Longevity News

Obituary Page Cancelled

posted on August 31, 2010

This is what we work toward. It’s what gets us up in the morning. We look forward to the day when death is so rare and infrequent that it will make the main news section.

Many of my friends who still live in my hometown, routinely read the obits in the local paper. As they aged, they gradually became morbidly interested in which of their friends died. When they were young, they rarely read that page. Why should have they? Life was good with few worries, and it offered a sense of hope and immortality. So what happened?

They got a taste of their mortality. They started noticing neighbors, relatives and friends dying from aging related diseases and conditions. As time passed, they passively accepted this as their fate, not something to resist. Unknowingly, they got in line.

Gone was their sense of immortality, hopes and plans for a bright future, and few, if any, concerns over their health.

When confronted with the finality of aging and death, they usually fire back with pre-programmed responses such as “I’m aging gracefully”, “I’ll be going to a better place”, or “You can’t cheat Father Time.”

Why accept aging gracefully when we are on the verge of reversing it? Sure, it will take a lot of work, and it’s not guaranteed, but look at the rewards!

Are you sure you’re going to a better place? If so, why haven’t you decided to go there by now? Let’s say you had an opportunity to pop a youth pill versus a choice to keep aging and eventually going to your better place. Which would you choose? I’m not saying with certainty there is no better place. I simply don’t know. So I decided to hang around this imperfect place as long as I can and actively create what I can to help fix it. How about you? If you’re sitting on the sidelines of life, waiting for the “inevitable”, why not at least give life the old college try?

Father Time? He can be your friend, not your enemy. How about instead of giving in to the passage of time, you use time to your advantage? It will take time to solve this aging puzzle. So instead of passively watching it slip by, why not use it to improve your health while researchers use it to close the gap between what we know about aging and what we need to know to reverse it? And of course, they can use your support as well.

Life without hope is terminal and depressing. Hope based on hype will give you a short-term boost but will end up crashing you on the rocks of despair. But hope based on your awareness of the facts, on continually acquiring knowledge and on keeping up with the newest advances can deliver the opposite. Sure, anything can go wrong at any time. As I said, there are no guarantees. But staying aware and hopeful should help you prevent many of the things that can go wrong and reverse the “guarantee” that you will age and die.

Personal creativity is the name of the game. In the worst case, it will enrich you and make life more interesting and more worth living. In the best case, it can propel you into an indefinite future of youth and prosperity.

Here’s one way to start: Drop the obit habit, and replace it with empowering pursuits. Remember “epigenetics?” Every one of your thoughts or actions, positive or negative, either strengthens or erodes every one of your trillions of cells.

Long Life,
David Kekich
____________________________

LATEST HEALTHY LIFE EXTENSION HEADLINES

DREXLER ON AUTOPHAGY (August 27 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4874
A post on autophagy at Metamodern: "I’d like to say a few words about one of the hottest and, in my view, most important areas in biomedicine: Autophagy, a process crucial to health, disease, and aging. Autophagy research is expanding rapidly. In autophagy ('self eating'), cells engulf and digest their own macromolecules and organelles. Autophagy serves two functions: providing critical nutrients in times of scarcity, and recycling damaged cellular structures. It seems that lab animals and human beings fed ad-libitum do too little autophagic recycling. The resulting accumulation of damaged machinery causes a wide range of functional deficits, and accumulation of damaged mitochondria, in particular, increases the production of reactive oxygen species, accelerating further damage. In a range of organisms, dietary restriction both induces autophagy and results in wide-ranging health benefits, including the extension of healthy lifespans. Blocking autophagy blocks the most important of these effects. Rapamycin induces autophagy and extends lifespan, as does sirtuin-1. Autophagy again appears to be central to these effects. A recent review article examines genetic interventions that indicate 'tight connections between autophagy, health span and aging'."

MORE ON ARTIFICIAL CORNEAS (August 26 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4873
Work on artificial replacements for damaged corneas is showing promise: "A new study from researchers in Canada and Sweden has shown biosynthetic corneas can help regenerate and repair damaged eye tissue and improve vision in humans. Globally, diseases that lead to clouding of the cornea represent the most common cause of blindness. More than a decade ago, [researchers] began developing biosynthetic corneas in Ottawa, Canada, using collagen produced in the laboratory and molded into the shape of a cornea. Together, they initiated a clinical trial in 10 Swedish patients with advanced keratoconus or central corneal scarring. Each patient underwent surgery on one eye to remove damaged corneal tissue and replace it with the biosynthetic cornea, made from synthetically cross-linked recombinant human collagen. Over two years of follow-up, the researchers observed that cells and nerves from the patients' own corneas had grown into the implant, resulting in a 'regenerated' cornea that resembled normal, healthy tissue. Patients did not experience any rejection reaction or require long-term immune suppression, which are serious side effects associated with the use of human donor tissue. The biosynthetic corneas also became sensitive to touch and began producing normal tears to keep the eye oxygenated. Vision improved in six of the ten patients, and after contact lens fitting, vision was comparable to conventional corneal transplantation with human donor tissue."

SEEKING A WAY TO BREAK DOWN GLUCOSEPANE (August 25 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4870
A press release from InnoCentive and the SENS Foundation announces a short-term incentive program "seeking innovative ideas to biologically reverse one of the causes of aging and age-related diseases believed to be attributed to glucosepane, a protein crosslink that reduces elasticity throughout the body. This is a Theoretical Challenge, so Solvers need to submit a detailed and thorough description of their solution. The Challenge runs for 60 days and one Solver will receive $20,000 if their solution is chosen. Finding an innovative solution to breaking down glucosepane, or what we call 'public enemy number one,' is our Foundation's top priority in the category of protein crosslinks, as it is the most abundant protein crosslink in aged humans. We believe there are several radical possibilities to solving this Challenge - things we haven't even thought of - and will keep an open mind to solutions we receive. Our goal is to discover solutions that can be implemented and reverse stiffening, therefore restoring youthful health and vigor to the world's population. Evidence suggests that glucosepane may play a role in osteoporosis, cardiovascular diseases like hypertension, inflammation and diabetes. Scientists have studied the accumulation of glucosepane for 30 years with little success, so SENS Foundation is reaching out to InnoCentive's 200,000+ Solvers for innovative solutions to find a way to break the formation of glucosepane." This seems like a good way to draw attention to aspects of the SENS program that are not greatly studied - very few groups are working seriously on crosslink breakers at the present time.

OLD CHEMOTHERAPIES MADE BETTER, SAFER BY TARGETING (August 24 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4868
Cancer chemotherapy is harrowing is because it is indiscriminate. But all of the old chemotherapies can be made much better and safer when used as the payload in one of the new cell targeting nanotechnologies: researchers "have developed a nano-sized vehicle with the ability to deliver chemotherapy drugs directly into cancer cells while avoiding interaction with healthy cells, increasing the efficiency of chemotherapeutic treatment while reducing its side effects. Inside the nano-vehicle itself are tiny particles of chemotherapy drugs. When the delivery vehicle comes into contact with cancer cells, it releases the chemotherapeutic payload directly into the cell. The nanomedical device can be used to treat many different types of cancer, including lung, blood, colon, breast, ovarian, pancreatic, and even several types of brain cancers. The key to the drug delivery platform is the molecule used to create the outer coating of this cluster nano-vehicle, a sugar recognized by receptors on many types of cancer cells. When the nano-vehicle interacts with the receptor on the cancerous cell, the receptor undergoes a structural change and the chemotherapy payload is released directly into the cancer cell. [This] leads to more focused chemotherapeutic treatment against the diseased cells. Clinical trials [should] begin in two years or less."

STEM CELL INFRASTRUCTURE CONTINUES TO IMPROVE (August 23 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4867
Researchers continue to produce improvements to infrastructure technologies needed for stem cell research and development: "Human pluripotent stem cells, which can become any other kind of body cell, hold great potential to treat a wide range of ailments, including Parkinson's disease, multiple sclerosis and spinal cord injuries. However, scientists who work with such cells have had trouble growing large enough quantities to perform experiments - in particular, to be used in human studies. Furthermore, most materials now used to grow human stem cells include cells or proteins that come from mice embryos, which help stimulate stem-cell growth but would likely cause an immune reaction if injected into a human patient. To overcome those issues, MIT chemical engineers, materials scientists and biologists have devised a synthetic surface that includes no foreign animal material and allows stem cells to stay alive and continue reproducing themselves for at least three months. It's also the first synthetic material that allows single cells to form colonies of identical cells, which is necessary to identify cells with desired traits and has been difficult to achieve with existing materials."

EVEN MODEST WEIGHT GAIN CAN BE HARMFUL (August 23 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4866

From the Mayo Clinic: "researchers found that healthy young people who put on as little as 9 pounds of fat, specifically in the abdomen, are at risk for developing endothelial cell dysfunction. Endothelial cells line the blood vessels and control the ability of the vessels to expand and contract. Researchers recruited 43 healthy Mayo Clinic volunteers with a mean age of 29 years. They were tested for endothelial dysfunction by measuring the blood flow through their arm arteries. The volunteers were assigned to either gain weight or maintain their weight for eight weeks, and their blood flow was tested. The weight-gainers then lost the weight and were tested again. Endothelial dysfunction has long been associated with an increased risk for coronary artery disease and cardiovascular events. Gaining a few pounds in college, on a cruise, or over the holidays is considered harmless, but it can have cardiovascular implications, especially if the weight is gained in the abdomen. Among those who gained weight in their abdomens (known as visceral fat), even though their blood pressure remained healthy, researchers found that the regulation of blood flow through their arm arteries was impaired due to endothelial dysfunction. Once the volunteers lost the weight, the blood flow recovered. Blood flow regulation was unchanged in the weight-maintainers and was less affected among those who gained weight evenly throughout their bodies."

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