One of the themes on Future Blogger and for fans of accelerating
change in general is life extension and the prospect of relative
immortality. 
We covered this topic in our very first interview with
Aubrey de Grey and Dick
Pelletier has addressed it many times. One of the core
arguments in this debate is that, regardless of increasing life
expectancy rates, humans have an upper limit. This is probably best
categorized as the Hayflick
limit argument . That there is a maximum number of years that a
human can live and if nothing gets to you before reaching that
threshhold, when you do, that’s it – it’s over. That limit is about
120 years of age, with the oldest documented lifespan being the 122
attained by Jean Calumet
Increases in life expectancy are ultimately discounted by this
assumption. In response to Jack Uldrich’s
recent piece on the prospect of living to 1000, John
Frink correctly points out that the radical increase in life
expectancy that developed societies have experienced over the last
170 years or so (roughly doubling) is largely due to advances in
health/medicine and hygiene. He cites the vast reduction in the
infant mortality rate as being of particular note. But that is more
reflective of initial gains and merely part of a larger trend at
work. (cont.)
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(Cross-posted from
Ouroboros: Research in the biology of aging.)
A transgenic mouse that lives twice as long as controls is also
stronger and faster, arguing against the idea of inherent negative
tradeoffs associated with lifespan extension. 
Increased expression of a metabolic enzyme, phosphoenolpyruvate
carboxykinase (PEPCK, an enzyme that most of us learned about in
freshman biology and then promptly forgot, reasoning that the
descriptive name and the ability to look it up if necessary would
suffice if it ever came up again) results in mice that are
muscular, have lower body fat than a runway model, and able to run
25 times farther than a wildtype control.
Even more interesting, according to proud parents Hanson and Hakimi, the females of the PEPCK-Cmus strain mate and have
normal-sized litters at 35 months, an age when the blood of
wildtype mice has cooled substantially (and, indeed, the mice
themselves are starting to check out). The implication is that
aging is slowed, and longevity extended, as a result of the
transgene.
It’s become reflexive to ask whether a long-lived mutant is
living longer because it’s calorie-restricted for some reason,
incidental to the main phenotype conferred by the mutation, but
this is not the case here: In order to preserve their enviable
bods, PEPCK-Cmus mice eat 60%
more than controls — so they’re not extending their lifespan
by dieting. If anything, they’re anti-dieting: their increased
metabolic efficiency means they’re harvesting more calories per
gram of carb or fat than normal animals. No word yet on what
happens if you do try to calorie-restrict them; I can imagine it
going either way but am holding out hope for tiny
explosions. (cont.)
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(cross-posted from
Ouroboros: Research in the biology of aging)
Stress resistance at the cellular level is correlated with
longevity at the organismal level, to such an extent that one can
screen for longevity mutants by first identifying
stress-resistant animals. Conversely, the cells of prematurely
aging mutants tend to be
hypersensitive to stress. The idea here is that longevity is
controlled in part by basal and inducible molecular defenses like
antioxidants and chaperones, and that high levels of such factors
confer both stress resistance and enhanced longevity.
What’s interesting about this pattern is that it seems to apply
to a wide range of multiple stresses, with very different physical
bases: oxidation, irradiation, starvation, heavy metal toxicity,
and temperature, to name a few. Without a great deal of
experimental proof to support it, one can imagine some central
homeostatic integrator of cellular well-being, upon which all
manner of perturbations might impinge and which might in turn
control both the appropriate defensive responses and factors that
determine longevity.
It would therefore come as a surprise if a long-lived organism
turned out to be unusually sensitive to stress — and in particular,
sensitive to particular stresses. In one fell swoop, this
would falsify both the general, well-accepted correlative pattern
(stress resistance = longevity) and the somewhat more fanciful
model of a central homeostatic integrator.
align=”right” width=”100”>Lo, the naked mole rat,
Heterocephalus glaber. A eusocial rodent roughly
intermediate in size between a mouse and a rat (depending on where
you shop), and slightly less aesthetically pleasing than an
overcooked boudin blanc with teeth, the naked mole rat has
recently drawn the attention of model-hungry biogerontologists
worldwide: Perhaps because of the
quirky selection pressures on eusocial animals, H.
glaber is unusually long-lived compared to animals of similar
size and body plan (like mice and rats). Like, ten times
longer-lived. So, compared to mice and rats, mole rats should be
much more resistant to all stresses, right? (cont.)
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(cross-posted from
Ouroboros: Research in the biology of aging)
Our understanding of aging in animals owes a great debt to a
large body of careful work in a single-celled organism, the
brewer’s yeast Saccharomyces cerevisiae. Indeed, as I’ve
argued
before, yeast is one of the two organisms with the strongest
credible claim to have started modern biogerontology. An unusually
large crop of yeast aging papers have appeared over the last few
months, and I thought it would be appropriate to spend a few
paragraphs describing them — in honor of this humble organism that
rises our bread, ferments our beer, and has done so much to open
our eyes to the fundamental mechanisms of aging.
For those unfamiliar with the yeast field or simply wishing a
clearly written and nearly comprehensive summary, Steinkraus et al. provide the historical
perspective. The piece thoroughly reviews the development of yeast
as a model system in aging, as well as the arguments in favor of a
connection between results in yeast and well-established (but
sometimes hard-to-test) hypotheses in animals.
Based on the influence that yeast has already had on
biogerontology as a whole, it seems fair to claim that it will
continue to reveal fundamentals of aging that are conserved across
evolution. (cont.)
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Much has been made of Caloric Restriction (CR) and how it is the one true life-extension strategy currently available. In countless articles and videos it has been given much attention and 
there are a bunch of folks whose stomachs are growling as we speak that will be disappointed to learn that this strategy may be flawed.
A new study by Raj Sohal and Michael Forster recapped on EurekAlert! shows that CR is essentially only effective when "an animal eats more than it can burn off." The problem it seems is that it really only works for obese mice and has little or no benefit for those who aren't.
The study looked at two different genetically altered strains of mice - basically a fat mouse and a skinny mouse (I think this may have sitcom potential). The takeaway was that calorie restriction helped the mouse that had been programmed to double its weight over its lifespan while it did not extend the life of the skinny mouse. In fact, when CR is started later in life they found that it actually shortened the lifespans of leaner test subjects. The authors noted that previous studies have also demonstrated that wild mice experience minimal life-extension benefits from CR.
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By Jack Uldrich
Cross-posted from www.jumpthecurve
I ask this question from neither a deep-seated fear of dying nor an egotistical desire to live forever. I simply ask it from the perspective of someone who is deeply interested in the accelerating pace of change and is concerned we are heading into a future for which few of us are really prepared.
Let me begin by sharing a couple of recent news items which speak to the astounding progress being made in the field of health care.
To begin, if I am in need of surgery sometime within the next few years, it is likely that that surgery will be conducted with the assistance of a robot. Given that these robots are already better than many human surgeons, this suggest I will not only get out of the hospital faster but that I will be in better condition when I do so. Continued advances in robotics will only improve surgical outcomes over the coming years.
Next, say, I am in an accident. There is now a very good chance – due to advances in the Nationwide Health Information Network, personal electronic records and the ever-improving capability of the Internet – that my providers will be able to rapidly access a growing wealth of medical knowledge in order to keep me alive.
Much of this knowledge will likely be genetic in nature and it is not unreasonable to believe – given the extraordinary advances in genomics as well as the possibility that I will within a few years be able to sequence my own genome for less than $1000 dollars - that I will soon be able to avail myself to a growing category of drugs individually tailored to treat me for everything from heart disease and diabetes to a wide variety of cancers.
Assuming then that I dodge some of these pesky middle-age risks, there is a very real chance, according to this article, that I’ll soon be able to “grow replacement body parts.” We can already replace our aging hips and knees, but what happens when I can replace my lungs and, eventually, my heart?
The question is a serious one because society is closer to this future than most people realize.
Alas, these advances – which I remind you are only from the past few days – are just the beginning. I am now 44 years and it is not unreasonable to think, given recent medical progress, that I will live to 100.
But even this is the wrong way to think about this issue. The question I – and all of us, really – need to ask is what further advances will be made in the next 56 years of my life and how might they extend my life past 100 years of age?
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