Healthy Life Extension

How Understanding “Cultural Inertia” Will Preserve Your Youth

posted on May 12, 2010

Last Thursday, an old close friend, Joe Polish, popped into town on a speaking engagement. I enjoyed a wonderful evening and dinner with him at a local raw foods/vegetarian restaurant. (By the way, if you’re ever near Fountain Valley, CA, make sure you stop at Au Lac for an over-the-top meal)

During the course of our conversation, which always seems to get around to life extension, one of the guests, Tim Ringgold, introduced a new term to my vocabulary.

We were lamenting over how many people will die unnecessarily because of inheriting the deathist memes that are ingrained in our culture. By that, I mean humans have longed for eternal youth and have been frustrated by the inevitability of aging and death from aging since the dawn of consciousness. This is not a pleasant prospect for our future, and we were not successful in stemming the aging tide, so what did we do? Simple. We did what we had to do to keep from being depressed by the prospect of steady decline until it all ends. We rationalized death, often as a good thing.

We came to terms with it through religion, painted death as a positive, invented various descriptions of an afterlife and the necessity of making room for future generations along many other arguments, some supporting the notion that living for a very long time is bad… and even evil.

OK, I know I’m treading on thin ice here when I challenge some of the most sacred religious beliefs regarding afterlife. I’m not trying to stir up arguments, in fact I can even think of science-based arguments in favor of it. What I am saying is, we don’t KNOW for sure. There is no proof, and faith is not proof, no matter how strong. I hope there is an afterlife, and it would be comforting to know for sure. Meanwhile, we suffer and die from slow agonizing deaths just like our ancestors.

Now here is what is going to happen. I am going to hear from some subscribers whose belief is so powerful that they will claim they know beyond a shadow of a doubt that there is an afterlife. And that’s the point. In the event they are wrong, many will miss the opportunity for extreme life extension by resisting the notion that science will deliver it to them. Clinging to these beliefs dampens support for radical life extension science for everyone else as well. It slows down research today and is causing millions of premature deaths. And that is what Tim calls Cultural Inertia.

For thousands of years, we wanted something that was impossible to deliver. Now times are suddenly different. We are on the cusp of restored youth and extreme life extension. Eternal life? Immortality? Trauma will most likely limit our lives. But isn’t age-reversal something to work toward, regardless of your beliefs – and regardless of whether we tack on just a few, or many quality years? Isn’t ending suffering and premature death a noble goal, even if you don’t care about it for yourself?

So recognize the power of cultural inertia, overcome it in these exciting times, and…

Live Long,
David Kekich
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LATEST HEALTHY LIFE EXTENSION HEADLINES

LOOKING TO THE FUTURE OF PERSONALIZED MEDICINE (April 30 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4704
Sequencing our own DNA and cross-referencing the results against the best of present scientific knowledge will soon be cheap and routine. This is an example of the sort of incremental progress in medical technology that is increasing human life expectancy year after year: a little more prevention here, a little better insight into how to cure there. From ScienceDaily: "For the first time, researchers have used a healthy person's complete genome sequence to predict his risk for dozens of diseases and how he will respond to several common medications. The risk analysis [also] incorporates more-traditional information such as a patient's age and gender and other clinical measurements. The resulting, easy-to-use, cumulative risk report will likely catapult the use of such data out of the lab and into the waiting room of average physicians within the next decade, say the scientists. The $1,000 genome is coming fast. The challenge lies in knowing what to do with all that information. We've focused on establishing priorities that will be most helpful when a patient and a physician are sitting together looking at the computer screen. Information like this will enable doctors to deliver personalized health care like never before. Patients at risk for certain diseases will be able to receive closer monitoring and more frequent testing, while those who are at lower risk will be spared unnecessary tests. This will have important economic benefits as well, because it improves the efficiency of medicine."

ON ATTACKING CANCER STEM CELLS (April 29 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4703
This EurekAlert! release looks at some of the challenges facing the increasing number of research groups who are attempting to destroy cancer stem cells: "Many of the colon cancer cells that form tumors can be killed by genetically short-circuiting the cells' ability to absorb a key nutrient, a new study has found. While the findings are encouraging, the test tube study using human colon cancer cells also illustrates the difficulty of defeating these cells, known as cancer stem cells (CSCs). It is becoming more evident that only a small number of cells in the tumor are capable of forming the tumor, namely the cancer stem cell. So the new strategy is to eliminate the cancer stem cells and thus lower the recurrence of cancer. Because CSCs have properties similar to normal stem cells, we have to find a way to attack them while keeping the adult stem cells alive. To do that, the research team inactivated a receptor that is found in increased amounts in colon cancer cells: the insulin-like growth factor receptor (IGF-1R). The colon cancer CSCs seem to need a fair amount of IGF to live, more than other cells, and they can't function without the IGF receptor. Working with human colon cancer cells, the researchers manipulated the cellular genetics using small interfering RNA (siRNA) to prevent the synthesis of IGF-1R. In this way, they reduced the number of IGF receptors by half, and reduced the number of CSCs by 35%."

AN INTERVIEW WITH THE DEPARTING SIRTRIS CEO (April 28 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4701
An interesting article: "In what turned out to be his final official engagement as CEO of Sirtris Pharmaceuticals, Christoph Westphal offered some key lessons in how to build a successful biotech company. It's pretty amazing. In the last 20 years, we've gone from zero understanding of the genes that play a role in aging to a pretty clear understanding that IGF1 plays a role, MTOR, the Sirtuins play a role, there's 10-15 genes play a role. Many of those are going to be druggable targets. Will Sirtris be successful? I don't know. It's still going to be very risky. But I'll be shocked if there are not drugs in the next 10-15 years that target genes that control aging. Westphal did not shirk from addressing the ongoing controversy surrounding the physiological activity of some Sirtris compounds. There's a debate in the academic world. We don't know the specific molecular mechanism of why you need a specific substrate on the in vitro screen to find Sirt1 activators. It's a numbers game and it's gotten harder with the FDA. People are spending less on pharma R&D and more on consumer health care and trying to diversify into developing countries and away from Europe and the United States. Fewer drugs are getting approved, revenues are going down, margins are going to go down."

THE COST OF NEGLIGENCE (April 27 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4698
From MSNBC: "Four common bad habits combined - smoking, drinking too much, inactivity and poor diet - can age you by 12 years, sobering new research suggests. The findings are from a study that tracked nearly 5,000 British adults for 20 years, and they highlight yet another reason to adopt a healthier lifestyle. Overall, 314 people studied had all four unhealthy behaviors. Among them, 91 died during the study, or 29 percent. Among the 387 healthiest people with none of the four habits, only 32 died, or about 8 percent. The risky behaviors were: smoking tobacco; downing more than three alcoholic drinks per day for men and more than two daily for women; getting less than two hours of physical activity per week; and eating fruits and vegetables fewer than three times daily. These habits combined substantially increased the risk of death and made people who engaged in them seem 12 years older than people in the healthiest group. The findings don't mean that everyone who maintains a healthy lifestyle will live longer than those who don't, but it will increase the odds." This study joins many others in putting a number on the harm we do to ourselves by failing to keep up with the health basics.

SARCOPENIA, METABOLIC SYNDROME, AND OVERNUTRITION (April 26 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4697
This paper outlines the overlap between the ways in which both processes of aging and eating too much lead to the loss of muscle mass and strength: "Sarcopenia, which is defined by the loss of skeletal muscle mass, predisposes skeletal muscle to metabolic dysfunction which can precipitate metabolic disease. Similarly, overnutrition, which is a major health problem in modern society, also causes metabolic dysfunction in skeletal muscle and predisposition to metabolic disease. It is now the prevailing view that both aging and overnutrition negatively impact skeletal muscle metabolic homeostasis through deleterious effects on the mitochondria. Accordingly, interplay between the molecular pathways implicated in aging and overnutrition that induce mitochondrial dysfunction are apparent. Recent work from our laboratory has uncovered the stress-responsive mitogen-activated protein kinase (MAPK) phosphatase-1 (MKP-1) as a new player in the regulation of metabolic homeostasis in skeletal muscle and mitochondrial dysfunction caused by overnutrition. These observations raise the intriguing possibility that MKP-1 may function as a common target in the convergence between sarcopenia and overnutrition in a pathophysiological pathway that leads to a loss of skeletal muscle mitochondrial function." Going the other way, you might recall that calorie restriction helps to maintain muscle mass with age.

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