual beauty. The dane went on to make a further bril- age and die after a mere two to three essence of it was originally seen back liant observation. If natural selection weeks. The whole of the C. elegans 32 HASTINGS CENTER REPORT July-August 2003 genome has been sequenced, and a promising and exciting areas of work funded research is successful. high proportion of C. elegans genes in biology, yet biologists are strangely BBSRC-funded work has involved have equivalents in humans. Thus, if reluctant to advocate the extension of treatments that dramatically increase the genes controlling aging in C. ele- human life, or sometimes even to lifespan in nematodes, fruitflies, ro- gans are found, they could potentially admit that life extension may be a dents, and yeast. Yet it is easy to un- be used to identify genes controlling consequence of their work. Consider derstand how we have arrived at this human aging. the following justifications for aging peculiar attitude of denial. Treating In classical genetics, the art is to research grant applications in the the aging process would have two identify genes that control the forma- United Kingdom: major consequences. First, it would tion of any particular facet of biology dramatically reduce the incidence of “Unless we can identify ways by looking for instances where a sin- many of the principal killer diseases through which healthspan can be gle gene has malfunctioned (mutat- of the developed world, such as car- increased as we age, the strain on ed), producing a defective animal. diovascular disease, cancer, diabetes, healthcare costs owing to the vol- The geneticist then works back to Alzheimer’s disease, and Parkinson’s ume of age-related pathologies will infer the normal function of the gene.

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