Is Aging an Accident? (article)

note: this issue may be important for longevity/immortality cultivators. It implies that one’s intention to live longer might activate (or de-activate) the genes needed to live longer. It also suggests that one must shift things not just at the organ level of cultivation, but at a deep jing (=DNA) level. That is main function of neidangong (internal alchemy).
michael

IS AGING AN ACCIDENT OF EVOLUTION? STANFORD SCIENTISTS SAY “YES”
Posted by Casey Kazan
Daily Galaxy
July 29, 2008

http://www.dailygalaxy.com/my_weblog/2008/07/is-aging-an-acc.html

Prevailing theory of aging challenged by Stanford University Medical School
researchers. Their discovery contradicts the prevailing theory that aging is
a buildup of tissue damage similar to rust. The Stanford findings suggest
specific genetic instructions drive the process. If they are right, science
might one day find ways of switching the signals off and halting or even
reversing aging.

³We were really surprised,² said Stuart Kim, who is the senior author of the
research.

Kim¹s lab examined the regulation of aging in C. elegans, a millimeter-long
nematode worm whose simple body and small number of genes make it a useful
tool for biologists. The worms age rapidly: their maximum life span is about
two weeks.

Comparing young worms to old worms, Kim¹s team discovered age-related shifts
in levels of three transcription factors, the molecular switches that turn
genes on and off. These shifts trigger genetic pathways that transform young
worms into social security candidates.

The question of what causes aging has spawned competing schools, with one
side claiming that inborn genetic programs make organisms grow old. This
theory has had trouble gaining traction because it implies that aging
evolved, that natural selection pushed older organisms down a path of
deterioration. However, natural selection works by favoring genes that help
organisms produce lots of offspring. After reproduction ends, genes are
beyond natural selection¹s reach, so scientists argued that aging couldn¹t
be genetically programmed.

The alternate, competing theory holds that aging is an inevitable
consequence of accumulated wear and tear: toxins, free-radical molecules,
DNA-damaging radiation, disease and stress ravage the body to the point it
can¹t rebound. So far, this theory has dominated aging research.

But the Stanford team¹s findings told a different story. ³Our data just
didn¹t fit the current model of damage accumulation, and so we had to
consider the alternative model of developmental drift,² Kim said.

The scientists used microarrays — silicon chips that detect changes in gene
expression — to hunt for genes that were turned on differently in young and
old worms. They found hundreds of age-regulated genes switched on and off by
a single transcription factor called elt-3, which becomes more abundant with
age. Two other transcription factors that regulate elt-3 also changed with
age.

To see whether these signal molecules were part of a wear-and-tear aging
mechanism, the researchers exposed worms to stresses thought to cause aging,
such as heat (a known stressor for nematode worms), free-radical oxidation,
radiation and disease. But none of the stressors affected the genes that
make the worms get old.

So it looked as though worm aging wasn¹t a storm of chemical damage.
Instead, Kim said, key regulatory pathways optimized for youth have drifted
off track in older animals. Natural selection can¹t fix problems that arise
late in the animals¹ life spans, so the genetic pathways for aging become
entrenched by mistake. Kim¹s team refers to this slide as ³developmental
drift.²

³We found a normal developmental program that works in young animals, but
becomes unbalanced as the worm gets older,² he said. ³It accounts for the
lion¹s share of molecular differences between young and old worms.²

Kim can¹t say for sure whether the same process of drift happens in humans,
but said scientists can begin searching for this new aging mechanism now
that it has been discovered in a model organism. And he said developmental
drift makes a lot of sense as a reason why creatures get old.

³Everyone has assumed we age by rust,² Kim said. ³But then how do you
explain animals that don¹t age?²

Some tortoises lay eggs at the age of 100, he points out. There are whales
that live to be 200, and clams that make it past 400. Those species use the
same building blocks for their DNA, proteins and fats as humans, mice and
nematode worms. The chemistry of the wear-and-tear process, including damage
from oxygen free-radicals, should be the same in all cells, which makes it
hard to explain why species have dramatically different life spans.

³A free radical doesn¹t care if it¹s in a human cell or a worm cell,² Kim
said.

If aging is not a cost of unavoidable chemistry but is instead driven by
changes in regulatory genes, the aging process may not be inevitable. It is
at least theoretically possible to slow down or stop developmental drift.

³The take-home message is that aging can be slowed and managed by
manipulating signaling circuits within cells,² said Marc Tatar, PhD, a
professor of biology and medicine at Brown University who was not involved
in the research. ³This is a new and potentially powerful circuit that has
just been discovered for doing that.²

Kim added, ³It¹s a new way to think about how to slow the aging process.²

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