Aging Stealing Our Extended Lives

Reverse Aging Research

Funding Aging Research

Aging is Slowly Stealing Our Lives


posted on November 17, 2008

You and I are both aware that aging is slowly stealing our health, our vigor and our lives. Yet we function without a sense of urgency to do something about aging. Why? Because we™re bombarded with our personal and career responsibilities and daily distractions. And those squeaky wheels are what get our attention. This is totally normal and logical. We have to take care of our families, get our haircuts and pay attention to endless details. Who has time to really make a commitment to being proactive when it comes to something as abstract as age-reversal?

That™s the way I used to think. But taking paths of least resistance normally leads us down reactive paths. In other words, we usually let outside forces control our lives. It isn™t until we™re faced with a crisis that those forces take a backseat to focusing on something that may have been avoided in the first place. Sometimes, that crisis means life or death.

This really hit home when I just found out a close and loved associate was diagnosed with one of the deadliest forms of cancer. What™s even more tragic is he™s an active life extension researcher. That™s the worst of ironies.

I am saddened to report that Dr. Chris Heward, one of the original participants of MaxLife™s first international scientific brainstorm sessions to reverse aging, is fighting an uphill battle for his life. Chris is Director of the Kronos Science Laboratories of Phoenix, AZ. He has been diagnosed with terminal, Stage-IV Esophageal Cancer.  The cancer has metastasized to several other organs, and consequently his condition has a poor prognosis (50% mortality in 90 days and about 99% in a year). 

Since surgery is no longer a realistic option, Chris has proposed to undergo an experimental but very promising immunotherapy treatment in Boca Raton, FL.  However, this treatment requires blood donors less than 30 years old with "A" or "O" positive or negative blood types and no prior history of cancer in their families. If you are in”or if you know anyone in this category who would be willing to donate several units of blood to retrieve the granulocyte cells, please get in touch with me as soon as possible. Not only could this experimental treatment save Chris, but it could lead to a universal cure for many types of cancer. Here™s an opportunity to contribute to a great cause that could ultimately save many lives by making a simple referral.

Thank you in advance for your attention to this critical matter.
________________________________________

LATEST HEALTHY LIFE EXTENSION HEADLINES

Researchers on Aging (November 14 2008)  http://www.mcclatchydc.com/226/story/55835.html
An article of quotes from various noted aging reseachers: "Aging is caused by the gradual, lifelong accumulation of a wide variety of molecular and cellular damage. The free radical theory is the most widely accepted theory of aging. But the idea that aging is caused by one thing is naive. One general theory can never fit all. Clearly, it's the combination of genes that your parents dealt you and the lifestyle choices you make and the environmental toxins one is exposed to. One need only count the number of ways a car will fail to start to appreciate that aging can be caused by a large number of problems. Like any machine, it's going to wear out. About 25 percent of how a person ages is due to inherited genes. Certain genes control a cell's ability to repair damaged DNA. If those genes are defective, they can't do their job. Not everybody will be susceptible to diseases like Parkinson's or cancer as they age. But each one of us will lose muscle mass and muscle strength. That's why this research is so important. Frailty affects all of us."

Enhanced Longevity through Telomerase (November 14 2008) http://www.sciencenews.org/view/generic/id/38552/title/Telomere_enzyme_a_likely_key_to_longevity
From Science News: "the enzyme telomerase can extend the lifespan of mice by about 24 percent. Telomerase lengthens telomeres - the 'caps' on the end of chromosomes that protect DNA from damage. Like burning fuses, telomeres normally get shorter each time that most body cells divide. While the enzyme enables cells to keep dividing, it also takes cells one step closer to growing and proliferating out of control - that is, becoming cancerous. Lab animals with extra genes for telomerase often die young from tumors. [researchers] engineered mice to have not only an extra copy of the gene for telomerase, but also extra anti-tumor genes to combat the enzyme's cancer-causing potential. In the altered mice, signs of aging such as poor coordination or degraded tissue health were delayed compared to mice that had only the extra copies of anti-tumor genes." Most interesting; you might also want to look at recent research that suggests telomerase operates by protecting mitochondria, and less damaged mitochondria means better preservation of telomeres - but, more importantly for life span, less oxidative stress.

Better Synthetic Cartilage (November 13 2008) http://www.sciencedaily.com/releases/2008/11/081113075959.htm
From ScienceDaily: "Until now, creating synthetic cartilage was complex but not impossible. The problem was that it was impossible to imitate the perfection of human cartilage due to the difficulty in orienting the collagen nanofibers [in] a particular configuration: in parallel, in a circle, or crossed. The fibers that form the cartilage that protects the knee are aligned in parallel. [Researchers have now] achieved this using the electrospinning method. Collagen nanofibers are obtained by exposing the collagen to electrical discharges. The collagen is extruded, in the form of a nanofiber thread, through a fine needle and is deposited on an electric collector consisting of two grounded plates. The student placed a nonconductive material between the two conducting plates. The nanofibers aligned on top of each other perfectly in parallel lines between the two conducting plates." Innovations in engineering the simpler forms of human tissue have been arriving more rapidly of late - more scientists are involved, the tools are improving, and the cost of research is falling. This is all groundwork for the next decade and tissue engineering of complex replacement organs.

Steps towards Liver Regeneration (November 13 2008) http://www.uphs.upenn.edu/news/News_Releases/2008/11/liver-stem-cell-marker.html
Discovering a stem cell population is the first step to regenerating the tissue they support: "A novel protein marker has been found that identifies rare adult liver stem cells, whose ability to regenerate injured liver tissue has the potential for cell-replacement therapy. In the future, this marker will allow for the isolation and expansion of these stem cells, which could then be used to help patients whose livers can no longer repair their own tissue. In a healthy liver, proliferation of mature liver and bile-duct lining cells is sufficient to maintain the necessary size and function of the organ. This even works when the liver is confronted with mild and acute injury, but the situation changes when injury to the liver is chronic and severe. For chronic injury, the liver uses a back-up system that stimulates stem cells to proliferate and eventually differentiate into new liver cells. [Researchers] found that these dual-potential stem cells can be identified and potentially isolated from other liver cells."

More on Myelin Loss (November 12 2008)
http://www.eurekalert.org/pub_releases/2008-11/mnia-itw111208.php
You might recall that age-related thinning of the myelin that insulates nerves strongly correlates with declining brain function. Researchers investigating MS are making progress into the mechanisms by which this happens: the protein netrin-1 "is known to guide and direct nerve cell axons to their targets. Blocking the function of netrin-1 and one of its receptors in adult neural tissue causes the disruption of myelin. We've known for just over 10 years that netrin is essential for normal development of the nervous system, and we also knew that netrin was present in the adult brain, but we didn't know why. The new findings show that
netrin-1 and its receptor are needed to hold paranodal junctions in place, and thereby maintain the structure of myelin. The paranodal junction is a highly specialized region of contact where an oligodendrocyte cell attaches itself to the nerve cell's axon. This juncture acts as a molecular fence, which organizes and segregates the distribution of key proteins along the nerve cells axon and plays an imperative role in the proper conduction of electrical signals along the length of the nerve cell. When the function of netrin-1 and its receptor is disrupted, the organization of this adhesive junction comes apart, disrupting the function of nerve cells in the brain and spinal cord."

Brain Growth Receptors and Lifespan (November 10 2008) http://dx.doi.org/10.1371/journal.pbio.0060274
A very readable overview of recent research from PLoS Biology: "When resources are short, growing organisms face an existential choice: should you ignore the shortage and hope for better times soon, or scale back and live within your limited means? And if you do scale back, will there be any payoff later in life? For animals, these choices are played out hormonally, with environmental fluctuations leading to internal rearrangements in endocrine signal and response throughout the growing body. In mammals, two principal hormones - growth hormone (GH) and insulin-like growth factor 1 (IGF-1) - promote growth. Remarkably, inhibiting one or both of these two not only retards growth, but also extends lifespan, not just in lab animals, but possibly also in people: mutations that reduce the function of the IGF-1 receptor have recently been discovered in centenarians (who are also short). Growth occurs throughout the body, and receptors for IGF-1 are found in every organ on virtually every cell. But [researchers have now shown] that it is the IGF-1 receptors in the brain that set the pattern for growth and lifespan."

Mainstream Press on the Singularity and Longevity (November 10 2008) http://english.ohmynews.com/ArticleView/article_view.asp?menu=A11100&no=384115&rel_no=1
An interesting, if flawed, article on the singularity and engineered longevity via the Korean OhmyNews: "Amidst the rapid changes of society ranging from general advances in science and technology to politics and social policy, with respect to knowledge, there is an emergent issue that promises to radically change our lives and our reality. It is predicted that within less than 20 years, the human lifespan will be extended to perhaps 150 or more years. Scientists and futurists on the cutting edge of thought about science and society believe that the increase in lifespan is one step towards what will be known as the Singularity, at which time, life might be extended indefinitely depending upon environmental conditions. The Singularity is the term used for a technological integration unheard of; it is a theoretical future point of unprecedented technological progress, caused in part by the ability of machines to improve themselves using artificial intelligence. It was just over a hundred years ago, when the human lifespan began to double to what it is today. It is possible that most people who lived only to 35 years of age thought that to live to 72 years would be too long and that they would be too tired. Nevertheless, we have adjusted and found life to be meaningful, even in our current 'long' life of 72 years."

Back to Top