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posted on January 3rd, 2012

Dear Future Centenarian,

Historically, one of the great frustrations of all time is convincing others, and the world, to adopt new ideas which we are convinced will improve humanity. 

Humans tend to cling to established beliefs, so when radically new ideas are introduced, they are usually ignored at best or ridiculed at worst. This can be very frustrating, and even defeating, for those who champion new ideas.

Extreme life extension, although a dream for thousands of years, was only recently put forth as a workable solution to aging, decay and then death. An enticing concept, yes, but still fantasy to most people. In order to convince others, we need to teach them why the deeply ingrained deathist meme is antiquated.

But how do we do that? Educating the masses is not in the cards. It’s much too big a job, and there’s too much resistance. If we could demonstrate the concept by reversing the aging in an animal for example, people would not need to know how it was done. Most would just want to be led to the nearest rejuvenation center.

But we don’t have that demonstration… at least not yet. In order to do it, we need to convince people that it can be done in order to get them to support the research.

So this brings us back to square number one. Or does it?

Fortunately, no. There’s an answer.

A recent simulation of the way in which ideas spread through society reinforces what advocates already know: you don't need to persuade everyone. If only a minority, even just one in ten, support your vision, then you can still achieve the end goal. See the supporting article at:

http://www.fightaging.org/archives/2011/07/we-dont-need-to-persuade-everyone.php

Scientists at Rensselaer Polytechnic Institute have found that when just 10 percent of the population holds an unshakable belief, their belief will always be adopted by the majority of the society.

The scientists, who are members of the Social Cognitive Networks Academic Research Center (SCNARC) at Rensselaer, used computational and analytical methods to discover the tipping point where a minority belief becomes the majority opinion.

Considering this, it doesn't do to become discouraged when you are rejected in an attempt to persuade a friend of the merits of supporting extreme life extension, or to give more thought to longevity science. It wouldn't matter if a majority of your friends rejected these ideas. So long as a solid minority of supporters can grow to that one in ten estimate, most of the world will eventually follow along.

We don't need to get everyone on our side. Even those who don’t support us will eventually benefit.

Long Life,
David Kekich
____________________________

LATEST HEADLINES FROM FIGHT AGING!

OBESITY, AGING, FAT TISSUE, AND TELOMERES Friday, December 30, 2011 http://www.fightaging.org/archives/2011/12/obesity-aging-fat-tissue-and-telomeres.php
Pulling together the connections in a review paper: "Obesity is a condition in which excess or abnormal fat accumulation may present with adverse effects on health and decreased life expectancy. Increased body weight and adipose tissue accumulation amplifies the risk of developing various age-related diseases, such as cardiovascular disease, Type 2 Diabetes Mellitus, musculoskeletal disorders, respiratory diseases and certain types of cancer. This imbalance in body composition and body weight is now recognized as a state of increased oxidative stress and inflammation for the organism. Increasing oxidative stress and inflammation affect telomeres.

Telomeres are specialized DNA-protein structures found at the ends of eukaryotic chromosomes and serve as markers of biological aging rate. They also play a critical role in maintaining genomic integrity and are involved in age-related metabolic dysfunction. Erosion of telomeres is hazardous to healthy cells, as it is a known mechanism of premature cellular senescence and loss of longevity. The association of telomeres and oxidative stress is evident in cultured somatic cells in vitro, where oxidative stress enhances the process of erosion with each cycle of replication. Shorter telomeres have been associated with increasing body mass index, increased adiposity, and more recently with increasing waist to hip ratio and visceral excess fat accumulation. Furthermore, many of the metabolic imbalances of obesity (e.g. glycemic, lipidemic, etc.) give rise to organ dysfunction in a way that resembles the accelerated aging process."

INCREASED LONGEVITY VERSUS REDUCED REPRODUCTION IN HUMANS? Thursday, December 29, 2011 http://www.fightaging.org/archives/2011/12/increased-longevity-versus-reduced-reproduction-in-humans.php
Human studies may reveal a correlation between longevity and lower rates of reproduction: "A number of leading theories of aging, namely The Antagonistic Pleiotropy Theory (Williams, 1957), The Disposable Soma Theory (Kirkwood, 1977) and most recently The Reproductive-Cell Cycle Theory (Bowen and Atwood, 2004, 2010) suggest a tradeoff between longevity and reproduction.

While there has been an abundance of data linking longevity with reduced fertility in lower life forms, human data have been conflicting. We assessed this tradeoff in a cohort of genetically and socially homogenous Ashkenazi Jewish centenarians (average age ~100 years). As compared with an Ashkenazi cohort without exceptional longevity, our centenarians had fewer children (2.01 vs 2.53, p<0.0001), were older at first childbirth (28.0 vs 25.6, p<0.0001), and at last childbirth (32.4 vs 30.3, p<0.0001). The smaller number of children was observed for male and female centenarians alike. The lower number of children in both genders together with the pattern of delayed reproductive maturity is suggestive of constitutional factors that might enhance human life span at the expense of reduced reproductive ability."

OXIDATIVE STRESS AND GENDER LONGEVITY DIFFERENCES Wednesday, December 28, 2011 http://www.fightaging.org/archives/2011/12/oxidative-stress-and-gender-longevity-differences.php
Here is another of the many theories aiming to explain why women live longer than men: "One of the most significant achievements of the twentieth century is the increase in human lifespan. In any period studied, females live longer than males. We showed that mitochondrial oxidative stress is higher in males than females and that the higher levels of estrogens in females protect them against ageing, by up-regulating the expression of antioxidant, longevity-related genes.

The chemical structure of estradiol confers antioxidant properties to the molecule. However, the low concentration of estrogens in females makes it unlikely that they exhibit significant antioxidant capacity in the organism. Therefore we studied the mechanisms enabling estradiol to be antioxidant at physiological levels. Our results show that physiological concentrations of estrogens activate estrogen receptors and the MAPK and NFKB pathway. Activation of NFkB by estrogens subsequently activates the expression of Mn-SOD and GPx. Moreover, we have demonstrated that genistein, the most abundant phytoestrogen in soya, reproduces the antioxidant effect of estradiol at nutritionally relevant concentrations by the same mechanism. We conclude that estrogens and phytoestrogens up-regulate expression of antioxidant enzymes via the estrogen receptor and MAPK activation, which in turn activate the NFkB signalling pathway, resulting in the up-regulation of the expression of longevity-related genes."

MANIPULATING THE IMMUNE SYSTEM TO SABOTAGE AUTOIMMUNITY Tuesday, December 27, 2011 http://www.fightaging.org/archives/2011/12/manipulating-the-immune-system-to-sabotage-autoimmunity.php
An immunotherapy approach is turned to treating autoimmune conditions: scientists have "turned the tables on an autoimmune disease. In such diseases, including Crohn's and rheumatoid arthritis, the immune system mistakenly attacks the body's tissues. But the scientists managed to trick the immune systems of mice into targeting one of the body's players in autoimmune processes, an enzyme known as MMP9. [Researchers] have spent years looking for ways to home in on and block members of the matrix metalloproteinase (MMP) enzyme family. These proteins cut through such support materials in our bodies as collagen, which makes them crucial for cellular mobilization, proliferation and wound healing, among other things. But when some members of the family, especially MMP9, get out of control, they can aid and abet autoimmune disease and cancer metastasis. Blocking these proteins might lead to effective treatments for a number of diseases.

Rather than attempting to design a synthetic molecule to directly attack MMPs [an] MMP immunization would trick the body into creating antibodies that block the enzyme at its active site. [Researchers] created an artificial version of the metal zinc-histidine complex at the heart of the MMP9 active site. They then injected these small, synthetic molecules into mice and afterward checked the mice's blood for signs of immune activity against the MMPs. When they had induced an inflammatory condition that mimics Crohn's disease in mice, the symptoms were prevented when mice were treated with [the new synthetic molecules]. We are excited not only by the potential of this method to treat Crohn's, [but] by the potential of using this approach to explore novel treatments for many other diseases."

WORKING ON THE FOUNDATION OF A THERAPY FOR ANOSMIA Monday, December 26, 2011 http://www.fightaging.org/archives/2011/12/working-on-the-foundation-of-a-therapy-for-anosmia.php
Significant loss of the senses of smell and taste, a condition known as anosmia, can occur with aging. Here, researchers investigate stem cell related mechanisms; this may be another case of functionality fading because the stem cell population necessary to support it is shutting down with advancing age: "Experts estimate that about 2 percent of the U.S. population suffers from [a] lack of smell known as anosmia. And research by neuroscientists [provides] hope of new therapies for those who have lost their sense of smell, whether due to aging, trauma or a viral infection.

In the study published this month [the researchers found] a genetic trigger responsible for renewing smell sensors in the nose. That gene, known as p63, tells olfactory stem cells whether to replace themselves or to change into different types of cells. Under normal circumstances [there] is a balance between the two outcomes. But when p63 is absent, the cells only turn into other types of mature cells, which [could] eventually lead to the complete depletion of olfactory cells. One reason for the onset of anosmia could be that the stem cells age and are less able to regenerate, or they are just depleted. Finding a way to promote stem cell renewal could help maintain sensory functions, such as the sense of smell."

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