Longevity Road Paved by Julia Roberts

Longevity Research

Funding Aging Research

Will Julia Roberts Pave Your Road to Longevity?

posted on October 27, 2009

Scientists are starting to meet Hollywood, but they™re invisible to the general public.

Think about it. If most people accidently walked into a room full of leading scientists, they would head for the nearest exit. But if they walked into a room packed with Hollywood stars, they™d be well¦ star struck.  

Where most people are bored to death with scientists, they hang on every word uttered by celebrities. That means Paris Hilton gets more attention than Nobel Laureates. Sad but true.

But rather than agonize over the injustice of it all, think about how we can put it to our advantage if our goal is age reversal¦ and it is of course.

Who is more narcissistic than actors and actresses? Who depend more on youth and beauty than any other group?

So why fight an uphill battle trying to get the public to listen to researchers when they are already listening to their favorite celebs? Our job, if we want to heighten awareness and support for life extension research is the same as directors. Put words into stars™ mouths.

Educating and enthusing one top celebrity advocate like Arnold Schwarzenegger could influence millions. That in turn could open the floodgates of medical research funding. There are loads of investment opportunities in this unknown but emerging industry. There are also tons of deserving research projects seeking grants and donations. But hardly anyone knows about them, and hardly anyone understands the profound implications they will have on their health and longevity.

That™s why we are starting to introduce the scientists to Hollywood, especially to the aging stars.

I told you about one small event last month. The next is the Manhattan Beach Project “ Longevity Summit in November. Go to www.ManhattanBeachProject.com for details.

I don™t know which celebrity will take up the banner, but when one or more do, we can expect to see our efforts multiplied, maybe overnight. And then, your favorite star might end up being your savior.


THE STUDY OF CENTENARIANS AND SUPERCENTENARIANS (October 23 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4435
A look at some scientific studies of the present bounds of human longevity from Courant: "It's becoming clear that people who break through the 90-plus barrier represent a physical elite, markedly different from the elderly who typically die younger than them. Far from gaining a longer burden of disability, their extra years are often healthy ones. They have a remarkable ability to live through, delay or entirely escape a host of diseases that kill off most of their peers. Supercentenarians - people aged 110 or over - are even better examples of aging gracefully. As a demographic group, they basically didn't exist in the 1970s or '80s. They have some sort of genetic booster rocket and they seem to be functioning better for longer periods of time than centenarians. The average supercentenarian had freely gone about their daily life until the age of
105 or so, some five to 10 years longer even than centenarians, who are themselves the physical equivalent of people eight to 10 years their junior. This isn't just good news for the oldest old and for society in general; it also provides clues about how more of us might achieve a long and healthy old age."

GREGORY BENFORD ON GENESCIENT (October 23 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4434
Here is a Google Tech Talk video of Gregory Benford discussing his latest venture, Genescient, which seems to be close to commercializing its first results: "Genescient is the world's first computational biology company founded on the use of artificial biological selection to cure the diseases of aging. Our laboratory animals have been selected for longevity through 750 generations for the equivalent of 15,000 human years. I will describe Genescient's multiple pathways toward accelerating human longevity, with parallel enhancements of vigor and function. Genescient applies 21st century genomic technology to identify, screen and develop benign therapeutic substances at precise doses, to defeat the diseases of aging. Our singular approach addresses the complex genomic networks that underlie aging and aging-associated diseases such as cardiovascular disease, Type II diabetes and neurodegenerative diseases. I shall display some results and our first product, due in 2009."

TOWARDS RADIATION-RESISTANT HUMANS (October 22 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4432
Evolved human biochemistry is suboptimal in some intriguing ways - we don't heal as well as some other species, for example. Here, EurekAlert! notes that our biochemistry is not as radiation-resistant as it might be either: "More than half of all cancer patients are treated at least in part with radiation. But the same radiation that kills cancer cells can also destroy healthy ones, causing side effects such as nausea and vomiting, skin sores and rashes, and weakness and fatigue. Long-term radiation exposure can lead to the scarring and death of normal tissue. [Researchers] have identified a biochemical signaling pathway that can profoundly influence what happens to both cancerous and healthy cells when they are exposed to radiation. In mouse experiments, they found that blocking a molecule called thrombospondin-1 from binding to its cell surface receptor, called CD47, affords normal tissues nearly complete protection from both standard and very high doses of radiation. We almost couldn't believe what we were seeing. This dramatic protective effect occurred in skin, muscle and bone marrow cells, which is very encouraging. Cells that might have died of radiation exposure remained viable and functional when pre-treated with agents that interfere with the thrombospondin-1/CD47 pathway." Given enough time, many beneficial changes to human biochemistry will be possible and affordable.

A MASTER MECHANISM FOR REGENERATION? (October 21 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4431
Researchers continue to uncover the biochemistry of regeneration: "Biologists long have marveled at the ability of some animals to re-grow lost body parts. Newts, for example, can lose a leg and grow a new one identical to the original. Zebrafish can re-grow fins. These animals and others also can repair damaged heart tissue and injured structures in the eye. In contrast, humans have only rudimentary regenerative abilities, so scientists hoping eventually to develop ways of repairing or replacing damaged body parts are keenly interested in understanding in detail how the process of regeneration works. Using zebrafish as a model, researchers [have] found that some of the same genes underlie the process in different types of tissues. Genes involved in fin regeneration and heart repair are also required for rebuilding damaged light receptors in the eye, they found, suggesting that a common molecular mechanism guides the process, no matter what body part is damaged." A common mechanism, if confirmed, would mean that the task of introducing this sort of regenerative capacity into humans will be simpler than thought.

THE PROSPECTS FOR MEMORY ENHANCEMENT (October 21 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4430
Via EurekAlert!: "Over-expressing a gene that lets brain cells communicate just a fraction of a second longer makes a smarter rat. Dubbed Hobbie-J after a smart rat that stars in a Chinese cartoon book, the transgenic rat was able to remember novel objects, such as a toy she played with, three times longer than the average Long Evans female rat, which is considered the smartest rat strain. This adds to the notion that NR2B is a universal switch for memory formation. The finding also further validates NR2B as a drug target for improving memory in healthy individuals as well as those struggling with Alzheimer's or mild dementia. NR2B is a subunit of NMBA receptors, which are like small pores on brain cells that let in electrically-charged ions that increase the activity and communication of neurons. Dr. Tsien refers to NR2B as the 'juvenile' form of the receptor because its levels decline after puberty and the adult counterpart, NR2A, becomes more prevalent. While the juvenile form keeps communication between brain cells open maybe just a hundred milliseconds longer, that's enough to significantly enhance learning and memory and why young people tend to do both better."

AUBREY DE GREY'S BIG THINK VIDEOS (October 19 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4427
Aubrey de Grey's videos at Big Think made it onto the Independent's website recently: "At a certain point in time - perhaps sooner than most people think - the ever-increasing average human lifespan will begin accelerating faster than people age. This moment, according to anti-aging expert Aubrey de Grey, will be more important than the Singularity - when the human race achieves this 'longevity escape velocity,' we will essentially become immortal. And de Grey, who is in his mid-40s, argues that this moment has a 50/50 chance of occurring in time for him to live forever. Crazy talk? Maybe not - de Grey shared with Big Think some surprising aging research and explained why there are no more major breakthroughs necessary for us to defeat aging for good. He even provided a vision of how we might defeat cancer. De Grey's optimistic vision brings up some interesting questions; most importantly, wouldn't an ageless society present a logistical nightmare? Aubrey de Grey is confident that arguments about economic difficulties and overpopulation in an ageless society are unwarranted; he does, however, believe that society would change dramatically, but mostly for the better."

WATCHING STEM CELL INFRASTRUCTURE (October 19 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4426

Advances in infrastructure drive the pace of research: making tools better, cheaper, and faster means that established research groups can do more, and more new research groups can afford to enter the field. Here is some good news on that front: researchers have "developed a method that dramatically improves the efficiency of creating stem cells from human adult tissue. The new technique, which uses three small drug-like chemicals, is 200 times more efficient and twice as fast as conventional methods for transforming adult human cells into stem cells (in this case called 'induced pluripotent stem cells' or 'iPS cells'). In developing the improved method, Ding drew on his knowledge of biology. He decided he would focus his efforts on manipulating a naturally occurring process in cells, in particular in a type of adult cell called fibroblasts, which give rise to connective tissue. This naturally occurring process - called MET (mesenchymal to ephithelial cell transition) - pushes fibroblasts closer to a stem-cell-like state. If he could manipulate such a fundamental process to encourage MET and the formation of stem cells, Ding reasoned, such a method would be both safer and more direct than hijacking other aspects of biology, for example those directly involved in cancer. The safety profile of the new method is highly promising. Not only is the method based on natural biological processes, [but] also the type of molecules used have all been tested in humans."

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