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Healthy Life Extension
Is There a Free Lunch After All?
posted on March 15, 2011Nearly every year, I attend Natural Products Expo West in Anaheim, Calif., the world’s biggest industry trade show. That’s where you’ll find the newest supplements, natural foods, natural cosmetics and raw materials. I went last Friday, but it takes at least two to three days to walk the entire show and to sample the more interesting food and nutritional products.
This is always a high energy weekend, with some of the healthier and more informed people you’ll meet in a single location. One example is Steve Jennings.
Steve was aware of Maximum Life Foundation, the Manhattan Beach Project and the life extending initiatives we champion in general. He introduced himself, and we had a long and stimulating discussion about (what else?) longevity.
Let me tell you a little about this fascinating guy:
He is 56 years old, charismatic, and he looks like a walking billboard for wellness and fitness. But he shouldn’t have been there. He should be dead. In fact, he was pronounced dead twice from two near fatal accidents. One left him paralyzed for a long time, and it took him thirteen years to fully recover. Now, amazingly, he is national pentathlon champion and is one of the top twenty sprinters in the US for his age group. Not bad for someone who was never supposed to have walked again.
He’s become a longevity mentor to cancer patients, a second-chance for the dangerously unhealthy, and a ‘go-to guy’ for Olympians. Steve Jennings has been called “a leader who shows you how to soar and lift your life up to be the best that you can be.” He’s the guy everyone wishes was at their side during life’s greatest challenges. He’s the tough-love coach that learned in the trenches.
Steve Jennings is different. He’s one of the few who walk the talk. One of the reasons? He’s totally immersed in and committed to anti-aging. It’s his life.
Steve knows what being down is all about. Anyone who fights thirteen long years to recover what he lost knows a little about pain, commitment and results. Most of us are lucky enough to lead able bodied lives until we near the end. But that luck may actually work against us, since it can lead to complacency. We simply don’t value what we take for granted. So we squander opportunities to improve our health when they are still available.
Steve hit his physical bottom early in life. Now he treasures every day… every breath. He is so passionate about the importance of treasuring and improving health that he actually broke down and cried during our conversation.
We talked at length about how many people will die unnecessarily, because they take their health for granted. In last week’s newsletter, I told you about the tragic passing of Robert Bradbury. I’m still shaken up over it and have concluded he should be alive today. Robert was one of the great thinkers of our time. Maybe that was his undoing.
He spent most of his activities shaping the future. By doing so, he tended to neglect the present. Unfortunately, Robert didn’t treat his body with the respect it needed to hold up long enough to benefit from the very technologies he was developing. And he was not alone in this respect. I know several scientists working on extending lives who have horrible lifestyle habits.
Why do you suppose that is? Why do you suppose the vast majority ignore their health until it’s too late? Steve will be quick to tell you it’s because it takes work. Yep, there’s no free lunch. At least not yet. Someday, technology may allow us to eat whatever we want and live healthy, yet sedentary lives. But for now, if you want to increase your odds of avoiding a premature death and unnecessary suffering, if you want to survive to see the day when Robert’s and others’ youth restoring technologies are fully developed, you’ll need to do what Steve does. Sorry. You’ll need to do some work.
Maybe Steve’s injuries will end up being the best thing that ever happened to him. Maybe facing death early in life instead of late in life gave him the awareness he needed to routinely invest in his health. Do yourself a favor, and learn from his experiences and from his example.
Long Life,
David Kekich
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LATEST HEADLINES FROM FIGHT AGING!
TARGETING INFLAMMATION IN NEURODEGENERATIVE DISEASES Friday, March 11, 2011 http://www.fightaging.org/archives/2011/03/targeting-inflammation-in-neurodegenerative-diseases.php
Neurodegeneration has an inflammatory component, and some research groups use that as a starting point for treatment: "Neurodegenerative diseases like Alzheimer's and Parkinson's are partly attributable to brain inflammation. Researchers [now] demonstrate [that] a well-known family of enzymes can prevent the inflammation and thus constitute a potential target for drugs. Research suggests that microglial cells - the nerve system's primary immune cells - play a critical part in neurodegenerative diseases, such as Alzheimer's and Parkinson's. The over-activation of these cells in the brain can cause inflammation, resulting in neuronal death. Scientists [have] now found a way to prevent the activation of the microglia and consequently the inflammation they cause. The key is the blocking of enzymes called caspases, which the team has shown control microglial activation. By studying cell cultures and mice, the researchers show that certain caspases (3, 7 and 8) activate rather than kill microglial cells, which triggers an inflammatory reaction. Mice given caspase inhibitors displayed fewer activated microglia and less inflammation and cell death in the surrounding neurons."
MANIPULATING STEM CELLS TO TREAT VASCULAR DISEASE Friday, March 11, 2011 http://www.fightaging.org/archives/2011/03/manipulating-stem-cells-to-treat-vascular-disease.php
An example of a class of stem cell medicine that involves manipulation of existing populations of cells in the body: "Circulating through the bloodstream of every human being is a rare and powerful type of cell, one that can actually create new blood vessels to bypass blockages that cause heart attacks and peripheral artery disease. Though everyone has these cells - called endothelial progenitor cells - they are often dysfunctional in people prone to vascular disease. Now researchers [have] discovered that a molecule - called Wnt1 - can improve the function of endothelial progenitor cells, increasing the blood flow to organs that previously had been cut off from the circulation. The finding could enhance clinical trials already testing these powerful cells in patients hospitalized with cardiac arrest. A number of studies in the past few years have suggested that genes that play an important role during early development and get 'turned off' during adulthood may also get 'turned on' or expressed again in response to injury, such as heart attack. [Researchers] found that one gene in particular, Wnt1, was expressed during development of blood vessels, shut off during adulthood and then re-expressed in angiosarcoma, a cancer of endothelial cells. Treating these special cells with Wnt1 not only greatly increased their function but also their number. Next, [researchers] investigated what effect the protein would have on a mouse model of peripheral artery disease, an illness in humans caused by decreased blood flow to the extremities. They found that treating these animals with a single injection of the Wnt1 protein resulted in almost three fold increase in blood flow in the affected areas."
ADVANCES IN INDUCED PLURIPOTENCY Thursday, March 10, 2011 http://www.fightaging.org/archives/2011/03/advances-in-induced-pluripotency.php
EurekAlert! passes on an advance in the technology of reprogramming cells: "In the past few months, a slew of papers have indicated that the therapeutic potential of a promising type of stem cell, called induced pluripotent stem (iPS) cells, might be limited by reprogramming errors and genomic instability. iPS cells are engineered by reprogramming fully differentiated adult cells, often skin cells, back to a primitive, embryonic-like state. Given these problems, a team of researchers [wondered] if there might be a better way to regenerate lost tissue to treat conditions like heart disease and stroke.
They outline a method to obtain a new kind of stem cell they call 'induced conditional self-renewing progenitor (ICSP) cells.' It's amazingly cool that we can dial adult cells all the way back to embryonic-like stem cells, but there are a lot of issues that still need to be addressed before iPS cells can be used to treat patients. So we wondered... if we just want to treat a brain disease, do we really have to start with a skin cell, which has nothing to do with the brain, and push it all the way back to the point that it has potential to become anything? In this study, we developed ICSP cells using a cell from the organ we're already interested in - the nervous system, in this case - and pushed it back just enough so it continued to divide, giving us a quantity that we were able to apply efficiently, safely and effectively to treat stroke injury in a rodent model. The [reprogramming gene] used here is conditionally expressed. This means that ICSP cells can only produce [the gene] when the researchers add a compound called tetracycline to laboratory cultures. When tetracycline is removed, the cells cease dividing and start differentiating. Then, once transplanted into to an animal model, ICSP cells are no longer exposed to tetracycline and take their growth and differentiation cues from their new environment."
SINGULARITY HUB ON ARTIFICIAL RETINAS Wednesday, March 9, 2011 http://www.fightaging.org/archives/2011/03/singularity-hub-on-artificial-retinas.php
Another in a series of articles on this topic from Singularity Hub: "The blind in Europe have reason to rejoice, the world's most advanced artificial retina has just received the CE Mark, approved for use in new patients. The Argus II, developed by Lawrence Livermore National Laboratory and marketed by Second Sight, is on sale in the EU, but still awaiting FDA approval here in the US. Luckily, clinical trials are already underway and we could get the amazing device here soon. With the Argus II, blind patients use an external camera to pick up video that is wirelessly transmitted to an electrode array surgically implanted in the eye. While full vision is not restored, the 60+ electrodes allow for some distinction of outlines and other basic shapes. Definitely an improvement over blindness.
A camera embedded in a pair of glasses records the world in front of the patient. A wearable computer takes that image and transforms it into a basic series of impulses. That pattern is transmitted to the Argus II implant which rests inside the eye, and which is attached to the back of the eye through an electrode array. Although software improvements may arrive first, hardware upgrades are also on the horizon. The Argus II operates with about 60 electrodes in its array. That's 60 points of data for your eye to interpret. The Argus III, currently under development at LLNL, should have 200+ electrodes. Perhaps considerably more. It will take a thousand or so to make out human faces accurately, but the Department of Energy is pushing LLNL towards that goal, and beyond. As slow as the progress in artificial retinas has been, it shows no sign of stopping. There are other projects outside of the Argus series, at least two (one in MIT, another in Germany) show serious promise, and even have superior qualities to the Argus in some respects. I have no doubt that we could, eventually, reach a resolution that equals that of the human eye. Perhaps, with a different kind of interface, we could even see in greater detail than nature intended."
TISSUE ENGINEERING OF NEW URETHRAS Tuesday, March 8, 2011 http://www.fightaging.org/archives/2011/03/tissue-engineering-of-new-urethras.php
From CNN: "Engineering organs begins with something missing - a phantom organ in the body that causes a patient incredible discomfort, dysfunction or pain. It ends with a Star Trek-esque feat of engineering where missing organs are replaced using cells culled from a patient's own body. In a small pilot [study] scientists reported successfully reconstructing urethras in five young patients, using their own cells. We were able to create patients' own tissue that actually belongs there. If the tissue is supposed to be there, hopefully we will do better by the patient. Patients had their engineered urethras implanted between March 2004 and July 2007 at the Federico Gomez Children's Hospital in Mexico City. Their urethras continued to function after several years' follow-up. The urethra is a narrow tube that connects the bladder with the genitals, providing a conduit to usher waste out of the body. When it is damaged - sometimes congenitally, or as result of disease, pelvic fractures or other traumas - it is usually replaced using tissue harvested from the lining of a patient's cheeks or using skin grafted from another area of the body. Unfortunately for the narrow structures in the body (like urethras), they are kind of complex because they tend to collapse. Every organ has its own challenges.
The challenge with traditional urethra replacement is creating a viable tube, one that will not easily collapse. And that is where engineering urethras may offer some benefit. The first step for engineering a new urethra is to take a very small piece of the patient's own tissue (around half the size of a postage stamp) from the bladder area. Cells are scraped from the biopsied tissue, allowed to multiply, after which muscle cells are separated from urethral cells. It is the next few steps in the process that sound like science fiction. When there are a sufficient number of cells, scientists 'seed' them - much like you would seed a new lawn - onto a mesh scaffold that is shaped like a urethra. The inside of the mesh is coated with urethral cells while the outside gets muscle cells. The seeded structure is placed in an incubator for about two weeks, in a 'cooking' process that [simulates] how cell growth occurs inside the body. After that, the newly engineered urethra is ready to be implanted into the patient."
BOOSTING GARBAGE DISPOSAL IN BRAIN CELLS Tuesday, March 8, 2011 http://www.fightaging.org/archives/2011/03/boosting-garbage-disposal-in-brain-cells.php
The processes of cellular housekeeping appear to be important in aging, and here is an example of what can be achieved by selectively boosting their operation: "Gene therapy that boosts the ability of brain cells to gobble up toxic proteins prevents development of Alzheimer's disease in mice that are predestined to develop it. The treatment - which is given just once - could potentially do the same in people at the beginning stages of the disease. Giving brain cells extra parkin genes promotes efficient and effective removal of amyloid particles believed to be destroying the neurons from the inside.
This revved up protein disposal process prevents the cells from dying and spewing amyloid proteins into the brain, where they stick together and clump into plaque. Many neurodegenerative diseases are characterized by a toxic build-up of one protein or another, and this approach is designed to prevent that process early-on. Providing brain cells with about 50 percent more parkin protein activates two parallel garbage-removal processes within the brain. One is ubiquitination, in which errant proteins are targeted for destruction and recycling within the cell. The other process is autophagy, in which membranes form around damaged mitochondria (the cell's power plants) and these membranes fuse with lysosomes that destroys the contents. This is particularly important [because] damaged mitochondria have been found to clog the insides of neurons affected by Alzheimer's disease, and the extra parkin seems to help clear them. That allows the cells to produce new and healthy mitochondria. With a normal amount of parkin, the cells are overwhelmed and cannot remove molecular debris. Extra parkin cleans everything." This should have much wider application, possibly even for the slowing of aging, given the broad role of autophagy; it's the sort of therapy that everyone would want done, regardless of their present state of health.
CRITIQUING SENS ON NUCLEAR DNA DAMAGE Monday, March 7, 2011 http://www.fightaging.org/archives/2011/03/critiquing-sens-on-nuclear-dna-damage.php
Ben Best here offers a critique of SENS, the Strategies for Engineered Negligible Senescence assembled by Aubrey de Grey, based on the absence of nuclear DNA damage from the list of things to repair: "Dr. de Grey asserts that repairing aging damage is a more effective approach than attempting to slow or prevent aging, and I agree with him. Being an ardent supporter of SENS has not stopped me from simultaneously being a critic of aspects of his program that I think are flawed or deficient. I will attempt to outline some of my criticisms in simple language, assuming that my readers have some knowledge of basic science. [a] fundamental concern that I have that a significant form of aging damage may be being ignored by SENS.
There are many types of DNA damage, but for the purposes of this essay I will focus on breakage of both DNA strands - resulting in a gap in a chromosome. There are two mechanisms for repairing double-strand DNA breaks: Homologous Recombination (HR) and Non-Homologous End-Joining (NHEJ). HR usually results in perfect repair, but HR can only operate when cells are dividing. NHEJ is the more frequent form of double-strand break repair, but it is error-prone. NHEJ is the only DNA repair mechanism available for non-dividing cells. Even in cells that divide, 75% of double-strand breaks are repaired by NHEJ. It is hard to believe that it could be a coincidence that the most notorious 'accelerated aging' diseases are due to defective DNA repair. Nuclear DNA damage typically leads to mutation or DNA repair - or apoptosis or cellular senescence when DNA repair fails (a mechanism that is believed to have evolved for protection against cancer). But not all DNA damage is repaired, and NHEJ repair is often defective. Accumulating DNA damage and mutation can lead to increasingly dysfunctional cells." Everyone in the community should have a go at critiquing SENS - because doing so forces you to do some digging and think it through for yourself, at which point you'll find that many aspects of biotechnology and human cellular biology are not as intimidating or as hard to understand as they might appear at a distance.
COMMUNICATIONS TECHNOLOGY AND SCIENTIFIC PROGRESS TOWARDS LONGEVITY Monday, March 7, 2011 http://www.fightaging.org/archives/2011/03/communications-technology-and-scientific-progress-towards-longevity.php
Thoughts on large systems, communications, scientific progress, and evolutionary theory from h+ Magazine: "What do the Global Brain (GB) and human biological immortality have in common? At first, this appears to be a strange question. However, I believe that the realisation of the Global Brain will, perhaps inevitably, result in humans achieving extreme life extension, and eventually abolishing death due to aging. The GB is an emergent worldwide entity of distributed intelligence, one facilitated by communication and the meaningful interconnections between billions of humans, via technology such as the internet. When fully operational, the GB must rely on its individual constituents - individual human brains interconnected through technology. Without human input, the GB cannot exist. Furthermore, it cannot exist without technology.
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