What is Your Life Worth?

Life Extension Research

Funding Aging Research

What's Your Life Worth?

posted on Novemeber 10, 2009

If you were faced with the prospect of dying tomorrow and could buy your way out, what would you be willing to pay?

Think about this for a moment, because you may be faced with that decision. You may have a chance to buy your way out of a premature death.

There™s no doubt about it, if you live long enough (within reason), you may never have to endure the agony of death from aging, including all the horrible associated diseases.

For example, do you know we may be only a few short years from restoring your immune system to that of a young adult™s? Several years after that, we may be able to do the same for most of your vital organs. And how about this one? Even though it won™t extend your life, we may have a cure for baldness as early as next year!

Incredible things are happening at lightning speed, and they are pointing to full age reversal. Imagine how it will feel to have a 25 year-old body again.

One of these days, that will be normal. Young adults won™t age, and old adults will be rejuvenated. The younger generations may not need to worry about all this. It will develop naturally in their lifetimes. But for those of us who are chronologically challenged, there will be a price to pay.

In order for us to benefit from tomorrow™s youth restoring technologies, we™ll have to work for it. We™ll need to work to extend our lifespans by living sensibly. That means investing in yourself by learning how to live as long and as healthy as possible by incorporating today™s life extending knowledge into your life. The best place to start is by reading Life Extension Express.

Next, if you™re not already well-heeled, start saving your money. Depending on your age, you may need it to buy rejuvenating therapies as soon as they become available. Even though prices should drop rapidly, they will most likely be expensive at first. You may not have time to wait though.

Finally, if you are well-heeled, give serious thought to investing in companies that are developing technologies which could save your life. Money invested now could shave years off the time to when these technologies mature. We know what some of the key companies who are developing them are. Remember, some of us will be part of the last generation to die from aging, while others will be part of the first generation to enjoy open-ended youth and vitality.

The group you fall into may be determined by the commitments and investments you make today.


ILLUSTRATING THE POTENCY OF HORMESIS (November 06 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4455
Researchers are occasionally surprised when a genetic modification expected to reduce life span in fact extends it. In this example, a defense against lipid peroxidation is disabled in mice. (You might recall that lipid peroxidation is one of the ways in which oxidative damage originating in the mitochondria spreads throughout the body). Rather than reducing the life span of these mice due to greater damage, this actually has the effect of galvanizing further defensive mechanisms to greater activity. So in fact, such a mouse winds up with more effective repair and protection mechanisms over the long term. This is an example of hormesis - regular application of a little damage provokes an ongoing and massive response from the body's repair mechanisms, which leads to a longer healthy life span. From the paper: "The lipid peroxidation product 4-hydroxynonenal (4-HNE) forms as a consequence of oxidative stress. A major route of 4-HNE disposal is via glutathione conjugation, in the mouse catalyzed primarily by glutathione transferase mGSTA4-4. Unexpectedly, mGsta4-null mice, in which 4-HNE detoxification is impaired, have an extended life span. This finding could be explained by the observed activation of the transcription factor Nrf2 in the knockout mice, which in turn leads to an induction of [a] detoxification mechanism that contributes to enhanced longevity."

THEORIZING ON THE ROLE OF LONGEVITY GENES (November 06 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4454
It isn't completely clear exactly how many longevity genes affect our biochemistry. For example: "The researchers studied a family of transcription factors called FoxO known to be involved in proliferation, differentiation and programmed cell death. FoxO genes are required for the extreme longevity seen in some strains of laboratory roundworms, and a single mutation in the FoxO3 gene has recently been associated with long life in Japanese, German, American and Italian populations. We wanted to know if FoxO3 could be involved in regulating the pool of neural stem cells. Researchers examined laboratory mice in which the FoxO3 gene was knocked out. The few stem cells found in the adult mice without FoxO3 more rapidly churned out neural cell precursors - those cells destined to become new neurons - than did the mice with normal FoxO3 levels. In fact, the brains of the mice that lacked FoxO3 were heavier than the control group, perhaps because they were burning through their pool of neural stem cells by making too many new nerve cells. It's intriguing to think that genes that regulate life span in invertebrates may have evolved to control stem cell pools in mammals. [researchers] are working on creating a mouse in which FoxO3 levels are artificially elevated. If their theory about the function of the protein in the brain is correct, it's possible that the neural stem cell pools of these mice will be protected from the ravages of time. We're very interested in understanding how everything unravels during the aging process."

REPLACING SKIN GRAFTS WITH AUTOLOGOUS STEM CELLS (November 05 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4453
From the MIT Technology Review: "Traditionally, treatment for severe second-degree burns consists of adding insult to injury: cutting a swath of skin from another site on the same patient in order to graft it over the burn. The process works, but causes more pain for the burn victim and doubles the area in need of healing. Now a relatively new technology has the potential to heal burns in a way that's much less invasive than skin grafts. With just a small skin biopsy and a ready-made kit, surgeons can create a suspension of the skin's basal cells - the stem cells of the epidermis - and spray the solution directly onto the burn with results comparable to those from skin grafts. After removing a small swatch of skin near the burn site (the closer the biopsy, the better for precise matching of color and texture), the surgeon places it in the kit's tiny incubator along with an enzyme solution. The enzyme loosens the critical cells at the skin's dermal-epidermal junction, and the surgeon harvests them by scraping them off the epidermal and dermal layers and suspending them in solution. The resulting mixture is then sprayed onto the wound, repopulating the burn site with basal cells from the biopsy site."

ANOTHER PROMISING TARGETED CANCER THERAPY (November 05 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4452
The use of targeting mechanisms makes existing anti-cancer methodologies, such as radiation or toxic chemicals, work far more effectively and inflict less harm upon the patient. Via EurekAlert!: researchers used "a radiolabeled antibody to deliver targeted doses of radiation, followed by a stem cell transplant, to successfully treat a group of leukemia and pre-leukemia patients for whom there previously had been no other curative treatment options. All fifty-eight patients, with a median age of 63 and all with advanced acute myeloid leukemia or high-risk myelodysplastic syndrome - a pre-leukemic condition - saw their blood cancers go into remission. The key to success in this study was use of a radiolabeled antibody that has therapeutic iodine 131 attached and is designed to target leukemic bloods cells that carry a marker on the surface of the cell known as CD45. Delivered intravenously, the radiation looks for the CD45 antigen receptor on the surface of blood cells. This approach results in a two- to four-fold increase in the amount of radiation that reaches cancerous cells as compared to standard external beam radiation, which also radiates normal surrounding organs and tissue. The more radiation that can be applied, the more cancer cells will be killed in preparation for donor stem cells to take over the diseased immune system and kill off the remaining cancer cells." The survival rate after 3 years is around a third - somewhat better than the expected zero for existing options.

HOW EXCESS FAT CAUSES INFLAMMATION (November 04 2009) http://www.maxlifesolution.com/inflammex/
Researchers are delving deeper into the mechanisms that link fat tissue with chronic inflammation, a source of damage to the body that raises the risk of age-related disease: "Researchers have new evidence to explain how saturated fatty acids, which soar in those who are obese, can lead the immune system to respond in ways that add up to chronic, low-grade inflammation. The new results could lead to treatments and natural supplements like Inflammex designed to curb that inflammatory state, and the insulin resistance and type 2 diabetes that come with it. One key [is] an immune receptor (called Toll-like receptor 4 or Tlr4) at the surface of blood cells, including a particularly 'angry' class of macrophages known to pump out toxic molecules and spur inflammation. It now appears that fatty acids may in essence 'hijack' those immune cells via Tlr4. Tlr4 is out there to sense bacterial products, but one of those looks a lot like fatty acids. They don't know it's not bacteria. Scientists had suspected that Tlrs might be the 'sensors' linking obesity to inflammation. Indeed, earlier studies had supported that notion. In the new study, the researchers show that this interaction is particularly important in the bloodstream. Mice lacking Tlr4 only in blood cells grew obese when they were fed a high-fat diet, but they were largely spared the metabolic consequences of their obesity. The mice were fat, but metabolically they continued to 'look pretty normal.'"

AN INTERVIEW WITH KEVIN PERROTT (November 04 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4450
Kevin Perrott of the LifeStar Institute is featured in this Edmonton Sun article: "Kevin Perrott sees a future without heart disease, arthritis or cancer. And it's right around the corner. If people can get over their unfounded fear of stem-cell research.  'The potential is totally limitless,' Perrott says, his eyes widening with enthusiasm, 'But we have to get everybody on the same wavelength.' The problem, he says, is that the ethical debate over stem cells hasn't kept up with the research. Perrott, a local businessman and PhD student, hopes to change that. Earlier this year he founded the LifeStar Institute Canada to build public support for stem-cell research. In the near future, someone needing a kidney transplant could have a new organ manufactured out of cells taken from their own skin, potentially bringing an end to organ donor wait lists. It also opens the door for 'personalized cell replacement therapies.' For example, heart attack victims who've suffered permanent organ damage could be treated so that the dead tissue regenerates itself. Parkinson's disease, Alzheimer's disease and other incurable conditions could potentially be reversed."

THE IMPORTANCE OF PROTEIN FOLDING (November 02 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4447

Here is a glance at why protein folding is important: "Research indicates that ALS, in common with other neurological disorders, such as Alzheimer's and Parkinson's disease, is caused by our own proteins, which form aberrant aggregates that are fatally toxic to our nerve cells. However, it has not been known what causes these proteins to aggregate. [Researchers] have now revealed what happens with proteins during the very first, critical step towards forming larger aggregates. It turns out that the protein superoxide dismutase interchanges between its normal structure and a misfolded form. During a brief moment the structure becomes partially misfolded to expose sticky patches that normally are hidden in the interior. These patches cause two or several protein molecules to stick together, thereby forming the cornerstone of the larger structures that are believed to underlie ALS. Knowledge of the misfolded protein structure potentially makes possible future efforts to rationally design drugs that prevent the misfolding event and hence the development of ALS." This is why projects like Folding@home are important to the future of medical science: understanding a misfold makes it possible to work towards correcting it.

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