LongeCity - Longevity Meme Newsletter

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.longevitymeme.org/newsletter/

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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.fightaging.org/archives/001363.php

http://www.mfoundation.org/index.php?pagename=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.methuselahfoundation.org/2007/...s_research.html

http://blog.methuselahfoundation.org/2007/...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.methuselahfoundation.org/index....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

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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-unbound.org/2007/12/07/ron...-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/10.1371/journal.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-unbound.org/2007/12/05/dia...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.sciencedaily.com/releases/2007/...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-scientist.com/article/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.methuselahfoundation.org/index....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.eurekalert.org/pub_releases/200...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://discovermagazine.com/2007/dec/can-w...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.eurekalert.org/pub_releases/200...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-unbound.org/2007/12/03/aub...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."

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If you have comments for us, please do send e-mail to

newsletter@longevitymeme.org.

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