Rapid Responses to:
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Rapid Responses: Rapid Responses published:
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Fountains of youth
- Luc Bonneux (10 July 2008)
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A common misperception
- David S Stodolsky (16 July 2008)
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Proposed new model of health promotion for the 21st century: need more flesh and skin on the bone?
- Phyo K Myint, Miles D Witham, Clinical Lecturer in Ageing and Health, Section of Ageing and Health, University of Dundee, Dundee DD1 9SY ; Alasdair M J MacLullich, MRC Clinician Scientist Fellow, University of Edinburgh, Edinburgh, EH16 4TJ (22 July 2008)
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Response to Dr. Bonneux from Butler et al.
- S. Jay Olshansky, Robert N. Butler, Richard A. Miller, Daniel Perry, Bruce A. Carnes, T. Franklin Williams, Christine Cassel, Jacob Brody, Marie A, Bernard, Linda Partridge, Thomas Kirkwood, George M. Martin, S. Jay Olshansky (28 July 2008)
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Physical activity and exercise slow the negative consequences of ageing
- Marijke Hopman-Rock, Nico van Meeteren (physiotherapist) (7 August 2008)
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The "old health promotion model" has legs
- Paul Z Zimmet (28 September 2008)
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Luc Bonneux, Epidemiologist 3502 AR Den Haag, Netherlands
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The fountain of youth likely has obsessed humankind from its dawn. However, slowing rates of aging comes at a high price. It is an unethical policy, increasing inequity. Aging is defined as the increasing probability of disease, disability and death by increasing age. Slowing the rates of aging does not change the human life course, ending in senescence at the end of life. If we simplify senescence and the rate of aging as transition rates to three states in a multi state life table, healthy, senescent and death, slowing the rates of ageing implies extending dwelling times in all states, the healthy and the senescent state. This fountain of youth therefore promises increasing numbers senescent and disabled Struldbruggs at the end of life. Increasing levels of care dependence will increase further health care budgets. Many ageing societies do not know how to cope with future care dependence, facing always more dependent elderly and always less young people, able and willing to care for them. Enhancing immigration, one of the few workable solutions, will increase societal problems in the receiving countries and bleed the sending countries further from qualified health care personnel. Increasing health care budgets, sounding nice in the ears of doctors, increases inequity by starving other budgets, such as pensions for the surviving elderly and reduction of poverty here and in the rest of the world. We do not need medical or biological research to increase life expectancy in the world. That ought not to be difficult, with life expectancies under 50 in the whole of Sub Saharan Africa. We do need much, much more policy research to understand how we can increase the rates of development of countries, stuck into failure. Sending more aid seems, for the time being, as effective a cure for poverty as blood letting was for disease in the 18th and 19th century. Fighting disease is based on arguments of equity. Some of us have good luck, they are healthy. Some of us have bad luck, they have a disease. It is the duty of the strong to help the weak. The ethics of equity have always been pervasive in medicine. That changes dramatically if we attack an ubiquitous characteristic of the human life course, ageing. We will now create inequity, as it is hardly likely that reduction of rates of aging will be available to all. There will be the rich, who can afford to get very old, there will be the poor, who are allowed to die young. Nil novum sub sole, nothing new under the sun, but this is not an honorable aim of medicine. The biology of aging is an obvious and important target of scientific research. But it has little to do with humane medicine, centering on the needs of the patient: to cure sometimes, to relieve often, to comfort always. Competing interests: None declared |
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David S Stodolsky, Senior Scientist 2400 Copenhagen NV
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"If we simplify senescence and the rate of aging as transition rates to three states in a multi state life table, healthy, senescent and death, slowing the rates of ageing implies extending dwelling times in all states, the healthy and the senescent state. " This is a common misperception. Person's who reach extreme ages tend to have less disability than those that don't. It should be no surprise that healthy people live longer. Competing interests: None declared |
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Phyo K Myint, Clinical Senior Lecturer in Ageing and Stroke Medicine School of Medicine, Health Policy and Practice, University of East Anglia, Norwich, NR4 7TJ, Miles D Witham, Clinical Lecturer in Ageing and Health, Section of Ageing and Health, University of Dundee, Dundee DD1 9SY ; Alasdair M J MacLullich, MRC Clinician Scientist Fellow, University of Edinburgh, Edinburgh, EH16 4TJ
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Butler and colleagues make the case for “new model of health promotion for the 21st century” [1]. The authors argued for the potential contribution of basic science research into ageing to improving health span. We fully agree that understanding the biology of ageing is an important component of any research programme aimed at this goal. However, even if genetic variations resulting in quantitatively important changes to the ageing phenotype are discovered, this only the beginning of a very long and expensive process towards the development of safe and effective drugs. Two important points need to be made regarding our ability to translate laboratory knowledge of the ageing process into health gains for older people. Firstly, we have at least two powerful, pleiotropic interventions that are known to improve the function of many different bodily systems – these are exercise and nutrition [2]. Directing resources towards finding effective ways of implementing these interventions is the most likely way of retarding the ageing process in the near future. Shifting towards favourable risk profile of the whole population by taking small and simple steps towards the right direction has huge potential in reducing the burden of chronic disease worldwide. While better understanding of biological basis of ageing could potentially identify people who would benefit most from targeted interventions, without investment in clinical and social gerontology research, ageing research will not get anywhere. Secondly, insights from basic science will be wasted unless enough funding, personnel and structures are in place to perform clinical studies in older people. This is patently not the case at present [3]. If we are to be successful in further compressing morbidity and extending healthy lifespan, we need to put at least as many resources into recruiting and funding clinical academic geriatricians as we put into funding the basic science of ageing. References [1] Butler RN, Miller RA, Perry D, Carnes BA, Williams TF, Cassel C, Brody J, Bernard MA, Patridge L, Kirkwood T, Martin GM, Olshansky SJ. New model of health promotion and disease prevention for the 21st century. BMJ 2008;337:a399. [2] Kennedy ET. Evidence for nutritional benefits in prolonging wellness. Am J Clin Nutr. 2006; 83:410S-414S. [3] House of Lords Science and Technology Committee. Ageing: scientific aspects. London: Office of Technology and Science, 2005. Competing interests: None declared |
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S. Jay Olshansky, Scientist 60612, Robert N. Butler, Richard A. Miller, Daniel Perry, Bruce A. Carnes, T. Franklin Williams, Christine Cassel, Jacob Brody, Marie A, Bernard, Linda Partridge, Thomas Kirkwood, George M. Martin, S. Jay Olshansky
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Dr. Bonneux's reply makes four main claims, and we want to respond to each of these. First, he claims that "slowing the rates of ageing implies extending dwelling times in all states, the healthy and the senescent state," leading to increased numbers of unhappy and disabled elderly people. He assumes that anti-aging interventions are bound to increase, in proportion, all stages of the life course, as though one were stretching a rubber band by pulling on one end. The evidence on this point, though sparse, is fully consistent, and it all points in just the opposite direction. When aging is delayed, in laboratory mice or rats, whether by genetic or dietary means, the animals not only live longer, but they are also much less likely to have a serious chronic illness at the time of their (delayed) death. Rats on an anti-aging, low calorie diet, for example, if allowed access to an exercise wheel, continue to run for one to three kilometers per day even at ages where all of the control rats have long since died, i.e. at ages proportionally equivalent to 100-year old people (1). The incidence of cancer and kidney disease in slow-aging mice, at the time of their death, is also lower than that seen in normal animals dying much earlier (2,3). The ability to learn and to remember is also retained longer in slow-aging mutant mice than in their normal siblings (4). Thus although omnia flumina intrant in mare (all rivers run into the sea) (5), these mice and rats not only take a longer course in their journey, they also spend less time meandering through the delta at the end of the trip. Dr. Bonneux also argues that "we do not need medical or biological research to increase life expectancy in the world," calling instead for research in health policy to develop better strategies for addressing the diseases that plague those who live in sub-Saharan Africa and other impoverished areas. We agree that a combination of policy research, along with a resolve to pursue a more equitable distribution of food, water, and access to medicines, would improve life expectancies of those in third- world countries, and that this is a worthy goal. But unless Dr. Bonneux is proposing to stop all research on diseases that afflict the elderly, like cancer and Alzheimer's and heart attacks and adult-onset diabetes, we think his argument is off point. Our article did not address the complicated issue of how to address health inequalities, global and local. We are instead proposing an approach that in our view would make research on late-life illnesses more cost-effective and productive than it is as present, by focusing on the biology of aging and its causal links to diseases, rather than sticking to the current, disease-at-a-time approach that is now the dominant paradigm. Dr. Bonneux argues that research on aging is "unethical," because it will "create inequity" by allowing only rich people to grow old, while "the poor will be allowed to die young." In many countries – though perhaps not in the Netherlands where Dr. Bonneux lives – there already exists a considerable inequality between the health care provided to wealthy people and that available to the impoverished, and there is a strong correlation between socio-economic indices and health outcomes. This disparity arose in the absence of any useful anti-aging medicines, and there are better ways of dealing with the inequity than by lambasting biogerontologists. Dr. Bonneux seems to be assuming that if an anti-aging medicine could be developed, it would be so much more expensive than current preventive modalities that only wealthy people could afford it, and that these aristocrats, in their pursuit of their own longevity, would insist on gobbling up a larger share of health care resources than their already consume. Dystopias of this kind are a common trope in science fiction, but their assumptions do not stand up well under scrutiny. Lastly, Dr. Bonneux asserts that "the biology of aging… has little to do with humane medicine, centering on the needs of the patient: to cure sometimes, to relieve often, to comfort always." Here we disagree completely. Our proposal is "humane" for exactly the same reason that learning how to prevent or treat all the individual diseases of aging is humane. Research aimed at learning how to prevent a heart attack, by exercise or coronary bypass, or at helping those who have suffered an infarction to regain cardiovascular function and return to their work and family, is, appropriately, viewed as fully "humane." Investigations into the biology of cancers, diabetes, cataracts, Parkinson's disease, and hip fractures are all humane things to do because discoveries in these areas could, in the long run, help diminish suffering and increase the number of productive, happy years available to our patients, our friends, and ourselves. Research aimed to learning how to delay aging has the same humane goal, but, we believe, may provide a faster and cheaper way to make progress toward this objective. There will always be a need for physicians to relieve and comfort their patients when illness strikes and a cure is unavailable, but there is no shame in trying to put these late- life illnesses off for a decade or two before we have to place that call to the geriatrician. Reference List (1) McCarter R, Masoro EJ, Yu BP. Does food restriction retard aging by reducing the metabolic rate? Am J Physiol 1985; 248:E488-E490. (2) Ikeno Y, Bronson RT, Hubbard GB, Lee S, Bartke A. Delayed occurrence of fatal neoplastic diseases in ames dwarf mice: correlation to extended longevity. Journals of Gerontology Series A -Biological Sciences & Medical Sciences 2003; 58(4):291-296. (3) Vergara M, Smith-Wheelock M, Harper JM, Sigler R, Miller RA. Hormone- treated Snell dwarf mice regain fertility but remain long-lived and disease resistant. J Gerontol Biol Sci 2004; 59:1244-1250. (4) Kinney BA, Coschigano KT, Kopchick JJ, Steger RW, Bartke A. Evidence that age-induced decline in memory retention is delayed in growth hormone resistant GH-R-KO (Laron) mice. Physiol Behav 2001; 72(5):653-660. (5) Ecclesiastes 1:7 Competing interests: None declared |
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Marijke Hopman-Rock, Epidemiologist, psychologist, biologist TNO Quality of Life, P.O Box 2215, 2301 CE Leiden, The Netherlands, Nico van Meeteren (physiotherapist)
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Robert Butler and colleagues (BMJ, 19 July 2008, 149-150) wrote an interesting article about a recommendable paradigm shift from research targeted at individual diseases to multidisciplinary ageing research. We certainly support this view, and would like to add some comments. Already in 1981 Fries and Crapo1 revealed their theory of compression of morbidity in their pioneering work called ‘Vitality and Aging’. The idea behind this was that strategies for health promotion such as stimulation of physical activity and improvement of other lifestyle behaviours, could enhance quality of life and decrease the time spent with diseases. In the eighties of the last century an exiting new branch of science started in the area of physical activity and exercise. An overwhelming amount of evidence has since then been published on substantial benefits of physical activity, including physical and cognitive functioning of older people. As the well known geriatrician Archie Young2 stated already in 1986: “not only can exercise reverse the effects of immobilization, it can readily produce a further 10 to 20% improvement in strength and aerobic power, effectively postponing functionally important thresholds for some 10 to 20 years”. Knowing these facts, it is amazing that the medical field in general is still reluctant to advise and prescribe physical activity to (older) people. This can partly be explained by the fear that people could experience a fall or get heart complaints. During the last World Conference of Physical Activity and Aging in Japan (July 2008) it was stated however, that a visit to the toilet is much more dangerous for older people than getting started with physical activity (such as for instance walking). In our eyes the practical interventions that slow the negative consequences of ageing are relatively easy to achieve: prescription of physical activity and exercise, be it as an elixir of life such as recommended by Nelson et al3 or as a (preventive) medicine in case of a potential hazardous major life event (e.g. Hulzebos et al4). 1 Fries JF, Crapo LM. Vitality and Aging. San Francisco: WH Freeman, 1981. 2 Young A. Exercise physiology in geriatric practice. Acta Med Scand Suppl. 1986; 711: 227-232. 3 Nelson ME et al. Physical activity and public health in older adults: recommendation from the American College of Sports Medicine and the American Heart Association. Med Sci Sports Exerc 2007; 38(8): 1435-1445. 4 Hulzebos HJ et al. Prevention of postoperative pulmonary complications in high-risk patients undergoing CABG surgery preoperative intensive inspiratory muscle training. A randomized clinical trial. JAMA 2006; 296(15): 1851-1857. Competing interests: None declared |
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Paul Z Zimmet, Director of International Research Baker IDI Heart Nad Diabetes Institute, Melbourne 3181
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Butler and colleagues have published on a “new model of health promotion for the 21st century” (1). I found their comments about current strategies to prevention of chronic disease rather outdated and not consistent with the current paradigms. Do we really need a "new model"? They state that the traditional approach to amelioration of modern chronic diseases has been to tackle them individually. They also note that their article arose from their efforts to get physicians, scientists and politicians to understand and appreciate the public health benefits that would accrue from efforts to slow ageing, and distinguish those benefits from the current medical approach to attacking one disease at a time. While their "new model" certainly is attractive, how relevant really is it to the current public health. Other than an additionally strategy. It is certainly a novel suggestion but the rationale for its proposal does not stand up to the reality of current approaches to the prevention of non- communicable diseases (NCD). For over 2 decades now, WHO has championed an integrated helth promotion approach to the prevention and control of NCD with many nations adopting that strategy. The lifestyle strategy has the potential,and has been demonstrated to address prevention of type 2 diabetes, cardiovascular diseases, certain cancers etc. Perhaps "old is new again"! [1] Butler RN, Miller RA, Perry D, Carnes BA, Williams TF, Cassel C, Brody J, Bernard MA, Patridge L, Kirkwood T, Martin GM, Olshansky SJ. New model of health promotion and disease prevention for the 21st century. BMJ 2008;337:a399. Competing interests: None declared |
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