A Tiny Enemy Could Be Claiming Your Life

Extreme Life Extension Research

Funding Aging Research

Could a Tiny Enemy Be Claiming Your Life?

posted on October 6, 2009

Who™s in charge?

We work overtime to make extreme life extension a reality for you. But we fight an ongoing battle with a deadly enemy only you have control over.

That enemy is your personal lifestyle.

Since it™s probably going to be touch and go whether or not we can reverse aging in your lifetime, how long you keep yourself alive can be the difference between oblivion and open-ended youth. We™re doing all we can to push you over the finish line. Are you doing the same for yourself?

Remember, you are the one with most of the power over your destiny. It™s not your genes. It™s not your environment. It™s you!

By now, you understand your lifestyle can be the difference of up to twenty extra “ or twenty less years. You should also know what you can do to add (or subtract) those years, especially if you have read Life Extension Express.

So what are you doing about it? Are you focusing on the benefits you will receive? Or are you giving in to deadly short-term habitual temptations?

Stop right now, and do this exercise. Consider the things that are keeping you from being as healthy as you can be. What are those things you could change if you had a magic wand? You might want to stop and list them on a piece of paper.

Then go back in time to the first time you noticed those destructive habits creeping into your life. Step into your body at that time and feel the pain they have caused you. Now gradually bring yourself back to the present and review the pain, regret and even sickness they have caused you at each phase of your life. Consider how they have affected your health, appearance, self-esteem relationships and career. Now fast forward to the future and observe how they will continue to eat away at your happiness, shorten your life and cause you to miss out on endless youth.

Feel the pain and loss these habits will cause if you don™t change them. Consider the lost hope and the unfulfilled dreams.

Now come back and realize that you are the one with the ability to seize control of you life, your health, your long future and your happiness.

So who™s in charge? If not you, then consider the words of Ayn Rand.

œ¦if you choose to perish, do so with full knowledge of how cheaply how small an enemy has claimed your life.

Health Conference Alert

Please put this in your calendar, especially if you are a health practitioner. Age management Medicine Group (AMMG) is holding their annual Clinical Applications for Age Management Medicine conference in Las Vegas, November 5-8. Go to their website for information on this important conference.



EXPLORING THE MECHANISMS OF PROTEIN RESTRICTION (October 02 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4405
Lowered dietary protein leads to a longer life, acting in much the same way as calorie restriction. Here researchers delve more deeply into the underlying mechanisms: "Mitochondria act as the 'powerhouse' of the cells. It is well known that mitochondrial function worsens with age in many species. Our study shows that dietary restriction can enhance mitochondrial function hence offsetting the age-related decline in its performance. The researchers report the unexpected finding that while there is a reduction in protein synthesis globally with the low protein diet, the activity of specific genes involved in generating energy in the mitochondria are increased. That activity, which takes place at the level of conversion of RNA to protein, is important for the protective effects of dietary restriction. There have been correlative studies that show mitochondria change with dietary restriction, this research provides a causal relationship between diet and mitochondrial function. Mitochondrial genes are converted from RNA to protein by a particular protein (d4EBP). Flies fed a low protein diet showed an uptick in activity of d4EBP, which is involved in a signaling pathway that mediates cell growth in response to nutrient availability called TOR (target of rapamycin). ... d4EBP is necessary for lifespan extension upon dietary restriction. When the activity of the protein was genetically 'knocked out' the flies did not live longer, even when fed the low protein diet. When the activity of d4EBP was enhanced, lifespan was extended, even when the flies ate a rich diet."

ON REVERSIBLE CRYOPRESERVATION (October 02 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4404
From Depressed Metabolism: "I think in the next 20 years more small animal organs, and perhaps some human organs, may be reversibly cryopreserved. The best scenario for cryonics would be improved, and possibly demonstrably reversible, cryopreservation of animal brains. It has been long observed that if reversible solid-state brain preservation could be demonstrated, then cryonics revival becomes a purely technical problem (albeit very complex one) of tissue regeneration. There would be no remaining doubt about whether the preservation itself was viably preserving human beings. Reversible solid-state cryopreservation of whole mammals is a very difficult problem with existing technology. This is why when asked about it people will often defer to nanotechnology. References to nanotechnology as a solution to a medical problem basically say, 'We have no idea how to solve this problem with existing tools, but future abilities to completely analyze and repair tissue at the molecular level will be implicitly sufficient.' It's a valid argument, but saying that a medical problem will be solved when someday technology exists to solve every medical problem is not very illuminating about time lines or nature of the problem."

SENS RESEARCH WINS THE 3BANANA CONTEST (October 01 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4403
I see that, thanks to the vigorous response of the pro-longevity community, the SENS Foundation has won $5,000 for longevity research: "The challenge, launched this September, was sponsored by 3banana as a philanthropic crowdsourcing contest helping health, environment and education-focused non-profit organizations raise money and exposure for their respective causes while testing the sharing features of the company's online and mobile note-taking software. 'We are very honored to accept this prize. This contest has really opened our eyes to the possibilities of furthering our cause using social networks,' said Dr. Aubrey de Grey, Chief Science Officer for the SENS Foundation. 'Thousands of our supporters shared their words of encouragement for our mission, and this effort has created more dialog between our organization and our supporters.'" As the cost of biotech research falls, I think we're going to see much more grassroots fundraising of this nature - see, for example, the laser ablation of lipofuscin research that was funded earlier this year via online efforts.

TOWARDS THE RESTORATION OF AGED MUSCLES (October 01 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4402
Via ScienceDaily: "adult muscle stem cells have a receptor called Notch, which triggers growth when activated. Those stem cells also have a receptor for the protein TGF-beta that, when excessively activated, sets off a chain reaction that ultimately inhibits a cell's ability to divide. The researchers said that aging in mice is associated in part with the progressive decline of Notch and increased levels of TGF-beta, ultimately blocking the stem cells' capacity to effectively rebuild the body. This study revealed that the same pathways are at play in human muscle, but also showed for the first time that mitogen-activated protein (MAP) kinase was an important positive regulator of Notch activity essential for human muscle repair, and that it was rendered inactive in old tissue. For old human muscle, MAPK levels are low, so the Notch pathway is not activated and the stem cells no longer perform their muscle regeneration jobs properly. When levels of MAPK were experimentally inhibited, young human muscle was no longer able to regenerate. The reverse was true when the researchers cultured old human muscle in a solution where activation of MAPK had been forced. In that case, the regenerative ability of the old muscle was significantly enhanced. In practical terms, we now know that to enhance regeneration of old human muscle and restore tissue health, we can either target the MAPK or the Notch pathways. The ultimate goal, of course, is to move this research toward clinical trials."

UTILITY AND ENGINEERED LONGEVITY (September 30 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4401
Here's a long post on the utility of contributing to engineered longevity versus the other foreseeable technology most likely to dramatically reshape the world - self-improving artificial intelligence (AI). The author puts that goal in advance of contributing now to advancing longevity science, but I think that a point is missed along the way. Even if your contributions made now don't lead to technologies arriving in time to extend your life, they will bring forward the dates at which the medicine of engineered longevity does emerge in each region of the world. Every day gained in this fashion saves approximately 100,000 lives at present population levels. From the post: "The crux of my conflict is whether there is greater utility in putting money toward longevity or strong AI. And for now, let's pretend that longevity escape velocity (LEV) occurs 25 years from now without any of my investment. Now lets say I buy 5 years of 'progress' in longevity, so it happens only 20 years from now. I think it's likely that within the first few decades of LEV, most of the change in life expectancy will come from wealthy old people in prosperous nations. I just saved and improved many lives, but not a whole bunch probably under half a billion. Infectious and lifestyle diseases, accidents and wars still exist, and those who can't afford treatment still die when they get old, even when AI shows up."

NOTE: Why would it be a choice? Fund both approaches. The Manhattan Beach Project sees both at integral parts of the aging puzzle.

MODERN GENETICS: DISABLE THE GENE AND SEE WHAT HAPPENS (September 29 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4399
Here is a good example of the way in which modern genetic studies tend to proceed: genes of interest are disabled one by one to confirm exactly what it is they do. This is how researchers are exploring the complex feedback loops and interlinked mechanisms surrounding calorie restriction induced longevity, for example: "Dietary restriction is the most widely used intervention to promote longevity; however, the mechanisms underlying the effect of dietary restriction remain elusive. In a previous study, we identified two novel genes, nlp-7 and cup-4, required for normal longevity in Caenorhabditis elegans. nlp-7 is one of a set of neuropeptide-like protein genes; cup-4 encodes an ion-channel involved in endocytosis by coelomocytes. Here, we assess whether nlp-7 and cup-4 mediate longevity increases by dietary restriction. [RNA interference] of nlp-7 or cup-4 significantly reduces the life span of the eat-2 mutant, a genetic model of dietary restriction, but has no effect on the life span of long-lived mutants resulting from reduced insulin/IGF-1 signaling or dysfunction of the mitochondrial electron transport chain. The life-span extension observed in wild-type N2 worms by dietary restriction [is] prevented significantly in nlp-7 and cup-4 mutants. We conclude that two novel pathways, NLP-7 signaling and endocytosis by coelomocytes, are required for life extension under dietary restriction in C. elegans."

OBESITY AND AGING (September 29 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4398
In Search of Enlightenment ponders obesity and aging: "When it comes to a disease like progeria, which is an extreme form of accelerated aging, I assume we would all agree that we should seek ways of preventing the disadvantage that comes with the disease. No child deserves to be robbed of the opportunity to have a healthy childhood and develop into a healthy adult. Progeria is very rare, affecting about 1 in 8 million births. When it comes to obesity, which also accelerates aging (though is less severe than progeria, but much, much more prevalent) we also think we should strive to prevent this. No one deserves diabetes or heart disease in their 50's or 60's. But what about the 'regular' rate of aging, which is less severe but much, much more prevalent than obesity, what should our attitude be? The inborn aging process limits average life expectancy of humans to around 85. Shouldn't we aspire to retard that rate of molecular and cellular damage if it would help prevent disease and death? Does anyone actually believe people (or to make the point more vivid, their parents, children or spouse) deserve heart disease, stroke, AD, cancer, etc. in late life? [Yet] aging research is grossly underfunded and that young scientists who want to make the world a better place gravitate towards goals like trying to control the global climate or finding a cure for just one disease of aging (e.g. cancer) rather than investigating the aging process itself."

REVISITING OVARIES AND LONGEVITY IN MAMMALS (September 28 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4397
It has been known for some years that manipulation or transplant of ovaries can influence longevity in mammals, a fact that might be compared with the mechanisms linking germ cells to nematode longevity. Here is a recent demonstration: "Previously we reported that prepubertally ovariectomized mice that received young transplanted ovaries at a postreproductive age showed a 40% increase in life expectancy. To study this phenomenon in greater detail, 11-month-old ovariectomized and ovary-intact CBA/J mice underwent ovarian transplantation with 60-day-old ovaries or a sham surgery. Results from observations on transplant recipients in the current study extended our previous results. Whereas intact control mice lived an average of 726 days, transplant recipients lived an average of 770 days (i.e., 780 days for intact recipients and 757 days for ovariectomized recipients). If intact recipients had ceased reproductive cycling by the time of transplant, we observed a further increase in mean life span to 811 days. These results demonstrate that young ovaries enhanced longevity when transplanted to old mice and that ovarian status, examined by means of ovariectomy and ovarian transplantation, clearly influenced the potential of young transplanted ovaries to positively impact longevity." We still await an understanding of the biochemical mechanisms involved in this method of life extension.

THE THIEL FOUNDATION (September 28 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4396

The Thiel Foundation is the public face of investor Peter Thiel, noteworthy for his funding of SENS Foundation research. "Freedom is always under siege. Around the world, authoritarian regimes deprive millions of people of basic economic and social rights. Even elected governments can burden their citizens with labyrinthine bureaucracies and complex, unnecessary laws. And while some regimes are obviously worse than others, they all have apologists who obscure these conditions by twisting the relationship between freedom and human fulfillment. The Thiel Foundation defends and promotes freedom in all its dimensions: political, personal, and economic. How do we do this? (a) By supporting innovative scientific research and new technologies that empower people to improve their lives. (b) By championing organizations and individuals who expose human rights abuses and authoritarianism in all its guises. (c) By encouraging the exploration of new ideas and new spaces where people can be less reliant on government and where freedom can flourish." The goal of freedom taken to its logical ends means not just freedom from human-engineered oppression, but also freedom from the limitations, suffering, and cruelties inherent in the human condition and human biology - such as degenerative aging.

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