Longevity News

Use a Monkey Claw to Get Wider Support for Longevity Research

posted on August 03, 2010

One of the reason’s lots of money is not being raised for research that could radically extend your life is, not enough people know it is possible in our lifetimes.

Why do you think that is?

One reason is, those of us who truly understand how and why we may be able to reverse aging while we are still here to take advantage of it, say something like I just did. In other words, we offer what are generally construed as far-fetched conclusions before we give our audience enough data to prepare them for and to understand our conclusions. So we lose credibility, and along with it, potential donors and investors. When that happens, progress slows down, and millions of people ultimately die prematurely.

Do you know what a monkey claw is? If you spent much time on the high seas, you probably do. You’ve seen little tiny tugboats towing huge ocean liners, right? Did you ever wonder how the sailors managed to connect those thick heavy cables to each vessel? Obviously, they didn’t just toss the cable from one boat to the other. No. What they do is tie a thin light rope to a weight, a monkey claw, and throw the monkey claw from one boat tot the other.

Then, when they are connected by a light rope, they attach a heavier rope to that one, and they may keep doing it multiple times until they get the right sized cable, depending on the size of the ship that needs to be towed.

Therein lies our lesson.

Hitting someone with a radical conclusion without leading them down the gradual path of knowledge they need to understand and accept the conclusion, is like trying to throw a one ton cable from one vessel to another.

So what you need to do is start with something they understand and agree with, and build on that. Step by step, they will get where you want them to go.

My good friend and marketing maven Joe Sugarman takes this a step farther when he educates his markets. He uses a psychological trigger that he calls “linking”. He starts by taking some familiar thing or event and links it to his product. You might link weight loss to longevity if someone is weight conscious. You might gently lead them into some genetic engineering information that is designed to cure obesity. Now that they understand some basics of genetic engineering, it’s much easier to illustrate how manipulating genes that are related to aging could extend lives.

Then you go on to gradually disclosing how science is marching toward reversing aging. Now they can relate to it, where before they couldn’t.

We all use mobile phones, right? But how many people had them twenty years ago?

One reason over 70% of the people in the world own these tiny powerful computers is because of the exponential or geometric growth of technology. Once you point this out and then link to similar tools driving aging research, people tend to understand and appreciate how and why a similar technology explosion is now taking place in biotech.

What is barely understood today will be widely applied tomorrow. But between now and then, we need to learn to communicate better in order to make age-reversal a reality in our lifetimes.

Long Life,
David Kekich

P.S. Want to see a fun anti-aging blog? Go to Ellen Wood’s site at http://growyoungguide.wordpress.com/. Ellen is the youngest 73 year old you’ll ever know. See how she does it.
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LATEST HEALTHY LIFE EXTENSION HEADLINES

HARNESSING HORMESIS (July 29 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4833
Hormesis is here examined in the context of exploiting it to slow aging: "The process of aging is accompanied by a progressive reduction of biological dynamical sophistication, resulting in an increased probability of dysfunction, illness, and death. This loss of sophistication is inherent in all aging organisms. However, it may be possible to retard the rate of loss of biological complexity [by] exploiting the multiple effects of hormesis, through a wide range of challenges including physical, mental, and biological stress. Hormesis is widely encountered in biological systems, and its effects are also seen in humans. It is possible to use hormetic strategies [to] enhance the function of repair processes in aging humans and therefore prevent age-related chronic degenerative diseases and prolong healthy lifespan. Such techniques include dietary restriction and calorie restriction mimetics, intermittent fasting, environmental enrichment, cognitive and sense stimulation, sexuality-enhancing strategies, exposure to low or to high temperatures, and other physicochemical challenges. Current research supports the general principle that any type of a hormetic dose-response phenomenon has an effect that does not depend on the type of stressor and that it can affect any biological model. Therefore, novel types of innovative, mild, repeated stress or stimulation that challenge a biological system in a dose-response manner are likely to have an effect that, properly harnessed, can be used to delay, prevent, or reverse age-related changes in humans."

CONSIDERING CRYONICS AND NEURONAL SURVIVAL (July 28 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4831
From Depressed Metabolism: "The debilitating effects of a stroke are the result of the (delayed) neuronal death that follows an ischemic insult to the brain. In cryonics, biochemical or freezing damage to cells does not necessarily produce irreversible cell death because damaged cells are stabilized by cold temperatures. As such, morphological preservation of brain cells can co-exist with loss of viability. Therefore, securing viability of brain cells is a sufficient but not a necessary condition for resuscitation of cryonics patients. Future cell repair technologies are assumed to infer the original viable state of the cells from their morphological properties. This does not mean that conventional stroke research does not have any relevance for evaluating the technical feasibility of cryonics. Extensive delays between the pronouncement of legal death and the start of cryonics procedures could alter the structural properties of cells to such a degree that meaningful resuscitation is even problematic with advanced nanomedical cell repair technologies. This is one of the reasons why Alcor complements the cryopreservation process with stabilization procedures to secure viability of the brain after pronouncement of legal death."

SOCIAL CONNECTIVITY AND MORTALITY RISK (July 28 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4830
This study crunches the numbers to show that being socially connected has an effect on life expectancy comparable to that of exercise. Why this correlation exists is still up for debate, but it is worth considering that skill at networking and possessing a large social network enable success in other aspects of life: "These findings indicate that the influence of social relationships on the risk of death are comparable with well-established risk factors for mortality such as smoking and alcohol consumption and exceed the influence of other risk factors such as physical inactivity and obesity. Furthermore, the overall effect of social relationships on mortality reported in this meta-analysis might be an underestimate, because many of the studies used simple single-item measures of social isolation rather than a complex measurement. Although further research is needed to determine exactly how social relationships can be used to reduce mortality risk, physicians, health professionals, educators, and the media should now acknowledge that social relationships influence the health outcomes of adults and should take social relationships as seriously as other risk factors that affect mortality, the researchers conclude."

EXERCISE: GOOD AT ANY AGE (July 27 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4829
Failing to exercise damages your prospects for healthy life in the future: "one in three men and one in two women over the age of 75 are not physically active at all. A recent study led by the National Institute on Aging (NIA) says this lack of exercise makes these seniors three times more likely to die sooner than their counterparts who do only light day-to-day activities. Any movement is better than no movement at all to lower your risk of death. For every 287 calories per day a senior expended, there was a 32 percent reduction in death rate over the six-year period encompassed by the study. It is well-established that exercise leads to the reduction of heart disease, cancer and diabetes, and it can preserve mental sharpness. What is significant about the current findings is that the study is the first to provide credible evidence that everyday activity might be beneficial. Researchers ask how much activity do we need, but the public approaches it by asking how little can I get away with.
Experts caution against using the study as a basis to give up exercise, a conclusion not supported by the data." A little is better than none, but more is better than a little. Rejuvenation medicine is on the far horizon, and if you want the best chance of being alive and healthy to benefit from it, you'd better take care of the health basics here and now.

LYSOSOMAL DYSFUNCTION AND ALZHEIMER'S DISEASE (July 27 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4828
Your lysosomes are recycling units, but their function slowly fails with age - meaning your cells degrade as they fill with waste and junk. More rapid and selective lysosomal failure in brain cells is implicated in a variety of neurodegenerative conditions. Here, researchers dig more deeply: "Neurodegenerative disorders, like Alzheimer's disease, are a devastating group of conditions that exact a heavy toll on patients and their families. Research over the past two decades has strongly suggested that a fundamental problem in affected nerve cells relates to accumulation of cellular 'garbage,' or proteins and other material that is too old to function properly. Thus, understanding how the neuron handles these outdated molecules is of great significance. Here we find that upregulation of one such cellular degrading pathway, the lysosome, can have significant deleterious effects to the neuron. We specifically show that expanding the lysosomal compartment can markedly increase production of a very toxic form of tau, a protein strongly implicated in neuronal dysfunction and death in Alzheimer's disease and related disorders. Our findings have important implications for the development of neurodegenerative disease therapies that seek to manipulate the lysosome and the proteins within the lysosome." Therapies that can repair failing lysosomes may have general application to rejuvenation medicine - so the more groups working on that, the better.

MDR PROTEINS AND CELLULAR LONGEVITY (July 26 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4826

An interesting study that provides another view of the relationship between accumulating damage, repair systems, and life span in cells: "Yeast cells, much like our own cells, have a finite ability to reproduce themselves. A 'mother' cell can only produce 20-30 'daughters' before it loses the ability to replicate and dies. Multidrug resistance (MDR) proteins are best known for helping cancer cells expel anticancer drugs - hence their name - but they also ferry compounds in and out of normal cells. [Researchers] found that yeast lacking certain MDR proteins have a shorter reproductive lifespan; they produce fewer daughter cells. Yeast engineered to contain more of these pumps, however, can produce more daughters. During division, the mother conserves damaged proteins and other cellular components that could prove harmful to the bud. Indeed, some research groups have posited that the mother's finite reproductive capability is the result of accumulating these damaged and toxic compounds. Yeast division also results in an unequal distribution of MDR proteins. The mother cell retains the original MDR proteins while the bud gets young, newly formed MDR proteins. Because the mother's supply is never replenished, she has to rely on the pool of MDR proteins that she's born with. Over time these proteins decay. Some lose only part of their function; others may stop working altogether."

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