Life Extension Research
Youthfulness in a Plain Brown Wrapper
posted on June 2, 2009
First, a reminder:
Thursday at 3 PM Pacific, I will be speaking on a webinar. I sent you a notice about two weeks ago.
If you haven™t registered yet, go to www.nolimitshealthintensive.com. There™s no cost to register. It is a twelve week program with twelve fascinating presenters (well eleven, anyway) giving you lots of inside health secrets that you may have never heard before.
Now I™d like to introduce you to Ellen Wood.
Ellen is a dynamic teenager living in a georgous 72 year-old body. She™s also got a beautiful soul. Check her and her book out at www.howtogrowyounger.com.
My chapter on Attitude in Life Extension Express may be my most important chapter. If you animated that chapter, Ellen would pop out. Here is what she sent me on Saturday in the form of a newsletter:
Youthfulness in a Plain Brown Wrapper
I noticed her when she came into the room “ one of the last to arrive for my talk on how to grow younger. This small woman with gray hair was smartly dressed in a navy blue suit with the collar of a crisp white blouse peeking over the edges of her suit lapels.Â Her black heels were stylish but perhaps a little too high since they made her teeter as she walked. A serious expression on her beautiful face was in stark contrast to the animated faces of the others who were greeting friends and bringing the noise level near the crescendo of a comedy club.
What drew my attention to her was the way she looked furtively from side to side and then slunk down into a seat in the back, as though she was being hunted by someone and this seemed a good place to hide.
It was later, after my talk was over and the line for book signings and questions had thinned to a precious few, that I noticed her again.Â All the other seats were empty but she was still hunkered down, just waiting.Â For the police?Â A jealous ex-lover?Â Gotcha, you™re It?
Actually¦ none of these.Â After everyone else left, she came up to me and the intrigue was over.Â She just wanted to ask me a question but didn™t want anyone she knew to see her at a workshop about growing younger.
In a timid voice she told me her friends discussed my workshop and criticized it as vain attempts to hold back what™s natural and inevitable.
She told me they concluded, œIt™s against nature.Â We should just grow old gracefully.Â Wanting to grow younger is just vanity.
I told her I deeply respect those who feel we should grow old gracefully, but I don™t agree that we should accept the inevitability of decline.Â
Accepting that decline™s going to happen no matter what - brings with it all the programming we™ve accumulated over the years that associates age with progressive deterioration of mind and body.Â
And no, it™s not vanity to want to enjoy life with vigor; to live passionately; to feel good and share joy, love, accomplishment and adventure.Â That just doesn™t have to change because we live longer.
I noticed she was perking up. She straightened her shoulders and I swear she grew two inches. œThat™s how I feel, she told me and excitement began to creep into her voice.
I was back on my soapbox: this method is not about glorifying youthful appearance so you can get flattering remarks and admiring glances.Â But don't be surprised if you do.
If we, individually and collectively, change our image of aging, just think of the incredible contribution people our age can make to humankind.Â
We can be the pivotal generation group that bridges the old human way to the new. We can envision all of humanity living lives that are empowered and grow better and better as the years progress.Â I don't know what that looks like exactly - but the baby boomers, especially, are ripe for pioneering a new frontier of transformation and renewal.
I was giving my speech all over again and it felt so good! She gets it, I thought, as she broke into a big smile and we both hugged like we meant it.
I could tell there would be no more hiding for her.Â No more putting youthfulness ideas and techniques in a plain brown wrapper so people won™t know she™s partaking of something forbidden.
Dear Readers, let™s all come out in the open about our desire to be vital and healthy and fresh and alive!Â And if that™s called youthfulness, let™s embrace it with gusto.
Don™t you just love Ellen? Visit her site to get more.
RATIONALE FOR THE œMY BRIDGE 4 LIFE INITIATIVE
As a part of recent reorganization, the Methuselah Foundation introduced its first short-term initiative: My Bridge 4 Life. Dave Gobel, the Foundation CEO, recently explained the rationale behind the initiative:
"The reason for MB4L is that we are working to reduce the 'aha! gap' or conceptual hurdle for the billions of folks for whom a leap straight to the idea of extending healthy life is too vast and daunting a gap.
"The new effort - focused on the short term and exemplified by MB4L - is designed to gain the positive attention of the 99.9% of the population who have been too busy to pay attention to the real underlying problems [of degenerative aging], but to whom life has handed a very sad but compelling imperative - i.e. "I (or my loved one) has Cancer (or some other life-threatening condition)!" The goal of MB4L is to provide serious, valid and relevant medical information, family and community support, education and hopefully lifesaving insights to such people at very low cost. At the same time while adding supporters and generating donations in behalf of the foundation and its longer-term mission.
"During their involvement with MB4L it will become clear to MB4L's participants that the real enemy to defeat is the insidious underlying process that made them or their loved ones vulnerable to the disease that eventually attacked them. In a sense, MB4L is a real bridge that saves lives both in the present AND in the future. It is a bridge that brings people to understand the larger goals at a time when they are willing and able to listen."
LATEST HEALTHY LIFE EXTENSION HEADLINES
Forbes on Medical Tourism (May 29 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4225
The FDA forbids the development of new medical technologies long past the point at which any sane person would consider them a good risk, and in the process makes these technologies vastly more expensive. Medical tourism is a sane response to heavy-handed and unaccountable government employees: "Gregg Victor is one of the 1.5 million Americans who traveled abroad to get medical treatments last year. More than a few were pursuing new stem-cell-based treatments unavailable in the States.Â 'I am not waiting for the FDA to rule to get treatments,' says Gregg Victor, who chose her clinic in Germany after spending a year and a half looking into stem cell treatments available all over the world. Jordan happened upon TheraVitae, a Bangkok-headquartered biotechnology company that markets 'VesCell stem cell treatments' via licensing agreements with four clinics in Thailand. Thai doctors injected 25 million of his own stem cells into Jordan's heart. Twenty thousand miles, 22 days, a cardiac arrest and $43,000 later, he came home to his wife with an ejection fraction between 30% and 35%. Even Jordan's doctor had to admit he was happy with the results." Results are mixed, much as you'd expect. Caveat emptor, and do your research - but a great many people are materially benefiting from technologies still forbidden by their own governments.
Another Look at Hormesis (May 29 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4224
A little damage can be a good thing in a self-repairing system: "Oxidative stress has been linked to aging, cancer and other diseases in humans. Paradoxically, researchers have suggested that small exposure to oxidative conditions may actually offer protection from acute doses. One major contributor to oxidative stress is hydrogen peroxide, converted from a type of free radical that leaks from the mitochondria as it produces energy. [Researchers] used the rich functional genomics toolbox of yeast to identify pathways involved in the cell's adaption to hydrogen peroxide. Adaption (or hormesis) is an effect where a toxic substance acts like a stimulant in small doses, but is an inhibitor in large doses. This finding may explain recent studies suggesting that eating less may, in fact, raise [oxidant] levels - and, in doing so, provide protection from acute doses of oxidants.Â This is counter to the hypothesis that caloric restriction extends lifespan in some species because it reduces [oxidants] produced as a by-product of the energy generated by mitochondria. It may be that adaption to oxidative stress is the main factor responsible for the lifespan-expanding effects of caloric restriction." Possibly, but my money is still on enhanced autophagy as the major mechanism.
Telomere Length and Years of Healthy Life (May 27 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4221
Shorter telomeres appear to be a bad thing, but their relationship to longevity is not straightforward: "Although telomere length (TL) is known to play a critical role in cellular senescence, the relationship of TL to aging and longevity in humans is not well understood. In a large biracial population-based cohort, we tested the hypotheses that elderly persons with shorter TL in peripheral white blood cells have poorer survival, shorter life span, and fewer years of healthy life (YHL). ... TL [was] not associated with overall survival or death from any specific underlying cause including infectious diseases, cancer, or cardiac and cerebrovascular diseases. TL, however, was positively associated with more YHL. Findings suggest that TL may not be a strong biomarker of survival in older individuals, but it may be an informative biomarker of healthy aging."
Which suggests to me that telomere length is broadly associated with all sorts of poor health and age-related decline, but modern medicine is blunting the resulting hit to life expectancy. Questions of cause and effect remain, however: is telomere shortening merely a reflection of other age-related damage, or a fundamental damage-causing process itself?
Working with Neurogenesis (May 27 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4220
What could medical science do with a reliable way of generating new neurons in the brain? "Researchers have identified a new mechanism that plays a central role in adult brain stem cell development and prompts brain stem cells to differentiate into neurons. Their discovery, known as Integrative FGFR1 Signaling (INFS) [is] considered capable of repopulating degenerated brain areas, raising possibilities for new treatments for Parkinson's disease, Alzheimer's disease and other neurodegenerative disorders. The approach uses gene engineering and nanoparticles for gene delivery to activate the INFS mechanism directly and promote neuronal development. The INFS-targeting gene can prompt these stem cells to differentiate into neurons. The research team set out to see if it is possible to generate a wave of new neurons from stem cells and direct them to the affected areas. [There is] the need for further development of gene delivery methods for the treatment of neuronal loss. Targeting the INFS mechanisms by small molecules could potentially replace the need for gene transfers and create a classical drug therapy for the neuronal loss."
Update on Catalase in the Mitochondria (May 25 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4217
You might recall that mice genetically engineered to generate more of the antioxidant catalase in their mitochondria live longer in good health. Similarly, ingested antioxidant compounds engineered to migrate to the mitochondria have much the same effect (but don't go looking for that in the stores - it's only in the lab so far). Other ingested antioxidants are a wash - no effects, or negative effects. Here's an update from the group working on catalase-producing mice: "Age is a major risk for cardiovascular diseases. Although mitochondrial reactive oxygen species have been proposed as one of the causes of aging, their role in cardiac aging remains unclear. We have previously shown that overexpression of catalase targeted to mitochondria (mCAT) prolongs murine median lifespan by 17% to 21%. Cardiac aging in mice is accompanied by [a number of characteristic biochemical and structural forms of damage and change in the heart, heart tissue, and heart cells]. All of these age-related changes were significantly attenuated in mCAT mice." Much as one would expect: less damage to cells and tissues means a longer life, on average.