Maximum Life Foundation - Accelerating Progress in Anti-Aging Medicine Research for Life E

Healthy Aging, Longevity and Life Extension

2009-01-26T09:50:00.000-08:00

Dear Future Centenarian,

Almost twenty years ago, I bought some furniture from one of the nicest, most gentle men I ever knew. He owned a furniture store in my hometown, Johnstown, PA. That was the first time I met him, even though I went to high school with his son.

He came to my home to ensure delivery went well, and we got into a long conversation. I don’t remember much of the discussion, but a lot of it had to do with aging and how great his life was up to recently. One sentence stuck with me for twenty years and helped shape my future. That sentence was:

“I never thought it would be like this.”

Mr. Gearhart was probably in his 70’s at the time, and he was not aging well. He was afflicted with early-stage Parkinson’s which prompted him to explain to me how aging absolutely sucked. He went on to say he always knew he would grow old, and then he laid that haunting sentence on me. It was a distressing conversation for me and a sad time for his family. I’m sure he’s gone by now, and his death must have been agonizing. He wasn’t one of the “lucky” ones with a squared mortality curve.

A squared mortality curve is where a person stays healthy until he or she dies. Most gerontologists try to square mortality curves to alleviate old age suffering. Most mortality curves decline from birth to death, especially in the later stages of life. That means your health gradually declines as you age, usually severely in the last ten years or so, just like Mr. Gearhart’s. So squaring the curve generally means a quick comfortable death.

A squared curve is not my goal. A horizontal one is. That would be where you stay in top shape with no end in sight. You would see no decline, because you wouldn’t age. (Yes, I know a “horizontal curve” is technically not a curve, but a line. I hardly ever get to coin a term though, so I’m going to keep using it.)

Then, if an accident suddenly ended your life, your curve would then become squared.

If you’re not yet convinced that keeping your mortality curve horizontal is possible, I’m sure you most certainly prefer a squared curve to that of a declining one. Personally, I’m holding out for quality AND quantity.

But whichever your goal is, you will advance toward it by keeping up with the weekly information in Longevity News Digest.

By the way, a horizontal curve is my goal for you as well as for me.

P.S. If you have donated to Maximum Life Foundation and are waiting for your final premiums, your wait is almost over. Stem Cell Products is taking delivery next week of their first inventory of Signals, the breakthrough skin care line. You will be receiving yours soon, and your wait will have been worth it. If you have had a change of address, please let me know.
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AVOID CHRONIC INFLAMMATION

Chronic inflammation is a potent source of biochemical damage that contributes to age-related disease. A reminder of the way in which that works and what can be done:

http://www.fightaging.org/archives/001659.php

The best short term way of evading chronic inflammation, and thereby increasing your chances to living more healthy years, is to avoid carrying excess visceral fat. But that only gets you so far: eventually even the healthiest immune system in the healthiest body starts to fall into a permanent condition of chronic inflammation called inflammaging. Evolution didn't produce a system that can be used for as long as we modern humans would like."

So when Reason says 'avoid chronic inflammation' he’s not really talking about sane lifestyle choices, although that's very necessary as well. He really means 'do what you can to help advance medical research into repairing our aged immune systems.' As time goes by, you'll find that the greatest determinant of your health and longevity is medical technology that can repair the damage of aging. While we're healthy and active, we should do what we can to advance that medical research; it'll pay off later.
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LATEST HEALTHY LIFE EXTENSION HEADLINES

Indy Longevity Mutation Works through Mitochondria (January 23 2009) http://news.brown.edu/pressreleases/2009/01/aging
Another longevity mutation is shown to work by reducing the all-important emission of free radicals from the mitochondria: "first discovered in 2000 [a] mutation in the Indy ('I'm Not Dead Yet') gene [extends] the life span of fruit flies. Subsequent studies of the Indy flies have led to the new finding that a mechanism in those genetically altered fruit flies appears to reduce significantly the production of free radicals, a cellular byproduct that can contribute to the aging process. This intervention takes place with few or no side effects on the quality of life for the fruit fly. The discovery could lead to the development of new anti-aging treatments. There are very few, if any, interventions that are known to dramatically extend healthy lifespan. Understanding how [the] Indy mutation alters the metabolic state of the fruit fly would allow someone to come up with pharmacological interventions that could mimic it and give you the benefit of genetic manipulation without having to do genetics."

Geron Going to Trials with Stem Cell Therapy (January 23 2009) http://www.nytimes.com/2009/01/23/business/23stem.html
As the New York Times reports, Geron's embryonic stem cell therapy for spinal injuries is soon entering phase I human trials. Make what you will of timing, and consider that in the absence of the FDA this would already be in clinics: "The clearance of the clinical trial - of a treatment for spinal cord injury - is to be announced Friday. Geron's trial will involve 8 to 10 people with severe spinal cord injuries. The cells will be injected into the spinal cord at the injury site 7 to 14 days after the injury occurs, because there is evidence the therapy will not work for much older injuries. Geron's therapy involves using various growth factors to turn embryonic stem cells into precursors of neural support cells called oligodendrocytes, which are then injected into the spinal cord at the site of the injury. The hope is that the injected cells will help repair the insulation, known as myelin, around nerve cells, restoring the ability of some nerve cells to carry signals. There is also some hope that growth factors produced by the injected cells will spur damaged nerve cells to regenerate." By way of a reminder, we should all be interested in technologies for myelin repair, given the evidence for a general decline in myelin during aging.

Rebuilding Nerves with Viruses (January 22 2009) http://www.technologyreview.com/biomedicine/21991/
From the Technology Review: "Researchers working on tissue engineering hope to eventually be able to use a patient's own cells to grow replacement tissue for damaged hearts, livers, and nerves. But mimicking the structure and function of the body's tissue has proved difficult. Matrices of supportive, fibrous proteins sustain the cells of the heart, lungs, and other tissues in the body. These scaffolds provide both structural support and chemical signals that enable an organ or nerve tissue to function properly. Viruses that mimic supportive nerve tissue may someday help regenerate injured spinal cords. While other tissue-engineering materials must be synthesized and shaped in the lab, genetically engineered viruses have the advantage of being self-replicating and self-assembling. They can be designed to express cell-friendly proteins on their surfaces and, with a little coaxing, be made into complex tissue like structures. Preliminary studies show that scaffolds made using a type of virus called a bacteriophage (or phage) that infects bacteria but cannot invade animal cells can support the growth and organization of nerve cells."

Beyond Stem Cells (January 21 2009) http://www.agemed.org/default.asp?page=ShaneLaskyBeyondStemCellsJan09
A fascinating article: "stem cells are an imprecise physiological system to directly communicate to cellular networks of a host organism. The future of stem cell research will not necessarily be in the transplantation of stem cells to a specific pathogenic tissue region, but rather in reeducating or reprogramming that particular cellular network. Each organism has an exacting molecular blue print, which as a function of epigenetics, is either enhanced or mollified through its interfacement with a particular environmental milieu. Stem cell transplantation is not a precise strategy for amelioratively reprogramming cellular networks, which are compromised. In most instances, the stem cells, which have been transplanted are only inducing a minimum benefit in terms of their medicinal efficacy. Stem cell transplantation is not a therapeutic pantheon, but rather a way to comprehend how to modify a tissue's proteomics or physiological processes. Clinical medicine in the future will not involve providing imprecise cellular substrates, which vaguely impact genetic transcription and translation or millions of stem cells to a pathophysiologic tissue. Medical therapies will [instead] be a precise utilization of peptides which can ardently reprogram an overall.

Regenerating Stroke Damage (January 19 2009) http://news.bbc.co.uk/2/hi/health/7795586.stm
The BBC looks at a clinical trial for Reneuron's foetal-derived stem cell line: "A Glasgow team is to launch a major trial to assess whether stem cells can be used to treat stroke patients. If it works, as it has done in animal model systems, it may allow new nerve cells to grow or regeneration of existing cells and actual recovery of function in patients who would not otherwise be able to regain function. For the high proportion of patients who make an incomplete recovery [you] can reorganize the brain, you can help that reorganization with physiotherapy but you cannot cause new nerve cells to grow. The hope with stem cell therapy is that by putting in new cells and new tissue that you can further improve on that recovery. We have only taken one donation of tissue to make this product. We have a technology that is able to scale up an individual cell into all of the cells that are required to treat thousands of patients. We think this is a major plus in the technology we have and really negates the ethical concerns about the original use of fetal tissue."

A Look at Osiris Therapeutics (January 19 2009) http://pharmexec.findpharma.com/pharmexec/ArticleStandard/Article/detail/575911?contextCategoryId=47505
An interview with the Osiris Therapeutics president is as revealing of the way in which the FDA constrains progress as it is of the work being done. Broadly promising scientific applications are held back for years and squashed down to minor, narrowly approved uses - and everyone involved has to speak as though this is wonderful and the best of all possible worlds lest they are targeted for retribution. It's a sorry state of affairs. From the interview: mesenchymal stem cells or MSCs "do three things: They downregulate inflammation, they work to regenerate the damaged connective tissue, and they prevent scarring or fibrosis. That's the Holy Trinity of the mesenchymal stem cell. It's the natural progression or sequence of how we respond to injury. When we're young, that process works well. Children heal in miraculous ways. Conversely, an elderly person will die of something like a fractured hip. This is because children have 1,000-fold more MSC in their body than adults do. What happens is an adult ends up with a very exaggerated inflammatory response, a weak regenerative response, and a lot of scarring. We can reverse that trend by administering MSC. Because MSCs naturally have a broad range of things they can respond to, our job is to package them as something that will satisfy the FDA."

Value Reflections

2009-01-13T13:40:00.000-08:00

One of the advantages of old age is your increased ability to reflect. You can reflect on the mistakes you made and on your regrets as some people choose to do most of the time. That’s called dwelling. Or, you can briefly reflect on those negative experiences and learn from them. That’s called wisdom.

An even more positive form of reflection is value reflection. No matter whom you are or how you measure your levels of happiness and success, you definitely have created and/or experienced values during your lifetime. Value reflection is one of the most rewarding and pleasurable experiences of life. Who doesn’t like to relive happy memories? Who doesn’t take pride and pleasure in looking back on the positive contributions you made to society, your market, your family, your friends and to yourself?

We all carry within us a treasure of values to be proud of, and with each passing year, that treasure grows, whether you are aware of it or not.

With extended longevity, imagine your possibilities. Not only is technology growth exponential, but so is personal growth. And if you remain vibrant, your enthusiasm can actually intensify with age.

In past issues, I wrote about how the power of technology doubles every year, including the technology that contributes to radical life extension. That means next year will see a doubling of all that power we made since the beginning of history. And here is what that means to you:

If you take the healthy steps to live an extra year, the technology that could lead to your open ended lifespan doubles in that year. If you decide to adopt a lifestyle that adds ten more quality years to your life, life enhancing technology will increase by over 1000 times! And then if you try just a little harder and add another extra year, the power of that technology will double to 2000 times. That means your 11th extra year was just as beneficial to you as those first extra ten.

Then add another year and… well, you get the idea. Before you know it, we will have cracked the longevity code, and you will be on your way to endless youth.

And what could one of the most pleasurable things about that be? As I said, more and more years to add happiness and value and even better value reflection. Imagine what you can accomplish in two lifetimes. In three or more. Imagine how big your values treasure chest will grow as you exponentially acquire wisdom.
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LATEST HEALTHY LIFE EXTENSION HEADLINES

The Life Expectancy Puzzle of Left-Handedness (December 05 2008) http://pmid.us/19044215
Many identified differences in human longevity between groups lack conclusive explanations, such as why women have a greater life expectancy. Differences in life expectancy due to handedness are another puzzle: "Many studies report that left-handers have a shorter longevity than right-handers, and the present study may provide a possible explanation for that finding. In a Cardiac Rehabilitation Unit for the elderly with a mean age of 75.2 years the prevalence of left-handers was 16.7%. This latter value was significantly different from the 6.7% in controls of similar age. These data suggest that heart disease may be one reason for a reduced longevity among left-handers. Left-handers use the right hemisphere for movement, and unilateral activation of that hemisphere in the form of EEG desynchronization and deactivation in the form of EEG slow waves are both related to cardiac abnormalities." In the grand scheme of things these differences are unimportant: the greatest determinant of our future longevity is progress in the application of aging research.

On Immunosenescence (December 05 2008) http://pmid.us/19047800
Researchers discuss the failing, age-damaged immune system: "At present, individuals can live up to 80-120 years, a time much longer than that of our ancestors, as a consequence of the improvements in life conditions and medical care. Thus, the human immune system has to cope with a lifelong and evolutionarily unpredicted exposure to a variety of antigens, which are at the basis of profound age-related changes globally indicated as immunosenescence, a multifaceted phenomenon that increases morbidity and mortality due to infections and age-related pathologies. The major changes occurring during immunosenescence are the result of the accumulation of cellular, molecular defects and involutive phenomena (such as thymic involution) occurring concomitantly to a hyperstimulation of both innate and adaptive immunity (accumulation of expanded clones of memory and effector T cells, shrinkage of the T cell receptor repertoire, progressive activation of macrophages), and resulting in a low-grade, chronic state of inflammation defined as inflammaging. It is unknown whether inflammaging, which represents a risk factor for most age-related pathologies, is a cause or rather an effect of the aging process. Centenarians seem to be equipped with gene variants that allow them to optimize the balance between pro- and anti-inflammatory molecules, and thus to minimize the effects of the lifelong exposure to environmental insults and stressors."

Dormant Emergency Stem Cells (December 04 2008) http://www.eurekalert.org/pub_releases/2008-12/haog-dsc120408.php
An intriguing discovery from a cancer research group that I suspect has more promise for the field of regenerative medicine: "Up to now, scientists have assumed that adult stem cells have a low division rate. According to theory, they thus protect their DNA from mutations. [Researchers] have now discovered a group of stem cells in mouse bone marrow that remain in a kind of dormancy [and] divide only about five times throughout the life of a mouse. Translated to humans, this would correspond to only one cell division in 18 years. In contrast, stem cells of the larger group, the 'active' stem cells, divide continuously about once a month. However, in an emergency such as an injury of the bone marrow or if the messenger substance G-CSF is released, the dormant cell population awakes. Once awakened, it shows the highest potential for self-renewal ever to be observed in stem cells. If transplanted into irradiated mice, these cells replace the destroyed bone marrow and restore the whole [blood] system. It is possible to isolate new dormant stem cells from the transplanted animals and these cells are able to replace bone marrow again – this can be done several times in a row. The situation is different with 'active' stem cells, where bone marrow replacement can successfully be carried out only once."

Evidence Against the Cancer Stem Cell Theory (December 03 2008) http://www.eurekalert.org/pub_releases/2008-12/uom-usp112608.php
It would be good for all of us if the cancer stem cell theory turns out to be true for even a majority of cancer types - as this would mean that a side-effect of stem cell research will be a cure for cancer. Unfortunately, there are good reasons to believe that this will not be the case; nothing in human biochemistry is as simple as we'd like. From EurekAlert!: "the cancer stem-cell model [must] be reassessed because it is based largely on evidence from a laboratory test that is surprisingly flawed when applied to some cancers. I think the cancer stem-cell model will, in the end, hold up for some cancers. But other cancers, like melanoma, probably won't follow a cancer stem-cell model at all. Scientists previously estimated that only one in 1 million melanoma cells has the ability to run wild, exhibiting the kind of unchecked proliferation that leads to new tumors. These aggressive interlopers are the cancer stem cells, according to backers of the model. But after updating and improving the laboratory tests used to detect these aberrant cells, [researchers] determined that at least one-quarter of melanoma cells [have] the ability to form new tumors. The assay on which the field is based misses most of the cancer cells that can proliferate to form tumors. Our data suggest that it's not going to be possible to cure melanoma by targeting a small sub-population of cells."

Senescent Cells and Cancer (December 03 2008) http://dx.doi.org/10.1371/journal.pbio.0060301
One of the consequences of an aging immune system is that it stops removing senescent cells - certainly, senescent cells increase dramatically with age. Here is a look at why that process is likely to increase your cancer risk: "Although 'cellular senescence' can suppress tumor formation from damaged cells by blocking the cell division that underlies cancer growth, it has also been implicated in promoting cancer and other age-related diseases. To understand how this might happen, we measured proteins that senescent human cells secrete into their local environment and found many factors associated with inflammation and cancer development. Senescent cells promote the growth and aggressiveness of nearby precancerous or cancer cells. Our findings support the idea that cellular senescence can be both beneficial, in preventing damaged cells from dividing, and deleterious, by having effects on neighboring cells; this balance of effects is predicted by an evolutionary theory of aging." Senescent cells are a prime target for the same sorts of discerning therapies being developed to kill cancer cells with no side-effects.

Towards Tuning the Immune System (December 02 2008) http://www.sciencedaily.com/releases/2008/11/081130153102.htm
Researchers are making good progress towards control over immune cells, and future goals seems likely to be applicable to the restoration of some function to an age-damaged immune system. Researchers have identified "seven different receptors on T cells that can tamp down immune responses during a prolonged battle with an infectious pathogen or against developing cancer. Chronic over-stimulation of the immune system can lead to poor control of infections and cancer, so the results explain why it is that these key immune cells gradually become 'exhausted' and ineffective over time. We are starting to see a picture emerging of a really tuneable array of inhibitory receptors expressed on T cells. That suggests it may be possible to not only dramatically enhance antiviral or antitumor T cell responses, but also to fine tune which response you want to enhance in order to reverse T cell exhaustion and continue fighting an infection or disease. This presents us with a great clinical opportunity. T cells have a lot of weapons at their disposal to control viral infection and most of them are disarmed when these cells become exhausted. It may be possible to selectively rearm T cells while generally reinvigorating them."

More on Exercise and the Aging Brain (December 01 2008) http://www.eurekalert.org/pub_releases/2008-12/rson-ehp112508.phpIt's well worth remembering that regular exercise brings benefits that no present medical technology can match-and at a fraction of the cost of medicines that do far less. EurekAlert! notes that researchers compared "brain scans of older adults who exercise to brain scans of those who do not. The researchers recruited 12 healthy adults, age 60 to 76. Six of the adults had participated in aerobic exercise for three or more hours per week over the last 10 years, and six exercised less than one hour per week. All of the volunteers underwent MRI to determine cerebral blood flow and MR angiography to depict blood vessels in the brain. Researchers were able to make 3-D models of the blood vessels and examine them for shape and size. They then compared the blood vessel characteristics and how they related to blood flow in both the active and inactive groups. The results showed that the inactive group exhibited fewer small blood vessels in the brain, along with more unpredictable blood flow through the brain. The active adults had more small blood vessels and improved cerebral blood flow. These findings further point out the importance of regular exercise to healthy aging."

Kekich’s Credo

2009-01-12T13:34:00.000-08:00

Dear Future Centenarian,

About 21 years ago, I was reflecting on some really dumb mistakes I made in my life and what I could do to keep from repeating them. So I drew on almost all the positive lessons I learned and on all the wisdom of people and mentors whose paths I crossed. The result was personal rules of life encapsulated in 100 credos. I named it Kekich’s Credo” and studied it religiously.

A friend of mine got a copy and published it in his newsletter. Then it spread to another newsletter and so on, and in some circles I became known as “The Credo Guy”.

Last October, Pete Hilgartner, a very bright and fascinating chiropractor, called me to ask permission to publish some of my credos in his newsletter. He went on the say he wanted to write a little essay on each as they pertain to health and well-being. Since then, he did about twenty. From time-to-time, I will share some of Dr. Pete’s gems with you, starting with this one:

1. People will do almost anything to stay in their comfort zones. If you want to accomplish anything, get out of your comfort zone. Strive to increase order and discipline in your life. Discipline usually means doing the opposite of what you feel like doing. The easy roads to discipline are 1) setting deadlines, 2) discovering and doing what you do best and what's important and enjoyable to you and 3) focusing on habits by replacing your bad habits and thought patterns, one-by-one, over time, with good habits and thought patterns.

What health habits (or lack thereof) are you holding on to that are keeping you from your goals?

Are you trying to lose weight? Get strong? Get rid of back pain? Maybe you're ignoring your high blood pressure or triglycerides. "Yumm! that pizza just looks too good! I'll be more disciplined tomorrow..."

Here's a wake up call... NO YOU WON'T!

If you want a different outcome in your life, on any dynamic, you have to DO something different, NOW! The same-ol', same-ol 'is gonna get you the same-ol', same-ol'.

Yes, new habits are tough. They take you out of your comfort zone.

Getting up in the morning to stretch before you do anything else (OK, you can go pee first) is going to be new... but what will you gain? Is the pleasure of what you will gain worth the short term discomfort of doing what you haven't done before? What about giving up the donuts and replacing it with an egg? How about taking a walk instead of watching TV?

Change is actually easy once you decide what it is that you really want and don't let anything stand in the way of making that decision a reality. Excuses are simply a way for you to stay in your comfort zone.

When you hear that little voice in your head start to make excuses or rationalize, shout "STOP! Thank you for sharing...now go away...I choose to _______ (fill in the blank.) I'm DONE with my comfort zone!"

You can certainly stay in that warm bed and not go for that walk you planned. After all you can start tomorrow...

The choice is yours... but so are the results.

How are your choices working for you?

This guy is something else, isn’t he? How’d you like to have someone like Dr. Pete as your personal chiropractor? You can find more about him at www.drshilgartner.com.
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LATEST HEALTHY LIFE EXTENSION HEADLINES

The Age of the Cyborg (January 09 2009) http://www.publicaffairs.ubc.ca/ubcreports/2009/09jan08/cyborg.html
The cyborg age is sneaking up on us by way of the tools of tissue engineering and improvements in nanoscale manufacture. Sooner or later most of us will have artificial structures in our bodies - though perhaps not the ones we imagined having when we were young: "With age, the human body wears out. And engineered materials - metals, polymers and ceramics - increasingly help repair or replace injured or destroyed body parts. As we become more sophisticated in our ability to design materials, particularly at the nanoscale, we open all kinds of opportunities for repairing damaged body parts. The potential is really unlimited. Considering the great strides materials engineers are making in developing materials that are readily accepted by the body and that accelerate the process of recovery and healing, the age of the Cyborg seems not so much science fiction as it does science fact - a good thing given the increasing life expectancy and enduring desire to lead active lives."

Most Likely Not Programmed Aging (January 08 2009) http://www.eurekalert.org/pub_releases/2009-01/sumc-sru010509.php
From EurekAlert!: "Two previously identified pathways associated with aging in mice are connected. The finding reinforces what researchers have recently begun to suspect: that the age-related degeneration of tissues [is] an active, deliberate process rather than a gradual failure of tired cells. Derailing or slowing this molecular betrayal, although still far in the future, may enable us to one day tack years onto our lives ... There is a genetic process that has to be on, and enforced, in order for aging to happen. It's possible that those rare individuals who live beyond 100 years have a less-efficient version of this master pathway." I suspect that one reason that theories of programmed aging remain somewhat popular is that the reactions of our cells to a slow stochastic accumulation of biochemical wear and tear do look something like the unfolding of a program. Gene expression steadily changes as the damage mounts. So you see research like this, said to support programmed aging but which could just as well support aging as an accumulation of damage. Researchers are linking changes in gene expression previously noted to be important to aging and longevity, but without evidence of the root cause of these changes, it's premature to declare aging programmed.

Provoking Regeneration (January 08 2009) http://www.eurekalert.org/pub_releases/2009-01/icl-scu010709.php
From EurekAlert!: "When a person has a disease or an injury, the bone marrow mobilizes different types of stem cells to help repair and regenerate tissue. New research [shows] that it may be possible to boost the body's ability to repair itself and speed up repair, by using different new drug combinations to put the bone marrow into a state of 'red alert' and send specific kinds of stem cells into action. In the new study, researchers tricked the bone marrow of healthy mice into releasing two types of adult stem cells - mesenchymal stem cells, which can turn into bone and cartilage and that can also suppress the immune system, and endothelial progenitor cells, which can make blood vessels and therefore have the potential to repair damage in the heart. The researchers were able to choose which groups of stem cells the bone marrow released, by using two different therapies. Ultimately, the researchers hope that their new technique could be used to repair and regenerate tissue, for example when a person has heart disease or a sports injury, by mobilizing the necessary stem cells. The researchers also hope that they could tackle autoimmune diseases such as rheumatoid arthritis, where the body is attacked by its own immune system, by kicking the mesenchymal stem cells into action."

More on Tissue Engineering of Bone Marrow (January 07 2009)
http://www.economist.com/science/tm/displaystory.cfm?story_id=12883495
From the Economist: "tissue engineers have mastered the arts of artificial skin and bladders, and recently they have managed to rig up a windpipe for a patient whose existing one was blocked. But more complicated organs elude them. And simpler ones, too. No one, for instance, has managed to grow bone marrow successfully. At first sight, that is surprising. The soft and squishy marrow inside bones does not look like a highly structured tissue, but apparently it is. That does not matter for transplants. If marrow cells are moved from one bone to another they quickly make themselves at home. But it matters for research. Bone marrow plays an important role in the immune system, and also in bodily rejuvenation. Stem cells that originate within the marrow generate various sorts of infection-fighting blood cells and also help to repair damaged organs. However, many anti-cancer and anti-viral drugs are toxic to marrow. That leaves patients taking them susceptible to disease and premature ageing. Experiments intended to investigate this toxicity using mice have proved unsatisfactory. Nicholas Kotov of the University of Michigan in Ann Arbor and his colleagues have therefore been trying to grow human marrow artificially."

Continued Improvement in iPS Cells (January 07 2009) http://www.eurekalert.org/pub_releases/2009-01/bu-cas010709.php
Researchers continue to rapidly improve the technology of production for induced pluripotent stem (iPS) cells: a "research team has discovered a more efficient way to create [iPS] cells, derived from mouse fibroblasts, by using a single virus vector instead of multiple viruses in the reprogramming process. The result is a powerful laboratory tool and a significant step toward the application of embryonic stem cell-like cells for clinical purposes such as the regeneration of organs damaged by inherited or degenerative diseases. Prior research studies have required multiple retroviral vectors for reprogramming - steps that depended on four different viruses to transfer genes into the cells' DNA - essentially a separate virus for each reprogramming gene. Upon activation these genes convert the cells from their adult, differentiated status to what amounts to an embryonic-like state. However, the high number of genomic integrations - 15 to 20 - that typically occurs when multiple viruses are used for reprogramming, poses a safety risk in humans, as some of these genes [can] cause cancer. The major milestone [was] combining the four vectors into a single 'stem cell cassette' containing all four genes. The cassette (named STEMCCA) [was] able to generate iPS cells more efficiently - 10 times higher than previously reported studies."

More on Skulachev's Research and SkQ1 (January 06 2009) http://pmid.us/19120018
One of the items I'd like to see reasonably settled soon is whether longevity can be reliably engineered by targeting antioxidant compounds to the mitochondria and thereby slowing the accumulation of damaged mitochondria and their contribution to aging. We have good demonstrations that it can, and good demonstrations that it can't. Something interesting is clearly going on (as indicated by mice living significantly longer than they ordinarily would), but the details are still fuzzy. One of the lines of this research I've been following for a while is the work of Skulachev and colleagues in Russia, who seem to have developed an ingested compound called SkQ1 that can perform the mitochondrial targeting trick without the need for gene engineering of the sort employed by Rabinovitch. Here's the latest paper from that group: "Very low (nano- and subnanomolar) concentrations of 10-(6'-plastoquinonyl) decyltriphenylphosphonium (SkQ1) were found to prolong lifespan of [an] insect (Drosophila melanogaster) and a mammal (mouse). The lifespan increase is accompanied by rectangularization of the survival curves (an increase in survival is much larger at early than at late ages) and disappearance of typical traits of senescence or retardation of their development. Data summarized here and in the preceding papers of this series suggest that mitochondria-targeted antioxidant SkQ1 is competent in slowing down execution of an aging program responsible for development of age-related senescence."

Enthusiasm for Regenerating Teeth (January 06 2009) http://seattletimes.nwsource.com/html/nationworld/2008593860_teeth06.html
From the Seattle Times: "the real news about the future of dentures is that there isn't much of one. It turns out wisdom teeth are prolific sources of adult stem cells needed to grow new teeth for you. From scratch. In your adult life, as you need them. In the near future. Regenerating a whole tooth is no less complicated than rebuilding a whole heart. Not only do you have to create smart tissue (nerves), strong tissue (ligaments) and soft tissue (pulp), you've got to build enamel - by far the hardest structural element in the body. And you have to have openings for blood vessels and nerves. And you have to make the whole thing stick together. And you have to anchor it in bone. And then you have to make the entire arrangement last a lifetime in the juicy stew of bacteria that is your mouth. It's a nuisance, but researchers are closing in on it. They think the tooth probably will be the first complex organ to be completely regenerated from stem cells. In part, this is because teeth are easily accessible. Nobody is predicting when the first whole tooth will be grown in a human, although five to 10 years is a common guess."

An Interview with Jason Silva (January 05 2009) http://www.bravenewtraveler.com/2009/01/05/interview-jason-silva-on-how-science-will-make-you-live-forever/An interesting interview: "I believe humans have always overcome their biological limitations. It is what has brought us out of the caves and onto the moon. We have cured ourselves of diseases, we fly remarkable machines through the air at 500 miles per hour. We communicate instantly and wirelessly across the world. Why is it such a stretch to imagine us re-programming our biochemistry (much like computer software) so that we may alleviate suffering, decay, and death? Death is a profound tragedy. Human consciousness is basically a profound (and valuable) pattern of information residing in a complex biological machine. This machine can repair itself for a certain period, but over time it wears out and decays at a faster rate than it can fix itself. This is why we die. Today, however, we are at the verge of correcting this. Death is the loss of everything that matters - It is our memories, our loves, the images and dreams that define us - the songs that moved us and the films that shaped us. Death takes this all away. I argue that in the same way we feel compelled to preserve the works of Shakespeare and other great works of art, why shouldn't we extend this into our physicality?"

New "Miracle" Anti- Aging Products

2008-12-16T16:45:00.000-08:00

It was a fun week.

I just returned from a large annual anti-aging conference and trade show. Every year unveils new “miracle” anti-aging products. Doctors and others lectured for almost a week, and the trade show lasted three days. Thousands attended, mostly physicians.

It was an interesting mix of practitioners, serious scientists, some serious and not so serious participants and a few hundred companies and individuals promoting a huge mix of anti-aging products and services.

I especially enjoyed meeting new people in this exciting field and getting together with old friends. Saturday evening was most stimulating, because I had a chance to take part in brain-stretching discussions with very legitimate scientists, physicians and activists at a private event. We even had a chance to discuss some of the newer products and services on the market. Some credible, backed by scientific studies. Some were worthless snake oil. And there were a whole lot in between that I just couldn’t figure out. I’m not the only one either.

So out of the hundreds or thousands of anti-aging products displayed at shows like this… or especially on the Internet, how do you know what works and what doesn’t? That’s an important question, since your life may depend on it.

How’s that? Your life?

Sure. And here’s why.

As you’ve heard me say over and over, we are going to be able to reverse the damage aging does to you one of these days. And when that happens, you, if you are still alive, could be transformed from the old person you are growing into, to a twenty-something improved version of your former self. And then, you will essentially have a youthful open-ended lifespan ahead of you.

But whether or not you live long enough to see that day could be largely up to you. Don’t forget, your genes only account for 25-35% of your destiny. (And science is working on fixing that 25-35% too.) You largely control the rest.

That’s why knowing which supplements or medical treatments work, and which don’t, might save your life. The extra few or more years the effective ones could add to your lifespan could very well be the difference between your living long enough to take advantage of tomorrow’s life extending miracles… or just barely missing out.

I had a very interesting conversation with two separate gentlemen at the event which led me to a conclusion. Maximum Life Foundation may be positioned to filter most of the anti-aging claims and information that overwhelm us. If we can find out what actually works and what doesn’t, then you will have a handy source of information. It will take several months to work out the details and to determine if we have the time to do this. And if we or someone else can, you will benefit.

Meanwhile, I just finished my longevity book, Life Extension Express, "7 steps you can take now, to catch the emerging wave of medical breakthroughs… for a youthful, indefinite (yes, indefinite) lifespan."

You can get a big jump on boosting your longevity by reading it. You’ll be able to get a copy from Amazon soon, but better yet, you can have a FREE downloadable copy by going to www.MaxLife.org now.
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LATEST HEALTHY LIFE EXTENSION HEADLINES

Gene Therapy Versus Periodontitis and Arthritis (December 12 2008) http://www.eurekalert.org/pub_releases/2008-12/uom-gte121008.php
Via EurekAlert!: "Using gene therapy, [researchers] found a way to help certain cells using an inactivated virus to produce more of a naturally-produced molecule soluble TNF receptor. This factor is under-produced in patients with periodontitis. The molecule delivered by gene therapy works like a sponge to sop up excessive levels of tumor necrosis factor, a molecule known to worsen inflammatory bone destruction in patients afflicted with rheumatoid arthritis, joint deterioration and periodontitis. Targeted Genetics released human trial results that showed the same gene therapy approach [had] positive affects in human patients with rheumatoid arthritis. The company tested 127 human subjects and showed a 30 percent improvement in pain relief, and gain of function, among other enhancements using the gene treatment. The gene also delivers quite a bit of genetic bang for the buck. The periodontal tissues were spared from destruction by more than 60-80 percent with the use of gene therapy. If you deliver the gene into the target cells once, it keeps producing in the cells for a very long period of time or potentially for the life of the patient. This therapy is basically a single administration, but it could have potentially life-long treatment effects in patients who are at risk for severe disease activity."

Manipulating Heart Cells into Regeneration (December 11 2008) http://www.eurekalert.org/pub_releases/2008-12/haog-hra121108.php
Via EurekAlert!: "Up until today scientists assumed that the adult heart is unable to regenerate. Now, researchers and cardiologists [have] been able to show that this dogma no longer holds true. [They] were able to show that the body`s own heart muscle stem cells do generate new tissue and improve the pumping function of the heart considerably in an adult organism, when they suppress the activity of a gene regulator known as beta-catenin [which] plays an important role in the development of the heart in embyros. [Researchers] could now show that beta-catenin is also important for the regeneration of the adult heart. They suppressed this factor in the nucleus of the heart cells in mice. This way they activated heart precursor cells (stem cells) to turn on the regeneration of heart in adult mice. Four weeks after blocking beta-catenin, the pumping function of the heart of the animals had improved and the mice survived an infarction much better than those animals with a functioning beta-catenin gene."

CR Mimetics Are Not CR (December 10 2008) http://pmid.us/19056839
By way of a reminder that there's still a world of difference between calorie restriction (CR) and a CR mimetic drug that reproduces some of the same observed biochemical changes: "resveratrol may produce calorie restriction-like effects on metabolic and longevity endpoints in mice. In this study, we sought to determine whether resveratrol treatment elicited other hallmark changes associated with calorie restriction, namely bradycardia and decreased body temperature. We found that during short-term treatment, wild-type mice on a calorie-restricted diet experienced significant decreases in both heart rate and body temperature after only 1 day whereas those receiving resveratrol exhibited no such change after 1 [week]. We also used [obese] mice to study the effects of long-term treatment because previous studies had indicated the therapeutic value of resveratrol against the linked morbidities of obesity and diabetes. After 12 [weeks], resveratrol treatment had produced no changes in either heart rate or body temperature. Strikingly, and in contrast to previous findings, we found that resveratrol-treated mice had significantly reduced endurance in a treadmill test. We conclude that the bradycardia and hypothermia associated with calorie restriction occur through mechanisms unaffected by the actions of resveratrol."

Another Approach to Restoring Hair Cells (December 10 2008) http://www.google.com/hostednews/ukpress/article/ALeqM5hI6vwfg3SuetvGrNdvVr1wKBUq6Q
Researchers are exploring a range of options to restore the hair cells of the ear that are lost with age, leading to deafness: "Damage to hair cells in the inner ear due to ageing and overstimulation is a major cause of deafness, affecting 10% of the worldwide population. The cell loss is irreversible because the cells have a limited capacity to regenerate. However, a new study suggests that the ependymal layer of the lateral ventricle of the brain contains stem cells which share characteristics with inner ear hair cells and which have the potential to reproduce. According to the scientists, these cells could potentially be transplanted from a person's brain into their ear, where they would undergo a functional switch to enable them to replace the damaged ones. The authors concluded that transplanted cells could alter their functions to work as inner ear hair cells and thus restore hearing. They suggested their findings on the flexible function of certain cells could also be extended to offer treatment for other problems affecting the nervous system."

Hourglass VI (December 09 2008)
http://ouroboros.wordpress.com/2008/12/09/hourglass-vi-a-carnival-of-biogerontology/
The sixth edition of the Hourglass blog carnival on aging and longevity science is up at Ouroboros. One of the linked posts is a series of thoughts on the way in which we humans cut ourselves short by discounting the
future: "The best example of human’s irrational dealing with the future is what is called hyperbolic discounting (also called: temporal discounting, or future discounting). Hyperbolic discounting is the human preference for small immediate reward over larger future payoffs. The further the time in the future of the reward the greater the discounting. Humans are generally bad at delaying rewards and hence we too easily take the immediate smaller reward rather than delaying our immediate gratification for a greater reward in the future. I propose here that unless humans soon become better at thinking about the future - and not discounting it so much - we might not be able to make the changes we need for a better world and society. The same could be said about longevity research - if we can not imagine ourselves living longer and healthier lives - and not imagine it as only happening to a 'stranger' we [are] unlikely as a society to invest in this imagined future."

Newsweek on Mainstream Longevity Science (December 08 2008) http://www.newsweek.com/id/172561/output/print
Newsweek has a general interest article up online on the topic of mainstream longevity science: projects aimed at the hard target of metabolic manipulation to slow aging. "Since the days of Ponce de Leon, if not before, people have been seeking the elusive Fountain of Youth. Until recently, such pursuits were the realm of quacks and charlatans. And there are still plenty of snake-oil salesmen out there on the Internet and in so-called anti-aging clinics, hawking everything from longevity-bestowing Ecuadoran waters (which are probably harmless) to growth hormones (which could be downright dangerous for adults). But serious scientists are now bringing respectability to the field, unraveling the secrets of aging on a cellular level and looking for ways to slow it down. And while the science is still young (so to speak), legitimate longevity-boosting treatments could be available in 10 to 15 years - although the gains would be [modest]. Some critics of the scientific quest for longevity say it's God's will that we should die when our time comes. But in the past century, a clean water supply, antibiotics, vaccines and improved medical care have boosted life expectancy at birth by roughly 50 percent in the United States - from 48 for men and 51 for women in 1900 to 75 for men and 80 for women today. No one seems to object to that."

A Viral Cause for Alzheimer's? (December 08 2008) http://www.sciencedaily.com/releases/2008/12/081207134109.htmThis release via EurekAlert! is very compelling - but how does it fit in with the good evidence that Alzheimer's is a form of diabetes? "The virus behind cold sores is a major cause of the insoluble protein plaques found in the brains of Alzheimer's disease [AD] sufferers. [researchers] investigated the role of herpes simplex virus type 1 (HSV1) in AD. Most people are infected with this virus, which then remains life-long in the peripheral nervous system. HSV1 DNA is located very specifically in amyloid plaques: 90% of plaques in Alzheimer's disease sufferers' brains contain HSV1 DNA, and most of the viral DNA is located within amyloid plaques. The team had previously shown that HSV1 infection of nerve-type cells induces deposition of the main component, beta amyloid, of amyloid plaques. Together, these findings strongly implicate HSV1 as a major factor in the formation of amyloid deposits and plaques, abnormalities thought by many in the field to be major contributors to Alzheimer's disease."

Life Expectancy

2008-11-24T09:19:00.000-08:00

Can your expectations determine how long you will live?

I believe lots of us actually die because of our expectations. We're conditioned to believe the average lifespan is around eighty years, so we wind down and die right on schedule. We usually get what we expect, not what we want. What if you expected to live to 100? Wouldn't you naturally gravitate toward the habits that will make that happen? Wouldn't your thoughts and emotions be more positive? How about longer? Loads of research tells us we should stay healthy for up to 100 years. But why don't we? Could it start with your attitude? Don't cop out by blaming it on your genes or on luck. Really, 65–75% of it is the choices you make. Your genes account for less that 35%.

This is backed up by hard science. Studies have shown that people who just think they are aging faster actually do age faster!

If you always think the glass is half full, you're on the right track. Mayo Clinic research shows that people with positive outlooks typically live 19% longer than people who see the glass as half empty. Although it's questionable if this can be attributed to optimists being more likely to seek medical help when they're ill, or if their immune systems strengthen as a result of their sunny outlook. The end result is though, they live longer. Optimists are also less likely to suffer depression and helplessness than their pessimistic counterparts.

To support the hypothesis that their immune systems are actually strengthened, Dr. Bruce Lipton’s experiments, and that of other leading-edge scientists, have examined in great detail the processes by which your cells receive information. The implications of this research radically change our understanding of life. It shows that genes and DNA do not control your biology. Instead, DNA is controlled by signals from outside your cells, including the energetic messages emanating from your positive and negative thoughts.

He clearly describes the connection between your core thoughts, beliefs and attitudes and how your cells function as a result. Happy thoughts put your cells’ functions in balance. Hateful, angry and resentful thoughts do the exact opposite. They suppress your immune system, alter your hormones, upset your digestive system, and diminish your brain function and respiration.

Dr. Lipton’s profoundly hopeful synthesis of the latest and best research in cell biology and quantum physics is being hailed as a major breakthrough showing your body can be changed as you retrain your thinking. His book, The Biology of Belief is a groundbreaking work in the field of New Biology.

In addition, an often repeated study showed that when a person’s living cells from different organs are put in separate dishes, cells from one organ would respond when cells from a different organ in a different dish were stimulated. If the cells were from two different people, they would not get the reaction. This means the trillions of cells in your body are always in direct communication with one another, even if they are not in direct contact by chemical or neurological pathways.

Stub a toe, and all your cells react. Poison your body with cigarette smoke or toxic food, and you stimulate every cell. Subject yourself to uncontrolled stress, and you stress tens of trillions of cells. Now can you see why stress management and attitude are so critical to your health and longevity?

Now that you know your thoughts affect every single cell in your body, what are you going to do about it? Since you now realize positive, loving and grateful thoughts keep you healthy and make you live longer, while negative thoughts destroy you from the inside out, you have a big anti-aging advantage. What happens to you usually doesn’t matter one bit. How you react means everything.

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LATEST HEALTHY LIFE EXTENSION HEADLINES

Cryonics as Emergency Medicine (November 21 2008) http://www.depressedmetabolism.com/2008/11/19/cryonics-sets-example-for-emergency-medicine/
From Depressed Metabolism: "One of the most neglected aspects of cryonics is that its procedures, and the research to support them, can have important practical applications in mainstream fields such as organ preservation and emergency medicine. Contrary to popular opinion, cryonics does not just involve an optimistic extrapolation of existing science but can set the standard for these disciplines. As a matter of fact, that is exactly what cryonics, and cryonics associated research, has been doing over the last 25 years. It is encouraging to observe that some of the procedures that are routine in cryonics stabilization protocol are starting to catch on in mainstream emergency medicine practice as well. For example, contemporary cryonics stabilization protocol has been strongly shaped by the idea that the best strategy to limit brain injury after cardiac arrest is to combine a number of different interventions: cardiopulmonary support, induction of hypothermia, and administration of circulation-supporting and neuroprotective medications. It is therefore very encouraging to learn that the Wake County EMS group in North Carolina has achieved impressive results in treating out-of-hospital cardiac arrest victims using a protocol that closely follows elements of current cryonics stabilization protocol."

Building New Pancreatic Cells (November 21 2008) http://www.sciencedaily.com/releases/2008/11/081120130539.htm
Regenerative medicine advances, step by step: "researchers have developed an unlimited number of pure insulin-producing cells from mouse embryonic stem cells (ESCs). These pure insulin-producing cells, which according to electron microscopy studies, have the same sub-cellular structures as the insulin-producing cells naturally found in the pancreas, were highly effective in treating diabetes in the mouse model. The transplants of pure insulin-producing cells reduced the blood glucose levels of diabetic mice with high blood glucose levels. None of the diabetic mice involved in the transplant experiments developed teratoma, which are a type of tumor often associated with ESCs and which could complicate their use in human therapeutic treatment. Furthermore, the pure insulin-producing cells managed to retain their insulin-production and glucose-sensing capacity over time. Besides providing a tool to facilitate basic research in test tubes and animals, these insulin-producing cells may be also used to replace the isolated native pancreatic cells that are hard to obtain in a large amount, for pharmacological tests."

Towards Accurate Biomarkers of Aging (November 20 2008) http://www.eurekalert.org/pub_releases/2008-11/bifa-but111208.php
From EurekAlert!: researchers "have identified for the first time biomarkers of aging which are highly predictive of both chronological and physiological age. Biomarkers are biochemical features that can be used to measure the progress of disease or the effects of treatment. The research involves nematode worms, microarrays which measure changes in gene expression, and complex computer algorithms. This is the first step toward identifying similar biomarkers in humans which would provide a means of scientifically validating anti-aging therapies. This is the first evidence that physiological age can be predicted non-subjectively. This is a first step; our results were not perfect, but we were able to predict the ages of the animals 70% of the time, which is far better than anything that has been done before. Research into the biology of aging in humans has been hampered by the lack of irrefutable biomarkers that correlate with the aging process. I am confident that at some point there will be a non-subjective method of determining how old someone is with a high level of confidence."

Inflammation and Alzheimer's (November 19 2008) http://pmid.us/19014446
A prodrome is an early set of non-specific symptoms that herald a particular disease. Here, researchers point to chronic inflammation as a prodrome of Alzheimer's (AD): "Recently, the term 'inflammaging' was coined [to] characterize a widely accepted paradigm that ageing is accompanied by a low-grade chronic up-regulation of certain pro-inflammatory responses. Inflammaging differs significantly the from [traditional] acute inflammation in that it is characterized by a relative decline in adaptive immunity. While the over-active innate immunity characteristic of inflammaging may remain subclinical in many elderly individuals, a portion of individuals (postulated to have a "high responder inflammatory genotype") may shift from a state of "normal" or "subclinical" inflammaging to one or more of a number of age-associated diseases. Although conditions of enhanced innate immune response with overproduction of pro-inflammatory proteins are associated with both healthy aging and AD, it is suggested that those who age 'well' demonstrate anti-inflammaging mechanisms and biomarkers that likely counteract the adverse immunity of inflammaging. Thus, opposing the features of inflammaging may prevent or treat the symptoms of AD."

Regeneration via Embryonic Stem Cells (November 19 2008) http://www.reuters.com/articlePrint?articleId=USTRE4AI02220081119
From Reuters: "Stem cells from tiny embryos can be used to restore lost hearing and vision in animals, researchers said Tuesday in what they believe is a first step toward helping people. One team repaired hearing in guinea pigs using human bone marrow stem cells, while another grew functioning eyes in tadpoles using frog cells. They grew the stem cells into neuron-like cells in lab dishes and then transplanted them into the inner ears of the guinea pigs. Three months later, the animals appeared to have some hearing. The goal was to regrow the tiny hair cells that are essential for mammals to hear, although she is not sure yet how the stem cells made this happen. They would eventually like to try something similar in humans." These are early stage proof-of-concept demonstrations. It is an illustration of progress that they do not stand out as exceptional amidst advances in the many other lines of regenerative research presently taking place.

More on the Biochemical Value of Exercise (November 18 2008) http://www.eurekalert.org/pub_releases/2008-11/aps-eib111708.php
Exercise is good for you: "A new study confirms that exercise can reverse the age-related decline in the production of neural stem cells in the hippocampus of the mouse brain, and suggests that this happens because exercise restores a brain chemical which promotes the production and maturation of new stem cells. One hypothesis the researchers investigated is that the age-related decline in neurogenesis is tied to a rise in corticosterone in middle age. Elevation of corticosterone has been associated with a drop in the production of new stem cells in the hippocampus. The second hypothesis is that nerve growth factors -- which encourage new neural cell growth but which decrease with age -- account for the drop in neurogenesis. Production of neural stem cells improved by approximately 200% compared to the middle-aged mice that did not exercise. In addition, the survival of new nerve cells increased by 170% and growth by 190% compared to the sedentary middle-aged mice. ... Based on these results, it appears that nerve growth factor has more to do with these findings than the corticosterone."
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Aging is Slowly Stealing Our Lives

2008-11-17T09:33:00.000-08:00

You and I are both aware that aging is slowly stealing our health, our vigor and our lives. Yet we function without a sense of urgency to do something about aging. Why? Because we’re bombarded with our personal and career responsibilities and daily distractions. And those squeaky wheels are what get our attention. This is totally normal and logical. We have to take care of our families, get our haircuts and pay attention to endless details. Who has time to really make a commitment to being proactive when it comes to something as abstract as age-reversal?

That’s the way I used to think. But taking paths of least resistance normally leads us down reactive paths. In other words, we usually let outside forces control our lives. It isn’t until we’re faced with a crisis that those forces take a backseat to focusing on something that may have been avoided in the first place. Sometimes, that crisis means life or death.

This really hit home when I just found out a close and loved associate was diagnosed with one of the deadliest forms of cancer. What’s even more tragic is he’s an active life extension researcher. That’s the worst of ironies.

I am saddened to report that Dr. Chris Heward, one of the original participants of MaxLife’s first international scientific brainstorm sessions to reverse aging, is fighting an uphill battle for his life. Chris is Director of the Kronos Science Laboratories of Phoenix, AZ. He has been diagnosed with terminal, Stage-IV Esophageal Cancer. The cancer has metastasized to several other organs, and consequently his condition has a poor prognosis (50% mortality in 90 days and about 99% in a year).

Since surgery is no longer a realistic option, Chris has proposed to undergo an experimental but very promising immunotherapy treatment in Boca Raton, FL. However, this treatment requires blood donors less than 30 years old with "A" or "O" positive or negative blood types and no prior history of cancer in their families. If you are in—or if you know anyone in this category who would be willing to donate several units of blood to retrieve the granulocyte cells, please get in touch with me as soon as possible. Not only could this experimental treatment save Chris, but it could lead to a universal cure for many types of cancer. Here’s an opportunity to contribute to a great cause that could ultimately save many lives by making a simple referral.

Thank you in advance for your attention to this critical matter.
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LATEST HEALTHY LIFE EXTENSION HEADLINES

Researchers on Aging (November 14 2008) http://www.mcclatchydc.com/226/story/55835.html
An article of quotes from various noted aging reseachers: "Aging is caused by the gradual, lifelong accumulation of a wide variety of molecular and cellular damage. The free radical theory is the most widely accepted theory of aging. But the idea that aging is caused by one thing is naive. One general theory can never fit all. Clearly, it's the combination of genes that your parents dealt you and the lifestyle choices you make and the environmental toxins one is exposed to. One need only count the number of ways a car will fail to start to appreciate that aging can be caused by a large number of problems. Like any machine, it's going to wear out. About 25 percent of how a person ages is due to inherited genes. Certain genes control a cell's ability to repair damaged DNA. If those genes are defective, they can't do their job. Not everybody will be susceptible to diseases like Parkinson's or cancer as they age. But each one of us will lose muscle mass and muscle strength. That's why this research is so important. Frailty affects all of us."

Enhanced Longevity through Telomerase (November 14 2008) http://www.sciencenews.org/view/generic/id/38552/title/Telomere_enzyme_a_likely_key_to_longevity
From Science News: "the enzyme telomerase can extend the lifespan of mice by about 24 percent. Telomerase lengthens telomeres - the 'caps' on the end of chromosomes that protect DNA from damage. Like burning fuses, telomeres normally get shorter each time that most body cells divide. While the enzyme enables cells to keep dividing, it also takes cells one step closer to growing and proliferating out of control - that is, becoming cancerous. Lab animals with extra genes for telomerase often die young from tumors. [researchers] engineered mice to have not only an extra copy of the gene for telomerase, but also extra anti-tumor genes to combat the enzyme's cancer-causing potential. In the altered mice, signs of aging such as poor coordination or degraded tissue health were delayed compared to mice that had only the extra copies of anti-tumor genes." Most interesting; you might also want to look at recent research that suggests telomerase operates by protecting mitochondria, and less damaged mitochondria means better preservation of telomeres - but, more importantly for life span, less oxidative stress.

Better Synthetic Cartilage (November 13 2008) http://www.sciencedaily.com/releases/2008/11/081113075959.htm
From ScienceDaily: "Until now, creating synthetic cartilage was complex but not impossible. The problem was that it was impossible to imitate the perfection of human cartilage due to the difficulty in orienting the collagen nanofibers [in] a particular configuration: in parallel, in a circle, or crossed. The fibers that form the cartilage that protects the knee are aligned in parallel. [Researchers have now] achieved this using the electrospinning method. Collagen nanofibers are obtained by exposing the collagen to electrical discharges. The collagen is extruded, in the form of a nanofiber thread, through a fine needle and is deposited on an electric collector consisting of two grounded plates. The student placed a nonconductive material between the two conducting plates. The nanofibers aligned on top of each other perfectly in parallel lines between the two conducting plates." Innovations in engineering the simpler forms of human tissue have been arriving more rapidly of late - more scientists are involved, the tools are improving, and the cost of research is falling. This is all groundwork for the next decade and tissue engineering of complex replacement organs.

Steps towards Liver Regeneration (November 13 2008) http://www.uphs.upenn.edu/news/News_Releases/2008/11/liver-stem-cell-marker.html
Discovering a stem cell population is the first step to regenerating the tissue they support: "A novel protein marker has been found that identifies rare adult liver stem cells, whose ability to regenerate injured liver tissue has the potential for cell-replacement therapy. In the future, this marker will allow for the isolation and expansion of these stem cells, which could then be used to help patients whose livers can no longer repair their own tissue. In a healthy liver, proliferation of mature liver and bile-duct lining cells is sufficient to maintain the necessary size and function of the organ. This even works when the liver is confronted with mild and acute injury, but the situation changes when injury to the liver is chronic and severe. For chronic injury, the liver uses a back-up system that stimulates stem cells to proliferate and eventually differentiate into new liver cells. [Researchers] found that these dual-potential stem cells can be identified and potentially isolated from other liver cells."

More on Myelin Loss (November 12 2008)
http://www.eurekalert.org/pub_releases/2008-11/mnia-itw111208.php
You might recall that age-related thinning of the myelin that insulates nerves strongly correlates with declining brain function. Researchers investigating MS are making progress into the mechanisms by which this happens: the protein netrin-1 "is known to guide and direct nerve cell axons to their targets. Blocking the function of netrin-1 and one of its receptors in adult neural tissue causes the disruption of myelin. We've known for just over 10 years that netrin is essential for normal development of the nervous system, and we also knew that netrin was present in the adult brain, but we didn't know why. The new findings show that
netrin-1 and its receptor are needed to hold paranodal junctions in place, and thereby maintain the structure of myelin. The paranodal junction is a highly specialized region of contact where an oligodendrocyte cell attaches itself to the nerve cell's axon. This juncture acts as a molecular fence, which organizes and segregates the distribution of key proteins along the nerve cells axon and plays an imperative role in the proper conduction of electrical signals along the length of the nerve cell. When the function of netrin-1 and its receptor is disrupted, the organization of this adhesive junction comes apart, disrupting the function of nerve cells in the brain and spinal cord."

Brain Growth Receptors and Lifespan (November 10 2008) http://dx.doi.org/10.1371/journal.pbio.0060274
A very readable overview of recent research from PLoS Biology: "When resources are short, growing organisms face an existential choice: should you ignore the shortage and hope for better times soon, or scale back and live within your limited means? And if you do scale back, will there be any payoff later in life? For animals, these choices are played out hormonally, with environmental fluctuations leading to internal rearrangements in endocrine signal and response throughout the growing body. In mammals, two principal hormones - growth hormone (GH) and insulin-like growth factor 1 (IGF-1) - promote growth. Remarkably, inhibiting one or both of these two not only retards growth, but also extends lifespan, not just in lab animals, but possibly also in people: mutations that reduce the function of the IGF-1 receptor have recently been discovered in centenarians (who are also short). Growth occurs throughout the body, and receptors for IGF-1 are found in every organ on virtually every cell. But [researchers have now shown] that it is the IGF-1 receptors in the brain that set the pattern for growth and lifespan."

Mainstream Press on the Singularity and Longevity (November 10 2008) http://english.ohmynews.com/ArticleView/article_view.asp?menu=A11100&no=384115&rel_no=1
An interesting, if flawed, article on the singularity and engineered longevity via the Korean OhmyNews: "Amidst the rapid changes of society ranging from general advances in science and technology to politics and social policy, with respect to knowledge, there is an emergent issue that promises to radically change our lives and our reality. It is predicted that within less than 20 years, the human lifespan will be extended to perhaps 150 or more years. Scientists and futurists on the cutting edge of thought about science and society believe that the increase in lifespan is one step towards what will be known as the Singularity, at which time, life might be extended indefinitely depending upon environmental conditions. The Singularity is the term used for a technological integration unheard of; it is a theoretical future point of unprecedented technological progress, caused in part by the ability of machines to improve themselves using artificial intelligence. It was just over a hundred years ago, when the human lifespan began to double to what it is today. It is possible that most people who lived only to 35 years of age thought that to live to 72 years would be too long and that they would be too tired. Nevertheless, we have adjusted and found life to be meaningful, even in our current 'long' life of 72 years."

A Valuable Lesson

2008-11-10T15:06:00.000-08:00

As promised, I’m going to pass on a valuable lesson from Dr. Pete Hilgartner.

What is your first reaction to a crisis? Let’s say you get diagnosed with a serious illness. First your heart skips a beat and then thunders like a jackhammer. Maybe you break out in a cold sweat. Then when reality sets in, do you retreat? Do you roll up in a fetal position, pull the covers over your head and hope your problems disappear? Do you tend to sleep more, head for the liquor cabinet or pray harder than you had in years?

How about when you life’s savings gets wiped out overnight due to mismanagement, theft, the economy or just by hard luck?

Or what do you do when the economy slows down, and your customers’ orders slow to a trickle, or you get laid off?

What about when all the real estate equity you built over the years vanishes overnight?

Time to retreat, right? Batten down the hatches. Cut expenses. Downsize. Deprive yourself until things get better. That’s what most people do, and that’s one reason the press tells you our economy sucks.

What if there was a better way to handle crises? Well there is. In fact there are two. The first is offered up by Dr. Pete. The second by yours truly.

Dr. Pete is a fascinating guy and a successful student of life. He was very sickly as a child, way sicker than most people could tolerate. But his illnesses motivated him to set lofty goals. He decided to win an Olympic gold metal, to become an officer in the Marine Corps and to become a physician. He was well on his way to a shot at the gold when his aching back tripped him up. So he joined the Marines and later became a successful physician.

The Marines taught him one of life’s great lessons. They taught him how to survive an ambush.

Capt. Pete survived six ambushes in fact. He realized he survived them the same way he survived his childhood injuries and the same way he’s surviving today’s economic climate. When you’re ambushed, the Marines teach you to head for an escape route. But what is there is none? What do you do when the enemy closes off all escape? Then you make yourself as small a target as possible, right? Wrong!

If you want to escape, to survive, you do the counter-intuitive. You do the unexpected. You expand… and attack. But don’t just sort of expand. Expand with decisiveness, purpose, order and with a plan. Play offense instead of defense. Overcome your fear and take the fight to the enemy. Dr. Pete and most of the company he commanded live today because of that one critical lesson.

Have you noticed that when people are filled with fear, they tend to withdraw? They stop communicating. If they do communicate, it’s usually to complain about how bad things are. When you’re down, be a beacon of optimism. Take charge of your situation. Every cell in your body will react and rally you to your recovery.

Can you force yourself to expand, when every fiber of your existence wants to do what everyone else is doing; succumbing and contracting to fear? Yes, you can!

I have another way to not only survive, but to prosper as well. It’s your surest path to sound health and longevity. In a word, it’s “prevention”. Expand now, and avoid your ambushes. Head off disease and illness by taking precautionary measures now and forever.

It’s a well-known fact that people will go to the ends of the earth searching for cures but will ignore preventative measures. Terminal diseases and what is happening now are concretes. The threat of disease and the future are abstracts. So we live for the moment while internal time bombs tick away. Sooner or later, one catches up with you. And more often than not, it’s too late. If you catch it early enough and/or expand and attack, you have a chance to beat it back. But not all of Capt. Pete’s soldiers got out alive.

Will tomorrow’s technologies obsolete death from aging and other diseases? I’m certain of it. Will we all live to see the day? Unfortunately, no. And most of those who miss the extreme longevity boat will miss it because of inattention to prevention. Some will make it because they will expand when their crisis catches up with them. But with so much at stake, why roll the dice? Play to win, not to not lose. Expand right now, before it’s too late.

Now getting back to reacting to a health crisis. I’m afraid I have some terrible news for you. You have a terminal disease that no one has ever survived. You were born with it, and you too will die from it – unless you improve your odds by expanding and by preventing. It’s called aging. Instead of complaining about it, or even joking about it, for the first time in history, you can actually do something about it. One contribution many of us can make is supporting the research that will conquer the effects of aging while you are still alive. The other is simply taking a proactive approach to your health to keep yourself alive until emerging medical miracles will give you a new lease on life.
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LATEST HEALTHY LIFE EXTENSION HEADLINES

The Most Important Research (November 07 2008) http://www.exchangemagazine.com/morningpost/2008/week45/Friday/1107018.htm
From the Exchange Morning Post, a statist, public funding viewpoint on longevity science: "Learning how to turn back time - or at least how to slow the aging process - may be more important for improving our overall health than the discovery of a cure for cancer. There are real, tangible benefits, for society as well as individuals, to slowing down the aging process. 'By extending the life span, people would remain in the workforce longer, personal income and savings would increase, age entitlement programs would face less pressure from shifting demographics, and national economies would flourish'. Almost half of the current population over 75 years old is limited in their activity by chronic conditions, with costs to society set to rise dramatically. Given the current predicament we face, we can't ignore the call to tackle aging more aggressively. To those who ask: 'Can we really afford to invest more in such research?' we can reply: 'Can we really afford not to tackle aging?' The greatest obstacle will be convincing the general public that slowing the aging process is both feasible and deserving of a larger share of the funds available for scientific research."

An Overview of Cryonics (November 07 2008) http://kn.theiet.org/magazine/issues/0819/science-without-deadline.cfm
A good article on cryonics from Engineering and Technology: "The field of cryonics, which made its debut in the 1960s, continues to push the envelope and search for a solution to death. The process consists of preserving legally dead humans or pets at very low temperature (below -130C) in the hope that future science can restore them to life, youth, and health. The advancement of medicine and science is so much faster than it used to be. Science fiction is becoming science fact on a daily basis. All of a sudden, cryonics doesn't look quite so far-fetched. Most cryonicists believe reanimations will occur within 50 to 100 years for those currently being cryopreserved. Within that time frame, virtually all current diseases should be curable and elderly people can probably be rejuvenated to a youthful condition. With full disclosures and signed consent, [cryonics] is highly ethical. When you think about the grand scheme of things, cryonics is a lot more conservative than burial or conventional cremation. Tissue preserved at the temperature of liquid nitrogen does not deteriorate, even after centuries of storage. Therefore, if current medical technology can’t keep us alive, we can instead choose to be preserved in liquid nitrogen, with the expectation that future medical technology should be able to reverse any cryopreservation injury and restore good health.

Cells as Vectors for Targeted Therapies (November 06 2008) http://www.eurekalert.org/pub_releases/2008-11/miot-mct110508.php
The possibilities of bioengineering are endless, and one of the most energetic branches of the research community is involved in developing methods of precisely targeting therapies: "MIT engineers have outfitted cells with tiny 'backpacks' that could allow them to deliver chemotherapy agents, diagnose tumors or become building blocks for tissue engineering. The polymer backpacks allow researchers to use cells to ferry tiny cargoes and manipulate their movements using magnetic fields. Since each patch covers only a small portion of the cell surface, it does not interfere with the cell's normal functions or prevent it from interacting with the external environment. Researchers worked with B and T cells, two types of immune cells that can home to various tissues in the body, including tumors, infection sites, and lymphoid tissues - a trait that could be exploited to achieve targeted drug or vaccine delivery. The researchers found that T cells with backpacks were able to perform their normal functions, including migrating across a surface, just as they would without anything attached. By loading the backpacks with magnetic nanoparticles, the researchers can control the cells' movement with a magnetic field."

Towards a Rejuvenated Thymus (November 06 2008) http://www.uga.edu/news/artman/publish/081106_Manley_Research.shtml
One approach to the issue of declining naive T-cells with age - and consequence failure of the immune system - is to boost production by manipulating the thymus: "a key gene may be crucial to maintaining the production of the thymus and its disease-fighting T-cells after an animal's birth. The discovery could help scientists find out how to turn the thymus back on so it could produce T-cells long after it normally shuts down most of its function, which, for humans, occurs by early adulthood. If the finding leads to further ways to manipulate the gene, the result could be a new avenue for the body to fight disease more effectively as the body ages. Such things as infectious diseases, inflammation and heart problems are all related to immune response. You don't have to think far to see how understanding the effect of this gene could affect the quality of life for older people and others as well. If [physicians] were able selectively to turn T-cell production back on, then many diseases that currently afflict older people could become manageable if not, in cases, entirely absent."

Boosting the Aging Immune System (November 05 2008) http://pmid.us/18981163
Many research groups are working on ways to boost the effectiveness of an exhausted immune system - due to either chronic viral infection or aging - without necessarily aiming to address the root causes: "In contrast to most normal somatic cells, which show little or no telomerase activity, immune cells up-regulate telomerase in concert with activation. Nevertheless, during aging and chronic HIV-1 infection, there are high proportions of dysfunctional [immune cells] with short telomeres. Exposure of CD8(+) T lymphocytes from HIV-infected human donors to a small molecule telomerase activator (TAT2) modestly retards telomere shortening, increases proliferative potential, and, importantly, enhances cytokine/chemokine production and antiviral activity. The enhanced antiviral effects were abrogated in the presence of a potent and specific telomerase inhibitor, suggesting that TAT2 acts primarily through telomerase activation. Our study is the first to use a pharmacological telomerase-based approach to enhance immune function."

Incremental Improvements in Scaffolding (November 03 2008) http://www.technologyreview.com/printer_friendly_article.aspx?id=21625&channel=biomedicine&section=
From the MIT Technology Review: "Engineering heart tissue presents particularly tough problems for researchers, since the heart is an active organ. Scaffolds designed for other kinds of tissues did not have the right mechanical properties for heart tissue. Heart tissue must be flexible enough to change shape as the heart contracts, but also strong enough to withstand the intense forces generated by these contractions. The researchers designed the scaffold to encourage cells to align themselves in the same direction to better mimic this property of natural heart muscle tissue. Using a laser cutting technique, they created a pattern of oblong holes in the polymer; the result is a flexible, honeycomb-like structure that is stiffer in one direction than another. Just as rowers line up in one direction to propel a boat forward, 'all the heart muscle cells in a given region have to be lined up and contracting in the same direction' in order for the heart to beat efficiently. The honeycomb-like scaffold [represents] a 'substantial jump' toward that goal. If we had a biodegradable biomaterial, which had beating heart cells, we might be able to return function to [damaged parts] of the heart."

A General Interest Calorie Restriction Article (November 03 2008) http://afp.google.com/article/ALeqM5i8eh2v_zPiht03CZWKvVulsaPYqAAs the science advances, these articles get more positive. Recall the ridicule heaped upon the practice of calorie restriction even just a few years ago. "Some people are doing it strictly to enhance longevity. Others do it to avoid age-related disease, or because they already have diabetes, high cholesterol or clogged arteries and want to clean up their bodies by using diet. In rich countries, 90 percent of the population probably eats, on average, about 50 percent too much. Even if they were to reduce their calorie intake by half, they would still only be at baseline. A wealth of scientific evidence has confirmed that maintaining that balance helps prevent type-2 diabetes, cardiovascular disease and cancer. But experiments with both animals and humans have also shown that pushing one's calorie intake 10 to 20 percent below that baseline threshold -- without lowering nutrients -- may provide additional health advantages. Will this add 10 years to your life? Nobody knows. But one thing is sure -- calorie restriction will help you reach your maximum lifespan potential, which is different for all of us depending on our genetic profile."

A Jobe Kind of Year

2008-11-05T16:39:00.000-08:00

Dear Future Centenarian,

It’s been a Jobe kind of year so far. Let me count the ways:

We launched a market trading technology that took 12 years to develop that was designed to raise hundreds of millions of dollars for life extension research. Good news, right? Wrong! We launched it on the exact day the markets fell apart. A bunch of money vanished, and critical life extending projects are on hold..
I hired a contractor to build a real estate project. He promised a 10 month delivery date. Here it is, over three years later, and still not quite done. Meanwhile, the bottom fell out of the market this year, and poof, a couple of million plus – up in smoke.
The same contractor got into a dispute with a sub contractor, who put a lien on the property since the contractor won’t pay. Legal fees and headaches all last week. He cost me hundreds of hours wasted on a project that was supposed to be turnkey.
Father Time stole another year from me.
A borrower defaulted on a big loan.
Verizon inadvertently disconnected my Internet service 17 days ago… and it took 15 of those days to get me back online. When I checked to see why, they inactivated my account instead of reconnecting it. Almost four hours spent on phone calls with about a dozen different representatives. Sound familiar?
There is a situation as bad as #2 that I don’t even want to talk about.
There’s another as bad as #7.
A funder for a key longevity technology was not able to perform on his commitment. Meanwhile, the markets hit the skids, and now it will be 10 times harder to get funding. I believe thousands of lives may ultimately terminate as a result, and a small fortune is jeopardized.
My electric bed took on a mind of its own. From time-to-time, without any warning, the head and foot rise in unison, trapping me in a wedge. The last time it happened, the head inclined just fast enough to barely keep me from reaching the remote. The more I stretched, the farther out-of-reach it got. I had to get rescued. A little joke on Dave.
The final straw. My Vita-Mix (my most important health drink tool) gave out yesterday J.

You might be wondering why I’m sharing my tales of woe with you. Sure, I know, you have your own challenges to cope with. Once again, all this has something to do with your health and longevity.

I’m one of those guys you might hate running into when you are troubled. Instead of getting sympathy, you’ll get an irritating dose of sunshine and a pep talk, just when you wanted someone to share your misery with. Well, I should say, I’m usually that optimistic guy. I have to admit that numbers 1-11 above started consuming my thoughts. And that’s bad. It’s bad because it’s extremely unhealthy, life-shortening and counterproductive… and because I know better.

Do you know your thoughts affect every single cell in your body? Positive, loving grateful thoughts keep you healthy and make you live longer. Negative thoughts destroy you from the inside out. What happens to you usually doesn’t matter one bit. How you react means everything. A new friend reminded me of this in a very interesting way. His name is Dr. Pete Hilgartner, and I’m going to share his words of wisdom with you next week.

I don’t care what your situation is. You have plenty to be grateful for. I know I do. I have lots of positive things and people in my life. I’ve been fortunate enough to have attracted better friends, partners and relationships than most could ever hope for. I also lucked out in the health department. And get this. Just yesterday, a close friend and associate told me a benefactor pledged enough funding to finish developing a technology which may allow you and me to actually live as long as we want someday.

Then there are the little things I tend to take for granted. I started yesterday with a nutritious, delicious breakfast and ended it with a fabulous dinner. I live in one of the best climates in the world. I have a warm comfortable bed, even though it attacks me once in a while. My shoes fit. I have shoes. I have feet! And I have a couple of pages of more things to be grateful for. Just writing this makes me feel a lot better, because when you think a grateful, happy or loving thought, there’s no room in your mind for anything else. So happiness is simply deciding what you want to dwell on. And happiness equates to healthfulness. Sure, you have to face your problems, health and otherwise. But when you do, think of solutions rather than dwelling on the negatives.
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LATEST HEALTHY LIFE EXTENSION HEADLINES

Unregulated Prices Fall, While Quality Improves (October 31 2008) http://www.lef.org/magazine/mag2008/sep2008_Would-You-Tolerate-This-Abuse_01.htm
A piece from the LEF Magazine that makes the points about modern medical research that most people don't think about: "the public today tolerates federal and state laws that enable pharmaceutical companies to conduct business as a virtual monopoly. The result is that Americans pay outlandish prices for mediocre drugs that are often laden with side effects. Unlike regulated prescription drugs, the cost of dietary supplements has plummeted over the past three decades. In a free market environment, technological breakthroughs that occurred in telecommunications will also happen in medicine. More frightening is the suffocating effect that regulation has on the discovery of life-saving therapies. Just imagine if advancement in clinical medicine progressed at the same rapid rate as telecommunications. If it did, we would probably have cures for most killer diseases today!" Heavily regulated markets are bloated, slow markets, in which the incentives are so set as to discourage progress. Present regulation is a very real threat to the future of your health and longevity.

Incremental Improvements in Stem Cell Therapy (October 31 2008) http://www.eurekalert.org/pub_releases/2008-10/hms-scp102908.php
Researchers continue to find ways to alter stem cells to produce better therapies: "Adult stem cells resemble couch potatoes if they hang out and divide in a dish for too long. They get fat and lose key surface proteins, which interferes with their movement and reduces their therapeutic potential. Now, via a simple chemical procedure, researchers have found a way to get these cells off the couch and over to their therapeutic target. To do this, they simply added a molecule called SLeX to the surface of the cells. The procedure took just 45 minutes and restored an important biological function. Delivery remains one of the biggest hurdles to stem cell therapy. The blood stream offers a natural delivery vehicle, but stem cells don't move through blood vessels normally after being expanded in culture. Our procedure promises to overcome this obstacle. Karp cautions that his lab's discovery must be validated in animals, before doctors can apply it in the clinic. He's collaborating with another lab to test the homing ability of the SLeX-dotted cells in mice."

A Little More on IGF-1 and Growth Hormone (October 30 2008) http://dx.doi.org/10.1371/journal.pbio.0060254
Following up on a recent Fight Aging! post, more on the role of IGF-1 in longevity: "Using a mouse model relevant for humans, we showed that lifespan can be significantly extended by reducing the signaling selectively of a protein called IGF-I in the central nervous system. This caused growth retardation, smaller adult size, and metabolic alterations, and led to delayed mortality and longer mean lifespan. Thus, early changes in neuroendocrine development can durably modify the life trajectory in mammals. The underlying mechanism appears to be an adaptive plasticity of somatotropic functions allowing individuals to decelerate growth and preserve resources, and thereby improve fitness in challenging environments. Continuously low IGF-I and low growth hormone levels favor extended lifespan and postpone age-related mortality. Our results further challenge the view that administration of GH can prevent, or even counteract human aging. This knowledge is important since growth hormone is often prescribed to elderly people in an attempt to compensate the unwanted effects of aging."

Ouroboros on Mitochondrial Uncouplers (October 30 2008) http://ouroboros.wordpress.com/2008/10/30/mitochondrial-uncouplers-mimic-the-effects-of-calorie-restriction/
From Ouroboros: researchers "suggest that mitochondrial uncoupling is an effective mimic of [calorie restriction (CR)]. In mitochondria, the electron transport chain uses electrons from glucose and lipids to pump protons across a membrane. This proton gradient can be used to make energy in the form of ATP through oxidative phosphorylation. The process is kind of like generating hydropower. Uncouplers work by putting a leak in the dam, which lets water through without going to the generator. They 'uncouple' the electron transport chain from oxidative phosphorylation, thus reducing the efficiency of energy production. Although animals have uncoupling proteins (these proteins are important for thermogenesis, especially during hibernation), so far there are no known agonists. The researchers instead used low doses of the mitochondria uncoupler DNP.
The DNP treated mice ate the same amount of food as control mice but had lower body mass [and] showed many phenotypes observed in calorie restricted mice. Like CR mice, DNP treated mice had higher rates of respiration with lower production of ROS. Most importantly, DNP treated mice showed an extended lifespan. This study suggests that mitochondrial uncouplers are an effective mimic of calorie restriction and might be a realistic therapeutic intervention for delaying aging and extending lifespan."

Lipids and Alzheimer's (October 28 2008) http://www.medicalnewstoday.com/articles/126012.php
The brain is complex organ, and Alzheimer's is a complex disease: a wide range of strategies produce results that look promising while not addressing the root cause. Indeed, distinguishing symptoms from root causes in Alzheimer's is still an ongoing concern. Here is a potential strategy I have not seen mentioned before: "scientists working with laboratory mice have discovered that complete or partial removal of an enzyme that regulates fatty acid levels lessened the memory and learning deficits of Alzheimer's. The most striking change we discovered in the Alzheimer mice was an increase in arachidonic acid and related metabolites in the hippocampus, a memory center that is affected early and severely by Alzheimer's disease. An enzyme called group IVA phospholipase A2 (or PLA2) released arachidonic acid [in] the brain. Removal or even partial reduction of PLA2 prevented memory and learning deficits and other behavioral abnormalities in the Alzheimer mice." It is worth noting that PLA2 is upstream in biochemical signaling processes that lead to inflammation - I suspect this has more to do with inflammation than fatty acids per se.

Save for the Future

2008-10-13T09:03:00.000-07:00

What a week!

If you are in any market, you probably got slaughtered last week. If you didn’t, I want you to handle my investments.

Although I attribute most of the sudden losses to panic selling, it’s still very sobering. We’ll see lots of ripple effects that could last for a long time. We’ll also see more controls which will lead to more erosion of your freedoms.

Meanwhile, I’m working on keeping you alive for a long time, so if the markets are stressing you out, relax and review my previous commentaries on stress.

But this market made one more thing crystal clear to me. You may need money, if you want to dodge the grim reaper. Lots of it. If you didn’t lose money last week, it might be because you don’t have any to lose. And yes, that could be bad if you want to live for an extremely long time.

Let’s face it… the first people who are going to get effective life-extending treatment are those who will be able to afford it. If you’re old and broke when the longevity boat arrives, you might miss it. Sure, prices will come down, and pretty rapidly too. But many of us are on the bubble as it is, and not being near the front of the line could just cost you your life. So what are you going to do about it?

All your life, you have been told to save for the future, and you’re most certainly familiar with the magic of compound interest. As we age, we may regret not starting to save years ago. Now, many people who didn’t save figure it’s too late to amass any kind of fortune, so they live day-to-day, paycheck-to-paycheck. But what if you knew beyond a shadow of a doubt, you would be biologically transformed into a 25-year old, twenty or thirty years from now, if you had $500,000 in the bank at that time. Do you realize that if you socked away about $30,000 in a segregated investment account that compounded at around 10% growth per year, you would have your $500,000 in less than thirty years? (10% is roughly the historical annual growth of the stock market.)

In other words, $30,000 could be the difference between your being part of the last generation to die from aging or part of the first to live endlessly. What if you don’t have $30,000? That’s easy. Save $3,000 now and $3,000 every year in the same type of account, and presto! You’ll have your magical $500,000 in less than thirty years.

I have no idea what full rejuvenation will cost when it’s available, so plan for more, not less. Wouldn’t it be nice to be young again with a pile of money in the bank?
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LONGEVITY AND THE COMPOSITION OF MITOCHONDRIA

Comparisons of mitochondrial biochemistry between species of differing innate longevity is one several branches of research to demonstrate the importance of our mitochondria to aging:

http://www.fightaging.org/archives/001584.php

"Mitochondria, the power plants of your cells, generate damaging reactive oxygen species (ROS) in the course of their operation: ROS will race off to damage the first thing they can find by reacting with it, such as a cell membrane. Mitochondria themselves have membranes, and are first in line to be damaged by the ROS they generate. Eventually damage accumulates and cascades to change the surrounding cellular environment very much for the worse. This process is an important root cause of degenerative aging."

This process is why those species more resistant to the damaging effects of reactive oxygen species live longer than their peers. "Resistance" here means that the membranes of mitochondria and other cellular components are built of tougher stuff: proteins less likely to be succumb to ROS attack. Even in primates, mitochondrial composition differences are significant between species and highly correlated with longevity. This all reinforces just how central our mitochondria are to aging, and how vital it is to speed research into repairing damaged mitochondria in humans:

http://www.fightaging.org/archives/001395.php
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LATEST HEALTHY LIFE EXTENSION HEADLINES

Update on Viruses Versus Cancer (October 10 2008) http://www.sciencedaily.com/releases/2008/10/081008151320.htm
A number of groups are presently working on ways to use viruses to precisely target and kill cancer cells. Here's an update on one of them from ScienceDaily: "The Senecavirus [is] harmless to normal human cells, but could infect certain solid tumors, such as small cell lung cancer, the most common form of lung cancer. Scientists at Neotropix say that, in laboratory and animal studies, the virus demonstrates cancer-killing specificity that is 10,000 times higher than that seen in traditional chemotherapeutics, with no overt toxicity. The company has developed the 'oncolytic' virus as an anti-cancer agent and is already conducting early phase clinical trials in patients with lung cancer. Researchers went on to identify several areas on the viral protein coat that they think might hook onto receptors on cancer cells in the process of infecting them. It will be critically important to find out what region of its structure the virus is using to bind to tumor cells, and what those cancer cell receptors are. Then we can, hopefully, improve Senecavirus enough to become a potent agent that can be used with many different cancers."

Cuervo On Autophagy (October 10 2008) http://websites.afar.org/site/PageServer?pagename=IA_spotlight_main
A piece from earlier this year at InfoAging: "Aging is characterized primarily by the decline of function in various cellular and molecular systems in the body. These changes are influenced by three factors:
genetics, metabolism, and the environment. The focus in Dr. Cuervo's lab is the metabolic changes and resulting damage from these changes that are experienced with age, specifically damage to proteins. Every person experiences this damage to some degree, regardless of their age, but when it comes to repairing or removing the damage, the difference between young and old is clear. In younger people, the damaged or misfolded proteins can be repaired by what are known as chaperone proteins. Yet, like an old car, proteins that have undergone too much repair are not worth maintaining and so they are transported by the chaperone to the lysosome as 'trash' where they bind to a receptor and undergo autophagy (literally, self-eating) inside the organelle. Dr. Cuervo's research focuses on this pathway and how a major decline in its functionality is seen in older organisms." The piece goes on to describe how researchers restored this functionality to youthful levels in aged mice.

A Good Example of a Cell Signaling Application (October 09 2008) http://www.xconomy.com/boston/2008/10/09/provasculon-a-biogen-backed-startup-testing-regenerative-medicine-on-hearts/
An important field resulting from stem cell research is the discovery and application of biochemical signals to direct existing stem cells in the body - they can be made to repair damage where they would ordinarily remain inactive. Only where stem cells themselves are damaged would new cells be needed: in most situations, greater control over the cells you have is good enough. Via Xconomy: "Provasculon is tackling one of the bigger ideas in regenerative medicine - how to stimulate growth of new blood vessels after they've been damaged by a heart attack. Iin rat studies that a novel protein was able to stimulate a certain type of stem cells (better known to scientists as endothelial progenitor cells) to migrate to damaged heart tissue, promote growth of new blood vessels, and ultimately help the heart pump better after a heart attack. The trick here is that Provasculon is trying to make a genetically engineered form of the key protein, SDF-1, that is able to avoid certain enzymes in the body that would like to chop the protein up and render it useless."

All Problems Are a Matter of Atoms (October 08 2008) http://www.acceleratingfuture.com/michael/blog/2008/10/physical-basis-for-problems/
The ultimate goal of medicine is to be able to reliably and precisely manipulate any the molecules in our bodies: all disease, all aging, is a matter of the wrong molecules being in the wrong place at the wrong time. From Accelerating Future: "It's important to realize the obvious: that every human problem, every malady, every concern, every evil, is at root simply a suboptimal arrangement of atoms and molecules. If this sounds quasi-spiritual, it's because it is - for millennia, pre-scientific humans have attributed all ills to various agents - the gods, magicians, and other humans. This is because these ills demand an explanation, and we didn't have a plausible one, so we made it up. Now, at least in the abstract, we have a concrete, very likely correct answer: suboptimal atomic arrangements. This realization is neither trivial nor too broad to be useless. If your problems are caused by the gods (that some people sadly still believe in...), then to solve them, you either need to give up, on engage in rituals [that] have an empirical impact of precisely zero." There is a simple criteria by which to judge whether new technologies will enable better medicine: do they give us the ability to more precisely and easily move atoms around? Modern biotechnology and the molecular manufacturing that will follow are both good examples.

Pondering Aging Stem Cells in the Gut (October 08 2008) http://www.sciencenews.org/view/generic/id/37382/title/Old_age_causes_problems_for_gut_cells
From Science News: "Old age can hit animals in the gut. That's where elderly fruit flies experience a signaling imbalance that disrupts renewal of the gut wall, new research shows. The discovery could help scientists understand why the body's organs malfunction in old age, and why intestinal cancer is so common among older people. Normally, 'adult' stem cells in the intestinal wall churn out a steady stream of new cells to replenish the lining [but] in older animals, this balance seems to be breaking down. The imbalance appears to be triggered by stress - not psychological stress, but the chemical stresses put on cells by free radicals or by chronic inflammation, both of which get worse as an animal ages. Cells in the gut lining respond to this stress by activating a protective gene [which] is part of a signaling pathway that spurs intestinal stem cells to grow and divide. In response, another signaling pathway - called the Delta/Notch pathway - ramps up to try to keep that growth in check. But too much Delta/Notch can also derail the natural conversion of these stem cells into mature gut cells, causing an abnormal accumulation of halfway converted cells. [This] malfunctioning of adult stem cells in old age [is] very similar to what happens in certain human stem cell populations."

Attacking Macrophages in Fat (October 07 2008) http://www.eurekalert.org/pub_releases/2008-10/cp-ki093008.phpYou might recall that the reason excess fat tissue is so damaging seems to be due to roaming macrophages that release inflammatory biochemicals. Via EurekAlert!, a demonstration that reinforces this point: "Over the past decade, it has become quite clear that obesity gives rise to a state of chronic, low-grade inflammation that contributes to insulin resistance and type 2 diabetes [researchers] recently found that a specific subset of macrophages invades obese fat and muscle tissue. Although little was known about them, those macrophages are defined by a CD11c marker expressed on their surfaces. They also produce high levels of proinflammatory chemicals that are linked to the development of obesity-associated insulin resistance. We used a genetic 'trick' that allowed us to rapidly kill these macrophages. The treatment killed these cells within hours, and insulin resistance simply reversed itself. It argues strongly that macrophages are causative for the inflammation that leads to diabetes [in those who are obese]. The most interesting thing is that this reversal occurs very rapidly. Twenty-four hours later the animals' insulin response had completely normalized. They were still obese, but no longer insulin resistant."

Hub of NanoMedicine

2008-10-06T08:29:00.000-07:00

Dear Future Centenarian,

To continue last week’s discussion of nanomedicine, here’s why you’d be interested in living long enough to see it get fully developed:
Nanotechnology refers to the control of matter on a scale normally between 1-100 nanometers. One nanometer is a billionth of a meter or 80,000 times smaller than a human hair.
We work with the world’s recognized authorities on medical applications and implications of molecular nanotechnology, or Nanomedicine. They have launched a program aimed at developing a provable nanomedical life extension technology. This may be the ultimate technology which can cure aging and reverse its effects.
They constructed a preliminary R&D roadmap and have already achieved some of their objectives. They have even established six currently active collaborations.
The technology should have commercially useful early applications. If successful, the company will eventually own a must-have product – indefinite life extension and aging reversal. In a nutshell, nanomedicine could eventually build or repair almost every cell in your body, from the bottom up, atom by atom. When we get to the 2020s, we will ultimately have perfected the machines of nanotechnology, nanobots, which are blood cell-sized devices that can go inside your body and brain to perform therapeutic functions, as well as to advance the capabilities of our bodies and brains.
If that sounds too futuristic, I'll point out that we already have blood cell-size devices that are nano-engineered, working to perform therapeutic functions in animals. For example, one scientist cured type I diabetes in rats with this type of nanoengineered device. And some of these are now approaching human trials. The 2020s will be the "golden era" of nanotechnology.
If you want to see who is at the hub of nanomedicine, visit these two websites:
http://www.MolecularAssembler.com/Nanofactory
http://www.MolecularAssembler.com/Nanofactory/Media/PressReleaseAug08.htm
Nanomedicine promises to give us complete control of matter and a very efficient way to cure aging damage, injuries and diseases. So keep fit and lean in the meantime. You don’t want to miss this boat.
______________________________________________

SLOW AND STEADY WINS THE RACE

Some food for thought on the way in which you approach the health basics - exercise, diet, supplementation, and relationships with physicians:

http://www.fightaging.org/archives/001582.php

"Following up on growing evidence that higher levels of conscientiousness are associated with greater health protection, the authors conducted a meta-analysis of the association between conscientiousness-related traits and longevity. Higher levels of conscientiousness were significantly and positively related to longevity. Associations were strongest for the achievement (persistent, industrious) and order (organized,
disciplined) facets of conscientiousness. Results strongly support the importance of conscientiousness-related traits to health across the life span."

The persistent application of good habits and good choices pays well. The basics are not rocket science, but they do make a significant difference over the years.
______________________________

LATEST HEALTHY LIFE EXTENSION HEADLINES

More on Comparative Longevity (October 03 2008) http://www.bucknell.edu/x45446.xml
Researchers continue to try to learn from differences in longevity and metabolism between species: "Haussmann studied cacti and turtles before zeroing in on a small, marine bird that contradicts traditional assumptions about aging. Leach's storm-petrels should die young but live a long life and break the conventional rules. First of all, they're small, and there tends to be a relationship between body size and life span. Elephants live longer than humans. Humans live longer than mice. So this bird shouldn't live long, but it does. His studies of storm-petrels have shown that certain characteristics of DNA - specifically lengths of the protective telomeres at the tips of DNA - are associated with species that live longer lives and possibly with how susceptible they are to cancer-causing tumors. [Bird species] with shorter life spans, such as zebra finches, lost their protective telomere caps quickly over time. Species such as the common tern, which lives to be about 30 years old, had less shortening over time." The petrels apparently produce more antioxidants as well - which may tie into the evidence suggesting that mitochondrial damage is the cause of shortened telomeres. Antioxidants slow the rate of that damage. The question remains as to where telomere length sits in the spectrum of cause and effect.

The Novel Paradigm of Longevity Science (October 01 2008) http://www.acceleratingfuture.com/people-blog/?p=2366
Over at Future Current, one of the presentations from Aging 2008: "What can each of us do to advance a new paradigm for health promotion and disease prevention in the 21st century that makes as its central tenet the slowing of aging? Recently, the board of directors of [the Alliance for Aging Research] committed to an aggressive effort to speak out for longevity science, which I think is a more elegant way of saying biogerontology, in order to hasten the social benefits extending healthy aging, a goal that we have referred to as 'pursuing the longevity dividend.' Now, the members of my board are not naive. They know very well that longevity science continues to be a tough sell. Let's face it, call it by any name, the quest for significantly extended lifespan has an image problem. Most established scientific leaders have been brought up to believe that aging is not only unchangeable, but not even very interesting. Now let's move to lay people. Most of them think there is not anything you can do about aging. They believe that even if you could, it would be a social and an economic catastrophe. Too many sick, old people sitting around, not pulling their weight. Even if people believed there could be some scientific breakthrough that would make it possible to extend the healthy years of life, many will set themselves up in opposition because it sounds unnatural or upsetting to social norms or religious beliefs. What will it take to overcome negative assumptions among the public?"

Life is the Road to Utopia, If You Can Stay on It (September 30 2008) http://jetpress.org/v19/bostrom.htm
From JET, a Nick Bostrom fiction in the spirit of the Fable of the Dragon Tyrant: "Your body is a deathtrap. This vital machine and mortal vehicle, unless it jams first or crashes, is sure to rust anon. You are lucky to get seven decades of mobility; eight if you be fortune's darling. That is not sufficient to get started in a serious way, much less to complete the journey. Maturity of the soul takes longer. Why, even a tree-life takes longer. Death is not one but a multitude of assassins. Do you not see them? They are coming at you from every angle. Take aim at the causes of early death - infection, violence, malnutrition, heart attack, cancer. Turn your biggest gun on aging, and fire. You must seize the biochemical processes in your body in order to vanquish, by and by, illness and senescence. In time, you will discover ways to move your mind to more durable media. Then continue to improve the system, so that the risk of death and disease continues to decline. Any death prior to the heat death of the universe is premature if your life is good. One day you or your children should have a secure home. Research, build, redouble your effort!" The road to Utopia is to continue to live well - which, as Bostrom notes, will require great labor devoted to new medical technologies of engineered longevity.

Axolotl Biochemistry as a Goal to Aim for (September 29 2008) http://pmid.us/18814845
It is plausible that mechanisms of unlimited tissue regeneration will be learned from lesser species and then ported to humans: "Urodele amphibians such as the axolotl are the champions of tissue regeneration amongst vertebrates. These animals have mastered the ability to repair and replace most of their tissues following damage or amputation even well into adulthood. In fact it seems that the ability of these organisms to regenerate perfectly is not affected by their age. In addition to being able to regenerate, these animals display a remarkable resistance to cancer. They therefore represent a unique model organism to study regeneration and cancer resistance in vertebrates. The need for this research is even more pressing at the dawn of the 21st century as we are faced with an ever aging world population which has to deal with an increase in organ failure and cancer incidence. Studying tissue regeneration in salamanders could yield significant knowledge to help regenerative medicine achieve the desired goal of allowing humans to repair and regenerate some of their own tissues as they age."

Mechanisms of Osteoarthritis (September 29 2008) http://www.eurekalert.org/pub_releases/2008-09/uorm-nsp092508.php
Researchers continue to learn more about the underlying biochemistry of common age-related conditions: "Until relatively recently, osteoarthritis was believed to be due solely to wear and tear, and an inevitable part of aging. Recent studies have revealed, however, that specific biochemical changes contribute to the disease, changes that might be reversed by precision-designed drugs. Our study provides the first solid proof that some of those changes are related to pain processing, and suggests the mechanisms behind the effect. The study revealed that pain signals originating in arthritic joints, and the biochemical processing of those signals as they reach the spinal cord, worsen and expand arthritis. In addition, researchers found that nerve pathways carrying pain signals transfer inflammation from arthritic joints to the spine and back again, causing disease at both ends. We believe this to be a vitally important process contributing to orthopaedic and neurological diseases in which inflammation is a factor."

Nanofactory Collaboration Colleague Awarded $3 Million

2008-10-06T08:27:00.000-07:00

Dear Future Centenarian,

Are you plagued with information overload? It gets worse every day, doesn’t it? If it weren’t for Reason at www.longevitymeme.org, I’d never have the time to sort through all the daily longevity news that you see in this letter. He does a terrific job, I distill it down and slightly edit it, and presto, you spend a few minutes every week to pick and choose whatever hits your hot button. There’s something for almost everybody in each issue, maybe even some life-saving info for you or a loved one.

Here is an excerpt from a release that I got from another source. An article like this might not catch your attention. On the surface, it looks like just another narrow-niche, hi-tech article aimed toward a limited audience. In reality though, it could hold the key to your full age-reversal plus open-ended youth in a super-human body. I’ll tell you why in a moment.
Nanofactory Collaboration Colleague Awarded $3M to Conduct First Diamond Mechanosynthesis Experiments
Professor Philip Moriarty of the Nanoscience Group the School of Physics at the University of Nottingham (U.K.) has been awarded a five-year $3M grant by the U.K. Engineering and Physical Sciences Research Council (EPSRC) to perform a series of laboratory experiments designed to investigate the possibility of diamond mechanosynthesis (DMS). DMS is a proposed method for building diamond nanostructures, atom-by-atom. Moriarty’s experiments begin in October 2008.
The Nottingham work grew out of continuing discussions on DMS between Moriarty and Robert Freitas, a Senior Research Fellow at the Institute for Molecular Manufacturing (IMM) (Palo Alto, California, U.S.).
Freitas and Ralph Merkle, also a Senior Fellow at IMM, founded the Nanofactory Collaboration in 2001 to pursue molecular manufacturing via DMS. Moriarty is interested in testing the viability of positionally-controlled atom-by-atom fabrication of diamondoid materials as described in the Freitas-Merkle minimal toolset theory paper. Moriarty’s efforts will be the first time specific predictions of DFT in the area of mechanosynthesis will be rigorously tested by experiment.
The article goes into more detail, but the implication for your longevity is this:
DMS is the first step on the way to full-blown nanomedicine. Nanomedicine may be the holy grail of indefinite lifespans. Next week, we’ll go a little deeper and take a peek into the future that nanomedicine has in store for you.
______________________________
LATEST HEALTHY LIFE EXTENSION HEADLINES

Calorie Restriction: Animals Versus People (September 25 2008) http://www.sciencedaily.com/releases/2008/09/080924151018.htm
The present scientific consensus on calorie restriction in humans is that it will do wonderful things for your health and resistance to age-related disease, but won't extend the maximum human life span to the same degree that is seen in lower animals: "In the majority of the animal models of longevity, extended lifespan involves pathways related to a growth factor called IGF-1 (insulin-like growth factor-1). In calorie-restricted animals, levels of circulating IGF-1 decline between 30 percent and 40 percent. We looked at IGF-1 in humans doing calorie restriction [and] found no difference in IGF-1 levels between people on calorie restriction and those who are not. We know there are two major influences on IGF-1 levels: calorie intake and protein intake. So we decided to look at the influence of protein. Six [human testers] agreed to lower their protein intake and after three weeks their circulating IGF-1 declined dramatically. It's much easier to restrict protein than to restrict calories. If our research is on the right track, maybe humans don't need to be so calorie restricted. Limiting protein intake to .7 or .8 grams per kilogram per day might be more effective. That's just a hypothesis. We have to confirm it in future studies."

Nitric Oxide and Aging Blood Vessels (September 24 2008) http://pmid.us/18805864
Nitric oxide is important in the operation of the endothelium - the lining of blood vessels - but diminishes with age: "The normal endothelium exerts a major vascular protecting role by secreting substances, above all nitric oxide (NO). In disease conditions (such as the presence of cardiovascular risk factors) the activation of endothelial cells can lead to the production and release of contracting factors, which counteract the beneficial effects of NO, and reactive oxygen species (ROS), which in turn cause NO breakdown. Aging has been demonstrated to be associated to a progressive impairment in endothelial function both in conduit arteries and resistance vessels, mainly because of an increased production of ROS.

Therefore, it is conceivable that endothelial dysfunction plays a major role in favoring age-related increased cardiovascular risk in the elderly. "This is an example of the way in which age-damaged cells cause problems in the normal operation of surrounding tissue: cells taken over by damaged mitochondria are exporting reactive oxygen species that breakdown NO, and senescent cells are pushing out their own cocktail of unhelpful chemical instructions as well.

Out of Context, Many Old Cells Work Just Fine (September 23 2008) http://pmid.us/18802086
It is a recurring theme in stem cell and immune system research that cells removed from the context of the aging cellular environment can do their jobs just as well as cells in a young environment: "Understanding how aging impacts the function of memory CD4 T cells is critical for designing effective vaccines. Our studies show that immunological memory generated during youth functions well into old age, whereas that generated later in life functions poorly. This is the result of declines in the function of naive CD4 T cells from aged individuals and contributes to reduced efficacy of vaccines in the elderly. To begin to identify the cause of this defect, we examined the function of memory T cells generated from bone marrow precursor cells (BMPC) from young or aged mice in young hosts. In two different models, memory cells derived from young and aged BMPC exhibit good ex vivo and in vivo function. Importantly, memory CD4 T cells generated from aged BMPC exhibit potent cognate helper function for humoral responses, which are critical for effective immunization. These results indicate that there are no apparent age-related intrinsic defects in BMPC with regards to generation of functional memory T cells." As for many aspects of aging, the problem is one of failing systems and signal controls, not failing components.

NOTE: Maybe many do work fine, but we believe most don’t, due to accumulated mutations.

A Recellurization Update (September 23 2008) http://www.popsci.com/node/24069
Via Popular Science: "Some people say they can grow a heart from scratch in 10 years, which is ridiculous. But Dr. Taylor's approach is more realistic because it's so simple and elegant. By using an existing heart, she's taken away all of the structural issues. Taylor's system involves flushing animal hearts of cells using a cleanser, at which point only the extracellular matrix remains and 'the hearts look almost clear'. The next step is to infuse the hearts with a mix of mature and progenitor cardiac cells, which can come from a patient's own body to ensure compatibility. Incredibly, for reasons the team still doesn't understand, the cells seem to know how to divide and proliferate into cardiac tissue inside the empty-shell hearts. This year, Taylor has continued to forge ahead toward her goal of creating transplantable, made-to-order human organs. Soon after she published her rat-heart results, she started working on making recellularized pig hearts - closer in size and shape to the human equivalent - that could pump blood and generate electrical impulses. Our hope is that someday we'll be able to take a cadaver or pig organ, decellularize it, and transplant your own cells into the matrix to make an organ that matches your body."

A Potential Downside to Exercise Mimetics (September 22 2008) http://ouroboros.wordpress.com/2008/09/22/amp-activated-kinase-the-target-of-exercise-mimetics-may-contribute-to-photoaging-and-cell-death/
From Ouroboros: "AMP-activated kinase (AMPK) agonists mimic the effects of exercise, raising the possibility of a 'workout pill' that could simulate the effects of vigorous activity. The applications to human health are, to mildly understate the case, significant; it sounds almost too good to be true, and it leaves one looking for the catch. It turns out that AMPK is activated by certain types of genotoxic stress, and contributes to UV-induced apoptosis in the skin. Activation of AMPK could exacerbate the pro-aging effects that UV light exerts on the skin. Judging from the peroxide results, this also applies to endogenously generated reactive oxygen species (ROS) - which one can't avoid by simply staying out of the sun. Before we panic and throw the exercise mimetic baby out with its carcinogenic bathwater, I'd want to see whether AMPK agonists like AICAR do in fact synergize with stresses like UV and peroxide to increase apoptotic cell death in the skin. If they do, well, I think we found that catch."

More Multipotent Stem Cells Discovered (September 22 2008) http://www.eurekalert.org/pub_releases/2008-09/chop-pri092208.phpFrom EurekAlert!: "The scientists [identified] cells known as pericytes that are multipotent, meaning they have broad developmental potential. Pericytes are found on the walls of small blood vessels such as capillaries and microvessels throughout the body and have the potential to be extracted and grown into many types of tissues. We believe pericytes represent one of the most promising sources of multipotent stem cells that scientists have been searching for in the quest to make regenerative medicine possible. These cells can be extracted easily and painlessly from convenient sources such as fat tissue, dental pulp, umbilical cord and placental tissue, then grown in culture to large numbers and, possibly, re-injected into the patient to heal a broken bone, a failing joint or an injured muscle. Researchers were able to identify pericytes in all human tissues they analyzed, including muscle, fat, pancreas, placenta and many other samples. Through purification in the lab, these pericytes could then be coaxed into becoming whatever type of tissue the scientists desired. For instance, the researchers took pericytes from the pancreas and then reinjected them into an injured muscle. The cells immediately began regenerating muscle tissue."

Artificial General Intelligence

2008-09-29T08:14:00.000-07:00

I wish you could have been with me Wednesday evening. I was treated to a personal demonstration of a technology that could change the world in ways we can’t even imagine. One of the changes that will affect you could lock in full age reversal and open-ended youth and health ahead of even my ambitious schedule.

The technology I’m describing is Artificial General Intelligence (AGI).

AGI is a new kind of computer application. This technology will allow computers to learn, think and respond like humans. They will exhibit REAL intelligence. Such intelligent systems do not exist yet – however, the required knowledge to build them does, and it has already led to an embryonic prototype. That’s what I experienced Wednesday.

AGI makes up one part of the MaxLife plan to accelerate extreme life extension capabilities. Research aims to create this broad human-like intelligence, rather than narrowly "smart" systems that can operate only as tools for human operators in well-defined domains such as tracking inventory or landing airplanes.

Imagine machine intelligence with the ability to think and learn on its own as well as humans do. That’s in our future. For example, if it gets an education equivalent to a biotech researcher, it could do the research. The developers estimate a sophisticated working system could take less than 10 years to complete. Two years later, we could potentially have a fully-trained PhD-equivalent AGI doing research.

Imagine a PhD lab assistant which would have total recall and tirelessly work around the clock. It would be able to download all the data it needs from the Internet almost instantaneously. It could collaborate with humans and other AGI. And then, it could be quickly copied as many times as necessary.

Imagine unleashing 100,000 AGI researchers. Imagine how much faster they would develop real anti-aging therapies.

So keep posted and hang on for a long ride Methuselah.
_________________________________________________
$1 BILLION ALREADY INVESTED IN SOMETHING YOU CAN DO FOR FREE

"Two pilot studies were undertaken to examine the effects of alternate day fasting and calorie restriction on indicators of health and longevity in humans. In this study, we used sera collected from those studies to culture human cells and assessed the effects on growth, stress resistance and gene expression. Cells cultured in serum collected at the end of the dieting period were compared to cells cultured in serum collected at baseline (before the dieting period). This resulted in increased stress resistance and an up-regulation of genes proposed to be indicators of increased longevity."

As of late 2008, I'd guesstimate that something in the order of one to two billion dollars have been invested into developing drugs that will produce some fraction of the effects of calorie restriction on mammalian biochemistry - such as increasing the expression of Sirt1. They aren't done yet, and years of trials and further development lie ahead. Most people can get these benefits today and for free, however, by simply eating a less calorie-packed diet. You should look into it: calorie restriction isn't anywhere near as hard as those who have never tried it make it out to be. You can find an introduction at the Longevity Meme website:

http://www.longevitymeme.org/topics/calorie_restriction.cfm

TRY NOT TO STAB YOURSELF REPEATEDLY

Words of wisdom:

http://www.fightaging.org/archives/001572.php

"On March 19, 2008 a Symposium on Pathophysiology of Aging and Age-Related diseases was held in Palermo, Italy. Here, the lecture of V. Nicita-Mauro on Smoking, health and ageing is summarized. Smoking represents an important ageing accelerator, both directly by triggering inflammatory responses, and indirectly by favoring the occurrence of several diseases where smoking is a recognized risk factor. Hence, non-smokers can delay the appearance of diseases and of ageing process, so attaining longevity.

"Forms of slow self-destruction are many and varied amongst us humans: Smoking, not practicing calorie restriction, failing to keep up a good relationship with a physician, piling on the visceral fat, failing to exercise, and so forth. The vast majority of people are quite comfortable engaging in habits that cause great harm to the old person they will one day be - cutting off years or even decades of health. This is all a good example of time preference at work: we are hardwired to deeply discount the value of the future, even when it's our own future. What we don't value, we squander - you can see that maxim in action everywhere."
______________________________

LATEST HEALTHY LIFE EXTENSION HEADLINES

Lurking Behind the TOR Gene (September 19 2008) http://www.eurekalert.org/pub_releases/2008-09/uouh-lca091808.php
Researchers have known for a few years that the TOR gene is important in calorie restriction and other related ways of extending healthy life. Recent research follows the chain of biochemical cause and effect beyond TOR: "In C. elegans, the tiny roundworm that our lab studies, as well as some other animals, a loss of TOR has been shown to slow aging. Our work with C. elegans reveals that TOR depends on a second gene called pha4/FoxA to control the aging process. When there's lots of food, TOR gets active, which decreases the action of pha4/FoxA down the line, and that in turn shortens the lifespan of C. elegans. When there's little food, there'slittle TOR and more pha4/FoxA, and that results in a longer lifespan. Many organisms have a TOR gene and a gene similar to pha4/FoxA, such as single-cell yeasts, roundworms, and mammals including humans. In mammals, FoxA controls cell metabolism and there is a lot of it in breast and prostate cancers. The findings of this research establish that animals use both genes to sense the amount of food that is available and control the length of lifespan. Further research will be required to establish whether a similar relationship between these factors can control metabolism, longevity or disease in humans."

Early Experiments in Cryonics (September 18 2008) http://www.depressedmetabolism.com/2008/09/15/early-total-body-washout-experiments-in-cryonics/
Depressed Metabolism takes another look at the early days of cryonics: "The question of whether cryonics 'works' or not is too general and hides the point that progressive breakthroughs can make the concept more plausible. During its existence as a research program, cryonics researchers have shown great interest in recovering animals from ultra-profound hypothermic temperatures (lower than 5 degrees Celsius). The ability to routinely lower the temperature of mammals to temperatures close to zero degrees Celsius and recover them without adverse effects to the brain does make the initial stages of cryonics reversible. Less known than those record setting experiments are earlier explorations in cryonics into whole body asanguineous hypothermia. The following document by cryonics researcher and Alcor patient Jerry Leaf documents a Trans Time experiment during the early days of total body washout experiments in cryonics. This account was published in the November/December 1977 issue of Long Life Magazine."

Struggling to Break Out of the Old Paradigm (September 17 2008) http://www.redorbit.com/news/health/1558015/listening_to_resveratrol/
From RedOrbit, an example of someone caught halfway between paradigms: learning about the potential of longevity science, but having trouble envisaging the changes it will herald for institutions of insurance, development, and regulation. "Currently our drug development and approval systems aim at disease-specific treatments. Indeed, the Food and Drug Administration approves medications only for specific indications, and 'mortality,' a universal condition, would seem unlikely to qualify under the current system. Further, if senescence begins in one's 30s but the outcome (that is, death) can be measured only in one's 70s or 80s, how will researchers be able to perform timely clinical trials in humans? Health insurance is based on the principle of risk pooling. Because nobody can be certain that they will remain healthy, the disease-free are willing to share the cost burden with the sick. But if resveratrol-like drugs are recommended for everybody over 30 at risk for mortality (a universal condition), there would be no risk pooling." When you catch yourself asking"how will this ever fit?" then the answer is usually "it won't fit, and will never fit in the present structure, because things will change in the future so as to accommodate it."

Learning from AIDS (September 17 2008) http://www.sciencedaily.com/releases/2008/09/080916143900.htm
There are similarities between the progression of AIDS and what happens (more slowly) to our immune systems with aging. Forced overactivation and exhaustion of resources are the focus here. AIDS researchers are making steps towards understanding mechanisms that would allow the immune system to be tuned down for specific threats, to prevent it grinding itself into oblivion. "During both HIV infection in humans and SIV infection in macaques, the host immune system becomes highly activated, experiences increased destruction and decreased production of key immune effector cellsand progressively fails as a result. In contrast, natural hosts for SIV infection, like sooty mangabeys, do not exhibit aberrant immune activation and do not develop AIDS despite high levels of ongoing SIV replication. Sooty mangabeys, dendritic cells produce much less interferon alpha - an alarm signal to the rest of the immune system - in response to SIV. As a result, the dendritic cells are not activated during the initial or chronic stages of SIV infection, and mangabeys fail to mount a significant immune response to the virus." It seems reasonable to expect this knowledge to be applicable to the long-term response to CMV in humans, an important contributor to age-related immune system failure.

A Better Lifestyle Means More Telomerase? (September 16 2008) http://www.sfgate.com/cgi-bin/article.cgi?f=/c/a/2008/09/16/MNEL12UBJ5.DTL
The San Francisco Chronicle reports on an intriguing, if small, study: researchers "studied the levels of an enzyme called telomerase in the prostate tissue of the 30 cancer patients who had volunteered to follow a low-fat diet, exercise moderately and reduce their stress. After only three months, 24 patients showed a highly significant increase in their telomerase levels - an indication that the cell-protecting telomeres in their cells were being restored. The long telomere proteins protect the ends of chromosomes in the body, but they shorten naturally and ultimately die unless the telomerase enzyme acts to repair them and increase their length. Even with only 30 patients [the] association between their extremely healthy habits and the increased amount of telomerase proved highly [statistically] significant." Telomerase is apparently also involved in reducing age-related damage to mitochondria, which in turn slows the rate at which failing mitochondria cause telomeres to shorten.

Mitochondrial Function and Aging (September 16 2008) http://www.boston.com/news/health/articles/2008/09/15/power_outage/?page=fullThose of you familiar with the mitochondrial free radical theory of aging -damage to mitochondrial DNA leads to loss of function and a spreading chainof biochemical dysfunctions - will notice a subtle disconnect between this research and the popular science view of mitochondrial function and aging, as outlined in this Boston Globe article. The popular view is very much concerned with contribution to particular diseases, and in finding drugs that improve mitochondrial function as a way of slowing that contribution -without necessarily understanding why those drugs work. We know enough to do much better than that - repairing mitochondrial damage completely, for example, and thus totally removing its contribution to aging. But until thepublic at large realizes this, funding will continue to move towards the established old-school drug discovery programs. These programs focus on treating specific diseases of aging by patching over or slowing down root causes - as opposed than aiming to repair them fully

Las Vegas Longevity Workshop

2008-09-11T08:57:00.000-07:00

Last week, I mentioned the longevity workshop I attended in Las Vegas. This week, I’m going to illustrate how hanging out with the participants energized me, and I’m going to talk a little about the workshop itself.

First, let me tell you why it was such a positive event for me.

We had 16 attendees, plus me. Every one of them, all 16, shared a positive upbeat outlook on life.

Can you think of someone who brightens up your day by just walking into the room? Don’t you have someone in your life who you just love hanging around, someone who lifts your spirits by their mere presence? How about someone who shares your values, aspirations and plans?

OK, now roll those people into one… then multiply that person by 16. That’s who I spent the weekend with… 16 energizers.

In fact, it gets better. Half the attendees were geniuses and leaders in their respective fields. I’m totally in awe of some of them. They’re so brilliant, they totally humble me.

Now if that’s not enough, the workshop topic was something I am passionate about – life insurance!

What? Life insurance? I know, I know, you’re probably thinking I’ve gone off the deep end, or I’m some sort of closet life insurance salesman. Nothing could be further from the truth. I did in fact sell life insurance in a previous life, but that was traditional life insurance… and I hated it.

No, this workshop was about the only “pure” form of life insurance. Not the kind you can only benefit from by dying (which is actually “death insurance”), but the kind that could keep you from dying in the first place… Cryonics! More specifically, our topic was the strategy to preserve your assets if you experience clinical death, get cryonically preserved and get resuscitated. In other words, maybe you can “take it with you” after all.

If you’re not familiar with cryonics, research has shown that dying is a gradual process which starts after, not when, our hearts or brain waves stop. Our cells die gradually, over time. Cryonics is the science that halts this dying process with low-temperature technologies, stemming from the field of cryobiology.

If the cryonics rescue team reaches patients in time after legal death, they may be able to place them into suspended animation until such time as cures for what “killed” them are developed, and when age-reversal technologies are mature. At that time, they plan on fixing you and waking you up.

A long-shot? Maybe. Whacky? If you think so, consider this:

Cryonics depends largely on two technologies. One is cryobiology, a well-proven field that deals with ultra-low temperatures. In this case, that means storing human tissue at liquid nitrogen temperatures for future therapies. This has been routinely done for many years.

The other is neurobiology, again, a totally legitimate and non-controversial field.

So it follows that it is just as legitimate to store and recover the brain (where your memory resides) as it is to store and recover any other tissue. So cryonics should work.

Then we add another emerging, and soon to be maturing tool… regenerative medicine. We’re already growing replacement organs, and soon, they promise to be as good, or even better than the originals. You have read a lot about this in previous issues of this newsletter. Again, a well-accepted field.

As these technologies are fine-tuned, they may be more than enough for resuscitating patients. But there’s more.

Another technology that may be enormously helpful for even more perfect rescue from suspension is nanotechnology. There’s already more work in this field than I can ever hope to keep up with. Full-blown nanomedicine may be developed in as little as 19 years.

So you might look at cryonics as the purest form of life insurance. Insurance is something you hope you never need but are glad you have when you do need it… when it is no longer for sale.
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LATEST HEALTHY LIFE EXTENSION HEADLINES

Progress in Bypassing Mitochondrial Damage (September 05 2008) http://www.eurekalert.org/pub_releases/2008-09/cp-gtp082808.php
Allotopic expression of genes normally found in mitochondrial DNA is a core portion of the Strategies for Engineered Negligible Senescence. It is the process of inserting a copy of vital mitochondrial genes into the cell nucleus, and then figuring out how to get the proteins produced by those genes back to the mitochondria where they are needed. This could eliminate the contribution of mitochondrial DNA damage to aging. A technique for doing all this is now demonstrated in rats: "We obtained a complete and long-term restoration of mitochondrial function in human fibroblasts in which the mitochondrial genes ATP6, ND1, and ND4 were mutated. ND1 and ND4 are mutated in nearly all cases of Leber hereditary optic neuropathy (LHON). LHON is the most common mitochondrial disorder and is characterized by a loss of vision. They introduced the human ND4 gene with the mutation present in the majority of LHON patients into rat eyes. The treatment caused retinal ganglion cells (RGCs) to degenerate significantly when compared to those from control eyes and was associated with decreased visual performance. Importantly, reintroducing normal ND4 led to prevention of RGC loss and visual impairment, effectively rescuing the animals from impending blindness. These data represent the 'proof of principle' that optimized allotropic expression is effective in vivo and can be envisaged as a therapeutic approach for mtDNA-related diseases."

Reactive Carbonyl Species, ALEs, and Aging (September 04 2008) http://pmid.us/18721793
Free radicals (such as reactive oxygen species) are increasingly generated with age - this is the end of a long chain of consequences that starts with damaged mitochondrial DNA. How do those oxidizing agents actually cause widespread harm to bodily systems? This paper gives an overview of one broad set of mechanisms, wherein step one is the creation of reactive carbonyl species (RCS) by free radicals: "Most of the biological effects of RCS [are] due to their capacity to react with cellular constituents, forming advanced lipoxidation end-products (ALEs). Compared to reactive oxygen and nitrogen species, lipid-derived RCS are stable and can diffuse within or even escape from the cell and attack targets far from the site of formation. Therefore, these soluble reactive intermediates, precursors of ALEs, are not only cytotoxic per se, but they also behave as mediators and propagators of oxidative stress and cellular and tissue damage. The causal role of ALEs in aging and longevity is inferred from the findings that follow: a) its accumulation with aging in several tissues and species; b) physiological interventions (dietary restriction) that increase longevity, decrease ALEs content; c) the longer the longevity of a species, the lower is the lipoxidation-derived molecular damage; and finally d) exacerbated levels of ALEs are associated with pathological states."

Update on the Longevity Science Amex Members Project (September 04 2008) http://blog.methuselahfoundation.org/2008/09/an_update_on_your_votes_and_un.html
From the Methuselah Foundation blog: "I'm pleased to say that the pro-longevity science community rallied to vote the Amex Members Project submission "Undergrads Fighting Age Related Disease" into the top 25 projects by vote totals - and made it the most discussed project of all. Thank you! That discussion is still ongoing, by the way, and people unfamiliar with longevity research have questions about the project. Feel free to jump in and help answer them. What comes next? Well, between now and September 9th - less than a week away - the Members Project advisory panel will look at the projects, votes, and discussions, and announce the final 25. Those 25 projects will be voted on by Amex card holders to determine which 5 will be funded. So, all you generous folk who rounded up your friends and spread the word: we're going to do it all again for those with American Express cards starting on the 9th. We here at the Methuselah Foundation are looking forward to it!"

Another Regenerative Strategy for Hearing Loss (September 03 2008) http://www.eurekalert.org/pub_releases/2008-09/ctco-hrm090308.php
Following on from the gene therapy approach for age-related deafness mentioned a few days ago, here's a cell-based therapy via EurekAlert!: "hearing loss due to cochlear damage may be repaired by transplantation of human umbilical cord hematopoietic stem cells. The team used animal models in which permanent hearing loss had been induced by intense noise, chemical toxicity or both. Cochlear regeneration was only observed in animal groups that received HSC transplants. Researchers used sensitive tracing methods to determine if the transplanted cells were capable of migrating to the cochlea and evaluated whether the cells could contribute to regenerating neurons and sensory tissue in the cochlea. Our findings show dramatic repair of damage with surprisingly few human-derived cells having migrated to the cochlea. A fraction of circulating HSC fused with resident cells, generating hybrids, yet the administration of HSC appeared to be correlated with tissue regeneration and repair as the cochlea in non-transplanted mice remained seriously damaged."

Metformin as Calorie Restriction Mimetic (September 02 2008)
http://pmid.us/18728386
This paper is illustrative of the thinking that leads to trying anti-diabetic drugs as calorie restriction mimetics: "Studies in mammals have led to the suggestion that hyperglycemia and hyperinsulinemia are important factors both in aging and in the development of cancer. It is possible that the life-prolonging effects of calorie restriction are due to decreasing IGF-1 levels. A search of pharmacological modulators of
insulin/IGF-1 signaling pathway (which resemble effects of life span extending mutations or calorie restriction) could be a perspective direction in regulation of longevity. Antidiabetic biguanides are most promising among them. Here we show the chronic treatment of female outbred SHR mice with metformin (100 mg/kg in drinking water) slightly modified the food consumption but decreased the body weight after the age of 20 months, slowed down the age-related switch-off of estrous function, increased mean life span by 37.8%, mean life span of last 10% survivors by 20.8%, and maximum life span by 2.8 months (+10.3%) in comparison with control mice." Full calorie restriction does better than that (30-40% maximum life span extension), but this is a strong argument for its effects on insulin metabolism to be one cause of enhanced health and longevity.

Another Human Longevity Gene Association (September 02 2008) http://www.telegraph.co.uk/earth/main.jhtml?view=DETAILS&grid=&xml=/earth/2008/09/01/sciage101.xml
The Telegraph reports on confirmation that a class of longevity genes indentified in lower animals also has an effect on human populations: "The gene linked with better health and a longer life is called FOXO3A and although similar genes have been shown to prolong life span in other species, this is the first time that FOXO has been linked directly to longevity in humans. Each gene comes in two copies and the team found the longevity effect of this letter was additive: those with one copy doubled their odds of living an average 98 years. Men who had two G copies did even better and almost tripled their odds of living nearly a century, and were markedly healthier at older ages. We screened 213 of the long-lived participants' DNA and 402 of the average-lived, focusing on five genes. These genes were selected for good reason because they involved in the insulin pathway and signaling, which studies of other animals have shown is linked with longevity." This doesn't tell us laypeople more than we already knew: that insulin metabolism is significant in health and longevity variations within a species.

On the Way to Controlling Telomerase (September 01 2008) http://www.eurekalert.org/pub_releases/2008-08/twi-lso082608.php
Researchers are making progress in figuring how to control telomerase, and through it influence telomeres, cancer, and aging. From EurekAlert!: Researchers "have deciphered the structure of the active region of telomerase, an enzyme that plays a major role in the development of nearly all human cancers. The landmark achievement opens the door to the creation of new, broadly effective cancer drugs, as well as anti-aging therapies. Researchers have attempted for more than a decade to find drugs that shut down telomerase - widely considered the No. 1 target for the development of new cancer treatments - but have been hampered in large part by a lack of knowledge of the enzyme's structure. The findings [should] help researchers in their efforts to design effective telomerase inhibitors. Telomerase is an ideal target for chemotherapy because it is active in almost all human tumors, but inactive in most normal cells. That means a drug that deactivates telomerase would likely work against all cancers, with few side effects." Long-term deactivation will cause massive issues, of course, but that's not the intent for the moment. Given new information about telomerase and mitochondria in aging, there are potentially more interesting end results than good cancer therapies.

Two Kinds of Friends

2008-09-03T08:11:00.001-07:00

I divide my close friends into two general groups.

1. The Miscellaneous Group: This includes lifelong friends as well as recent acquaintances. I share either/or history and some values with this group. I see some frequently but most infrequently. All-in-all, group is shrinking in size. That’s because many of us have grown or are growing apart. In other words, we don’t have much in common anymore. And outside of rehashing old times (which I find more-and-more boring), hanging out together is pretty much a waste of time. The few that I do enjoy spending with share common goals and typically look forward rather than backwards.

2. Life Extensionists/Futurists: This is my favorite and larger group of the two. It’s also expanding rapidly. It’s rare to hear these members talking of the past, and they are far more stimulating. They typically live actively in the present with long-term positive views of the future. And for the most part, they do their best to insure a profound future for all of us. They may take various paths and contribute in a number of ways such as doing research, volunteering for various future-focused movements, building positive value-laced enterprises, running companies and foundations, marketing positive products and services and actively participating in events, seminars and workshops that point toward noble goals such as (my favorite) radical life extension.

All too often, I get bogged down in the sea of minutia and the distractions of business and life that tends to bury us if we’re not constantly on guard. One of the challenges in my life is to evaporate that sea to a puddle. I’m gradually succeeding, but I’m not there yet. So when I have the chance to shut everything else out and spend time with Group #2, it breathes new life into me. I enjoyed that pleasure the past two weekends.

Two weeks ago, I and a couple of M.D.s got to address a group of life extensionists.

Pure rapture.

Just associating with like-minded people energizes me beyond description. It also validates and reinforces my resolve to conquer aging in our lifetimes.

This past Saturday, I took part in a life extension workshop in Las Vegas. The personal and business challenges that sometimes consume me did not enter my mind the entire weekend. How could they? Almost every minute was spent with some very close friends and with some not as close, but still enormously treasured acquaintances. Every single one of them shares most of my deepest goals and aspirations.

Most people take a two week or longer vacation to recharge. For me, it only takes a day in the company of members of Group #2. If you consider yourself a member of this group, you’re invited to a get-together at my home in Huntington Beach, CA, tentatively scheduled for Sat, Nov 22nd. If so, email me for directions and a final date and time.

Next week I’ll tell you a little about last weekend’s workshop.
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LATEST HEALTHY LIFE EXTENSION HEADLINES

Thinking About Replacing the Brain (August 29 2008) http://www.memebox.com/futureblogger/show/827-our-future-brain-damage-resistant-with-unique-new-abilities
Some thoughts on the decades following the biotechnology revolution from FutureBlogger: Once nanotechnology is as far advanced as biotechnology is today, what sorts of capabilities start to look plausible? "By the mid-2030s, we could be replacing brain cells with damage-resistant nanomaterials that process thoughts much faster than today's biological brains. The new brain would include our same consciousness, memories and personality that existed before the conversion, but it would run much faster and would increase our memory a thousand-fold. A daily pill would supply nanomaterials and instructions for nanobots to format new neurons and position them next to existing biological brain cells to be replaced. These changes would be unnoticeable to us, but within six months, we would be enjoying our new brain. Should a person with the new damage-resistant brain die in an accident, their body could be a total loss, but the brain would survive. Biological brains die within minutes after the heart stops; our new brain will simply turn itself off and wait for a new power supply. All memories and consciousness would remain intact after a fatal accident. Rescue workers would remove the brain from the deceased body and reinstall it into a newly-cloned body." A lot of work remains to be accomplished before the golden future becomes a reality - first things first.

Vote For Amex Funding For Longevity Science (August 28 2008) http://www.membersproject.com/project/view/BVVE2C
The Methuselah Foundation volunteers are looking for more signatures in the next five days to help put the "Undergrads Fighting Age Related Disease" project high in the top 25 Amex Members Projects - and thus eligible for some of the $2.5 million in funding offered by American Express. There are five days left to put your name to this project in support: 1200 signatures have been gathered in the past two weeks, putting longevity science solidly in the running. At least that many more votes are needed before voting closes - which is where you and your friends come in. Visit the Methuselah Foundation blog or the project Facebook group to find out how to sign up - or just click through to this project and follow the directions. You don't have to be an American Express member, but you do have to be a US resident. One last thing: it's important to note that of all the projects submitted to date, Undergrads Fighting Age Related Disease has by far the most comments. This counts heavily in the final selection, so jump into the project comments section and tell the world why you support longevity science and the defeat of age-related disease.

Another Advance In Reprogramming Cells (August 28 2008) http://www.sciencedaily.com/releases/2008/08/080828082819.htm
As ScienceDaily notes, researchers "report having achieved what has long been a dream and ultimate goal of developmental biologists - directly turning one type of fully formed adult cell into another type of adult cell. The team is able to turn mouse exocrine cells, which make up about 95 percent of the pancreas, into precious and rare insulin-producing beta cells. Unlike the process involved in creating induced pluripotent stem cells (iPS) [this] direct reprogramming technique does not require turning adult cells into stem cells and then figuring out how to induce them to differentiate into a desired cell type. We're intrigued by the possibility that this approach, which has worked for pancreatic insulin-producing cells, could be more widely applied to many kind of cells, especially those that are lost in disease or following injury. And at the same time, we are exploring the possibility of using this general approach in a clinical context to make new beta cells for patients."

An Interview With Doug Melton (August 27 2008) http://www.technologyreview.com/printer_friendly_article.aspx?id=21307
The Technology Review interviews researcher Doug Melton: "If a patient has Parkinson's disease, their dopamine-producing cells are gone. We don't understand anything about what makes those cells go away - the field is kind of stuck because you can't watch the progression of the disease. Stem cells can make neurons in a dish. Imagine you have iPS cells from a healthy person and from a Parkinson's patient. If you make dopamine neurons from both sets of cells in separate dishes, you can look at what went wrong with the diseased stem cell. The same approach will work with different degenerative diseases, such as diabetes or ALS. I think it will change the way degenerative diseases are studied - we'll reduce the whole process of disease to a petri dish. Within a few years, researchers the world over should have access to disease-specific cells that can be turned into cell types defective in a particular disease. Science clearly works best when you have a lot of bright, motivated people working on these problems. The institute has sent thousands of human embryonic stem-cell lines to hundreds of labs all over the world. We like to think that has been helpful in encouraging basic research on embryonic stem cells."

Microglia Versus Alzheimer's (August 26 2008) http://www.sciencedaily.com/releases/2008/08/080825194705.htm
Researchers are attempting to convince the body's defenses to attack the amyloid plaques of Alzheimer's disease (AD): "by stimulating a brain cell called a microglia the cells will partially engulf the senile plaques ... [this is] the first time that this phenomenon, believed to take place in living brain, has been duplicated in the laboratory. The plaques themselves are not sufficient microglial activators. But when the microglia were treated with inflammatory stimulants, they attacked the plaques. In AD patients, microglia are not coping with the plaque build-up. Therefore plaques accumulate faster than the microglia can digest them. If we can enhance microglial digestion of these plaques, we will have a fighting chance to eliminate AD. The next step is to find a therapeutic drug that will stimulate the microglia to devour the plaques." Time will tell whether new methods of

The Bad Trends (August 25 2008) http://www.futurepundit.com/archives/005479.html
There are plenty of good trends in medicine research and development. The trend in bioinformatics and computational power, for example. Unfortunately, some of the bad trends are blocking movement of research into the clinic. Via FuturePundit: "Why do terminally ill patients have to wait so long to get access to the only treatments that hold any promise of saving their lives? And why is it not their right to decide? The FDA approved just 16 new drugs last year, and is on pace to approve only 18 this year. That's down from a high of 53 in 1996 and 39 in 1997. This trend does not bode well for the development of rejuvenation therapies. The FDA will hold off approval of an anti-cancer drug for people who have a fatal disease. Never mind that people who have a fatal disease are going to die anyway. The FDA won't let people take a risk when they have little to lose. That makes no sense to me. Rejuvenation therapies are going to treat that fatal disease called aging. Absent those therapies we are all going to die from complications of aging. Faced with rising risks of death combined with increasing pain and disablement people should be given wider latitude to try new and unproven therapies." The FDA should turn down completely; it is a roadblock to progress, and the cause of great and ongoing suffering.

Two Groups of Friends

2008-09-02T15:22:00.000-07:00

Funding Extreme Life Extension Research

2008-08-25T10:51:00.000-07:00

For you serious readers, some say Dr. Leonid Gavrilov’s book, Biology of Life Span: A Quantitative Approach, has the potential to change the future of this country for the better, if its ideas reach members of Congress and other representatives of the U.S. government. Get more information at http://tinyurl.com/5x5ror

Now we’re going to wrap up our previous discussion about how we’re going to fund extreme life extension research.

How about all the private money? Where is it all going? Unfortunately, many popular investments may be ruining your health and shortening your life instead of extending it. And you may be unknowingly contributing to it. If you are invested in mutual funds, retirement funds, hedge funds, the chances are, you are invested in what I sometimes call “pro-death industries”. They include fast foods, processed foods, alcoholic and soft drinks and tobacco.

These industries make money… lots of it. That’s why savvy money managers invest in them. But they kill in two insidious ways. First, the products can shorten your life. Second, they divert sorely needed funds needed to develop life extending products, technologies and services.

Doesn’t it make sense to commit a portion of your wealth to technologies that cure diseases, promote wellness and extend healthy life?

Sure, we can wait until large funding sources finally catch up. Meanwhile though, over 100,000 lives get snuffed out every single day from aging. A five year delay equates to 185 MILLION more lost lives. Scientists tell us they can start making an impact with only a few million more dollars per year, so we simply can’t wait for nature to run its course. A delay could cost you or a loved one your life.

So I urge you to do three things:

Incorporate the 7 simple steps outlined in Life Extension Express into your life and gain 5-20 years... or more from the health steps you practice now. You will create a brighter tomorrow for yourself when you take some simple steps today.

Invest in some of these technologies or donate to Maximum Life Foundation, Methuselah Foundation, InnerSpace Foundation or Immortality Institute to support them.

Keep abreast of advances and breakthroughs that could push you over the longevity finish line.

As I see it, extreme life extension in our lifetimes will ultimately depend on several factors: (a) how much funding we can raise; (b) how soon we can raise the money; (c) how well you take care of yourself in the interim and (d) your ability to dodge accidents, warfare, terrorism, natural disasters or epidemics. Don’t wait until it’s too late – and then wish you would have spent a little time, money and effort for prevention.

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LATEST HEALTHY LIFE EXTENSION HEADLINES

More Compelling Reasons to Exercise (August 22 2008) http://pmid.us/18716044

Here is another study to add to the huge stack of research telling us that exercise is good for healthy longevity: "We determined whether reduced insulin sensitivity, mitochondrial dysfunction and other age-related dysfunctions are inevitable consequences of aging or secondary to physical inactivity. Insulin-induced glucose disposal and suppression of endogenous glucose production were higher in the trained young and older people but no age-effect was noted. Age-related decline in mitochondrial oxidative capacity was absent in endurance-trained individuals. Although endurance trained individuals exhibited higher expression of mitochondrial proteins, mtDNA, and mitochondrial transcription factors there were persisting effects of age. SIRT3 expression was lower with age in sedentary but equally elevated in endurance trained individuals. ... The results demonstrate that reduced insulin sensitivity is likely related to changes in [level of body fat] and physical inactivity rather than an inevitable consequence of aging. The results also show that regular endurance exercise partly normalizes age-related mitochondrial dysfunction, although there are persisting effects of age at the level of mtDNA abundance, nuclear transcription factors, and mitochondrial protein expression. Furthermore, exercise may promote longevity through pathways common to effects of caloric restriction."

Ouroboros on Biomarkers and Telomere Length (August 22 2008) http://ouroboros.wordpress.com/2008/08/21/telomere-dysfunction-markers-as-biomarkers-of-aging/

From Ouroboros: "How old are you? At present, the best experimental approach to that question is to inspect your driver's license; we are very good at measuring chronological age, but far worse at measuring physiological age. Until we have such a tool, questions like 'how rapidly is this individual aging?' and 'is this treatment having a positive effect on the rate of aging?' will be meaningless. So, the race is on to find useful biomarkers of aging. Telomere length is a tantalizing biomarker for the aging process: it's positively correlated with life expectancy and negatively correlated with stress and disease. If telomere shortening is a biomarker of aging, then the measurable consequences of telomere shortening should also function as biomarkers, i.e., aging bodies should contain high levels of factors secreted by cells with dysfunctional or critically short telomeres. According to a recent paper by Jiang et al., this is indeed the case. The proteins identified here accumulate with age - [and] they accumulate faster in subjects who are both aged and suffering from age-related disease; in other words, in people whom we might intuitively assign to the 'more rapidly aging' category."

Weight Gain Cast as a Result of Neural Damage (August 21 2008) http://www.eurekalert.org/pub_releases/2008-08/mu-kc082108.php

Hopefully you don't need more reasons to eat a sensible diet by now, but here's another. EurekAlert! passes on a theory to account for what happens to those of us who load up the carbohydrates over the years: "key appetite control cells in the human brain degenerate over time, causing increased hunger and potentially weight-gain as we grow older. Appetite-suppressing cells are attacked by free radicals after eating and [the] degeneration is more significant following meals rich in carbohydrates and sugars. People in the age group of 25 to 50 are most at risk. The neurons that tell people in the crucial age range not to over-eat are being killed-off. When the stomach is empty, it triggers the ghrelin hormone that notifies the brain that we are hungry. When we are full, a set of neurons known as POMCs kick in.. However, free radicals created naturally in the body attack the POMC neurons. This process causes the neurons to degenerate over time, affecting our judgement as to when our hunger is satisfied .The free radicals also try to attack the hunger neurons, but these are protected by the uncoupling protein 2 (UCP2)." So eat more over the years and suffer neural damage that makes it harder not to eat more. We all have free will, but why make it harder for yourself?

Menstrual Blood as Source of Adult Stem Cells (August 20 2008) http://www.sciencedaily.com/releases/2008/08/080818220609.htm

Like heart damage, peripheral artery disease is open to comparatively simple stem cell therapies based on cell transplants. All that is needed is a low-cost source of suitable stem cells. From ScienceDaily: "Cells obtained from menstrual blood, termed 'endometrial regenerative cells' (ERCs) are capable of restoring blood flow in an animal model of advanced peripheral artery disease. A new study demonstrates that when circulation-blocked mice were treated with ERC injections, circulation and functionality were restored. [Researchers have] already performed clinical trials with adult stem cells for patients with peripheral artery disease. The advantage of ERCs is that they can be used in an 'off the shelf' manner, meaning they can be delivered to the point of care, do not require matching, and are easily injectable without the need for complex equipment." The ease with which a therapy can be implemented makes a great deal of difference to the speed with which it moves from laboratory to clinic.

Building Blood from Stem Cells (August 20 2008) http://www.timesonline.co.uk/tol/life_and_style/health/article4567387.ece

The Times has more on growing blood from stem cells: "Vials of human blood have been grown from embryonic stem cells for the first time during research that promises to provide an almost limitless supply suitable for transfusion into any patient. The achievement by scientists in the United States could lead to trials of the blood within two years, and ultimately to an alternative to donations that would transform medicine. If such blood was made from stem cells of the O negative blood type, which is compatible with every blood group but is often in short supply, it could be given safely to anybody who needs a transfusion. One of the biggest safety hurdles that must be cleared before stem-cell therapies enter clinical trials is the risk of uncontrolled cell growth causing cancer. Red blood cells, however, do not have nuclei that carry the genetic material that goes wrong in cancer, and thus should not present this danger. While a few red blood cells have been created from embryonic stem cells before, the ACT team is the first to mass-produce them on the scale required for medical use. They also showed that the red cells were capable of carrying oxygen, and that they responded to biological cues in similar fashion to the real thing."

A Profile of Robert Lanza (August 19 2008) http://discovermagazine.com/2008/sep/19-fighting-for-the-right-to-clone/article_print

Discover Magazine looks at one of the noteworthies of the stem cell research community: "The value of therapeutic cloning has long been clear to Lanza, who did his early work with South African heart transplant pioneer Christiaan Barnard. Starting from those early days, Lanza understood that the barrier to tissue transfer was rejection by the recipient. From an entire organ to a dose of embryonic stem cells, if the tissue's DNA came from anyone else, the transplant would be rejected without the aid of harsh immunosuppressive drugs. 'The treatment could be worse than the problem,' Lanza found. But embryonic clones, the source of an endless supply of stem cells imprinted with one's personal DNA, could alter the equation in favor of the patient and augur a paradigm shift in medicine on par with the changes brought about by antibiotics and vaccines. With the ability to become all of the blood cells - including your immune cells, red blood cells, all of your blood system, as well as vasculature, [hemangioblasts] have been biology's holy grail. What we discovered is that we can create literally millions or billions of these from human embryonic stem cells. We can use transient, intermediate cells like hemangioblasts as a toolbox to fix the adult so you don't have to have limbs amputated, so you may not have to go blind, to prevent heart attacks."

More DNA Damage Research, In Mice This Time (August 18 2008) http://pmid.us/18565572

What does nuclear DNA damage have to do with aging? The correlation is clearly there - older animals have more random nuclear DNA damage - but the mechanism by which increased damage might lead to some portion of degenerative aging is up for debate. A recent paper shows that the correlation extends to calorie restriction and some genetic manipulations that extend life: "Genetic instability has been implicated as a causal factor in cancer and aging. Caloric restriction (CR) and suppression of the somatotroph axis significantly increase life span in the mouse and reduce multiple symptoms of aging, including cancer. To test if in vivo spontaneous mutation frequency is reduced by such mechanisms, we crossed long-lived Ames dwarf mice with a C57BL/6J line [to] measure mutant frequencies. Four cohorts were studied: (1) ad lib wild-type; (2) CR wild-type; (3) ad lib dwarf; and (4) CR dwarf. Results indicate that two major pro-longevity interventions in the mouse are associated with a reduced mutation frequency. This could be responsible, at least in part, for the enhanced longevity associated with Ames dwarfism and CR."

Financial Support for Aging Research

posted on August 18, 2008

Dr. Christoph Westphal, the chief executive of Sirtris, said of the potential of the resveratrol based drugs they are developing, “I think that if we are right, this could extend life span by 5 or 10 percent.” He added that his goal was to develop drugs against specific diseases, with the extension of life being “almost a side effect of our medicine.”

There is no FDA category for longevity drugs, so if the company is to submit a drug for approval, it needs to be for a specific disease. However, longevity is what has motivated the researchers and what makes the drugs potentially so appealing.

There you have the most serious problem facing longevity science today. The FDA does not allow its direct application. Until this changes, no serious investment will be made in the US to bring longevity science to the clinic. This is a tragedy of astronomical proportions and is beyond belief.

Congress did supplement scarce aging research dollars by establishing the National Institute on Aging in 1974, but that money has primarily gone to disease specific research, such as Alzheimer's disease, or towards the behavioral aspects of aging.

Next week, we’ll look at the possibilities of significant private money finally joining the hunt.

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VOTE FOR "UNDERGRADS AGAINST AGE RELATED DISEASE"

I don't know if you're familiar with the American Express Members Project: It is an open vote to determine how that company will set up a philanthropic program. One of the suggested projects was put forward by a Methuselah Foundation volunteer, and we're looking for enough votes to move it into the next round of consideration:

"You can help by voting: it's free and won't take more than a few minutes. We just need you to go to the Members Projects website and nominate the "Undergrads Against Age Related Disease" project. You don't need to be an Amex card holder, but you do need to be a US resident."

You'll find the project description at the following link:

http://www.membersproject.com/project/view/BVVE2C

"A program that utilizes college undergraduates to perform research in a variety of scientific venues surrounding fighting age related diseases such as Alzheimer's, Parkinson's, Heart Disease, [Cancer, and] overall extension of healthy human life. Hiring researchers is exceedingly expensive. By outsourcing projects to undergraduate students, laboratory use and labor costs are negligible, and the students receive college credit for their work"

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LATEST HEALTHY LIFE EXTENSION HEADLINES

Towards Tissue Engineered Corneas (August 15 2008) http://www.hindustantimes.com/storypage/storypage.aspx?id=34901c8e-1148-44b8-ae83-395922ea0f64

From the Hindustan Times: "Half a dozen eye hospitals in India are collaborating with a research centre in Chennai to create the inner layer of the cornea, the vital window of the human eye. Nichi-In Centre for Regenerative Medicine (NCRM) hopes to make corneal endothelium (inside cell layer) available on a commercial scale. About 100,000 people are in need of eye transplant every year, yet only about 10,000 are able to get donated eyes. The wait for a donor can be endless for the other 90,000. Imagine what a boon it will be if an eye stem cell bank could provide these lab generated endothelial layer of the cornea. The eye has three main parts. The first is the cornea, which is a transparent film like structure that transmits light into the eye. The other two are the lens and retina. During eye transplant, only the cornea is taken from the donor, not the whole eye. Nichi-In is now growing the animal and human corneal inner layer cells on a nano-scaffolding. The research centre is hoping to begin phase I clinical trials on humans in six months."

Ouroboros on Open Science (August 15 2008) http://ouroboros.wordpress.com/2008/08/14/opening-science-how-unconferences-changed-my-life/

Open science, analogous to open source software development, is the way of the future. It greatly increases diversity and speed of work by lowering the cost of information, and thereby allowing many more people to participate in research. In a world in which information transmission is easy, it makes no sense to lock up scientific data. Publish early, publish often should be the mantra. From Ouroboros: "The world implied by these concepts is one of radical sharing, in which credit still goes where credit is due but by dramatically different mechanisms. Open science isn’t so much 'pay it forward' (though there is a bit of that) as an effort to create a (scientific) world in which no one is paying at all, a world in which there's no incentive to withhold or protect ownership of data. The science fiction writer Iain M. Banks once wrote that 'money implies poverty' - indeed, many of the current models of data ownership and publication, and their accompanying 'currencies' of proprietorship, prestige and closed-access publication, imply a world in which data is scarce and must be hoarded. But data is not scarce anymore."

Cryonics Versus Rejuvenation Medicine (August 14 2008) http://www.depressedmetabolism.com/2008/08/13/thomas-donaldson-on-cryonics-and-anti-aging/

Via Depressed Metabolism, arguments for a present focus on the development of cryonics over the development of rejuvenation medicine: "In his article 'Why Cryonics Will Probably Help You More Than Antiaging' (2004), cryonics activist Thomas Donaldson contrasts cryonics with antiaging as a means to life extension and argues that a major advantage of cryonics is that cryobiology research can move at a much faster pace than anti-aging research, especially as it pertains to humans. Not only that, but its progress almost totally lacks the problems of proving that an advance has happened. The state of a brain, or even a section of brain, after vitrification and rewarming to normal temperature, shows directly whether or not the method used improved on previous methods. Cryonic suspension is able at least to preserve our brains in a reversible form, allowing restoration of vital functions and looks likely to come much sooner [than rejuvenation medicine]." Which is all true - but problems left to other people to solve have a way of remaining unsolved. We should work on both cryonics and rejuvenation medicine, not leave the latter for future generations.

Removing the Worst Aspect of Chronic Infection (August 13 2008) http://www.eurekalert.org/pub_releases/2008-08/eu-twb_1080808.php

An important aspect of immune system aging is the lack of naive T cells resulting from long periods of chronic infection by viruses like cytomegalovirus. What if we could reconfigure the immune system to behave more rationally when presented with recurring threats, and thus not exhaust its resources? That might be a possibility: "preventing white blood cells' circulation by trapping them in the lymph nodes can help mice get rid of a chronic viral infection. Laboratory mice can fight off infection by the Armstrong strain of lymphocytic choriomeningitis virus (LCMV), but are vulnerable to chronic infection by a variant called clone 13. Infecting mice with the Armstrong strain sequesters white blood cells in the lymph nodes, while clone 13 does so less stringently. Our hypothesis was that if we could artificially induce conditions like those produced by the Armstrong strain, it would help the immune system clear an infection by clone 13. An experimental drug called FTY720 [prevents] white blood cells from leaving lymph nodes. Even if mice have a stable chronic LCMV clone 13 infection, treatment with FTY720 can still improve their immune response against LCMV enough to have them rid it from their systems. FTY720 appears to prevent 'exhaustion' in the group of white blood cells called CD8+ T cells."

Hourglass II: A Carnival of Biogerontology (August 13 2008) http://ouroboros.wordpress.com/2008/08/12/hourglass-ii-a-carnival-of-biogerontology/

From Ouroboros: "Welcome to the second installation of Hourglass, a blog carnival devoted to the biology of aging. The entries are representatives of the excellent (and growing) community of bloggers who are writing about biogerontology, lifespan extension technologies, and aging in general. Anne C. shares a parable about taking care of her friend Nigel the Fish and what that led her to realize about longevity: specifically, that environment is critical, and that the combination of extrinsic factors that one might collectively term 'nurture' can make all the difference between a short unhappy life and a long fulfilled one. Old and damaged cells enter a permanent growth arrest known as senescence, which is both good (because they can’t initiate tumors) and bad (because persistent senescent cells behave in a ridiculously antisocial manner, secreting growth factors and proteases that both encourage nearby tumors to metastasize and degrade tissue function). At his new site Anti-Ageing Research, Dominick Burton discusses ways in which specifically targeted cancer therapies might be adapted to attack senescent cells instead."

Building Better Tendons (August 12 2008) http://technology.newscientist.com/article/dn14512-labgrown-tendons-gradually-fade-to-bone.html

Laboratory tissue engineering continues to improve in sophistication, as noted by the New Scientist: "only now have researchers managed to make different tissues blend into one another, as they do naturally in the body. Such gradients are necessary for some structures and organs to function properly. In the body, gradients like this strengthen the ends of tendons that attach to bones. Currently, lab-grown tendons put into the body often fail at the attachment end because they lack this property. The new technique should lead to more lifelike artificially-grown tendons, and better treatments for injuries like ruptured Achilles tendons.

The technique could also be applicable to other tissues, such as blood vessels. At the heart of the new technique is a gene that triggers the fibroblast cells that make up tendons to start forming bone. The team used viruses carrying that gene to transform a tendon made from normal fibroblasts into one with a gradient of bony properties. So far, the researchers have shown that tendons made this way are stable when implanted under the skin of rats. The next step is to graft a tendon to connect bone and muscle in a rat and see if it really does perform better."

Demonstrating the Value of Exercise (August 12 2008) http://www.medicalnewstoday.com/articles/117929.php

Via Medical News Today, another reminder of the value of exercise: "US scientists comparing middle aged and older regular runners with healthy equivalents for more than 20 years found that vigorous regular exercise was linked to longer life and less disability in old age. Fries and his team had 538 members of a nationwide running club and 423 healthy controls from northern California fill in questionnaires every year for as long as they could, from 1984 to 2005. The mean disability score was higher for the controls than the runners at all stages of the study and went up with age in both groups, but on average, for runners the onset of disability started later. Runners' initial disability was 16 years later than nonrunners. Runners had a significantly lower risk of having a disability score of 0.5. 19 years into the study, 15 per cent of the runners and 34 per cent of the controls had died, and after adjusting for possible confounders, runners showed a greater chance of living longer. The differences in disability and longevity between the runner group and the control group continued to diverge at the end of the study, as the participants approached their 80th birthday."

Full Paper on Visceral Fat and Longevity (August 11 2008) http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2504027

You may recall a solid demonstration that visceral fat tissue negatively affects longevity from earlier this year. The full paper is now open access and available at PubMed Central: "Visceral fat (VF) accretion occurs in obesity and with aging, and a reduction in VF is a common phenotypic change in calorie-restricted [CR] mammals. VF has been shown to be the single most important determinant of metabolic syndrome, and its removal in rats results in improved insulin action and delays the onset of diabetes. Given the hazards associated with abdominal obesity, it seems plausible that the beneficial effects of CR on longevity may be due at least in part to an attenuation of VF. Our data clearly demonstrate that in mammals, VF removal and CR are associated with an increase in mean and maximum lifespan. The mean and maximum lifespan of CR rats was greater than that seen in VF-removed animals, suggesting that the life-prolonging benefit of CR is mediated in part by pathways other than those modulated by an attenuation of VF. By comparing median lifespans, we estimate that the contribution of CR to longevity in this model was 47 weeks, whereas VF removal was 9.5 weeks, as compared to [ad libitum]-fed rats, suggesting that VF reduction offered approximately 20% of the effect of CR on longevity."

Financial Support for Aging Research

2008-08-19T15:38:00.000-07:00

Financial Support for Aging Research

Last week, we talked about the potential (optimistic) cost to reverse aging within the next couple of decades.
Historically financial support for aging research and efforts to extend the healthy lifespan has been spotty. Venture capital firms typically aim for profitable exits from their investments within two to four years. The research and product development we support typically takes longer to mature. Governments aren’t providing much funding. Pharmaceutical and biotech companies’ support of basic aging research is hindered due to the fact that there are no generally accepted biomarkers for human aging that would allow the FDA to approve a drug designed to slow the aging process. These companies are forced to develop drugs for specific diseases. And the FDA doesn’t recognize aging as a disease.
For example, The New York Times looks at Sirtris Pharmaceuticals: "The hope is that activating sirtuins in people would, like a calorically restricted diet in mice, avert degenerative diseases of aging like diabetes, heart disease, cancer and Alzheimer's.”

Dr. Christoph Westphal, the chief executive of Sirtris, said of the potential of the resveratrol based drugs they are developing, “I think that if we are right, this could extend life span by 5 or 10 percent.” He added that his goal was to develop drugs against specific diseases, with the extension of life being “almost a side effect of our medicine.”

There is no FDA category for longevity drugs, so if the company is to submit a drug for approval, it needs to be for a specific disease. However, longevity is what has motivated the researchers and what makes the drugs potentially so appealing.

There you have the most serious problem facing longevity science today. The FDA does not allow its direct application. Until this changes, no serious investment will be made in the US to bring longevity science to the clinic. This is a tragedy of astronomical proportions and is beyond belief.
Congress did supplement scarce aging research dollars by establishing the National Institute on Aging in 1974, but that money has primarily gone to disease specific research, such as Alzheimer's disease, or towards the behavioral aspects of aging.
Next week, we’ll look at the possibilities of significant private money finally joining the hunt.
_________________________________________________________

VOTE FOR "UNDERGRADS AGAINST AGE RELATED DISEASE"

I don't know if you're familiar with the American Express Members Project: It is an open vote to determine how that company will set up a philanthropic program. One of the suggested projects was put forward by a Methuselah Foundation volunteer, and we're looking for enough votes to move it into the next round of consideration:

"You can help by voting: it's free and won't take more than a few minutes. We just need you to go to the Members Projects website and nominate the "Undergrads Against Age Related Disease" project. You don't need to be an Amex card holder, but you do need to be a US resident."

You'll find the project description at the following link:

http://www.membersproject.com/project/view/BVVE2C

"A program that utilizes college undergraduates to perform research in a variety of scientific venues surrounding fighting age related diseases such as Alzheimer's, Parkinson's, Heart Disease, [Cancer, and] overall extension of healthy human life. Hiring researchers is exceedingly expensive. By outsourcing projects to undergraduate students, laboratory use and labor costs are negligible, and the students receive college credit for their work"
______________________________

LATEST HEALTHY LIFE EXTENSION HEADLINES

Towards Tissue Engineered Corneas (August 15 2008) http://www.hindustantimes.com/storypage/storypage.aspx?id=34901c8e-1148-44b8-ae83-395922ea0f64
From the Hindustan Times: "Half a dozen eye hospitals in India are collaborating with a research centre in Chennai to create the inner layer of the cornea, the vital window of the human eye. Nichi-In Centre for Regenerative Medicine (NCRM) hopes to make corneal endothelium (inside cell layer) available on a commercial scale. About 100,000 people are in need of eye transplant every year, yet only about 10,000 are able to get donated eyes. The wait for a donor can be endless for the other 90,000. Imagine what a boon it will be if an eye stem cell bank could provide these lab generated endothelial layer of the cornea. The eye has three main parts. The first is the cornea, which is a transparent film like structure that transmits light into the eye. The other two are the lens and retina. During eye transplant, only the cornea is taken from the donor, not the whole eye. Nichi-In is now growing the animal and human corneal inner layer cells on a nano-scaffolding. The research centre is hoping to begin phase I clinical trials on humans in six months."

Ouroboros on Open Science (August 15 2008) http://ouroboros.wordpress.com/2008/08/14/opening-science-how-unconferences-changed-my-life/
Open science, analogous to open source software development, is the way of the future. It greatly increases diversity and speed of work by lowering the cost of information, and thereby allowing many more people to participate in research. In a world in which information transmission is easy, it makes no sense to lock up scientific data. Publish early, publish often should be the mantra. From Ouroboros: "The world implied by these concepts is one of radical sharing, in which credit still goes where credit is due but by dramatically different mechanisms. Open science isn’t so much 'pay it forward' (though there is a bit of that) as an effort to create a (scientific) world in which no one is paying at all, a world in which there's no incentive to withhold or protect ownership of data. The science fiction writer Iain M. Banks once wrote that 'money implies poverty' - indeed, many of the current models of data ownership and publication, and their accompanying 'currencies' of proprietorship, prestige and closed-access publication, imply a world in which data is scarce and must be hoarded. But data is not scarce anymore."

Cryonics Versus Rejuvenation Medicine (August 14 2008) http://www.depressedmetabolism.com/2008/08/13/thomas-donaldson-on-cryonics-and-anti-aging/
Via Depressed Metabolism, arguments for a present focus on the development of cryonics over the development of rejuvenation medicine: "In his article 'Why Cryonics Will Probably Help You More Than Antiaging' (2004), cryonics activist Thomas Donaldson contrasts cryonics with antiaging as a means to life extension and argues that a major advantage of cryonics is that cryobiology research can move at a much faster pace than anti-aging research, especially as it pertains to humans. Not only that, but its progress almost totally lacks the problems of proving that an advance has happened. The state of a brain, or even a section of brain, after vitrification and rewarming to normal temperature, shows directly whether or not the method used improved on previous methods. Cryonic suspension is able at least to preserve our brains in a reversible form, allowing restoration of vital functions and looks likely to come much sooner [than rejuvenation medicine]." Which is all true - but problems left to other people to solve have a way of remaining unsolved. We should work on both cryonics and rejuvenation medicine, not leave the latter for future generations.

Removing the Worst Aspect of Chronic Infection (August 13 2008) http://www.eurekalert.org/pub_releases/2008-08/eu-twb_1080808.php
An important aspect of immune system aging is the lack of naive T cells resulting from long periods of chronic infection by viruses like cytomegalovirus. What if we could reconfigure the immune system to behave more rationally when presented with recurring threats, and thus not exhaust its resources? That might be a possibility: "preventing white blood cells' circulation by trapping them in the lymph nodes can help mice get rid of a chronic viral infection. Laboratory mice can fight off infection by the Armstrong strain of lymphocytic choriomeningitis virus (LCMV), but are vulnerable to chronic infection by a variant called clone 13. Infecting mice with the Armstrong strain sequesters white blood cells in the lymph nodes, while clone 13 does so less stringently. Our hypothesis was that if we could artificially induce conditions like those produced by the Armstrong strain, it would help the immune system clear an infection by clone 13. An experimental drug called FTY720 [prevents] white blood cells from leaving lymph nodes. Even if mice have a stable chronic LCMV clone 13 infection, treatment with FTY720 can still improve their immune response against LCMV enough to have them rid it from their systems. FTY720 appears to prevent 'exhaustion' in the group of white blood cells called CD8+ T cells."

Hourglass II: A Carnival of Biogerontology (August 13 2008) http://ouroboros.wordpress.com/2008/08/12/hourglass-ii-a-carnival-of-biogerontology/
From Ouroboros: "Welcome to the second installation of Hourglass, a blog carnival devoted to the biology of aging. The entries are representatives of the excellent (and growing) community of bloggers who are writing about biogerontology, lifespan extension technologies, and aging in general. Anne C. shares a parable about taking care of her friend Nigel the Fish and what that led her to realize about longevity: specifically, that environment is critical, and that the combination of extrinsic factors that one might collectively term 'nurture' can make all the difference between a short unhappy life and a long fulfilled one. Old and damaged cells enter a permanent growth arrest known as senescence, which is both good (because they can’t initiate tumors) and bad (because persistent senescent cells behave in a ridiculously antisocial manner, secreting growth factors and proteases that both encourage nearby tumors to metastasize and degrade tissue function). At his new site Anti-Ageing Research, Dominick Burton discusses ways in which specifically targeted cancer therapies might be adapted to attack senescent cells instead."

Building Better Tendons (August 12 2008) http://technology.newscientist.com/article/dn14512-labgrown-tendons-gradually-fade-to-bone.html
Laboratory tissue engineering continues to improve in sophistication, as noted by the New Scientist: "only now have researchers managed to make different tissues blend into one another, as they do naturally in the body. Such gradients are necessary for some structures and organs to function properly. In the body, gradients like this strengthen the ends of tendons that attach to bones. Currently, lab-grown tendons put into the body often fail at the attachment end because they lack this property. The new technique should lead to more lifelike artificially-grown tendons, and better treatments for injuries like ruptured Achilles tendons.
The technique could also be applicable to other tissues, such as blood vessels. At the heart of the new technique is a gene that triggers the fibroblast cells that make up tendons to start forming bone. The team used viruses carrying that gene to transform a tendon made from normal fibroblasts into one with a gradient of bony properties. So far, the researchers have shown that tendons made this way are stable when implanted under the skin of rats. The next step is to graft a tendon to connect bone and muscle in a rat and see if it really does perform better."

Demonstrating the Value of Exercise (August 12 2008) http://www.medicalnewstoday.com/articles/117929.php
Via Medical News Today, another reminder of the value of exercise: "US scientists comparing middle aged and older regular runners with healthy equivalents for more than 20 years found that vigorous regular exercise was linked to longer life and less disability in old age. Fries and his team had 538 members of a nationwide running club and 423 healthy controls from northern California fill in questionnaires every year for as long as they could, from 1984 to 2005. The mean disability score was higher for the controls than the runners at all stages of the study and went up with age in both groups, but on average, for runners the onset of disability started later. Runners' initial disability was 16 years later than nonrunners. Runners had a significantly lower risk of having a disability score of 0.5. 19 years into the study, 15 per cent of the runners and 34 per cent of the controls had died, and after adjusting for possible confounders, runners showed a greater chance of living longer. The differences in disability and longevity between the runner group and the control group continued to diverge at the end of the study, as the participants approached their 80th birthday."

Full Paper on Visceral Fat and Longevity (August 11 2008) http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2504027
You may recall a solid demonstration that visceral fat tissue negatively affects longevity from earlier this year. The full paper is now open access and available at PubMed Central: "Visceral fat (VF) accretion occurs in obesity and with aging, and a reduction in VF is a common phenotypic change in calorie-restricted [CR] mammals. VF has been shown to be the single most important determinant of metabolic syndrome, and its removal in rats results in improved insulin action and delays the onset of diabetes. Given the hazards associated with abdominal obesity, it seems plausible that the beneficial effects of CR on longevity may be due at least in part to an attenuation of VF. Our data clearly demonstrate that in mammals, VF removal and CR are associated with an increase in mean and maximum lifespan. The mean and maximum lifespan of CR rats was greater than that seen in VF-removed animals, suggesting that the life-prolonging benefit of CR is mediated in part by pathways other than those modulated by an attenuation of VF. By comparing median lifespans, we estimate that the contribution of CR to longevity in this model was 47 weeks, whereas VF removal was 9.5 weeks, as compared to [ad libitum]-fed rats, suggesting that VF reduction offered approximately 20% of the effect of CR on longevity."

Your perfect cure is prevention

2008-08-08T09:38:00.000-07:00

Dear Future Centenarian,

A very close friend of mine’s father seems to have lost his will to live. Here is an aging former soldier of fortune who once had a zest for life experienced by few. Now, he lost interest in eating, in seeing a doctor and seemingly everything else, including his will to live.

This bothers me for a couple of reasons. First, someone close to me may lose her dad. And on a larger scale, didn’t I say most people go to the ends of the earth to hang on to life towards the end? Well, apparently not all. Why is this?

Several months ago, I had a relevant conversation with another close friend about how some people cling to life at the end no matter how much suffering and pain they endure, while others simply throw in the towel. We concluded it may have something to do with declining hormone levels. So I gave my anti-aging physician a call a few days ago to discuss this possibility. His response was that yes, declining hormone levels lead to depression, which usually translates to loss of appetite, and of course, a diminished will to live. He routinely reverses this phenomena with closely monitored hormone replacement therapy (HRT).

Could declining hormone levels be evolution’s way to nudge us into going quietly into the night? Could savvy docs reverse deteriorating attitudes and improve and extend millions of lives with simple HRT?

I think the answer is a resounding YES!

Saturday, I enjoyed a wonderful lunch get together with one of the most esteemed psychologists and authors in history. In fact, he has been one of my personal heroes for about 40 years. He’s now experiencing moments of forgetfulness which he calls his “senior moments”. The difference between him and my friend’s father is he is attacking his challenge head on, while maintaining his witty sense of humor. He’s getting sophisticated diagnostics, will undergo cutting edge treatment and is determined to reverse it.

And reverse it he will, according to a medical consultant who specializes in neurodegenerative conditions.

The moral to this story is, don’t wait until you see serious decline to see an anti-aging specialist. In fact, see one before you experience any decline – period. After all, once you see signs of a condition or disease, it may be too late. Heart disease and cancer are two good examples. They eat away at you for years before you show symptoms. And one symptom from heart disease is often sudden death.

Your perfect cure is prevention.
__________________________________
THREE DECADES FROM NOW

Under the present weight of regulation, it looks to take about 30 years for a new medical technology to progress from first proof of concept through to widespread and cost-effective availability - for those that aren't buried young by the cost of red tape, that is. Compare that with something more like 20 years in less regulated industries. That difference adds up. But what can we expect to see in the 2030s, based on what has taken place in laboratories and trials in the past few years?

http://www.fightaging.org/archives/001537.php

"Replacement organs will be grown to order from your own cells.
Stem cells will be created, manipulated, and transplanted to direct extraordinary regeneration.
Age-damaged immune systems will be wiped clean and replaced afresh.
Gene therapy will be a mature technology, and genetic disorders curable.
Everyone will know their DNA sequence, and have access to a vast database of knowledge that describes risks, therapies, and best practices.
Cancer will be detected early, and even late-stage metastasis cured with few side-effects by nanoparticle-based, viral, or other therapies.
The important mitochondrial DNA will be replaced when damaged by disease or age.
Many of the biochemical processes underlying the benefits of exercise, calorie restriction, and known human longevity-associated genes will be reproduced by cheap drugs.”

ON STEM CELLS AND AGING

While perusing PubMed Central, Reason discovered a good overview of present thinking on stem cells, stem cell niches, and their role in aging:

http://www.fightaging.org/archives/001536.php

"If many adult tissues and organs are continuously replenished by cells derived from stem cells, then why do they show signs of aging? One possibility is that stem cells themselves age and senesce, resulting in a decreased ability to replace worn-out progeny and/or the fact that they pass on aged phenotypes to their progeny.

NOTE: Pending modest funding, a stem cell company will soon be launched that could solve this problem within a couple of years.

Somewhere at the end of this road of investigation lies the means to keep stem cell populations vital while not exaggerating the risk of cancer due to runaway failure in a stem cell - the most likely reason we have evolved mechanisms that diminish stem cell activity in response to age-related biochemical damage. At some point, the large and well-funded field of regenerative medicine is going to turn its attention to repairing the damage of aging. Many major lines of research presently address age-related disease, and it is becoming clear that the effectiveness of therapies is hindered by age-related damage in stem cells and their niches. We should encourage research in this direction.
______________________________

LATEST HEALTHY LIFE EXTENSION HEADLINES

Towards Long Life and Happiness (August 01 2008) http://www.canada.com/components/print.aspx?id=924ef76b-5103-4aad-a596-13278777f8eb
From Canada.com: "Aging - and more specifically, the aspiration to slow human aging - is the most important neglected issue of our time. There are many things that could kill the world's current 6.5 billion plus people, but the vast majority of those currently alive today, especially in the developed world, will die from age-related causes. The diseases of aging could be the real scourge of the 21st century. That is, unless we do something to remedy the biological vulnerabilities we have inherited from our evolutionary history. The current approach to medical research is to tackle individual diseases, one at a time. So we spend large amounts of public funding on basic research into cancer, heart disease, diabetes, Alzheimer's, etc. But we invest very little in understanding the biology of aging and how it impacts our health prospects. Supplementing the current medical approach with one that also tackles aging would help us take a more inclusive approach to health extension. Even if we find a cure for one of the diseases of aging - like cancer - it would only extend life by a few years, as most people will likely be afflicted by one of the other diseases of aging. But if we could modify the biological mechanisms underlying aging, we may be able to significantly increase the number of disease-free years humans can expect to live. This would reap enormous individual and societal benefits."

Exercise in a Pill? (July 31 2008)
http://www.eurekalert.org/pub_releases/2008-07/si-eia072808.php
If researchers could reproduce the biochemical basis for the health and longevity-enhancing results of exercise, the resulting drug would no doubt be as popular as calorie restriction mimetics. Exercise and calorie restriction are the two gold-standard items for health: little else even comes close yet. From EurekAlert!, news of small steps on this path: Researchers "identified two signaling pathways that are activated in response to exercise and converge to dramatically increase endurance. Previous work with genetically engineered mice [had] revealed that permanently activating a genetic switch known as PPAR delta turned mice into indefatigable marathon runners. In addition to their super-endurance, the altered mice were resistant to weight gain, even when fed a high-fat diet that caused obesity in ordinary mice. On top of their lean and mean physique, their response to insulin improved, lowering levels of circulating glucose. We wanted to know whether a drug specific for PPAR delta would have the same beneficial effects."

Short Telomeres and Accelerated Aging (July 31 2008) http://newswire.rockefeller.edu/?page=engine&id=791
All of the rare accelerated aging conditions appear to be caused by one aspect of "normal" aging exaggerated and run wild to cause great biochemical damage. Researchers now think they understand what underlies another of these conditions: "Sufferers of the disease, called dyskeratosis congentia, tend to have problems in tissues in which cells multiply rapidly - skin, hair, nails, tongue, gut and bone marrow - and usually die between the ages of 16 and 50 from bone marrow failure, or the inability to replenish their blood cells. Each time a cell divides, the protective caps at the ends of chromosomes shorten - and when these caps are gone, so are we. Now, by using an unconventional strategy to shorten telomeres in mice, [researchers] have not only created the first faithful mouse model for studying [dyskeratosis congentia], but they have revealed the molecular defect behind the disease. These results suggest that in patients suffering from dyskeratosis congenita, the enzyme telomerase can't elongate telomeres as fast as the nucleases chew them away. Clearly, the next step is to understand how telomeres are degraded in human cells. We need to identify the nucleases at work and find out how they are regulated."

Reduced Protein Intake and Immune Response (July 30 2008) http://pmid.us/18656703
Scientists here demonstrate the connection between reduced dietary protein and a better immune response, already known from the practice of calorie
restriction: "Manipulation of dietary variables is one the most described events to retard the aging process and maintain immune function. The present study deals with the effect of variable dietary protein-carbohydrate ratios (without caloric restriction) on the alteration of immune response of male albino rats. These results thus suggest that diets with variable dietary protein-carbohydrate ratios act as an exogenous modulator of immune response with age and [a low protein] diet may be beneficial to slow down/reduce the impairment of immune response in aged individuals." For comparison, you might also look at studies of methionine restriction without overall calorie restriction. Greater control of diet over the years adds up, and every extra year of health gained can make a big difference when the pace of medical development is rapid.

The Tithonus Error (July 29 2008)
http://www.dailymail.co.uk/news/article-1038717/MAX-HASTINGS-Growing-old-Britain-happy-experience-The-longer-live-worse-quality-life-becomes.html
So many, many people still believe that the result of longevity science will be that you are older and ever more frail for more years, with no hope of death. This is absolutely false: the goals are in fact rejuvenation of the old, repair of the biochemical damage of aging, and the extension of healthy, youthful life. But still people have the fate of Tithonus in mind, sunk into the collective consciousness through a hundred similar cautionary tales. So you'll see this sort of doleful op-ed from the Daily Mail: "To some of us, [longevity] seems a ghastly prospect. I am 62, and find life terrific. I get more work done than ever before, because my children have long ago left home and I remain fit. I take pills to keep my blood pressure down and waterworks functioning. It seems to some of us terrifying to imagine that we might survive to 100. Surely, the drear misery and loneliness that accompanies such age is not worth it for a birthday party, telegram from the Queen and maybe a paragraph in the local newspaper. Once mobility is gone, once the simplest actions of daily life become dependent upon others, it is hard to sustain self-respect. If science indeed continues to lengthen our lives, I believe that we shall have to be given a choice about opting out." The work of advocacy and education must continue - this is a sign that much remains to be done.

Futurist Musings on the Leap Ahead (July 29 2008) http://www.canada.com/topics/bodyandhealth/story.html?id=fa35f402-d10e-4c1e-a8c9-cc3f1cc12f92
From Canada.com: "Genetic science, stem-cell research and extreme caloric restriction are all part of a burgeoning 'immortality industry' that could soon point the way to a fountain of youth with the potential to stretch the human life span to 125 or 150 years, says a sociologist and consultant on future studies. Advances such as nanotechnology - the emerging ability to manipulate extremely small structures - could ultimately make it possible to regenerate every cell in the body. At that point, we can throw out every idea we have about longevity and even mortality itself. The effects of human life-extension will be far-reaching, [potentially] spawning second or third careers in people's extra decades and a society of lifelong students using the gift of more time to continually reinvent themselves with new education. The extension of human life will also depend on people's lifestyle [and] the current obesity epidemic, smoking habits and other unhealthy behaviors indicate they don't always make beneficial choices. People can be 'seduced' by breakthroughs they believe will save them from themselves. I think there is going to be a tremendous chasm between average life expectancy and life potential."

Michael West at Aging 2008 (July 28 2008)
http://www.acceleratingfuture.com/people-blog/?p=2338
Another Aging 2008 transcript from Future Current: "I have been entranced by the immortality of the species and how it's accomplished. A simple way of putting it: we are made of cells, trillions of them, that have been proliferating backward in time all the way through hundreds of millions of years to the beginning of life on the planet, leaving no dead ancestors in their wake ever - or we would not be here. It is our somatic cells that are destined to die. All the cells in our body have this immortal legacy going backward in time millions of years and will face death for the first time ever in our lifetime. What can we learn about the immortality of the species to transport those observations and discoveries of modern technologies into something that will really do something about human aging? How could these cells be used in the next ten years? There are numerous examples I could give you, but one hopeful one - macular degeneration. This is the leading cause of blindness, due to the aging of our retina. These cells have now been made in a form that is appropriate to begin human clinical trials. When they become lost or dysfunctional in the back of the retina, they cause this cascade of pathology that is a leading cause of blindness in the elderly. It is at least one of the top targets for how we hope these cells will eventually be used in medicine."

Cryonics as an Elective Medical Procedure (July 28 2008) http://www.depressedmetabolism.com/2008/07/24/cryonics-as-an-elective-medical-procedure/
From Depressed Metabolism: "The limitation that cryonics procedures can only be started after pronouncement of legal death reflects the unfortunate fact that the current medical establishment does not recognize cryonics as a credible form of advanced critical care. As a result, cryonics is currently practiced as a form of emergency medicine in which conventional resuscitation technologies such as chest compressions and ventilations are used to avoid the kinds of injury that follow after cardiac arrest. Although there will always be a place for cryonics as a form of emergency medicine to treat cases of trauma and sudden circulatory arrest, most patients who currently present for human cryopreservation would benefit from more hospital cooperation in choosing cryonics as an elective medical procedure. Although current cryonics organizations such as Alcor try to make the best of a bad situation by employing standby teams that allow rapid intervention after cardiac arrest to reduce brain injury, much improved quality of care of cryonics patients would be possible if cryonics procedures would start at a point where medical professionals (with informed consent of the patient and/or family) would determine that further treatment of the patient with contemporary technologies would be futile, or even counter-productive."
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DISCLAIMER: News summaries are reported by third parties, and there is no guarantee of accuracy. This newsletter is not meant to substitute for your personal due diligence and is not to be taken as medical advice. For originating report, please see www.longevitymeme.org/newsletter/.

If you would like to be removed from my list, I will stop sending you Longevity News Digest if you simply reply to this email with Unsubscribe in the subject line.

Aging, the New Frontier

2008-07-28T10:29:00.000-07:00

Dear Future Centenarian,
We are finally moving from an era where nothing could be done to defeat aging into an era where advancing technology will give us the tools to overcome it. All the old attitudes are no longer relevant.
We’re so used to people dying from age related causes that we accept it as a normal part of life. And we become desensitized to this death. But let’s look at it from a different angle and see if you think about it differently.
Robert Freitas, a brilliant scientist and perhaps the world’s utmost authority on Nanomedicine, offers some interesting ways to view aging. He points out the following:
100,000 lives are lost every single day from aging related causes. They’re scattered all over the world, so we hardly notice. But what if 400 jetliners fell out of the sky in a single day? We would be astonished, outraged and sickened. Yet effectively, that’s equivalent to 400 jetliner crashes.
If 400 planes crashed every day, wouldn’t the world marshal all its powers to insure aircraft safety, especially if we had no choice but to fly?
What if we could avoid… or at least postpone most aging related deaths?
Then why isn’t treating aging a #1 priority?
After all, if you or a loved one had a major medical condition such as cancer, heart disease or suffered a stroke, wouldn’t you ask for the very best medical care?
If we had a treatment that could reverse Alzheimer’s, Parkinson’s, osteoporosis, arteriosclerosis or diabetes… who in their right mind would turn it down?
Now it is aging, the new frontier. Since it kills everyone who survives or dodges diseases, might not aging be considered a disease as well? MaxLife looks at it as a curable disease, in fact the mother of most diseases. And we’re determined to do something about it.
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LATEST HEALTHY LIFE EXTENSION HEADLINES

The Dreaded Reactive Oxygen Species (July 25 2008) http://www.eurekalert.org/pub_releases/2008-07/uorm-ruk072108.php
It's good to see more research groups looking into targeting antioxidants to the mitochondria. From EurekAlert!: "Researchers have taken a first snapshot of how a class of highly reactive molecules inflicts cellular damage as part of aging, heart disease, stroke, cancer, diabetes, kidney disease and Alzheimer's disease to name a few. Researchers have discovered a tool that can monitor related damage and determine the degree to which antioxidant drugs effectively combat disease. Our study provides a better glimpse of why a cell under assault by disease makes 10 times as many reactive oxygen species [ROS] as the same cell when healthy. We have discovered a chemical tool for investigating how diseases cause damage, mitochondrion by mitochondrion. Efforts to develop antioxidant drugs (e.g. vitamin E) to treat diseases of increased oxidative stress have met with limited success to date because they tried to eliminate ROS, rather than maintain the right amount, Sheu said. He established the Mitochondrial Research & Innovation Group (MRIG) [in] 2002 with the goal of designing therapies to deliver precise amounts of antioxidants to the mitochondria of diseased cells only. MRIG teams are, for example, screening through compounds to confirm that oxidative stress can be reversed by mitochondria-specific drugs."

On Hormesis and Longevity (July 24 2008) http://pmid.us/18648625
A nice overview of hormesis: "Aging is characterized by a stochastic accumulation of molecular damage, progressive failure of maintenance and repair, and consequent onset of age-related diseases. Applying hormesis in aging research and therapy is based on the principle of stimulation of maintenance and repair pathways by repeated exposure to mild stress. In a series of experimental studies we have shown that repetitive mild heat stress has anti-aging hormetic effects on growth and various other cellular and biochemical characteristics of human skin fibroblasts undergoing aging in vitro. These effects include the maintenance of stress protein profiles, reduction in the accumulation of oxidatively and glycoxidatively damaged proteins, stimulation of the proteasomal activities for the degradation of abnormal proteins, improved cellular resistance to ethanol, hydrogenperoxide and ultraviolet-B rays, and enhanced levels of various antioxidant enzymes. Anti-aging hormetic effects of mild heat shock appear to be facilitated by reducing protein damage and protein aggregation by activating internal antioxidant, repair and degradation processes."

Yeast and Aging Research (July 22 2008) http://ouroboros.wordpress.com/2008/07/21/biogerontology-rising-recent-progress-in-yeast-aging-research/
Ouroboros looks at the humble yeast in context: "Our understanding of aging in animals owes a great debt to a large body of careful work in a single-celled organism, the brewer's yeast Saccharomyces cerevisiae. Indeed, as I've argued before, yeast is one of the two organisms with the strongest credible claim to have started modern biogerontology. An unusually large crop of yeast aging papers have appeared over the last few months, and I thought it would be appropriate to spend a few paragraphs describing them - in honor of this humble organism that rises our bread, ferments our beer, and has done so much to open our eyes to the fundamental mechanisms of aging. Yeast mutants in worm longevity genes are significantly more likely to be long-lived than randomly chosen mutants - suggesting [that] genes that modulate aging have been conserved not only in sequence, but also in function, over a billion years of evolution. Given this functional conservation, it is reasonable to use yeast to help answer questions about aging in general, so long as these questions as cell-biological in scope."

New York Times on Sirtris (July 22 2008) http://www.nytimes.com/2008/07/22/health/research/22long.html?pagewanted=all
The New York Times looks at Sirtris Pharmaceuticals: "The hope is that activating sirtuins in people would, like a calorically restricted diet in mice, avert degenerative diseases of aging like diabetes, heart disease, cancer and Alzheimer's. There is no Food and Drug Administration category for longevity drugs, so if the company is to submit a drug for approval, it needs to be for a specific disease. Nonetheless, longevity is what has motivated the researchers and what makes the drugs potentially so appealing. Dr. Christoph Westphal, the chief executive of Sirtris, said of the potential of the drugs, 'I think that if we are right, this could extend life span by 5 or 10 percent.' He added that his goal was to develop drugs against specific diseases, with the extension of life being 'almost a side effect of our medicine.'" There you have the most serious problem facing longevity science today: that its direct application is not permitted by the FDA. Until this changes no serious investment will be made in the US to bring longevity science to the clinic. This is a tragedy of so great a scale as to beggar belief.

Thoughts on Mortality and Its Evasion (July 21 2008) http://tacit.livejournal.com/250032.html
An interesting LiveJournal post: "A person immune to the ravages of old age would still not be immune to death; accident, violence, and other misadventure is perfectly capable of ending even a 25-year-old's life. It simply means that person no longer has a cap on the maximum time he can live, if he so chooses. And that's really what it's all about. Choice. If you go into the doctor's office, and he tells you that you have a bacterial infection, which will slowly grow progressively worse until it kills you painfully, then offers you an antibiotic pill that will completely eradicate the infection, I bet you'll take it. Even if you don't fancy the thought of living forever. There's an important point in that.

Even folks who don't much want to live forever still probably don't want to die today. Or tomorrow. Someday, perhaps, if that 'someday' is held in the abstract; some future time when things no longer seem interesting. But not today. And that's the point. A solution for aging puts the power to choose in your hands. Old age forces your hand; you don't get the choice to see your grandkids graduate from school, or to celebrate your fiftieth anniversary. The choice is made for you. And I don't see how that benefits anyone."

Growing Blood Vessels (July 21 2008) http://news.bbc.co.uk/2/hi/health/7514317.stm
Researchers continue to work at the blood vessel problem in tissue engineering. From the BBC: "Scientists have used human cells to grow new blood vessels in a mouse for the first time. The ability to develop swiftly a new network of tiny blood vessels - known as capillaries - would be a prize for scientists. There are dozens of potential applications in medicine, particularly in the treatment of conditions which involve damage to a tissue's blood supply, such as that to the heart muscle following a heart attack. However, the complex structure of these vessels has slowed progress. What's really significant about our study is that we are using human cells that can be obtained from blood or bone marrow rather than removing and using fully developed blood vessels. It could certainly assist in the connection of other engineered organs to the body's blood supply. Although this approach is not yet suitable for clinical use, it is interesting that they have demonstrated you have all the elements you need to create a functional network of capillaries from a small amount of blood."
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DISCLAIMER: News summaries are reported by third parties, and there is no guarantee of accuracy. This newsletter is not meant to substitute for your personal due diligence and is not to be taken as medical advice. For originating report, please see www.longevitymeme.org/newsletter/.
If you would like to be removed from my list, I will stop sending you Longevity News Digest if you simply reply to this email with Unsubscribe in the subject line.

Biological Evolution

2008-07-24T10:53:00.000-07:00

Dear Future Centenarian,
We’ve come a long way in our lifetimes. In fact, we have accomplished as much then as we did in all of recorded history. At least technologically. As a race, we really didn’t seem to have learned many lessons. Oh sure, maybe our justice systems are a little more fair (and maybe not), we may have developed a little more tolerance and compassion, and maybe we’re not quite as barbaric. All in all though, we react to intrusions about the same as prehistoric man.
We still settle disputes and differences about the same way. We either initiate or answer with violence for the most part. But instead of clubbing each other senseless and confining our rage, jealousies, pettiness and intolerances to an area roughly equivalent to our immediate reach and to one enemy or victim at a time, we now have these wonders of science at our disposal, capable of inflicting widespread death and destruction.
Then, we had clubs and primitive minds. Now we have nukes, biological and chemical weapons, potentially devastating nanotechnology capabilities… and primitive minds.
While we have evolved in some ways at light speed, our ability to solve social problems and disputes and our tendency to hate hasn’t changed since caveman days. Look, we’re on the cusp of breaking through to indefinite lifespans and solutions for health problems, poverty and pollution. But what good does it do us when emotionally unstable individuals have abilities to wipe out millions with no more effort or forethought than swinging a club?
Fortunately, the human race is extremely resilient and resourceful. We often respond to challenges in creative and unexpected ways. A relatively new foundation recognizes this challenge and is taking it on as part of its agenda. See more information at www.InnerSpaceFoundation.org.
They recognize that biological evolution is a somewhat haphazard and non-optimizing process that has produced many undesirable artifacts. Among a large number and wide variety of such artifacts, two stand out as the underlying causes of the most pervasive and extreme human suffering: mental and lifespan limitations. Mental inabilities, including the failure to resolve conflicts non-violently, are universal. They must ultimately serve to explain our ongoing failures to end human warfare, crime, poverty, and famine, and to completely cure diseases, disabilities, aging and death. Therefore, these inabilities are fundamentally even more harmful to humanity than the categories of biomedical dysfunction we currently labor to cure.
This belief forms the core of the Bioprogressive philosophy. The overall goal of the InnerSpace Foundation (IF) is to accelerate developing biomedical technologies for transcending these limitations. IF is taking specific steps toward enhancing memory, learning and cognition. These near-term goals should ultimately help us to eliminate or transcend other unwanted artifacts of Darwinian evolution.
IF, among others, have longer-term goals aimed at preserving memories. So hang on. We have some interesting times ahead.
____________________________________
CANCER AND IMMUNE SYSTEM PROFICIENCY

Are some immune systems much better than others at destroying cancer in its earliest stages? It seems that this is the case. Can we copy that proficiency and use it as a therapy? The prospects look promising:

http://www.fightaging.org/archives/001525.php

"First, we had cancer-resistant mice and asked, 'What can we learn from it?' The reason it's resistant is because it has very different white cells. So then that immediately prompted the concept of therapy, because you can easily transfer white cells. You can extract them as a therapeutic agent and give them to another mouse. It's a therapy. It's much better than to find the gene. If you find the gene, then you have to understand the mechanism, and you have to find a way to put the gene into the cell, into all the cells you want to, and that would not work very easily. The technology as we speak right now is not really mature for that area. You might have to wait another 10, 20 years before that technology catches up with the concept. However, what we found is a cell as a therapeutic agent, so why not go ahead and see how it works. It worked really well in mice, so the next question, very obviously, is can we find a similar cancer resistance for humans as a donor for a therapeutic agent. And the answer is yes, we did find quite a few of them ".

From a broad assessment of cutting edge cancer research, it seems that we are well on the way to turning cancer into a controllable chronic illness. You'll have outbreaks, they'll be caught early, and the medicine of the 2020s will eliminate them. The question is whether this is good enough: is a comprehensive suite of low-risk, safe cancer cures enough to remove cancer as a threat while our lives are extended by other medical technologies?
______________________________

LATEST HEALTHY LIFE EXTENSION HEADLINES

The Broadening Search for Longevity Genes (July 17 2008)
http://www.technologyreview.com/printer_friendly_article.aspx?id=21092
The MIT Technology Review looks at continued attempts to understand the degree to which present healthy human longevity is influenced by genes: "An ambitious plan to sequence 100 genes in 1,000 healthy old people could shed light on genetic variations that insulate some people from the ailments of aging, including heart disease, cancer, and diabetes, allowing them to live a healthy life into their eighties and beyond. Rather than focusing on genetic variations that increase risk for disease, scientists plan to focus on genes that have previously been linked to health and longevity. Advances in genetic screening technologies have allowed scientists to start searching the genome for clues to healthy aging and a lengthy life span. That work has revealed that the genomes of healthy old people are not blemish free. These people have genetic susceptibility markers for many serious diseases [but] they don't get any of these diseases. What is the explanation? What might account for their insulation from these diseases?" Genes are not fate - evidence to date suggests that lifestyle choices have much more weight for all but the most genetically unlucky, and those choices are reflected in epigenetic variations, not genetic variations.

Self-Assembly in Tissue Engineering (July 16 2008) http://www.technologyreview.com/printer_friendly_article.aspx?id=21080
The MIT Technology Review looks at a promising strategy in tissue engineering: "Tissue engineers are ambitious. If they had their way, a dialysis patient could receive a new kidney made in the lab from his own cells, instead of waiting for a donor organ that his immune system might reject. Likewise, a diabetic could, with grafts of lab-made pancreatic tissue, be given the ability to make insulin again. But tissue engineering has stalled in part because bioengineers haven't been able to replicate the structural complexity of human tissues. Now researchers have taken an important first step toward building complex tissues from the bottom up by creating what they call living Legos. These building blocks, biofriendly gels of various shapes studded with cells, can self-assemble into complex structures resembling those found in tissues. This will be an effective way to put the cells where we want them to be. You can probably generate a tissue with a higher complexity [using] the new method than is possible with a scaffold that has to be seeded with cells." Compare and contrast with the use of whole-organ cell matrix templates, another recent development aimed at solving the same problem.

Stress, Cortisol, and Shortened Telomeres (July 16 2008) http://www.eurekalert.org/pub_releases/2008-07/uoc--usi071508.php
Chronic stress correlates with shorter telomeres, as well as with worse health. Via EurekAlert! researchers are proposing a mechanism by which telomere length is reduced by stress, leading to a worse immune response: "Short telomeres are linked to a range of human diseases, including HIV, osteoporosis, heart disease and aging. An enzyme [called telomerase] keeps immune cells young by preserving their telomere length and ability to continue dividing. The stress hormone cortisol suppresses immune cells' ability to activate their telomerase. This may explain why the cells of persons under chronic stress have shorter telomeres. When the body is under stress, it boosts production of cortisol to support a 'fight or flight' response. If the hormone remains elevated in the bloodstream for long periods of time, though, it wears down the immune system. We are testing therapeutic ways of enhancing telomerase levels to help the immune system ward off cortisol's effect. If we're successful, one day a pill may exist to strengthen the immune system's ability to weather chronic emotional stress."

Why Fight Aging? (July 15 2008)
http://www.acceleratingfuture.com/people-blog/?p=2307
A Future Current transcript of one of Aubrey de Grey's presentations at Aging 2008: "Some people say, 'I don't want to live to a thousand.' I don't want to live to a thousand, necessarily. I don't even know if I want to live to a hundred. But I do know I want to make that choice when I am 99, rather than having it gradually removed from me by declining health. This is what it comes down to. The extension of lifespan by the defeat of aging is not the point - at least it is not the main point for me, and I do not think it is the main point for most people who are engaged in this crusade. The purpose is to alleviate the suffering that goes with getting decrepit, frail and dependent. Of course, this includes not just those who are suffering that, but the suffering of their loved ones. The extension of average lifespan is essentially a side benefit. It is something that will happen because the way that we are going to do this, using regenerative medicine, will also mean that you have only the same probability you did when you were a young adult of dying peacefully in your sleep without any of these diseases. In other words, a very low probability indeed. You will indeed on average live a great deal longer, and I don't think you’ll complain if you do. However, that is not the purpose. The purpose is to alleviate suffering."

On the Way to Longevity (July 14 2008)
http://www.dailybruin.ucla.edu/news/2008/jul/14/within-20-years-you-wont-have-grow-old/
The Daily Bruin talks to some of the folk who were at Aging 2008: "Defeating the effects of time by finding a cure for aging has become the focus of multiple areas of research, bringing the possibilities of achieving immortality from fantasy into the realm of science. The new possibilities offered by regenerative medicine illustrate how advancements in therapy on the molecular and cellular level may be able to extend the healthy human life span within the next 20 years. Finding a cure for aging is no longer a theoretical target or a fantasy, but on the way to becoming a practical target. Aging is the most universal degenerative condition and is now becoming the target of regenerative medicine. The body is a really complicated machine, but it's still a machine, so its healthy lifespan can be extended indefinitely by sufficiently comprehensive repair and maintenance, just like simple man-made machines. Aging is a complex phenomenon that affects many different systems. Understanding it and fixing the damage as it comes can potentially cure the harmful effects of aging and as a result, elongate the healthy human lifespan."
______________________________

DISCLAIMER: News summaries are reported by third parties, and there is no guarantee of accuracy. This newsletter is not meant to substitute for your personal due diligence and is not to be taken as medical advice. For originating report, please see www.longevitymeme.org/newsletter/.

If you would like to be removed from my list, I will stop sending you Longevity News Digest if you simply reply to this email with Unsubscribe in the subject line.

David A. Kekich
Maximum Life Foundation
714-641-0700/Fax 714-464-4135
www.MaxLife.org

"Where Biotech, Infotech and Nanotech
Meet to Reverse Aging by 2029"

The Problem… Population Size. The Solution… SuperLongevity

2008-07-14T15:08:00.000-07:00

Can super longevity solve, rather than create a population problem?

Consider these points edited from a paper presented several weeks ago by Herb Meyer at the World Economic Forum in Davos, Switzerland. Mr. Meyer is widely credited with being the first senior U.S. Government official to forecast the Soviet Union's collapse, for which he later was awarded the U.S. National Intelligence Distinguished Service Medal, the intelligence community's highest honor. Formerly an associate editor of FORTUNE, he is also the author of several books.

Some of His Conclusions

Maintaining a steady population requires a birth rate of 2.1. In Western Europe, the birth rate currently stands at 1.5, or 30 percent below replacement. In 30 years there will be 70 to 80 million fewer Europeans than there are today. The current birth rate in Germany is 1.3. Italy and Spain are even lower at 1.2. At that rate, the working age population declines by 30 percent in 20 years, which has a huge impact on the economy. When you don't have young workers to replace the older ones, you have to import them.

In Japan, the birthrate is 1.3. As a result, Japan will lose up to 60 million people over the next 30 years. Because Japan has a very different society than Europe, they refuse to import workers. Instead, they are just shutting down. Japan has already closed 2,000 schools, and is closing them down at the rate of 300 per year. Japan is also aging very rapidly. By 2020, one out of every five Japanese will be at least 70 years old.

The birth rate in Russia is so low that by 2050 their population will be smaller than that of Yemen.

Nobody has any idea about how to run an economy with those demographics. Europe and Japan, which comprise two of the world's major economic engines, aren't merely in recession, they're shutting down. This will have a huge impact on the world economy, and it is already beginning to happen.

When the birth rate drops below replacement, the population ages. With fewer working people to support more retired people, it puts a crushing tax burden on the smaller group of working age people. As a result, young people delay marriage and having a family. Once this trend starts, the downward spiral only gets worse.

These countries have abandoned all the traditions they formerly held in regard to having families and raising children. The U.S. birth rate is 2.0, just below replacement. We have an increase in population because of immigration. When broken down by ethnicity, the Anglo birth rate is 1.6 (same as France) while the Hispanic birth rate is 2.7.

In the U.S., the baby boomers are starting to retire in massive numbers. This will push the elder dependency ratio from 19 to 38 over the next 10 to 15 years. This is not as bad as Europe, but still represents the same kind of trend.

The world's most effective birth control device is money. As society creates a middle class and women move into the workforce, birth rates drop. Having large families is incompatible with middle class living. The quickest way to drop the birth rate is through rapid economic development.

Pretty sobering, isn’t it? So what’s the solution? Longevity… and lots of it. Keep the elderly alive, healthy and productive. Keep them out of retirement, hospitals and nursing homes where they drain resources, and have them contribute to the economy when they are at the peak of their productive capacity.

A Real Boost for Aging Research

2008-07-07T09:11:00.000-07:00

Friday, June 27th I attended Aging 2008 - Aging: the Disease, the Cure, the Implications at UCLA. It was sponsored by Dr. Aubrey de Grey and the Methuselah Foundation. About 700 people attended a stimulating three hour session featuring an All-Star lineup of aging researchers, advocates and personalities.

Most of the attendees spent the next couple of hours networking at an outdoor dinner. In my opinion, some of the more important and interesting people in the world were there, including some movers and shakers who are launching exciting companies and research projects – projects that could have a big impact on your health and longevity.

Here is a list of the speakers:
Dr. Bruce Ames, Professor of Biochemistry and Molecular Biology at UC Berkeley
G. Steven Burrill, Chairman of Pharmasset and Chairman of Campaign for Medical Research
Dr. Aubrey de Grey, Chairman and CSO of Methuselah Foundation and author of Ending Aging
Dr. William Haseltine, Chairman of Haseltine Global Health
Daniel Perry, Executive Director of Alliance for Aging Research
Bernard Siegel, Executive Director of Genetics Policy Institute
Dr. Gregory Stock, Director of Program on Medicine, Technology & Society at UCLA School of Medicine
Dr. Michael West, CEO of BioTime and Adjunct Professor of Bioengineering at UC Berkeley
I also got a Methuselah Foundation T-shirt, one of the coolest T-shirts I ever saw.

Aging 2008 was the opening session for the technically focused Understanding Aging conference which took place Saturday and Sunday. Thirty four scientists presented over the weekend. I believe this was the most extensive scientific longevity conference ever held in the US. Hopefully, the Methuselah Foundation will offer videos.

Open-forum events like this enable scientists to bounce ideas of one another, to cross pollinate ideas and to open up various research programs to debate and scrutiny. As a result, it fast tracks longevity research. Congratulations to Aubrey de Grey and all the Methuselah Foundation volunteers who made it happen.

Then last week, I attended a presentation to an investment banker to fund two very progressive adult stem cell companies. He made a verbal commitment, and funding might take place as early as this month. Once these companies are launched, human therapies could be accelerated. That could translate to the first round of therapies becoming available by next year. Anti-aging science is ratcheted up one more notch.
All-in-all that was a very productive week for life extension. Let’s look forward to many more.

Is Curing Aging Just a Scientific Challenge? The Answer Below May Surprise You.

2008-06-23T10:52:00.000-07:00

Dear Future Centenarian,

I wish you could have been with me last week. Please let me explain…

I attended a week-long conference for two reasons. First, my assistant went on his honeymoon then, and it was convenient for me to hole up and rest in a hotel for 5 days. Second, it gave me a good chance to spend some time with some friends who I hadn’t seen for a while. Oh and there was a third reason too… I figured I couldn’t help but pick up a nugget or two of valuable information.

Well, here’s what happened:

I didn’t get much rest. The conference started at 9 am each day and ran until almost 8 pm. And it was so captivating that I didn’t want to miss a word.
I hardly got to spend any time with my friends (See #1).
I picked up my nugget or two in the first 10 minutes. Five days and a whole tablet full of notes later, I looked back on the most insightful and valuable conference I ever attended.

Without going into detail, it was advertised as a business building and development conference. The organizer, Eben Pagan, walked nearly 200 attendees through the trials and tribulations he endured in building his business (and his incredible life) and how to shortcut them. Eben disclosed, step-by-step, how he built a business that triples every year. It already earns well over $2 million a month – and is still exploding. But there was more. Much more.

Why do I mention this in a life extension newsletter? Because solving the aging puzzle and delivering extreme life extension to you is as much a business and marketing challenge as a scientific one. Last week’s education is fast tracking that challenge for me. It could do the same for you, your project or your business.

If you’d like details, go to http://getaltitude.com.

Network Your Way to Immortality

2008-06-20T08:56:00.001-07:00

Dear Future Centenarian,

Saturday evening, I enjoyed life extension and stem cell technology conversation and dinner at an incredible couple’s home. Their guests were incredible as well. Not only were they bright, well informed and enthusiastic about extreme life extension, but they were a mix of savvy and successful scientists and business people. The latter will have as much to do with your longevity as the former. Maybe more. You’ll see what I mean when you read the attached PowerPoint.

Since 2000, Maximum Life Foundation designed a scientific and financial roadmap to reverse the human aging process. The attachment illustrates an aggressive approach to solving aging in your lifetime. You’ll notice what a surprisingly small investment we think it will take. But we can back up our scientific and financial assumptions. Now it’s time to implement the plan.

Reverse Aging by 2029 – Finally Becoming Believable?

2008-06-20T08:52:00.000-07:00

Dear Future Centenarian,

Last Friday energized me for almost three days… and counting.

Dr. Aubrey de Grey was in Los Angeles, and we cosponsored a Longevity Workshop. Of course Aubrey spoke brilliantly about the Methuselah Foundation and SENS and how it will reverse aging. www.sens.org

Dr. Stephen Coles opened the workshop with a Gerontology Research Group presentation. See www.grg.org for some fascinating life extension info.

The eminent evolutionary biologist Dr. Michael Rose followed Aubrey with a broad overview of how his 30 years of research is finally paying off in diagnostic tools and nutraceuticals that promise to have a huge impact on aging in the very near future. www.biology.ucr.edu/irpee/index

Then I chipped in by describing Maximum Life Foundation’s strategy to reverse aging in 21 years.

Finally, we had a lively panel discussion which included Peter Voss. Peter founded and manages Adaptive AI. See www.adaptiveai.com. Adaptive AI is aggressively pursuing Artificial General Intelligence (AGI). Once developed. Imagine the positive impact AGI, or machines with human level thinking abilities would have on life extension research!

So why am I so pumped up over info that you would think is old hat to me? Simply because just being around committed positive life extensionists supercharges me. And I don’t just mean the presenters. I mean people like Bruce Klein, founder of the Immortality Institute www.imminst.org and his wife Susan who spent so much time organizing this event. Bruce now works with Ben Goertzel in another AGI company called Novamente www.novamente.net. And I especially mean the enthusiastic audience, nearly 100% devoted to the prospect of indefinite youthful lifespans.

Afterwards, the speakers and organizers met for a dinner/social function hosted by super nice guy Elon Musk. Elon co-founded PayPal. His former partner, Peter Thiel, donated $500,000 to the Methuselah Foundation and ledged $3 million.

Actually, I’ve been energized for over two weeks. You almost always get positive feedback when you preach to the choir. No endless questions regarding what we’re going to do with all the people or how unnatural this is, etc. But a couple of weeks ago, I spoke to about 700 small business owners at a marketing conference. My topic was supposed to be the philosophy of certain success principals, but I spent about as much time on extreme life extension. Five years ago, an uninitiated audience like this would have thought I was a fruitcake. But of the 150 or so people who approached me afterwards, over half were as interested in the prospect of open ended lifespans as they were about marketing and business success.

Exhilarating!

There’s more good stuff, but I’ll save it for later.