You’ve seen it happen. Your favorite team or athlete builds a comfortable lead, turns conservative and blows the game. Or how about a business, or an industry, or even and entire country, that gets away from its aggressive innovative roots, only to see an upstart replace them at the top? This is why short-term survival mentalities often lead to long-term death. And closer to home, and entrepreneur or new company that tries to be another “me too” and never achieves greatness.
Finally, how about each individual who plays it too close to the vest, leads a comfortable life, but at the end regrets how his or her career, marriage or children turn out because they didn’t dare to take a chance, dig in their heels, or be aggressive from time-to-time?
You and I could discuss examples endlessly, so let’s narrow our focus.
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I assume you have more than a passing interest in health and longevity, or you wouldn’t be reading this letter. Accepting that assumption, let’s say you understand exactly why we can expect age-reversal capabilities toward the end of your projected lifespan. Then factor in, if the actuarial tables hold up, half the people your age will die before then, and half may have a chance at open-ended youth.
Then let’s allow room for error. Assume we miss our target by ten years.
If we do, and if our target is toward the end of your projected lifespan, that means instead of half the people your age missing the extreme longevity opportunity, well over 90% will miss it. Maybe 99% if you are on the bubble now. Even at younger ages, your odds drop dramatically as you age, since mortality rates increase with each passing year.
So if you’re not doing everything in your power now to reach what has been our unachievable dream for thousands of years, but which is now finally within our grasp, then not playing to win could, and probably will be the difference between your life and death.
I have lots of heroes. One such hero is Dr. Bill Andrews. Here’s a guy who plays to win. Not just in his personal life, but in his career as well. His is an extraordinary story. He had a cushy job as a chief scientist, working for a firm that lost its vision, and started playing not to lose. Bill would have noting of it, so he struck out on his own to achieve his dream of curing aging. You’ll be amazed at what he has accomplished, both personally and professionally.
Click on this link now.
Meet Bill Andrews: The Man who would be Immortal
Long Life,
David Kekich
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LATEST HEALTHY LIFE EXTENSION HEADLINES
SPURRING NEURAL GROWTH IMPROVES MEMORY (July 09 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4804
Via EurekAlert: “Scientists have discovered a compound that restores the capacity to form new memories in aging rats, likely by improving the survival of newborn neurons in the brain’s memory hub. This neuroprotective compound, called P7C3, holds special promise because of its medication-friendly properties. It can be taken orally, crosses the blood-brain barrier with long-lasting effects, and is safely tolerated by mice during many stages of development. Physical activity, social, or other enriching experiences promote neurogenesis – the birth and maturation of new neurons. This growth takes place in the dentate gyrus, a key area of the brain’s memory hub, the hippocampus. But even in the normal adult brain, most of these newborn neurons die during the month it takes to develop and get wired into brain circuitry. To survive, the cells must run a gauntlet of challenges. Newborn hippocampus neurons fare much worse in aging-related disorders like Alzheimer’s, marked by runaway cell death. In hopes of finding compounds that might protect such vulnerable neurons during this process, [researchers] tested more than 1000 small molecules in living mice. To find out if P7C3 could similarly stem aging-associated neuronal death and cognitive decline, the researchers gave the compound to aged rats. Rodents treated with P7C3 for two months significantly outperformed their placebo-treated peers on a water maze task, a standard assay of hippocampus-dependent learning. This was traced to a threefold higher-than-normal level of newborn neurons in the dentate gyrus of the treated animals.”
SHORTER TELOMERES, GREATER CANCER RISK (July 08 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4803
News of a study linking telomere length and cancer risk, but it’s still the case that the relationship could be indirect, such as both sides of the correlation being based on levels of biochemical damage. For example, it might reflect the state of mitochondrial biochemistry in a person: “A new study suggests that shorter length of leukocyte telomeres – chromosome markers of biological aging – are associated with an increased risk of cancer and death from cancer. Telomeres are a structure at the end of a chromosome involved in the replication and stability of the chromosome. Genetic factors and environmental stressors can shorten the length of the telomere, and telomere length has been considered to be an emerging marker of biological age. Some research has suggested that short telomeres and chromosomal instability contribute to malignant cell transformation. [Researchers] conducted a study to assess the association between leukocyte telomere length and risk of both new-onset cancer and cancer death. Leukocyte telomere length was [measured] in 787 participants, free of cancer in 1995. Analysis indicated that short telomere length at the beginning of the study was associated with new cancer independently of standard cancer risk factors. Compared with participants in the longest telomere length group, participants in the middle length group had about twice the risk of cancer, and those in the shortest length group had approximately three times the risk. Cancer incidence rates were inversely related to telomere length, with participants in the group with the shortest telomere length having the highest rate of cancer.”
GENERAL IMPROVEMENT IN CANCER MORTALITY RATES (July 08 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4802
Much like the slow and steady lengthening of life expectancy, there is a general improvement in cancer treatment outcomes thanks to progress across the board in modern medicine: “The continued drop in overall cancer mortality rates over the last 20 years has averted more than three-quarters of a million (767,000) cancer deaths according to a new report from the American Cancer Society. The American Cancer Society’s annual Cancer Statistics article reports that the overall death rate from cancer in the United States in 2007 was 178.4 per 100,000, a relative decrease of 1.3 percent from 2006, when the rate was 180.7 per 100,000, continuing a trend that began in 1991 for men and 1992 for women. In that time, mortality rates have decreased by 21 percent among men and by 12 percent among women, due primarily to declines in smoking, better treatments, and earlier detection of cancer. Cancer incidence rates decreased in men 1.3 percent per year from 2000 to 2006 and in women 0.5 percent per year from 1998 to 2006. Death rates for all cancer sites combined decreased 2 percent per year from 2001 to 2006 in males and 1.5 percent per year from 2002 to
2006 in females.”
ON MITOHORMESIS (July 07 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4801
A little stress improves our biochemistry: “Recent evidence suggests that calorie restriction and specifically reduced glucose metabolism induces mitochondrial metabolism to extend life span in various model organisms, including Saccharomyces cerevisiae, Drosophila melanogaster, Caenorhabditis elegans and possibly mice. In conflict with Harman’s free radical theory of aging (FRTA), these effects may be due to increased formation of reactive oxygen species (ROS) within the mitochondria causing an adaptive response that culminates in subsequently increased stress resistance assumed to ultimately cause a long-term reduction of oxidative stress. This type of retrograde response has been named mitochondrial hormesis or mitohormesis, and may in addition be applicable to the health-promoting effects of physical exercise in humans and, hypothetically, impaired insulin/IGF-1-signaling in model organisms. Consistently, abrogation of this mitochondrial ROS signal by antioxidants impairs the lifespan-extending and health-promoting capabilities of glucose restriction and physical exercise, respectively. In summary, the findings discussed in this review indicate that ROS are essential signaling molecules which are required to promote health and longevity. Hence, the concept of mitohormesis provides a common mechanistic denominator for the physiological effects of physical exercise, reduced calorie uptake, glucose restriction, and possibly beyond.”
THE SIMPLE ANSWER THAT NO-ONE WANTS TO HEAR (July 05 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4797
There’s nothing you can do right now that will have a greater immediate effect on your life expectancy than exercise and calorie restriction. The best thing you can do for future improvement is to help researchers raise funds to develop repair technologies for human aging. But no-one wants to hear that. Everyone wants a silver bullet now, and it doesn’t exist: “Friends occasionally ask me how they might best live healthy, longer. They inquire because I went to medical school, work in biotech, and focus professionally on developing drugs to treat diseases of aging by targeting aging genes. My response seems to surprise them, because it does not center on pharmaceutical products. The current answer on how to increase healthy human lifespan is simple: ‘Eat less, and exercise more.’ Modern medicine has discovered an impressive number of lifesaving new drugs for devastating diseases such as cancer, diabetes, heart disease, and infectious diseases. Nevertheless, for most of us, active lifestyles and less food will have a more profound effect than taking more medicines. Hard as it is, we should walk, run, and bike more, and reduce our food intake. The best way we can increase our chances to live healthy, longer is simple: eat less and exercise more.” Learn How to Get a Six Pack
