The possibility of intervening on the mechanisms of biological aging seems no longer so far off, and several studies are being carried out in this area.
One area of research, which has already given rise to relevant achievements in animal models, is caloric restriction. In protozoa, fruit flies, mice, rats, and even monkeys, it has been shown that diminishing caloric intake by 30-40% preserves all the nutrients needed for life while protecting the animals from many causes of illness and thus extending their lives by 40% and more (Sohal, Weindruch 1996). It has been speculated that low caloric diet has the effect of lowering body temperature, thus changing metabolism and lessening cell damage. However, this method is not plausibly transferable to humans, due to its undesirable side-effects: for one thing, it implies the psychological stress of being hungry all the time; second, it precludes physical activity and sports; third, it seems to negatively affect fertility rates and libido.
Another area that has been widely studied is the use of Human Growth Hormone (hGH), which has been reported to increase muscle mass, lessen body fat and strengthen the immune systems in small groups of older men and women (Blackman et al. 2002). However, it was also observed that mice genetically modified to produce lots of GH live less than controls and that hGH has a likely effect in the spreading of cancer (Coschigano et al. 2000); moreover, hGH has been shown to cause such side effects as diabetes, carpal tunnel syndrome, fluid retention, joint and muscle pain, and high blood pressure (Hintz 2004)). No safer results were reached with other hormones such as DHEA and melatonin (Pierrefiche, Laborit 1995).
According to the free radical theory of aging, a relevant role in cell, tissue and organ senescence is played by these reactive compounds, which are released by oxygen when producing energy (Harman 1984). Anti-oxidants such as vitamins A, C, and E are now largely used in order to fight the harmful effects of free radicals. These anti-oxidants are safe and have no negative side effect, but their alleged capacity to prevent cataracts and heart disease is still to be proven.
Probably the most relevant study in the area of senescence concerns the role which, according to the Hayflick limit theory of aging (Hayflick 1977), is played by telomeres in triggering the process by which cells progressively exhaust their capacity to maintain and repair themselves. Telomeres are the ends of chromosomes, made up by repeating DNA sequences that control the number of cell division; they increasingly shorten with every cell division, and the telomerase gene is finally repressed with cell differentiation. Major recent achievements in the effort to prolong human life-span include the insertion of a copy of an active form of the telomerase gene into some cell types, which allows for an extension of the capacity of the cell to divide before dying (Bodnar et al. 1998).
Another major achievement is the possibility to genetically program embryonic stem (ES) cells in order to repair and rejuvenate specific tissues or organs. ES cells in fact have permanently youthful telomeres that provide them with the theoretical capacity to indefinitely divide. If these cells could be safely introduced into somatic cell types, it would be possible to cope with the effects of such diseases as arthritis, diabetes and heart disease, which are significantly correlated with age; this may enhance human life-span by 10 to 20 years. If, however, ES cells expressing the telomerase gene could be programmed into the germ line at the embryonic stage, it would become possible to provide all of the body’s cells with the capacity to indefinitely divide; this may hypothetically extend human life up to 150 or 200 years.
Several questions have been raised, concerning the ethical evaluation of research into life-extension. Of course, the main perplexity has to do with the fact that, by intervening on a relevant control on normal cell senescence, there is the risk that we trigger uncontrolled cell proliferation, which would mean that the altered cells may give rise to tumours. The first ethical question is therefore whether research into life-span extension can be made safe, and may not risk being a cause of the shortening of human life.
Yet, even if the risk of increasing the incidence of cancer is removed, there are other relevant points to be considered. One surely has to do with the social consequences of a hypothetical future dissemination of these techniques. It seems very likely – though some raise doubts (Harris 2002) – that the general application of life-extending techniques would result in a relevant increase in the world population. This would raise serious questions concerning the quality of the life thus preserved: it seems very likely that life in this future world would be burdened by an increased competition for such scarce resources as food, water or health care. This may at least give rise to the temptation, on behalf of rulers, to curtail individual procreative liberty.
Since one effect of this process will be to alter the ratio between younger and older people in favour of the latter, it is also to be noted that the overall effect would be to put a serious pressure on intergenerational justice issues, with an ever smaller percentage of young people to work and fund medical care and social security taxes for an ever larger percentage of elderly people. This runs particularly against a relevant trend in the allocation of resources debate, according to which it is ethically sound to devote most of our health resources to grant all people the opportunity to reach the normal life-span, and the elderly who have passed it are an appropriate and justified target for withholding resources (Callahan 1987; Daniels 1988).
This trend is also related to the debate concerning the goals of medicine: supposing that it is possible to draw a sufficiently sharp line between therapy and enhancement, it may be maintained that the scarcity of health care resources compels to limit ourselves to therapy, renouncing everything that can be counted as an improvement on the ‘species-typical normal functioning’ (Parens 1998). In this case, life-extending technologies would be thought of as no therapy at all, since the species normal functioning, at the moment, is to allow a certain life span and no more, even in the absence of illness. One may reply that this field of research involves as much enhancement as therapy, since the goal of extending the life span cannot be pursued without striving to remove both the causes of those illnesses which in most cases procure an untimely death, and those conditions (impairment of cognitive and physical abilities) which negatively affect old age. It would be senseless to work for extended cellular life without working at the same time for a healthier (“normal”) life. Therefore, we may say, life extending technologies are a bundle of techniques in which it is quite hard to distinguish between therapy and enhancement.
Furthermore, the notions of “normal functioning” and “human nature” implied in the cautionary argument used against life-extending techniques are being put under dispute in this debate. The very idea of extending the “normal” life span runs against any presupposition of how long human life should “normally” be: species typical normal functioning is only a statistical variable, and there is nothing in that concept preventing one from thinking that these statistics should change, thanks to the new technologies. There does not seem to be any conceptual necessary link between a reasonable notion of human nature (e.g., «humans are rational living beings») and the present limits concerning life span; so why not extending those limits?
Further problems arise in the field of justice: it is to be expected that Western affluent societies, where these researches are being carried on, will be for many years the first to test and to enjoy the benefits of these technologies; it is therefore clear that the most likely prospect is one in which ever larger amounts of the world resources are devoted to keep alive and relatively healthy a small percentage of the world population, while the larger and younger part of the planet lies in a much less enviable condition. Though it is true that ethics does not require to withhold doing good to some until you can do it to all (Harris 2002), it seems ethically doubtful to devote much effort to prolong the lives of people who have reached and passed the biologically normal life-span, while most of the people in the third world lack the basic medical and non medical means to approach it. These questions focus on the issue of an appropriate distribution of resources.
Other problems of justice related to these technologies may arise in the distribution of benefits between the sexes. In fact, it is not clear what would happen of the reproductive ability of longer-living adults: the likely prospect is that while women would continue to be fertile during only a part of their much longer lives, men might be induced to pursue parental projects much later in life, since they are expected to live a longer time to look after their late offspring. In this case, women might reasonably call for a wider access to assisted procreation after menopause, in order not to be discriminated in their reproductive rights. Furthermore, one of the arguments against late assisted procreation, would lose its grip on reality: late mothers would definitely live enough to raise their children. On the other hand, as already noted, it is likely that the burden of a new child in an overwhelmingly aging society would be even greater than now is, creating a paradoxical situation: a longer reproductive life, with a heavily reduced social and material space for newborns.
Other objections have a much more philosophical character. For one thing, it may be noted that it is not clear that enjoying a much longer life would in fact be a benefit, or would really be appreciated by most people. (Williams 1973; Jonas1992;Glannon 2002a) One more point, raised by Glannon (2002b), has to do with the long-range effects of the extension of the human life-span and the possible negative effects of it for the early stages of life. Life-span enhancing technologies could in fact be unfair to future generations and create serious problems of justice among different generations.
Blackman M. R. et al. 2002, “Growth Hormone and Sex Steroid Administration in Healthy Aged Women and Men: A Randomized Controlled Trial”, JAMA 288: 2282-2292
Bodnar A.G. et al. 1998, “Extension of life-span by introduction of telomerase into normal human cells”, Science 279, pp. 349-352
Callahan D. 1987, Setting Limits: Medical Goals in an Aging Society, Simon & Schuster, New York
Coschigano K.T. et al. 2000, “Assessment of Growth Parameters and Life Span of GHR/BP Gene-Disrupted Mice”, Endocrinology 141, n. 7: 2608-2613
Daniels N. 1988, Am I My Parents’ Keeper? An Essay on Justice Between the Young and the Old, Oxford University Press, New York
Fries J.F. 1980, “Aging, natural death, and the compression of morbidity”, New England Journal of Medicine 303, pp. 130-135
Glannon W. 2002a, “Identity, prudential concern, and extending lives”, Bioethics 16, pp. 266-83
Glannon W. 2002b, “Extending the Human Life Span”, Journal of Medicine and Philosophy 27, pp. 339-354
Hayflick L. 1977, “The cellular basis for biological aging”, in Handbook of the Biology of Aging, L. Hayflick and C. Finch eds., Van Nostrand, New York: 159-186
Harman D. (1984), “Free radical theory of aging: the 'free radical' diseases”, Age 7: 111-31
Harris J. 2002, “A response to Walter Glannon”, Bioethics 16, pp. 284-291
Harris J. and Holm S. 2002, “Extending Human Lifespan and the Precautionary Paradox”, Journal of Medicine and Philosophy 27, pp. 355-368
Hintz, R.L. 2004, „Growth hormone: uses and abuses”, British Medical Journal 328: 907-908
Jonas H. 1992, “The burden and blessing of mortality”, Hastings Center Report 22, n. 1, pp. 34-40
Parens E. 1998, “Is better always good? The enhancement project”, Hastings Center Report 28, n. 1, pp. S1-S15
Pierrefiche G., Laborit H. (1995), “Oxygen free radicals, melatonin and aging”, Experimental Gerontology 30: 213-27
Sohal R., Weindruch, R. (1996) “Oxidative stress, caloric restriction, and aging”, Science 273: 59-63
Williams B. 1973, “The Makropulos case: reflections on the tedium of immortality”, in Problems of the Self, Cambridge University Press, Cambridge, pp. 82-100