Healthy Life Extension

I'm Coming Out of the Closet

posted on October 4th, 2011

Dear Future Centenarian,

An awareness came over me many years ago… and I’ve been keeping it secret… until now!

I’m addicted to instant gratification just as seriously as the sugar and other addicts I try to convert. If it weren’t for nearly-immediate benefits, I may have never started working out.

Only a minority, like me, train for wellness and longevity. But do we really? Sure, those are major, and in my opinion, primary benefits by far. But deep down inside, even at my age—I want to look good.

I must admit, when I was in my 20’s, I told myself I trained for health and fitness. I told myself I trained because it made me feel better and function better. But the reality was, I trained for ego and vanity, to get the girls and to boost my confidence.

Nothing much has changed in the past 40 years. Like most people at any age, I want to look good.

I realize the healthy habits I adopted decades ago were driven by short-term motivations more than long-term goals. Of course longevity still drives me. But I doubt I would be as religious about working out if it weren’t for the numerous short-term benefits. Those are what compel me to train when I don’t especially want to,  or when I think I don’t have the time.

Now, I discovered a new University of Michigan study which finds that the most convincing exercise message emphasizes immediate benefits that enhance daily quality of life. They don’t mention vanity, but that may be because the subjects are still hiding in that closet.

Health care, business and public health have presumed that promoting health and longevity benefits from exercise will motivate people to exercise. The new findings, however, indicate that these individuals exercised less than those who aimed to enhance the quality of their daily lives.

"The study showed that what an individual espouses as important does not necessarily translate into behavior," said Michelle Segar, research investigator for the U-M Institute for Research on Women and Gender. "While people say they value health and healthy aging, those distant benefits don't make exercise compelling enough to fit into their busy lives."

These findings challenge the current convention of promoting exercise for better health, longevity, or as medicine.

"Promoting exercise for health is logical, but people's daily decisions are more often connected to emotion than logic," Segar said. "A more effective 'hook' is to rebrand exercise to emphasize the immediate benefits that enrich daily living, such as stress reduction and increased vitality."

Individuals may also appreciate the subsequent benefits that make exercise more personally meaningful, such as being a patient parent, enjoying life, being creative and having focus at work, she says.

"By shifting our model from medicine to marketing, we can improve how we 'sell' exercise to the public by using principles like branding," Segar said.

For example, messages about immediate rewards from exercise that make life more enjoyable, such as "move more, get energy," may better motivate busy individuals than promotions focused on achieving distant and abstract benefits, such as "move more, get healthy."

Read the full release at: http://www.uofmhealth.org/news/exercise-rebrand-0927

Title: Rebranding exercise: 'Quality of life' a better motivator than 'Live longer'

This news release and a podcast can be found at this web address < http://bit.ly/rg8ffH  >

One of the most difficult parts of my mission is to get people to adopt the lifestyle habits I profess. I know if I could magically get every adult on the planet to do so, I would be able to save many millions of their lives.

Why? Simply because the last couple of decades of learning about aging from the masters convinced me that if we could all add just five active years to our lives, as many as 170 million people would have a much better chance to take advantage of emerging technologies that could restore their (our) youth in the future.

The trick is to be here when they are perfected. As it is, 37 million people die ‘prematurely’ from aging every year. If we could get everyone to 1) live five years longer, or 2) develop the technologies five years sooner, those 170 million people could get new leases on life.

We work every day on both #s 1 and 2. And I consider adding five years to lives on average is ridiculously conservative.

So what are you waiting for? Hit the gym, adopt a healthy diet and follow the other five simple steps outlined in Life Extension Express while keeping your eye on the short-term benefits. There are many more than you can imagine.

Go to www.MaxLife.org for a free downloadable copy of my book.

Long Life,
David Kekich

P.S. I'm a little late in passing this on, but if you're in the Los Angeles area this week you might consider dropping in on the SENS Foundation meeting on Wednesday eve. Instructions on how to RSVP are in the following Fight Aging! post:

http://www.fightaging.org/archives/2011/09/the-next-sens-foundation-los-angeles-chapter-meeting-is-wednesday-october-5th.php

Lots of fascinating people will be there. I’ll look for you.
____________________________

LATEST HEADLINES FROM FIGHT AGING!

WORKING WITH THE MITOSENS TEAM AT THE SENS FOUNDATION Friday, September 30, 2011 http://www.fightaging.org/archives/2011/09/working-with-the-mitosens-team-at-the-sens-foundation.php
Life science students intern at the SENS Foundation research center in the Bay Area as a part of the Foundation's broader academic initiative, working on the foundations of future rejuvenation therapies. Biotechnology has advanced to the point at which bright graduates can help to meaningfully advance the state of the art, and here is a report from one such: "Sarah Fazal joined our research center team as an intern for the summer. Over the past few months, she worked with our MitoSENS team, primarily verifying the integration of DNA transfected into cells and detecting RNA expression levels.  Her efforts contributed greatly to the progress our MitoSENS team has made over recent months, and she presented those results in a poster at our recent SENS5 conference in Cambridge.

The current project for mitoSENS is allotopic expression, which involves copying the mitochondrial DNA into the nucleus. My project required checking for integration of the DNA transfected into cells, and detecting RNA expression levels. By the end of the summer, I had done this successfully for 4 out of the 13 genes involved in oxidative phosphorylation that are still encoded by mitochondrial DNA. I spent my summer mostly doing PCRs (polymerase chain reaction), DNA and RNA isolations, cell culturing, and gel electrophoresis. I learned to perfect these techniques, to think critically when my results weren't as expected, and to design experiments. My experience at SENS helped shape me into a more confident and better experienced scientist. I would definitely recommend volunteering for this foundation; the experience was educational, the research is open-minded, determined, and bold, and the staff is friendly, welcoming, and helpful."

CONTINUED WORK ON AUTOPHAGY AND RAPAMYCIN Friday, September 30, 2011 http://www.fightaging.org/archives/2011/09/continued-work-on-autophagy-and-rapamycin.php
Rapamycin is known to extend life in mice, so researchers are looking into the mechanisms and possible uses as a therapy for age-related diseases. "Previous studies have shown that inducing autophagy ameliorates early cognitive deficits associated with the build-up of soluble amyloid-beta (Abeta). However, the effects of inducing autophagy on plaques and tangles are yet to be determined. While soluble Abeta and tau represent toxic species in Alzheimer's disease (AD) pathogenesis, there is well documented evidence that plaques and tangles also are detrimental to normal brain function. Thus, it is critical to assess the effects of inducing autophagy in an animal model with established plaques and tangles.

Here we show that rapamycin, when given prophylactically to 2-month-old 3xTg-AD mice throughout their life, induces autophagy and significantly reduces plaques, tangles and cognitive deficits. In contrast, inducing autophagy in 15-month-old 3xTg-AD mice, which have established plaques and tangles, has no effects on AD-like pathology and cognitive deficits. In conclusion, we show that autophagy induction via rapamycin may represent a valid therapeutic strategy in AD when administered early in the disease progression." This research is actually fairly indicative of the field as a whole: mechanisms that are potentially modestly useful as ways to slow aging across life are forced into consideration as late-stage therapies only. This happens because regulators will not permit commercialization of ways to treat aging in otherwise healthy people - they only permit treatments for named diseases. So progress is necessarily sub-optimal where it is permitted at all.

OBESITY AND REGIONAL DIFFERENCES IN LIFE EXPECTANCY Thursday, September 29, 2011 http://www.fightaging.org/archives/2011/09/obesity-and-regional-differences-in-life-expectancy.php
Here is a different way of looking at the material consequences of living a life that allows you to become obese: "The United States has the highest prevalence of obesity and one of the lowest life expectancies among high-income countries. We investigated the relationship between these 2 phenomena. We estimated the fraction of deaths attributable to obesity by country, age, and sex and reestimated life tables after removing these deaths. To allow for a possible secular decline in obesity risks, we employed alternative risks from a more recent period. In our baseline analysis, obesity reduced US life expectancy at age 50 years in 2006 by 1.54 years for women and by 1.85 years for men. Removing the effects of obesity reduced the US shortfall by 42% for women and 67% for men, relative to countries with higher life expectancies. Using more recently recorded risk data, we estimated that differences in obesity still accounted for a fifth to a third of the shortfall. The high prevalence of obesity in the United States contributes substantially to its poor international ranking in longevity."

ON OXIDATIVE STRESS Tuesday, September 27, 2011 http://www.fightaging.org/archives/2011/09/on-oxidative-stress.php
A review paper on the roles of oxidative stress in aging, both negative and positive: "Oxidative stress is considered to be a major detrimental factor limiting longevity, as originally postulated in the free radical theory of aging. The oxidative stress leads to accrual of damaged/misfolded proteins, increased mutagenesis rate and inflammation. Ironically, due to its ability to accumulate over time (as it was seen in many neurodegenerative disorders), oxidative damage also emerged as a consequence of longevity per se. The human life-span exceeds that of most mammalian species at least 4 times (median life span records across 900 mammalian species is ~16 years). Importantly, anti-oxidative stress adaptations are not subjects of evolutionary pressure at post-reproductive age, which further contributes to the buildup of oxidative damage in aging individuals. Yet, paradoxically, in short-lived Caenorhabditis elegans, oxidative stress might have beneficial effect on longevity by connecting to the nutrition signaling pathways [such as those activated through calorie restriction]. It was suggested that aging is driven by over-activation of signal-transduction pathways such as the nutrient-sensing pathway, while oxidative stress may be both one of its activators and effectors."

REPROGRAMMING MUSCLE CELLS TO A PROGENITOR STAGE Monday, September 26, 2011 http://www.fightaging.org/archives/2011/09/reprogramming-muscle-cells-to-a-progenitor-stage.php
Via ScienceDaily: researchers "have turned back the clock on mature muscle tissue, coaxing it back to an earlier stem cell stage to form new muscle. Moreover, they showed in mice that the newly reprogrammed muscle stem cells could be used to help repair damaged tissue. The achievement [opens] the door to the development of new treatments to combat the degeneration of muscle associated with muscular dystrophy or aging. Muscle formation has been seen as a one-way trip, going from stem cells to myoblasts to muscle fiber, but we were able to get a multi-nucleated muscle fiber to reverse course and separate into individual myoblasts. For many years now, people have wanted to do this, and we accomplished that by exposing the tissue to small molecule inhibitor chemicals rather than altering the cell's genome.

These tiny chemicals go inside the cell and change the way the cell behaves without changing its genome. The inhibitors were only used for 48 hours, enough time for the fused myofibers to split into individual cells, and then they were washed away. The cells can proceed to live and die as normal, so there is no risk of them dividing uncontrollably to become tumors. Rather than going back to a pluripotent stage, we focused on the progenitor cell stage, in which cells are already committed to forming skeletal muscle and can both divide and grow in culture. Progenitor cells also differentiate into muscle fibers in vitro and in vivo when injected into injured leg muscle. To test the viability of the newly regenerated myobasts, the researchers first cultured them in the lab to show that they could grow, multiply and fuse normally into new myofibers. The researchers then injected the de-differentiated myoblasts into live mice with damaged muscles. After two to three weeks, we checked the muscle and saw new muscle fibers that glowed green, proving that the progenitor cells we derived from mature muscle tissue contributed to muscle repair in vivo in mice."

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