What Ants Taught Me About Longevity

Healthy Life Extension

Funding Aging Research

What Ants Taught Me About Longevity


posted on August 23, 2011

Dear Future Centenarian,

I have ants in my kitchen.

At first, it wasn™t so bad. A few ants here and there scavenging for food. So I got some ant traps, which my assistant promptly threw out. She insisted the ants came inside because of the rainy season and that they would scurry away as soon as the sun shined regularly.

Phew, what a relief! What a simple solution to an infestation. Just stick your head in the sand, rely on nature, and your problems will disappear.

But the rain gave way to warm, dry sunny Southern California weather¦ and the ants didn™t pay attention. They found a home, decided to stay and to thrive. And thrive they did.

What started as a minor nuisance recently grew to a serious competitor for my food supply. So I decided to call an exterminator.

But no. My health-conscious nutritionist assistant insisted she could keep them at bay simply by keeping the sink clean. And for a short time, it worked, sort of. They never really disappeared. There were just fewer of them”at least from time-to-time. But then they started showing up in ever increasing numbers. Eventually, the smallest crumb would attract thousands.

Another plea to my assistant to finally get rid of them for good was answered by more symptom fighting. The dainty flower was concerned about the toxic effects the exterminator would have on her, even insisting she might end up in the hospital.

So the problem escalated. One day”not terrible. The next day”the sink and counter top would be covered.

As with all symptom fighting, it™s a losing battle. Ignore the cause, and the problem eventually consumes you.

And so it is with aging.

We spend hundreds and hundreds of billions every year researching and treating the diseases related to aging. We spend a huge fortune managing those diseases¦ and aging itself, hoping to stretch lifespans just a little and to put a lid on suffering.

Where does it get us? Trillions of dollars in debt, slightly longer lifespans and huge profits for the medical establishment. Don™t you think it™s time to exterminate aging and the budget-busting healthcare crisis once and for all? It can be done, and the answer is simple.

Invest a tiny fraction of the $100 billion spent on the broken healthcare system in the US every 16 days on cure instead of care!!!

We know how to solve aging. We know how to reverse the aging process. We really do. We just need a concerted effort like the Manhattan Project and the Apollo Project. When they were launched, we knew how to build the bomb and how to land on the moon. We just needed the commitment to do it. When we got those commitments, coupled with resources¦ success!

Don™t you think saving many of the 100,000 people who die from aging EVERY DAY is worth at least as much as building a war-ending bomb or walking on the moon?

Long Life,
David Kekich

P.S. My assistant and I reached a resolution, and the exterminators are on their way.
____________________________

LATEST HEADLINES FROM FIGHT AGING!

A PROFILE OF THE HALCYON MOLECULAR FOUNDERS Friday, August 19, 2011 http://www.fightaging.org/archives/2011/08/a-profile-of-the-halcyon-molecular-founders.php
This is a UK press article on Halcyon Molecular, one of the new companies that has emerged from the pro-engineered-longevity community in recent years. You might also look back in the Fight Aging! archives for more on the views of the founders: "Even by Silicon Valley standards, the grand design drawn up by William and Michael Andregg is hugely ambitious. Halcyon Molecular, the company that the brothers founded in 2008, is developing a way to sequence the human genome - and thus unlock the deepest secrets of DNA - faster and cheaper than ever before.

William is 29, Michael just a year older, and both are college drop-outs - but given Silicon Valley's impressive track record for nurturing and funding obsessive, unconventional young innovators, their age is hardly unusual. The surprise is the long-term mission of Halcyon Molecular: to solve "the biggest challenge humans can individually face - disease and mortality", as the mission-statement poster in their office reception says. Put another way, they're supercharging the effort to map life's biological code in almost unimaginable digital detail and, by doing so, ultimately, to attempt to conquer death itself." The difference between the here and now and 20 years ago is that you declare your plans to defeat aging and age-related death and both be taken seriously and raise large sums of money for research and development, both inside and outside the scientific community. There has been a sea change in attitudes towards engineered longevity as a goal, and that is one of the reasons that significant progress will be made in the years ahead: things happen when people start earnestly working to make them happen.

AN UPDATE ON THE SENS FOUNDATION ACADEMIC INITIATIVE Thursday, August 18, 2011 http://www.fightaging.org/archives/2011/08/an-update-on-the-sens-foundation-academic-initiative.php
The SENS Foundation Academic Initiative is a long-term project aimed at helping to build the research community of tomorrow - one interested in the repair and reversal of aging, rather than a next generation that is only interested in slowing down aging a little via manipulation of metabolism, a simple repeat of today's research community. Here is an update from the Foundation: "The SENS Foundation Academic Initiative's new structure is actively in the process of being implemented, and involves a number of significant changes. Among these are the separation of the Initiative into branches, an updated membership system that allows students to become involved more easily and in more ways, the creation of volunteer committees, and the addition of outreach projects to the Initiative's activities.

There will be three branches: Research, Outreach, and Education. The Research branch will be focused on the actual accomplishment of scientific research. This research will always be done with an eye to publication, but its most important function will be to provide our students with learning experiences, to help them develop into career scientists. The Outreach branch will be focused on spreading the word about the Academic Initiative and about the SENS Foundation, while the Education branch will be focused on educating students about science and SENS. While the Academic Initiative has long helped students to complete research projects, it has not done much in the past to encourage students to be advocates of the Initiative and the SENS Foundation. This will change with the implementation of outreach projects. These will generally be simple, off-the-shelf projects that students can finish in an afternoon, such as printing fliers from a pre-made template and distributing them at their university."

PROPOSING CONCURRENT MANIPULATION OF MULTIPLE METABOLIC PATHWAYS Wednesday, August 17, 2011 http://www.fightaging.org/archives/2011/08/proposing-concurrent-manipulation-of-multiple-metabolic-pathways.php
That part of the research community focused on manipulating metabolism to slow down aging has advanced to the point of considering multiple distinct simultaneous changes to achieve the desired end result: "Modern medicine is directed towards the prevention, detection and cure of individual diseases. Yet, current medical models inadequately describe aging-associated diseases. We now know that failure in longevity pathways including oxidative stress, multisystem dysregulation, inflammation, sarcopenia, protein deposition and atherosclerosis are associated with age-related diseases. Such longevity pathways are potential targets for therapeutic intervention.

Interventions in specific pathways have been shown to ameliorate and postpone the aging phenotype by activation of multiple genes. The strategy that we propose in this paper is to apply interventions simultaneously on complementary longevity pathways to achieve a synergistic result. For instance, aging is known to attenuate the HSF1 pathway leading to production of very toxic beta-amyloid fibrils. Consequently, the FoxO pathway is activated, resulting in the formation of less toxic high molecular weight aggregates as a defense mechanism. Thus the simultaneous upregulation of the HSF1 and FoxO pathways could potentially decrease protein deposition and proteotoxicity, thereby retarding or possibly preventing the onset of neurodegenerative diseases. Modulating these two pathways may also delay the onset of other age-related pathologies including cognitive decline, cancer, diabetes and cardiovascular disease due to its multi-gene effect. "

THE COST OF INACTIVITY Wednesday, August 17, 2011 http://www.fightaging.org/archives/2011/08/the-cost-of-inactivity.php
Researchers find what looks to be a proxy measure for the degree to which a person is sedentary - but of course there might be other important correlations here, such as with wealth or intelligence: "Watching TV for an average of six hours a day could shorten the viewer's life expectancy by almost five years. The impact rivals that of other well known behavioral risk factors, such as smoking and lack of exercise, the study suggests. Sedentary behavior - as distinct from too little exercise - is associated with a higher risk of death, particularly from heart attack or stroke. Watching TV accounts for a substantial amount of sedentary activity, but its impact on life expectancy has not been assessed, say the authors. They used previously published data on the relationship between TV viewing time and death from analyses of the Australian Diabetes, Obesity and Lifestyle Study (AusDiab), as well as Australian national population and mortality figures for 2008, to construct a lifetime risk framework.

AusDiab is a national survey of a representative sample of the population, starting in 1999-2000, and involving more than 11,000 adults aged 25 or older. The authors then constructed a risk framework for the Australian population in 2008, based on the answers the survey participants had given, when quizzed about the total amount of time they had spent in the previous week watching TV or videos. These figures compare with the impact of other well known lifestyle factors on the risk of death from cardiovascular disease after the age of 50, including physical activity and obesity. For example, other research has shown that lifelong smoking is associated with the shortening of life expectancy by more than 4 years after the age of 50, with the average loss of life from one cigarette calculated to be 11 minutes - equivalent to half an hour of TV watching, according to the authors' risk framework." I applaud the researchers for finding a way to present their work that will likely get a lot of play in the media.

QUANTIFYING THE BENEFITS OF MODEST EXERCISE Tuesday, August 16, 2011 http://www.fightaging.org/archives/2011/08/quantifying-the-benefits-of-modest-exercise.php
Gaining a large fraction of the estimated maximum possible long-term benefits from exercising can be achieved with only modest levels of regular exercise according to researchers. This recent paper is representative of earlier, similar findings: "The health benefits of leisure-time physical activity are well known, but whether less exercise than the recommended 150 min a week can have life expectancy benefits is unclear. We assessed the health benefits of a range of volumes of physical activity in a Taiwanese population. In this prospective cohort study, 416,175 individuals (199,265 men and 216,910 women) participated in a standard medical screening program in Taiwan between 1996 and 2008, with an average follow-up of 8.05 years.
On the basis of the amount of weekly exercise indicated in a self-administered questionnaire, participants were placed into one of five categories of exercise volumes: inactive, or low, medium, high, or very high activity.

We calculated hazard ratios (HR) for mortality risks for every group compared with the inactive group, and calculated life expectancy for every group. Compared with individuals in the inactive group, those in the low-volume activity group, who exercised for an average of 92 min per week or 15 min a day, had a 14% reduced risk of all-cause mortality, and had a 3 year longer life expectancy. Every additional 15 min of daily exercise beyond the minimum amount of 15 min a day further reduced all-cause mortality by 4% and all-cancer mortality by 1%. These benefits were applicable to all age groups and both sexes, and to those with cardiovascular disease risks. Individuals who were inactive had a 17% increased risk of mortality compared with individuals in the low-volume group."

A BRIEF LOOK AT MITOCHONDRIA IN AGING Tuesday, August 16, 2011 http://www.fightaging.org/archives/2011/08/a-brief-look-at-mitochondria-in-aging.php
A short piece on mitochondria and their role in aging: "Despite propaganda to the contrary, aging is rarely a pleasurable experience.  A lifetime of damage to cells and tissues results in malfunction, making old age a significant risk factor for ailments such as cancers and neurologic disabilities typified by Alzheimer's disease.  As a consequence, the graying of world populations has triggered a scientific frenzy to unravel the basic processes behind aging and find ways to slow down and perhaps even prevent age-related degeneration.

Two linked ideas are at the core of our current aging theory. The first is that proteins, RNA and DNA are bombarded with and damaged by reactive oxygen species (ROS) generated during normal cellular respiration and this results in eventual decline and disease.  The second is that mitochondria are the major culprits behind aging. Micro-injection of mitochondria from 'young' cells, those which haven't divided very much, can overcome senescence in cells that are reaching the natural end of their lives and will probably, in the usual course of things, undergo programmed cell death, or apoptosis which is also largely controlled by mitochondria. Further support for the 'mitochondrial theory' of aging [comes] from studies in a range of organisms including yeast, nematode worms, flies and mice showing that by silencing certain mitochondrial genes - mitochondria have their own circular genomes - life span is extended."

CLEANING UP ENGINEERED TISSUE Monday, August 15, 2011 http://www.fightaging.org/archives/2011/08/cleaning-up-engineered-tissue.php
A lesser but still important detail in tissue engineering is given some thought: "scientists are seemingly approaching a day when they will be able to make nearly any type of tissue from human embryonic stem cells. You need nerves or pancreas, bone or skin? With the right combination of growth factors, skill and patience, a laboratory tissue culture dish promises to yield therapeutic wonders. But within these batches of newly generated cells lurks a big potential problem: Any remaining embryonic stem cells - those that haven't differentiated into the desired tissue - can go on to become dangerous tumors called teratomas when transplanted into patients. Now researchers [have] developed a way to remove these pluripotent human embryonic stem cells from their progeny before the differentiated cells are used in humans.

We've used a combination of antibodies to weed out the few undifferentiated cells that could be left in the 10 or 100 million differentiated cells that make up a therapeutic dose. The researchers studied two sets of antibodies - one commercially available and one they generated themselves - to identify which among them bound most strongly to pluripotent, but not differentiated, cells. They found one newly generated antibody that was highly specific for a previously unknown marker on undifferentiated cells that they termed stage-specific embryonic antigen-5, or SSEA-5. The cells bound by this antibody, anti-SSEA-5, expressed high levels of pluripotent-specific genes and resembled embryonic stem cells in appearance. Anti-SSEA-5 also bound strongly to the inner cell mass of an early human embryo, the group of cells from which embryonic stem cell lines are derived. Anti-SSEA-5 recognizes and binds to a cell-surface carbohydrate structure called a glycan. As the pluripotent cell differentiates, this glycan is modified to other glycan structures not recognized by the antibody."

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