X-Message-Number: 24318
Date: Fri, 2 Jul 2004 20:39:03 -0700 (PDT)
From: Doug Skrecky <>
Subject: aging: the reality

J Gerontol A Biol Sci Med Sci. 2004 Jun;59(6):B579-86.
Aging: the reality: demography of human supercentenarians.
  An international committee of demographers has created a carefully
documented list of worldwide living supercentenarians (>/=110 years old)
that has been published by the Los Angeles Gerontology Research Group on
its web site and updated on a weekly basis for the past 6 years [see
"snapshot" for the year 2003 in the Appendix]. What can be learned by
studying this distinguished group of individuals? Also, what are the
implications for understanding the fundamental biological limits to human
longevity and maximum life span? Our conclusion: Although everyone agrees
that average life expectancy has systematically advanced linearly over the
last century, it is not realistic to expect that this pace can continue
indefinitely. Our data suggest that, without the invention of some new
unknown form of medical breakthrough, the Guinness Book of World Records
benchmark established by French woman Jeanne Calment of 122 years, set
back in 1997, will be exceedingly difficult to break in our lifetime.

J Gerontol A Biol Sci Med Sci. 2004 Jun;59(6):B573-8.
Aging: the reality: "anti-aging" is an oxymoron.
Hayflick L.
  No intervention will slow, stop, or reverse the aging process in humans.
Whether anti-aging medicine is, or is not, a legitimate science is
completely dependent upon the definition of key terms that define the
finitude of life: longevity determination, aging, and age-associated
diseases. Only intervention in the latter by humans has been shown to
affect life expectancy. When it becomes possible to slow, stop, or
reverse the aging process in the simpler molecules that compose inanimate
objects, such as machines, then that prospect may become tenable for the
complex molecules that compose life forms. Most of the resources available
under the rubric "aging research" are not used for that purpose at all,
thus making the likelihood of intervention in the process even more
remote. If age changes are the greatest risk factor for age-associated
diseases (an almost universal belief), then why is the study of aging
virtually neglected?

FASEB J. 2003 Apr;17(6):690-2. Epub 2003 Feb 05
Genotype and age influence the effect of caloric intake on mortality in mice.
  Long-term caloric restriction (CR) has been repeatedly shown to increase
life span and delay the onset of age-associated pathologies in laboratory
mice and rats. The purpose of the current study was to determine whether
the CR-associated increase in life span occurs in all strains of mice or
only in some genotypes and whether the effects of CR and ad libitum (AL)
feeding on mortality accrue gradually or are rapidly inducible and
reversible. In one experiment, groups of male C57BL/6, DBA/2, and B6D2F1
mice were fed AL or CR (60% of AL) diets beginning at 4 months of age
until death. In the companion study, separate groups of mice were
maintained chronically on AL or CR regimens until 7, 17, or 22-24 months
of age, after which, half of each AL and CR group was switched to the
opposite regimen for 11 wk. This procedure yielded four experimental
groups for each genotype, namely AL-->AL, AL-->CR, CR-->CR, and CR-->AL,
designated according to long-term and short-term caloric regimen,
respectively. Long-term CR resulted in increased median and maximum life
span in C57BL/6 and B6D2F1 mice but failed to affect either parameter in
the DBA/2 mice. The shift from AL-->CR increased mortality in 17- and
24-month-old mice, whereas the shift from CR-->AL did not significantly
affect mortality of any age group. Such increased risk of mortality
following implementation of CR at older ages was evident in all three
strains but was most dramatic in DBA/2 mice. Results of this study
indicate that CR does not have beneficial effects in all strains of mice,
and it increases rather than decreases mortality if initiated in advanced
age.

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