into the advanced years. Although technology, the built environment, and medical care advances may have yielded benefits in function and quality of life for the “greatest” generation, unless the health habits of the baby boomers change dramatically, future researchers may be trying to explain the cohort effect that found a short-lived reduction in the duration of age-related functional impairment.
Source: “The Compression of Morbidity Hypothesis: A Review of Research and Prospects for the Future” by Vincent Mor, PhD, in Journal of the American Geriatrics Society, 53(9), pp. 308–309. Copyright © 2005 by the American Geriatrics Society.
Notes
1. Fries J. Aging, natural death and the compression of morbidity. N Engl J Med 1980; 303: 130–133.
2. Katz S, Branch LG, Branson MU, et al. Active life expectancy. N Engl J Med 1983; 309: 1218–1224.
6. Cutler D. Declining disability among the elderly. Health Aff 2001;20:11–27.
9. Verbrugge LM, Patrick DL. Seven chronic conditions: Their impact on US adults’ activity levels and use of medical services. Am J Public Health 1995; 85: 173–182.
10. Freedman VA, Martin LG. Contribution of chronic conditions to aggregate change in old-age functioning. Am J Public Health 2000; 90: 1755–1760.
11. Crimmins EM, Saito Y. Trends in healthy life expectancy in the United States, 1970–1990: Gender, racial, and educational differences. Soc Sci Med 2001; 52: 1629–1641.
12. Crimmins EM, Saito Y. Change in the prevalence of diseases among older Americans: 1984–1994. J Dem Rsrch.
14. Cutler DM. The reduction in disability among the elderly. Proc Natl Acad Sci USA 2003; 98: 6546–6547.
15. Freedman VA, Martin MG, Schoeni RF. Recent trends in disability and functioning among older adults in the United States. JAMA 2002; 288: 3137–3146.
16. Fries J. Measuring and monitoring success in compressing morbidity. Ann Intern Med 2003; 139: 455–459.
17. Lakdawalla DV, Bhattacharya J, Goldman DP. Are the young becoming more disabled? Health Aff 2004; 23: 168–176.
18. Peeters A, Barendregt JJ, Willekens P, et al. Obesity in adulthood and its consequences for life expectancy: A life-table analysis. Ann Intern Med 2003; 138: 24–32.
19. Sturm R, Ringel J, Andreyeva T. Increasing obesity rates and disability trends. Health Aff 2004; 23: 199–205.
Reading 8: We Will Be Able to Live to 1,000
Aubrey de Grey
Aging is a physical phenomenon happening to our bodies, so at some point in the future, as medicine becomes more and more powerful, we will inevitably be able to address aging just as effectively as we address many diseases today.
I claim that we are close to that point because of the SENS (Strategies for Engineered Negligible Senescence) project to prevent and cure aging.
It is not just an idea: it’s a very detailed plan to repair all the types of molecular and cellular damage that happen to us over time.
And each method to do this is either already working in a preliminary form (in clinical trials) or is based on technologies that already exist and just need to be combined.
This means that all parts of the project should be fully working in mice within just 10 years and we might take only another 10 years to get them all working in humans.
When we get these therapies, we will no longer all get frail and decrepit and dependent as we get older, and eventually succumb to the innumerable ghastly progressive diseases of old age.
We will still die, of course—from crossing the road carelessly, being bitten by snakes, catching a new flu variant, etcetera—but not in the drawn-out way in which most of us die at present.
So, will this happen in time for some people alive today? Probably. Since these therapies repair accumulated damage, they are applicable to people in middle age or older who have a fair amount of that damage.
It is very complicated, because aging is. There are seven major types of molecular and cellular damage that eventually become bad for us—including cells being lost without replacement and mutations in our chromosomes.
Each of these things is potentially fixable by technology that either already exists or is in active development.
The Alternative View
Nothing in gerontology even comes close to fulfilling the promise of dramatically extended lifespan.
—S. Jay Olshansky
“Youthful Not Frail”
The length of life will be much more variable than now, when most people die at a narrow range of ages (65 to 90 or so), because people won’t be getting frailer as time passes.
The average age will be in the region of a few thousand years. These numbers are guesses, of course, but they’re guided by the rate at which the young die these days.
If you are a reasonably risk-aware teenager today in an affluent, non-violent neighbourhood, you have a risk of dying in the next year of well under one in 1,000, which means that if you stayed that way forever you would have a 50/50 chance of living to over 1,000.
And remember, none of that time would be lived in frailty and debility and dependence—you would be youthful, both physically and mentally, right up to the day you mis-time the speed of that oncoming lorry.
Should We Cure Aging?
Curing aging will change society in innumerable ways. Some people are so scared of this that they think we should accept aging as it is.
I think that is diabolical—it says we should deny people the right to life.
The right to choose to live or to die is the most fundamental right there is; conversely, the duty to give others that opportunity to the best of our ability is the most fundamental duty there is.
There is no difference between saving lives and extending lives, because in both cases we are giving people the chance of more life. To say that we shouldn’t cure aging is ageism, saying that old people are unworthy of medical care.
The Alternative View
There is no difference between saving lives and extending lives, because in both cases we are giving people the chance of more life.
—Aubrey de Grey
Playing God?
People also say we will get terribly bored but I say we will have the resources to improve everyone’s ability to get the most out of
