LONGEVITY MEME NEWSLETTER
December 10 2007
The Longevity Meme Newsletter is a weekly e-mail containing news, opinions
and happenings for people interested in healthy life extension: making use
of diet, lifestyle choices, technology and proven medical advances to live
healthy, longer lives. To subscribe or unsubscribe from the Longevity Meme
Newsletter, please visit http://www.longevity...org/newsletter/
______________________________
CONTENTS
- Short Videos by Aubrey de Grey Explaining Longevity Science
- Matching Funds Triple SENS Research Donations Until Year End
- Discussion
- Latest Healthy Life Extension Headlines
SHORT VIDEOS BY AUBREY DE GREY EXPLAINING LONGEVITY SCIENCE
You may not have seen these short introductory videos before: each briefly
explains a single concept in longevity science, starting with some of the
basic basics. They are the first in a new series of videos aimed at further
bridging the gap between an overview for the layman and scientific
publications:
http://www.fightagin...ives/001363.php
http://www.mfoundati...ename=video_faq
Online video has been a tremendously success in broadening awareness and
education for healthy life extension research, and the present state of
science. This will continue to be the case, so pick out a few from the
video FAQ page above, and forward them on to your friends.
MATCHING FUNDS TRIPLE SENS RESEARCH DONATIONS UNTIL YEAR END
Good news from the Methuselah Foundation, coming as the total pledged to
Strategies for Engineered Negligible Senescence (SENS) research passes $5
million. Donations to speed research into repairing the damage of aging and
extending the healthy human lifespan will be matched 2-to-1 until the end
of 2007, expanding your donation threefold:
http://blog.methusel...s_research.html
http://blog.methusel...n_matching.html
"You might recall in 2006 that Peter Thiel made a 3 million dollar Matching
Challenge to SENS Research, where he matches 50% of donations to research
until the end of 2009. Well, our performance and Thiel's example have
prompted a supporter and Three Hundred Member, Michael Cooper, to join
Peter Thiel. He is offering a $25,000 Matching Challenge of his own until
the end of this month.
"Thanks to these generous supporters, the donations are matched
cumulatively. That is, a $1 donation to research is first matched with $1
from Cooper. This $2 is then matched with a further $1 by Thiel's Matching
Challenge to bring the total donation to $3.
"In this way a donation of $100 is TRIPLED to $300 ...but this multiplier
only lasts until the end of this month. Perhaps you might be interested in
helping Cooper and Thiel turn their generous matching challenge dollars
into research?"
You can find out more on how the Foundation presently employs donations to
SENS research by following the link below:
http://www.methusela...gename=research
DISCUSSION
The highlights and headlines from the past week follow below. If you have
comments for us, please do send e-mail to newsletter@longevitymeme.org
Remember - if you like this newsletter, the chances are that your friends
will find it useful too. Forward it on, or post a copy to your favorite
online communities. Encourage the people you know to pitch in and make a
difference to the future of health and longevity!
Reason
reason@longevitymeme.org
______________________________
LATEST HEALTHY LIFE EXTENSION HEADLINES
To view commentary on the latest news headlines complete with links and
references, please visit the daily news section of the Longevity Meme:
http://www.longevitymeme.org/news/
Do We Need Death? (December 07 2007)
http://www.cato-unbo...-we-need-death/
Back to Cato Unbound we go, for Ronald Bailey's contribution to the present
debate. "Schaub offers no data nor even a plausible line of reasoning that
longer healthy lives will result in 'social sclerosis.' In fact, the
available evidence cuts the other way. Social and technological innovation
has been most rapid in those societies with the highest average life
expectancies. Yale University economist William Nordhaus estimates that the
huge increase in average life expectancy in the United States, from
forty-seven years in 1900 to seventy-seven years today, has been
responsible for about 40 percent of the increase in our standard of living.
... the highest expression of human nature and dignity is to strive to
overcome the limitations imposed on us by our genes, our evolution and our
environment. Future generations will look back at the beginning of the 21st
century with astonishment that some well-meaning and intelligent people
actually wanted to stop biomedical research just to protect their cramped
and limited vision of human nature. Our descendants will look back, I
predict, and thank us for making their world of longer, healthier lives
possible." Just so. Do we need death? "No. Next question."
Lamin A As a Biomarker of Aging in Skin (December 07 2007)
http://dx.doi.org/10...al.pone.0001269
More on the nuts and bolts of lamin A, the root of accelerated aging in
progeria (HGPS), from PLoS One: "90% of HGPS cases carry the [lamin A
mutation], activating a splice donor site that results in production of a
dominant negative form of lamin A protein, denoted progerin. Screening 150
skin biopsies from unaffected individuals (newborn to 97 years) showed that
a similar splicing event occurs in vivo at a low level in the skin at all
ages. While progerin mRNA remains low, the protein accumulates in the skin
with age in a subset of dermal fibroblasts and in a few terminally
differentiated keratinocytes. Progerin-positive fibroblasts localize near
the basement membrane and in the papillary dermis of young adult skin;
however, their numbers increase and their distribution reaches the deep
reticular dermis in elderly skin. Our findings demonstrate that progerin
expression is a biomarker of normal cellular aging and may potentially be
linked to terminal differentiation and senescence in elderly individuals."
This enlarges upon earlier work demonstrating the presence of lamin A
defects in normal individuals.
From the Camp of Mild-Mannered Deathism (December 06 2007)
http://www.cato-unbo...geless-mortals/
The first of the response essays to Aubrey de Grey's piece at Cato Unbound
epitomizes mild-mannered deathism; the instinct that any radical change to
the human condition brought on by healthy life extension must be bad. If I
had to pick out the one thing the archetypical human hates and fears above
all else, it'd be the prospect of change - and that always shows through in
discussions of radically increasing the healthy human life span. "Even
without the threat of vastly extended tyranny, a nation of ageless
individuals could well produce a sclerotic society, petrified in its ways
and views. Senescence escorts us, more or less gracefully, off the stage,
making room for fresh generations. The aging of individuals may be one
condition for societal renascence. Fascinatingly, longevity research in
animals suggests that one cost of age-retardation is sterility or decreased
fertility. If there are trade-offs between long life and new life, then the
quest for individual immortality may pose dangers for the well-being of the
human collective, whether at the level of the family, the nation, or the
species. While frailty and finitude don't seem such good things, they may
be inextricably entwined with other very good things that we would not want
to sacrifice." It is sad that so many people would choose the stasis of the
now - and death and suffering without end, over and over - rather than
immensely positive change and opportunity through longevity science.
Talking nonsense about petrified, unchanging ageless societies is
projection, methinks.
Stem Cells Point the Way (December 06 2007)
http://www.scienceda...71205140112.htm
If we knew exactly how stem cells, progenitor cells and other developing
cells can produce regeneration without generating new tissue themselves,
then we wouldn't need the cells. An example of that truism in action is
provided by ScienceDaily: "a protein called connexin43, expressed by the
transplanted embryonic heart cells, improved electrical connections to
other heart cells. The researchers showed that the improved connections
helped activate the transplanted cells deep within the damaged section of
the heart tissue. The technique reversed the risk of developing ventricular
arrhythmias after a heart attack ... In the past, scientists have
transplanted a variety of cell types into failing hearts with modest
improvement of function, although transplanting skeletal muscle cells made
things worse and led to more arrhythmias. Surprisingly, when [researchers]
transplanted embryonic cardiac cells, the hearts' electrical stability and
function returned to normal. ... we were able to see how cells used in
therapy are working with other cells in a complex organ within a living
animal, establishing the mechanism of the therapeutic effect ...
[researchers] engineered skeletal muscle to express connexin43 and achieved
the same restorative results as they did with the embryonic heart cells."
Viewing a Future of Engineered Eyes (December 05 2007)
http://www.the-scien.../display/53894/
The Scientist looks at the future of tissue engineered, perfect eyes:
"Picture-perfect vision, with lovely dark pupils and irises of any color
you want. Who wouldn't want that? Every person who wears glasses or contact
lenses, or who just has that classic wish of the pilot or bird watcher - to
see just a little bit better, farther, or more clearly at night - or who,
vanity of vanities, wants slightly brighter green eyes, would be delighted
to hear that stem cell research is moving us closer to the day when eyes
might be created in the lab and implantable. Looming is the prospect of
creating human eyes (or at the very least, central components of the eye)
for the purposes of replacing, repairing, or regenerating unhealthy or
damaged tissue. Scientists are finding pieces of the puzzle, those factors
that control the generation of eyes ... If you knew all the genes, and how
to turn them on, that you needed to make an eye, you could start with very
early embryonic cells and turn on all the right genes and grow an eye in a
dish."
$5 Million Pledged For SENS Research (December 05 2007)
http://www.methusela...dsdetaildisplay
If you head over to the Methuselah Foundation, you'll see that the total
pledged for Strategies for Engineered Negligible Senescence (SENS) research
has topped $5 million dollars - all raised in the past couple of years.
That's a hefty chunk of change, considering one can set up a noteworthy,
focused research institute at a major university with just twice that
amount these days. Much of the $5 million has been donated by people just
like you or I, who know the sort of world they'd like to live in, and who
stepped up to the plate to make a difference. This is the sort of thing we
all like to see, as supporters of meaningful longevity research and a
wide-open future of longer, healthier lives. Widespread support and
significant funding for direct, vocal scientific attempts to defeat aging
are the best foot forward on the road to that future. Aging will come for
us all until we band together and do something about it. When taking
advantage of the medical technology of the 2030s, don't you want to be one
of the people who can say "we made this technology happen, we saved
billions of lives?"
More Building of Better Mice (December 04 2007)
http://www.eurekaler...o-ape120307.php
From EurekAlert!, more experimental metabolic engineering: "the research
team bred large numbers of mice, fed them a normal chow diet and followed
each mouse until its natural death. Half were genetically engineered to
make more of a protein in their muscle tissue called uncoupling protein-1.
Their littermates did not make excess uncoupling protein. In muscle tissue,
uncoupling protein-1 converts the energy from food into heat and mimics the
effects of exercise. ... Uncoupling basically means generating inefficient
metabolism ... We were a little bit disappointed because we had hoped
uncoupling in muscle would slow aging, but maximum lifespan didn't
increase. However, the odds of reaching that maximum lifespan did improve
in the uncoupled mice. ... mice with the genetic alteration were more
likely to live longer, presumably because they were able to avoid
age-related diseases. One result appeared in all of the experiments:
Decreasing body fat and inflammation in the animals by accelerating muscle
metabolism with uncoupling protein delayed death and diseases, including
atherosclerosis, diabetes, hypertension and even cancer."
Discover on Inflammation and Aging (December 04 2007)
http://discovermagaz...g/article_print
The inflammaging model is starting to percolate into the popular science
press, such as Discover: "In recent years, gerontologists have overturned
much of the conventional wisdom about getting old. Aging is not the simple
result of the passage of time. According to a provocative new view, it is
actually something our own bodies create, a side effect of the essential
inflammatory system that protects us against infectious disease. As we
fight off invaders, we inflict massive collateral damage on ourselves,
poisoning our own organs and breaking down our own tissues. We are our own
worst enemy. This paradox is transforming the way we understand aging. It
is also changing our understanding of what diseases are and where they come
from. Inflammation seems to underlie not just senescence but all the
chronic illnesses that often come along with it: diabetes, atherosclerosis,
Alzheimer's, heart attack. ... Inflammatory factors predict virtually all
bad outcomes in humans. It predicts having heart attacks, having heart
failure, becoming diabetic; predicts becoming fragile in old age; predicts
cognitive function decline, even cancer to a certain extent." Strangely,
the article fails to talk about the pivotal role of excess body fat in
chronic inflammation.
Replacing Cells Lost to Parkinson's (December 03 2007)
http://www.eurekaler...i-rtc112807.php
As noted at EureAlert!, scientists are making progress in the quality of
their technology demonstrations: "Although [domamine or DA]
cell-replacement therapy by transplantation of human fetal mesencephalic
tissue has shown promise in clinical trials, limited tissue availability
means that other sources of these cells are needed. ... [researchers] have
identified a new source for DA cells that provided marked benefit when
transplanted into mice with a [Parkinson's or PD]-like disease. ... DA
cells were derived from ventral midbrain (VM) neural stem cells/progenitors
by culturing them in the presence of a number of factors - FGF2, sonic
hedgehog, and FGF8 - and engineering them to express Wnt5a. This protocol
generated 10-fold more DA cells than did conventional FGF2 treatment.
Further analysis revealed that these cells initiated substantial cellular
and functional recovery when transplanted into mice with PD-like disease.
Importantly, the mice did not develop tumors, a potential risk that has
precluded the clinical development of embryonic stem cells as a source of
DA cells." Tissue engineering is a fearsomely complex business, but great
improvement in quality and cost is inevitable.
Aubrey de Grey at Cato Unbound (December 03 2007)
http://www.cato-unbo...g-to-the-death/
An article by Aubrey de Grey appears at Cato Unbound, hammering on the
basics: "When thoroughly cornered on the question of whether the defeat of
aging would be a good thing, [apologists for aging] generally turn as a
last resort to the cry 'Okay, but first things first!' The fact that
efforts to postpone human aging will definitely not bear much fruit for at
least a few decades is held as a reason to deprioritize such efforts in
favor of combating already preventable problems. It is trivial to expose
the ethical bankruptcy of this position. We lock people up for the same
amount of time if they kill people with a gun or with a booby-trap bomb,
even though the interval between the murderer's action and the victim’s
death differs by several orders of magnitude in the two cases. The same
irrelevance of that interval applies to the saving of lives, since action
and inaction are morally indistinguishable. We are close enough today to
defeating aging that serendipity does not define the timeframe: the sooner
and harder we try to do it, the sooner we'll succeed. Thus, our inaction
today costs lives - lots of lives."
______________________________
If you have comments for us, please do send e-mail to
newsletter@longevitymeme.org.
December 10 2007
The Longevity Meme Newsletter is a weekly e-mail containing news, opinions
and happenings for people interested in healthy life extension: making use
of diet, lifestyle choices, technology and proven medical advances to live
healthy, longer lives. To subscribe or unsubscribe from the Longevity Meme
Newsletter, please visit http://www.longevity...org/newsletter/
______________________________
CONTENTS
- Short Videos by Aubrey de Grey Explaining Longevity Science
- Matching Funds Triple SENS Research Donations Until Year End
- Discussion
- Latest Healthy Life Extension Headlines
SHORT VIDEOS BY AUBREY DE GREY EXPLAINING LONGEVITY SCIENCE
You may not have seen these short introductory videos before: each briefly
explains a single concept in longevity science, starting with some of the
basic basics. They are the first in a new series of videos aimed at further
bridging the gap between an overview for the layman and scientific
publications:
http://www.fightagin...ives/001363.php
http://www.mfoundati...ename=video_faq
Online video has been a tremendously success in broadening awareness and
education for healthy life extension research, and the present state of
science. This will continue to be the case, so pick out a few from the
video FAQ page above, and forward them on to your friends.
MATCHING FUNDS TRIPLE SENS RESEARCH DONATIONS UNTIL YEAR END
Good news from the Methuselah Foundation, coming as the total pledged to
Strategies for Engineered Negligible Senescence (SENS) research passes $5
million. Donations to speed research into repairing the damage of aging and
extending the healthy human lifespan will be matched 2-to-1 until the end
of 2007, expanding your donation threefold:
http://blog.methusel...s_research.html
http://blog.methusel...n_matching.html
"You might recall in 2006 that Peter Thiel made a 3 million dollar Matching
Challenge to SENS Research, where he matches 50% of donations to research
until the end of 2009. Well, our performance and Thiel's example have
prompted a supporter and Three Hundred Member, Michael Cooper, to join
Peter Thiel. He is offering a $25,000 Matching Challenge of his own until
the end of this month.
"Thanks to these generous supporters, the donations are matched
cumulatively. That is, a $1 donation to research is first matched with $1
from Cooper. This $2 is then matched with a further $1 by Thiel's Matching
Challenge to bring the total donation to $3.
"In this way a donation of $100 is TRIPLED to $300 ...but this multiplier
only lasts until the end of this month. Perhaps you might be interested in
helping Cooper and Thiel turn their generous matching challenge dollars
into research?"
You can find out more on how the Foundation presently employs donations to
SENS research by following the link below:
http://www.methusela...gename=research
DISCUSSION
The highlights and headlines from the past week follow below. If you have
comments for us, please do send e-mail to newsletter@longevitymeme.org
Remember - if you like this newsletter, the chances are that your friends
will find it useful too. Forward it on, or post a copy to your favorite
online communities. Encourage the people you know to pitch in and make a
difference to the future of health and longevity!
Reason
reason@longevitymeme.org
______________________________
LATEST HEALTHY LIFE EXTENSION HEADLINES
To view commentary on the latest news headlines complete with links and
references, please visit the daily news section of the Longevity Meme:
http://www.longevitymeme.org/news/
Do We Need Death? (December 07 2007)
http://www.cato-unbo...-we-need-death/
Back to Cato Unbound we go, for Ronald Bailey's contribution to the present
debate. "Schaub offers no data nor even a plausible line of reasoning that
longer healthy lives will result in 'social sclerosis.' In fact, the
available evidence cuts the other way. Social and technological innovation
has been most rapid in those societies with the highest average life
expectancies. Yale University economist William Nordhaus estimates that the
huge increase in average life expectancy in the United States, from
forty-seven years in 1900 to seventy-seven years today, has been
responsible for about 40 percent of the increase in our standard of living.
... the highest expression of human nature and dignity is to strive to
overcome the limitations imposed on us by our genes, our evolution and our
environment. Future generations will look back at the beginning of the 21st
century with astonishment that some well-meaning and intelligent people
actually wanted to stop biomedical research just to protect their cramped
and limited vision of human nature. Our descendants will look back, I
predict, and thank us for making their world of longer, healthier lives
possible." Just so. Do we need death? "No. Next question."
Lamin A As a Biomarker of Aging in Skin (December 07 2007)
http://dx.doi.org/10...al.pone.0001269
More on the nuts and bolts of lamin A, the root of accelerated aging in
progeria (HGPS), from PLoS One: "90% of HGPS cases carry the [lamin A
mutation], activating a splice donor site that results in production of a
dominant negative form of lamin A protein, denoted progerin. Screening 150
skin biopsies from unaffected individuals (newborn to 97 years) showed that
a similar splicing event occurs in vivo at a low level in the skin at all
ages. While progerin mRNA remains low, the protein accumulates in the skin
with age in a subset of dermal fibroblasts and in a few terminally
differentiated keratinocytes. Progerin-positive fibroblasts localize near
the basement membrane and in the papillary dermis of young adult skin;
however, their numbers increase and their distribution reaches the deep
reticular dermis in elderly skin. Our findings demonstrate that progerin
expression is a biomarker of normal cellular aging and may potentially be
linked to terminal differentiation and senescence in elderly individuals."
This enlarges upon earlier work demonstrating the presence of lamin A
defects in normal individuals.
From the Camp of Mild-Mannered Deathism (December 06 2007)
http://www.cato-unbo...geless-mortals/
The first of the response essays to Aubrey de Grey's piece at Cato Unbound
epitomizes mild-mannered deathism; the instinct that any radical change to
the human condition brought on by healthy life extension must be bad. If I
had to pick out the one thing the archetypical human hates and fears above
all else, it'd be the prospect of change - and that always shows through in
discussions of radically increasing the healthy human life span. "Even
without the threat of vastly extended tyranny, a nation of ageless
individuals could well produce a sclerotic society, petrified in its ways
and views. Senescence escorts us, more or less gracefully, off the stage,
making room for fresh generations. The aging of individuals may be one
condition for societal renascence. Fascinatingly, longevity research in
animals suggests that one cost of age-retardation is sterility or decreased
fertility. If there are trade-offs between long life and new life, then the
quest for individual immortality may pose dangers for the well-being of the
human collective, whether at the level of the family, the nation, or the
species. While frailty and finitude don't seem such good things, they may
be inextricably entwined with other very good things that we would not want
to sacrifice." It is sad that so many people would choose the stasis of the
now - and death and suffering without end, over and over - rather than
immensely positive change and opportunity through longevity science.
Talking nonsense about petrified, unchanging ageless societies is
projection, methinks.
Stem Cells Point the Way (December 06 2007)
http://www.scienceda...71205140112.htm
If we knew exactly how stem cells, progenitor cells and other developing
cells can produce regeneration without generating new tissue themselves,
then we wouldn't need the cells. An example of that truism in action is
provided by ScienceDaily: "a protein called connexin43, expressed by the
transplanted embryonic heart cells, improved electrical connections to
other heart cells. The researchers showed that the improved connections
helped activate the transplanted cells deep within the damaged section of
the heart tissue. The technique reversed the risk of developing ventricular
arrhythmias after a heart attack ... In the past, scientists have
transplanted a variety of cell types into failing hearts with modest
improvement of function, although transplanting skeletal muscle cells made
things worse and led to more arrhythmias. Surprisingly, when [researchers]
transplanted embryonic cardiac cells, the hearts' electrical stability and
function returned to normal. ... we were able to see how cells used in
therapy are working with other cells in a complex organ within a living
animal, establishing the mechanism of the therapeutic effect ...
[researchers] engineered skeletal muscle to express connexin43 and achieved
the same restorative results as they did with the embryonic heart cells."
Viewing a Future of Engineered Eyes (December 05 2007)
http://www.the-scien.../display/53894/
The Scientist looks at the future of tissue engineered, perfect eyes:
"Picture-perfect vision, with lovely dark pupils and irises of any color
you want. Who wouldn't want that? Every person who wears glasses or contact
lenses, or who just has that classic wish of the pilot or bird watcher - to
see just a little bit better, farther, or more clearly at night - or who,
vanity of vanities, wants slightly brighter green eyes, would be delighted
to hear that stem cell research is moving us closer to the day when eyes
might be created in the lab and implantable. Looming is the prospect of
creating human eyes (or at the very least, central components of the eye)
for the purposes of replacing, repairing, or regenerating unhealthy or
damaged tissue. Scientists are finding pieces of the puzzle, those factors
that control the generation of eyes ... If you knew all the genes, and how
to turn them on, that you needed to make an eye, you could start with very
early embryonic cells and turn on all the right genes and grow an eye in a
dish."
$5 Million Pledged For SENS Research (December 05 2007)
http://www.methusela...dsdetaildisplay
If you head over to the Methuselah Foundation, you'll see that the total
pledged for Strategies for Engineered Negligible Senescence (SENS) research
has topped $5 million dollars - all raised in the past couple of years.
That's a hefty chunk of change, considering one can set up a noteworthy,
focused research institute at a major university with just twice that
amount these days. Much of the $5 million has been donated by people just
like you or I, who know the sort of world they'd like to live in, and who
stepped up to the plate to make a difference. This is the sort of thing we
all like to see, as supporters of meaningful longevity research and a
wide-open future of longer, healthier lives. Widespread support and
significant funding for direct, vocal scientific attempts to defeat aging
are the best foot forward on the road to that future. Aging will come for
us all until we band together and do something about it. When taking
advantage of the medical technology of the 2030s, don't you want to be one
of the people who can say "we made this technology happen, we saved
billions of lives?"
More Building of Better Mice (December 04 2007)
http://www.eurekaler...o-ape120307.php
From EurekAlert!, more experimental metabolic engineering: "the research
team bred large numbers of mice, fed them a normal chow diet and followed
each mouse until its natural death. Half were genetically engineered to
make more of a protein in their muscle tissue called uncoupling protein-1.
Their littermates did not make excess uncoupling protein. In muscle tissue,
uncoupling protein-1 converts the energy from food into heat and mimics the
effects of exercise. ... Uncoupling basically means generating inefficient
metabolism ... We were a little bit disappointed because we had hoped
uncoupling in muscle would slow aging, but maximum lifespan didn't
increase. However, the odds of reaching that maximum lifespan did improve
in the uncoupled mice. ... mice with the genetic alteration were more
likely to live longer, presumably because they were able to avoid
age-related diseases. One result appeared in all of the experiments:
Decreasing body fat and inflammation in the animals by accelerating muscle
metabolism with uncoupling protein delayed death and diseases, including
atherosclerosis, diabetes, hypertension and even cancer."
Discover on Inflammation and Aging (December 04 2007)
http://discovermagaz...g/article_print
The inflammaging model is starting to percolate into the popular science
press, such as Discover: "In recent years, gerontologists have overturned
much of the conventional wisdom about getting old. Aging is not the simple
result of the passage of time. According to a provocative new view, it is
actually something our own bodies create, a side effect of the essential
inflammatory system that protects us against infectious disease. As we
fight off invaders, we inflict massive collateral damage on ourselves,
poisoning our own organs and breaking down our own tissues. We are our own
worst enemy. This paradox is transforming the way we understand aging. It
is also changing our understanding of what diseases are and where they come
from. Inflammation seems to underlie not just senescence but all the
chronic illnesses that often come along with it: diabetes, atherosclerosis,
Alzheimer's, heart attack. ... Inflammatory factors predict virtually all
bad outcomes in humans. It predicts having heart attacks, having heart
failure, becoming diabetic; predicts becoming fragile in old age; predicts
cognitive function decline, even cancer to a certain extent." Strangely,
the article fails to talk about the pivotal role of excess body fat in
chronic inflammation.
Replacing Cells Lost to Parkinson's (December 03 2007)
http://www.eurekaler...i-rtc112807.php
As noted at EureAlert!, scientists are making progress in the quality of
their technology demonstrations: "Although [domamine or DA]
cell-replacement therapy by transplantation of human fetal mesencephalic
tissue has shown promise in clinical trials, limited tissue availability
means that other sources of these cells are needed. ... [researchers] have
identified a new source for DA cells that provided marked benefit when
transplanted into mice with a [Parkinson's or PD]-like disease. ... DA
cells were derived from ventral midbrain (VM) neural stem cells/progenitors
by culturing them in the presence of a number of factors - FGF2, sonic
hedgehog, and FGF8 - and engineering them to express Wnt5a. This protocol
generated 10-fold more DA cells than did conventional FGF2 treatment.
Further analysis revealed that these cells initiated substantial cellular
and functional recovery when transplanted into mice with PD-like disease.
Importantly, the mice did not develop tumors, a potential risk that has
precluded the clinical development of embryonic stem cells as a source of
DA cells." Tissue engineering is a fearsomely complex business, but great
improvement in quality and cost is inevitable.
Aubrey de Grey at Cato Unbound (December 03 2007)
http://www.cato-unbo...g-to-the-death/
An article by Aubrey de Grey appears at Cato Unbound, hammering on the
basics: "When thoroughly cornered on the question of whether the defeat of
aging would be a good thing, [apologists for aging] generally turn as a
last resort to the cry 'Okay, but first things first!' The fact that
efforts to postpone human aging will definitely not bear much fruit for at
least a few decades is held as a reason to deprioritize such efforts in
favor of combating already preventable problems. It is trivial to expose
the ethical bankruptcy of this position. We lock people up for the same
amount of time if they kill people with a gun or with a booby-trap bomb,
even though the interval between the murderer's action and the victim’s
death differs by several orders of magnitude in the two cases. The same
irrelevance of that interval applies to the saving of lives, since action
and inaction are morally indistinguishable. We are close enough today to
defeating aging that serendipity does not define the timeframe: the sooner
and harder we try to do it, the sooner we'll succeed. Thus, our inaction
today costs lives - lots of lives."
______________________________
If you have comments for us, please do send e-mail to
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