A Quick Fix for Your Lingering Health Issues

22 09 2010

Dear Future Centenarian, 

What do you call the person who graduates last in his or her class at medical school? “Doctor” 

I have had the good fortune to know some of the best anti-aging physicians in the country. I also met some of the worst. This specialty, just like every other, and every other profession for that matter, has its stars and its losers. But the big winners or losers are the consumers, and in this case, the patients.

A good doctor can change your life for the better… or the worst. They can perform miracles and save your life, but they can also kill you. Doctors, unlike any other professionals, do bury their mistakes.

So when it comes to something as precious as your health, how do you know whom to pick as your physician? If you want a top anti-aging doc, you can go to www.MaxLife.org and pick one of our Medical Advisory Board members if you are lucky enough to live near one of them. If not, and this goes for most of you, I may have your answer. I have never met anyone who knows more about the human body, or how to diagnose and treat as wide a variety of ailments, as one individual.

About eight years ago, I met Professor Joe Carrington. After I tell you a little about Joe, I will tell you how this info could help cure what you have now or what may be lurking in your future. Even better, how you can keep from getting knocked out by an unexpected disease or condition.

Joe is a research scientist and pioneer in Holistic and Clinical Nutrition. He has focused his 42 year career in anti-aging medicine and diseases of aging with heavy emphasis on neuro-degenerative conditions. He is an absolute genius, recognized early by Harvard University. Harvard skipped him over two college degrees (AA and BS) and admitted him directly into Harvard’s Master’s program. In many instances, Joe taught his Harvard Professors. 

During his study at Harvard, he cross registered, and was admitted at the same time, to The Massachusetts Institute of Technology (MIT), where he studied nuclear engineering with a focus on nuclear medicine, brain imaging and scanning.

Before dedicating himself to pure research in anti-aging medicine, Alzheimer’s and dementia, Professor Carrington practiced Clinical Nutrition for 42 years in an internationally renowned practice, solving problems for patients from all over the world who could not be helped by their regular, mainstream physicians. In fact, his patients include many Medical Doctors and other Physicians. He also teaches and trains Medical Doctors in anti-aging medicine, restoring brain neurochemistry and neuroendocrinology.

He is one of the few people I know with an encyclopedic memory. He jokes that he has no life, spending his time devouring every book and study on anti-aging he could lay his hands on that was published over the past fifty years.

Now here’s how Joe can help you get the best possible medical care, regardless of where you live.

You can keep your local primary care physician if you are happy with him or her. Joe would consult with you by phone as he has done for thousands of others. Then he would work hand-in-hand with your physician in getting you prescriptions for blood panels, other diagnostics and possibly medications. Once you receive your diagnostic reports, you would have them sent to Joe in Florida where he would analyze them and give his recommendations to you to share with your doctor.

Sometimes, you’ll find doctors whose egos are bigger than their motivation to help their patients. Sometimes, they resent “outsiders” advising them what is best for you. If this describes your doc, get a new one.

I am often asked to give referrals, and normally don’t. When I have a high level of confidence, I usually agree. In this case, Joe did not ask me, I asked him. Here’s his email address. carrington@post.harvard.edu. He charges way less than your doc, may be worth infinitely more, and he truly cares about you and your well-being. I can’t imagine you being in better hands.

Presently, Prof. Carrington works as a consultant, solving problems for Medical Doctors and scientific research institutions and creating formulations against disease.

In fact, he has completed a formula based on his clinical experience and over 1000 published studies, to slow, stop and reverse symptoms of Alzheimer’s Disease and dementia which will become available to the public when funding permits. 

Long Life,

David Kekich

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LATEST HEALTHY LIFE EXTENSION HEADLINES

 

HEAT SHOCK PROTEINS AS BIOMARKERS OF AGING (September 17 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4905

These researchers suggest that heat shock proteins might be used as a biomarker of aging, a way to determine biological age rather than chronological age, and hence predict life span or evaluate the effectiveness of potentially longevity-inducing therapies: “Since their discovery in Drosophila, the heat shock proteins (Hsps) have been shown to regulate both stress resistance and life span. Aging is characterized by increased oxidative stress and the accumulation of abnormal (malfolded) proteins, and these stresses induce Hsp gene expression through the transcription factor HSF. In addition, a subset of Hsps is induced by oxidative stress through the JNK signaling pathway and the transcription factor Foxo. The Hsps counteract the toxicity of abnormal proteins by facilitating protein refolding and turnover, and through other mechanisms including inhibition of apoptosis. The Hsps are up-regulated in tissue-specific patterns during aging, and their expression correlates with, and sometimes predicts, life span, making them ideal biomarkers of aging. The tools available for experimentally manipulating gene function and assaying healthspan in Drosophila provides an unparalleled opportunity to further study the role of Hsps in aging.”

WHY RESEARCHERS ARE INTERESTED IN CALORIE RESTRICTION (September 16 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4903

A great many research groups continue to investigate the biochemistry of calorie restriction, and this paper is a good illustration as to why this is the case: “It is well known that calorie restriction (CR) can retard the aging process in organisms ranging from yeast to non-human primates, and delay the onset of numerous age-related diseases including neurodegenerative disorders. Translation of the knowledge gained from CR research in animal models to disease prevention strategies in humans should provide therapeutic approaches for these diseases. Signaling pathways induced by CR are therefore potentially new therapeutic targets for neurodegenerative diseases. This review summarizes the evidence on key biological mechanisms underlying the beneficial effects of CR based on our current understanding, with particular emphasis on the recent impact of CR on neuroprotection, and on the emerging development of pharmacological agents that target signaling pathways induced by CR. We focus in particular on recent findings on sirtuins for skin care  and prevention of neurodegenerative diseases.” Even outside the context of aging, there is potentially much to learn about human biochemistry by following the effects of calorie restriction.

 

MILD MEMORY LOSS WITH AGING AS A DISEASE (September 16 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4902

The process of declaring parts of aging as a disease is driven by regulation: the FDA does not permit treatments for aging, only for named diseases. Since there is little funding for research that cannot be legally commercialized, the incentive is to carve off chunks of the process of aging and go through the process of having government employees add it to the list of diseases – which can take years and millions of dollars. Sarcopenia, for example, is still not recognized by the FDA, meaning that no potential treatment can be commercially developed in the US. Here is an example of this process at work for memory loss: “Simply getting older is not the cause of mild memory lapses often called senior moments, according to a new study. Even the very early mild changes in memory that are much more common in old age than dementia are caused by the same brain lesions associated with Alzheimer’s disease and other dementias. The very early mild cognitive changes once thought to be normal aging are really the first signs of progressive dementia, in particular Alzheimer’s disease. The pathology in the brain related to Alzheimer’s and other dementias has a much greater impact on memory function in old age than we previously recognized. Dementias are the root cause of virtually all loss of cognition and memory in old age. They aren’t the only contributing factors; other factors affect how vulnerable we are to the pathology and to its effects.  But the pathology does appear to be the main force that is driving cognitive decline in old age.”

 

CALORIE RESTRICTION CULLS SENESCENT CELLS (September 15 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4901

Calorie restriction has been shown to slow down almost every measure of degenerative aging examined to date. Here is another such open access study: “Dietary restriction (DR) extends the lifespan of a wide variety of species and reduces the incidence of major age-related diseases. Cell senescence has been proposed as one causal mechanism for tissue and organism ageing. We show for the first time that adult-onset, short-term DR reduced frequencies of senescent cells in the small intestinal epithelium and liver of mice, which are tissues known to accumulate increased numbers of senescent cells with advancing age. This reduction was associated with improved telomere maintenance without increased telomerase activity. We also found a decrease in cumulative oxidative stress markers in the same compartments despite absence of significant changes in steady-state oxidative stress markers at the whole tissue level. The data suggest the possibility that reduction of cell senescence may be a primary consequence of DR which in turn may explain known effects of DR such as improved mitochondrial function and reduced production of reactive oxygen species.” The telomere maintenance line item above might suggest that the shortest-telomere cells – i.e. senescent cells – are being destroyed and recycled, thus raising the average amongst remaining cells.

CREATING AN ARTIFICIAL OVARY (September 15 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4900

There are interesting intermediate destinations on the road to tissue engineered replacement organs. This is one of them: researchers have “invented the first artificial human ovary, an advance that provides a potentially powerful new means for conducting fertility research and could also yield infertility treatments for cancer patients. The team has already used the lab-grown organ to mature human eggs. An ovary is composed of three main cell types, and this is the first time that anyone has created a 3-D tissue structure with triple cell line. The ovary not only provides a living laboratory for investigating fundamental questions about how healthy ovaries work, but also can act as a testbed for seeing how problems, such as exposure to toxins or other chemicals, can disrupt egg maturation and health. To create the ovary, the researchers formed honeycombs of theca cells, one of two key types in the ovary, donated by reproductive-age (25-46) patients at the hospital. After the theca cells grew into the honeycomb shape, spherical clumps of donated granulosa cells were inserted into the holes of the honeycomb together with human egg cells, known as oocytes. In a couple days the theca cells enveloped the granulosa and eggs, mimicking a real ovary.”

 

WORKING TOWARDS REGENERATION OF THE ENTHESIS (September 14 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4899

An open access paper: “The enthesis, which attaches the tendon to the bone, naturally disappears with aging, thus limiting joint mobility. Tendons and ligaments are fibers made up of dense connective tissue and they are critical for physiological movement and the stability of joints because of their attachment to bone. Injury to these structures can significantly destabilize joints, resulting in the development of degenerative joint diseases, especially in the upper limbs. Surgery is frequently needed but the clinical outcome is often poor due to the decreased natural healing capacity of the elderly. This study explored the benefits of a treatment based on injecting chondrocyte and mesenchymal stem cells (MSC) [in rats] Damage was repaired by classical surgery without cell injection (group G1) and with chondrocyte (group G2) or MSC injection (group G3). The spontaneous healing rate in the G1 control group was 40%, close to those observed in humans. Cell injection significantly improved healing (69%). A new enthesis was clearly produced in cell-injected G2 and G3 rats, but not in the controls. Only the MSC-injected G3 rats had an organized enthesis with columnar chondrocytes as in a native enthesis 45 days after surgery. Cell therapy is an efficient procedure for reconstructing degenerative entheses. MSC treatment produced better organ regeneration than chondrocyte treatment. The morphological and biomechanical properties were similar to those of a native enthesis.”

INVESTIGATING THE ORIGIN OF AGGREGATES (September 13 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4897

Aggregates of unwanted proteins are important in aging, and researchers continue to investigate why it is that aggregates appear in the first place. Here, researchers “have solved a long-standing mystery of how cells conduct ‘quality control’ to eliminate the toxic effects of a certain kind of error in protein production. The new study suggests how cells in eukaryotic organisms, like humans, sense and destroy ‘non-stop’ proteins that remain stuck in the ribosome, the protein manufacturing plant of the cell. DNA is used to make RNA, which, in turn, is used to make proteins. In healthy cells, the ribosome translates the code carried by a messenger RNA (mRNA) to link together protein building blocks (amino acids) in a particular order to form specific proteins. But errors happen – which is why the body has a host of different quality control mechanisms to ensure that the proteins that emerge from this process are flawless. When aberrant proteins escape these surveillance mechanisms, they accumulate and form ‘aggregates’ that can be toxic to certain neuronal types, and disorders such as Alzheimer’s and Parkinson’s diseases can result. For some 15 years, scientists have understood the mechanism that identifies and destroys these problematic non-stop proteins in bacteria. In these organisms, non-stop proteins are tagged by a marker known as tmRNA or ssrA, which then leads to their destruction. In more complex eukaryotic organisms, which range from yeast to humans, though, the mechanism for identifying and eliminating such dangerous non-stop errors has remained a mystery – until now.”

TENGION WORKS ON KIDNEY REGENERATION (September 13 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4896

A press release from Tengion: “rodents with chronic kidney disease (CKD) were treated with healthy kidney cells to catalyze the regeneration of functional kidney tissue and delay disease progression, as evidenced by extended survival, improved kidney filtration, and reduced severity of kidney tissue pathology. The published data demonstrate that delivery of a selected population of kidney cells to the kidney significantly extended long-term survival and improved kidney function in rodents with chronic kidney disease during six months of follow-up. Further, the therapeutic effects reported in this study were more pronounced and more durable than have been previously reported with this animal model. Chronic kidney disease is a serious medical condition affecting millions of Americans and can lead to kidney failure requiring the need for transplant or lifelong dialysis. A treatment approach that can increase kidney tissue and improve function would be a significant advancement in the care of these patients. The scientific community has historically considered that CKD develops from an imbalance between tissue damage and the kidney’s ability to repair and regenerate itself. These preclinical data provide clear evidence that regeneration of functional renal tissue can delay progression of CKD.”

 
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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/.

David A. Kekich

Maximum Life Foundation

www.MaxLife.org

“Where Biotech, Infotech and Nanotech

     Meet to Reverse Aging by 2029”





The Difference Between Playing to Win and Trying to Not Lose

13 07 2010

You’ve seen it happen. Your favorite team or athlete builds a comfortable lead, turns conservative and blows the game. Or how about a business, or an industry, or even and entire country, that gets away from its aggressive innovative roots, only to see an upstart replace them at the top? This is why short-term survival mentalities often lead to long-term death. And closer to home, and entrepreneur or new company that tries to be another “me too” and never achieves greatness.

Finally, how about each individual who plays it too close to the vest, leads a comfortable life, but at the end regrets how his or her career, marriage or children turn out because they didn’t dare to take a chance, dig in their heels, or be aggressive from time-to-time?

You and I could discuss examples endlessly, so let’s narrow our focus.

]

I assume you have more than a passing interest in health and longevity, or you wouldn’t be reading this letter. Accepting that assumption, let’s say you understand exactly why we can expect age-reversal capabilities toward the end of your projected lifespan. Then factor in, if the actuarial tables hold up, half the people your age will die before then, and half may have a chance at open-ended youth.

Then let’s allow room for error. Assume we miss our target by ten years.

If we do, and if our target is toward the end of your projected lifespan, that means instead of half the people your age missing the extreme longevity opportunity, well over 90% will miss it. Maybe 99% if you are on the bubble now. Even at younger ages, your odds drop dramatically as you age, since mortality rates increase with each passing year.

So if you’re not doing everything in your power now to reach what has been our unachievable dream for thousands of years, but which is now finally within our grasp, then not playing to win could, and probably will be the difference between your life and death.

I have lots of heroes. One such hero is Dr. Bill Andrews. Here’s a guy who plays to win. Not just in his personal life, but in his career as well. His is an extraordinary story. He had a cushy job as a chief scientist, working for a firm that lost its vision, and started playing not to lose. Bill would have noting of it, so he struck out on his own to achieve his dream of curing aging. You’ll be amazed at what he has accomplished, both personally and professionally.

Click on this link now.

Meet Bill Andrews: The Man who would be Immortal

Long Life,

David Kekich

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LATEST HEALTHY LIFE EXTENSION HEADLINES

SPURRING NEURAL GROWTH IMPROVES MEMORY (July 09 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4804

Via EurekAlert: “Scientists have discovered a compound that restores the capacity to form new memories in aging rats, likely by improving the survival of newborn neurons in the brain’s memory hub. This neuroprotective compound, called P7C3, holds special promise because of its medication-friendly properties. It can be taken orally, crosses the blood-brain barrier with long-lasting effects, and is safely tolerated by mice during many stages of development. Physical activity, social, or other enriching experiences promote neurogenesis – the birth and maturation of new neurons. This growth takes place in the dentate gyrus, a key area of the brain’s memory hub, the hippocampus. But even in the normal adult brain, most of these newborn neurons die during the month it takes to develop and get wired into brain circuitry. To survive, the cells must run a gauntlet of challenges. Newborn hippocampus neurons fare much worse in aging-related disorders like Alzheimer’s, marked by runaway cell death. In hopes of finding compounds that might protect such vulnerable neurons during this process, [researchers] tested more than 1000 small molecules in living mice. To find out if P7C3 could similarly stem aging-associated neuronal death and cognitive decline, the researchers gave the compound to aged rats. Rodents treated with P7C3 for two months significantly outperformed their placebo-treated peers on a water maze task, a standard assay of hippocampus-dependent learning. This was traced to a threefold higher-than-normal level of newborn neurons in the dentate gyrus of the treated animals.”

SHORTER TELOMERES, GREATER CANCER RISK (July 08 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4803

News of a study linking telomere length and cancer risk, but it’s still the case that the relationship could be indirect, such as both sides of the correlation being based on levels of biochemical damage. For example, it might reflect the state of mitochondrial biochemistry in a person: “A new study suggests that shorter length of leukocyte telomeres – chromosome markers of biological aging – are associated with an increased risk of cancer and death from cancer. Telomeres are a structure at the end of a chromosome involved in the replication and stability of the chromosome. Genetic factors and environmental stressors can shorten the length of the telomere, and telomere length has been considered to be an emerging marker of biological age. Some research has suggested that short telomeres and chromosomal instability contribute to malignant cell transformation. [Researchers] conducted a study to assess the association between leukocyte telomere length and risk of both new-onset cancer and cancer death. Leukocyte telomere length was [measured] in 787 participants, free of cancer in 1995. Analysis indicated that short telomere length at the beginning of the study was associated with new cancer independently of standard cancer risk factors. Compared with participants in the longest telomere length group, participants in the middle length group had about twice the risk of cancer, and those in the shortest length group had approximately three times the risk. Cancer incidence rates were inversely related to telomere length, with participants in the group with the shortest telomere length having the highest rate of cancer.”

GENERAL IMPROVEMENT IN CANCER MORTALITY RATES (July 08 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4802

Much like the slow and steady lengthening of life expectancy, there is a general improvement in cancer treatment outcomes thanks to progress across the board in modern medicine: “The continued drop in overall cancer mortality rates over the last 20 years has averted more than three-quarters of a million (767,000) cancer deaths according to a new report from the American Cancer Society. The American Cancer Society’s annual Cancer Statistics article reports that the overall death rate from cancer in the United States in 2007 was 178.4 per 100,000, a relative decrease of 1.3 percent from 2006, when the rate was 180.7 per 100,000, continuing a trend that began in 1991 for men and 1992 for women. In that time, mortality rates have decreased by 21 percent among men and by 12 percent among women, due primarily to declines in smoking, better treatments, and earlier detection of cancer. Cancer incidence rates decreased in men 1.3 percent per year from 2000 to 2006 and in women 0.5 percent per year from 1998 to 2006. Death rates for all cancer sites combined decreased 2 percent per year from 2001 to 2006 in males and 1.5 percent per year from 2002 to

2006 in females.”

ON MITOHORMESIS (July 07 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4801

A little stress improves our biochemistry: “Recent evidence suggests that calorie restriction and specifically reduced glucose metabolism induces mitochondrial metabolism to extend life span in various model organisms, including Saccharomyces cerevisiae, Drosophila melanogaster, Caenorhabditis elegans and possibly mice. In conflict with Harman’s free radical theory of aging (FRTA), these effects may be due to increased formation of reactive oxygen species (ROS) within the mitochondria causing an adaptive response that culminates in subsequently increased stress resistance assumed to ultimately cause a long-term reduction of oxidative stress. This type of retrograde response has been named mitochondrial hormesis or mitohormesis, and may in addition be applicable to the health-promoting effects of physical exercise in humans and, hypothetically, impaired insulin/IGF-1-signaling in model organisms. Consistently, abrogation of this mitochondrial ROS signal by antioxidants impairs the lifespan-extending and health-promoting capabilities of glucose restriction and physical exercise, respectively. In summary, the findings discussed in this review indicate that ROS are essential signaling molecules which are required to promote health and longevity. Hence, the concept of mitohormesis provides a common mechanistic denominator for the physiological effects of physical exercise, reduced calorie uptake, glucose restriction, and possibly beyond.”

THE SIMPLE ANSWER THAT NO-ONE WANTS TO HEAR (July 05 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4797

There’s nothing you can do right now that will have a greater immediate effect on your life expectancy than exercise and calorie restriction. The best thing you can do for future improvement is to help researchers raise funds to develop repair technologies for human aging. But no-one wants to hear that. Everyone wants a silver bullet now, and it doesn’t exist: “Friends occasionally ask me how they might best live healthy, longer. They inquire because I went to medical school, work in biotech, and focus professionally on developing drugs to treat diseases of aging by targeting aging genes. My response seems to surprise them, because it does not center on pharmaceutical products. The current answer on how to increase healthy human lifespan is simple: ‘Eat less, and exercise more.’ Modern medicine has discovered an impressive number of lifesaving new drugs for devastating diseases such as cancer, diabetes, heart disease, and infectious diseases. Nevertheless, for most of us, active lifestyles and less food will have a more profound effect than taking more medicines. Hard as it is, we should walk, run, and bike more, and reduce our food intake. The best way we can increase our chances to live healthy, longer is simple: eat less and exercise more.” Learn How to Get a Six Pack





The Most Powerful Life Extender of All

7 07 2010

Dear Future Centenarian,

 For millions of years, we subsisted on a hunter/gatherer diet. That means we ate what we could find and kill. Those diets were actually much more diverse than typical modern diets. Average life spans were quite short due to the harshness and dangers of everyday life. But contrary to popular belief, maximum life spans may have been much longer than we can hope to reach today. And diseases associated with aging were largely unknown.

Around 10,000 years ago, we entered the Agricultural Age. We started growing crops and domesticating animals. That’s when we started eating grains, and later, dairy products, and we were not adapted to them.

 We’re not adapted to agricultural diets now either, because 10,000 years is nothing on the human evolutionary scale. We are still adapted to the hunter/gatherer diet. We’ve been on it for millions of years. We’re also adapted to eating cooked meat and some vegetables, since we’ve been eating those for well over a million years.

 By eliminating ALL grains and dairy products from your diet and by being physically active, you may be able to avoid most of the aging-related diseases. The sky is not the limit, but you could slow aging dramatically and may be able to add lots of healthy active years to your life. Find out more by reading Food and Western Disease by Staffan Lindeberg. This may be the single most important book you will ever read, if your goal is extreme longevity. If you’re young now, there is no need to eat this way until you are well over thirty. In fact, it could be counter-productive for children, since adaptation to recent changes drops drastically as we age.

 Most of the seven habits I describe in Life Extension Express can be fairly easy to implement once you grasp the incredible benefits. In fact, they can even be fun, especially once you experience the results. I thought this one would take lots of will power though, at least for me.

 I enjoy a cup of chocolate ice cream every month or so, and I do like cheese. There are fairly good healthy alternatives, even though they’re not quite the same. And although I seldom touch bread, I thought it would be tough to figure out how to replace my oatmeal and whole grain cereals. Well, I was wrong. I even found grainless alternatives to both bread and cereals. For example, you can get ones made from sunflower seeds. See www.LydiasOrganic.com for some tasty substitutes.

 The web is full of recipes for grain-free breads, cereals and pancakes as well as sources and recipes for non-dairy cheeses. And who needs dairy when you can enjoy delicious and nutritious almond milk?

 Sure, a hunter/gatherer diet is not as convenient, especially when you dine out. And it does take some trial and error and more creative grocery shopping. So the question you might ask yourself is, “Is it worth it”?

 The answer is a no-brainer for me. “Yes”! Why? Because it positions you and me better to take advantage of the emerging age-reversal and repair technologies described in Part I of Life Extension Express by extending our average lifespans now. In fact, this may be the greatest life-extender of them all. And yummies like honey, cacao, and avocado, or plants like them, have probably been in our diet for millions of years, so we are not talking total self-denial.

 There’s an additional benefit too, if weight loss is your goal. It’s next to impossible to be overweight if you adopt a hunter/gatherer lifestyle for a protracted period of time.

 Long Life,

David Kekich

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REGENERATIVE HEALING OF CAVITIES IN TEETH

The dental application of regenerative medicine is one of the more advanced areas in this field of research. Whole teeth have been grown from stem cells in animal studies, and here scientists demonstrate healing of cavities by regrowth of tooth enamel. After about one month, the cavities had disappeared.

http://www.fightaging.org/archives/2010/06/regeneration-of-tooth-enamel-cavities-healed-in-mice.php

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LATEST HEALTHY LIFE EXTENSION HEADLINES

INDUCED PLURIPOTENT STEM CELLS FROM BLOOD (July 02 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4795

From Wired: “Blood drawn with a simple needle stick can be coaxed into producing stem cells that may have the ability to form any type of tissue in the body, three independent papers report. The new technique will allow scientists to tap a large, readily available source of personalized stem cells. Because taking blood is safe, fast and efficient compared to current stem cell harvesting methods, some of which include biopsies and pretreatments with drugs, researchers hope that blood-derived stem cells could one day be used to study and treat diseases. Three research groups used similar methods to prod certain immune cells in human blood to become induced pluripotent stem cells. Because they are reprogrammed adult cells, these stem cells share many of the same regenerative abilities as true embryonic stem cells but may not have as much versatility. Scientists’ manipulations turned the stem cells in the new studies into several types of mature blood cells, including infection-fighting T cells. What’s more, all the groups showed that a batch of the stem cells implanted into mice developed into the three main types of progenitor cells found in human embryos.”

 

IMPROVED ASSOCIATION OF LONGEVITY GENES WITH LONGEVITY (July 02 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4794

Via ScienceNews: “In the new study, researchers looked at genetic markers called single nucleotide polymorphisms, or SNPs, in 1,055 centenarians and 1,267 younger people, all of European descent. The scientists found 150 genetic SNP variants linked to extreme longevity. Initially, the team identified only 33 SNPs found more often in people aged 90 to 114 years but not in a control group made up of people who will presumably live an average lifespan. Biostatistician Paola Sebastiani [devised] a different statistical method to identify additional SNPs that would improve the team’s ability to predict longevity. The team tested their predictions on a separate group of centenarians and controls. With the 150 SNPs, the researchers could correctly predict who was a centenarian 77 percent of the time. Now on one side, 77 percent is a very high accuracy for a genetic model, which means that the traits that we are looking at have a very strong genetic base. On the other hand, the 150 SNPs can’t explain why the remaining 23 percent of centenarians in the study have reached such ripe old ages. It could mean that those people have other, rare genetic variants or lifestyles responsible for their longevity or some combination of the two.”

ORGANS MADE TO ORDER (July 01 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4793

As the Smithsonian notes, “It won’t be long before surgeons routinely install replacement body parts created in the laboratory. Anthony Atala works in the body shop of the future. He and his colleagues use human cells to grow muscles, blood vessels, skin and even a complete urinary bladder. Much of the work is experimental and hasn’t yet been tested in human patients, but Atala has implanted laboratory-grown bladders into more than two dozen children and young adults born with defective bladders that don’t empty properly, a condition that can cause kidney damage. The bladders were the first lab-generated human organs implanted in people. If they continue to perform well in clinical tests, the treatment may become standard not only for birth defects of the bladder but also for bladder cancer and other conditions. Regenerative medicine’s once-wild ideas are fast becoming reality. Late last year, Organovo, a biotech company in San Diego, began distributing the first commercially available body-part printer. Yes, you read correctly: a printer for body parts. Using the same idea as an ink-jet printer, it jets laser-guided droplets of cells and scaffold material onto a movable platform. With each pass of the printer head, the platform sinks, and the deposited material gradually builds up a 3-D piece of tissue. Regenerative medicine laboratories around the world have relied on the printer to generate pieces of skin, muscle and blood vessels. Atala’s lab has used the technology to construct a two-chambered mouse-size heart in about 40 minutes.”

ARE OLD STEM CELLS LESS USEFUL? (June 30 2010)

http://www.longevitymeme.org/news/vnl.cfm?id=4791

Researchers are gathering evidence to suggest that stem cells from the old are less useful when transplanted – which means that some form of repair or other manipulations may need to be included in future stem cell therapies for the degenerative conditions of aging: “Clinical trials of cardiac cell therapy have indicated limited benefits in aging patients, even though preclinical studies using young animals consistently reported significant improvements. Animal studies have demonstrated reduced efficacy of donor cells isolated from older individuals. Here, we evaluated the effects of donor age on the function of human mesenchymal stem cells (hMSCs) in the context of cell therapy for ischemic cardiomyopathy. The regenerative capacity of hMSCs was significantly influenced by age. Transplanting young hMSCs improved functional outcomes after an MI by preventing matrix degradation and promoting angiogenesis. The clinical implication is that aged patients require an optimized source of stem cells for treatment.”

NOTE: There may be a solution on the horizon.

PROGRESS TOWARDS UNDERSTANDING MEMORY (June 29 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4789

Understanding the physical basis of human memory will enable therapies to both enhance youthful memory and reverse its decline with age. From ScienceDaily, an example of present investigations into the biology of memory: “We found one of the key proteins involved in the process of memory and learning. This protein is present in the part of the brain in which memories are stored. We have found that in order for any memory to be laid down this protein, called the M3-muscarinic receptor, has to be activated. We have also determined that this protein undergoes a very specific change during the formation of a memory – and that this change is an essential part of memory formation. In this regard our study reveals at least one of the molecular mechanisms that are operating in the brain when we form a memory and as such this represents a major break through in our understanding of how we lay down memories. This finding is not only interesting in its own right but has important clinical implications. One of the major symptoms of Alzheimer’s disease is memory loss. Our study identifies one of the key processes involved in memory and learning and we state in the paper that drugs designed to target the protein identified in our study would be of benefit in treating Alzheimer’s disease.”

MORE ON OVARIES AND LONGEVITY IN MICE (June 29 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4788

Another study to show that transplanting young ovaries into old mice extends life quite significantly: “successful ovarian transplants increased the lifespan of the mice by more than 40%. All the mice in both experiments that had received transplants resumed the normal reproductive behavior of young mice. They showed interest in male mice, mated and some had pups. Normally, old mice stay in the corner of the cage and don’t move much, but the activity of mice that had had ovarian transplants was transformed into that of younger mice and they resumed quick movements. Furthermore, the lifespan of the mice who received young ovaries was much longer than that of the control mice: the mice that had received two ovaries lived for an average of 915 days, and the mice that had received one ovary, for an average of 877 days. The newest of our data show the life span of mice that received transplants of young ovaries was increased by more than 40%. The average normal lifespan for this particular breed of mice [is] 548 days. It was not known why the ovarian transplant increased the lifespan of the mice, but it might be because the transplants were prompting the continuation of normal hormonal functions.”

MORE DECELLULARIZED LUNGS DEMONSTRATED (June 28 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4787

Following on from a demonstration of decellularized rat lungs, another team has produced similar work: “Researchers have been able to create tiny mouse lungs in the lab that are able to breathe. The lungs were created with stem cells and attached to a ventilator. They used a technique called decellularization, similar to the method used to create a beating mouse heart in a different lab at the University of Minnesota in 2008. In the cancer center, they took a mouse lung and stripped away all its cells. Then, injected the natural framework with stem cells. At first they used fetal mouse lung cells, but this year they had another breakthrough using adult stem cells called ‘induced pluriopotent stem cells.’ That’s basically a cell that we can take from anybody and re-program to act like an embryonic stem cell. The hope is one day human lungs could be re-created for transplant with a greater chance of success. Right now, there is no tissue matching for lung transplants. The beauty of that is that you can then create a tissue for an organ that’s transplantable that is derived from the patient and therefore would not be recognized as foreign by the immune system and not rejected. By adding the ventilator to make the lungs breathe, the stem cells are further trained to act like lung cells. It’s a huge success considering lungs are such complicated organs with some 60 different kinds of cells.”

______________________________

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/.

David A. Kekich

Maximum Life Foundation

www.MaxLife.org

“Where Biotech, Infotech and Nanotech

     Meet to Reverse Aging by 2029”





The Most Powerful Life Extender of All

7 07 2010

 Dear Future Centenarian,

 For millions of years, we subsisted on a hunter/gatherer diet. That means we ate what we could find and kill. Those diets were actually much more diverse than typical modern diets. Average life spans were quite short due to the harshness and dangers of everyday life. But contrary to popular belief, maximum life spans may have been much longer than we can hope to reach today. And diseases associated with aging were largely unknown.

 Around 10,000 years ago, we entered the Agricultural Age. We started growing crops and domesticating animals. That’s when we started eating grains, and later, dairy products, and we were not adapted to them.

We’re not adapted to agricultural diets now either, because 10,000 years is nothing on the human evolutionary scale. We are still adapted to the hunter/gatherer diet. We’ve been on it for millions of years. We’re also adapted to eating cooked meat and some vegetables, since we’ve been eating those for well over a million years.

By eliminating ALL grains and dairy products from your diet and by being physically active, you may be able to avoid most of the aging-related diseases. The sky is not the limit, but you could slow aging dramatically and may be able to add lots of healthy active years to your life. Find out more by reading Food and Western Disease by Staffan Lindeberg. This may be the single most important book you will ever read, if your goal is extreme longevity. If you’re young now, there is no need to eat this way until you are well over thirty. In fact, it could be counter-productive for children, since adaptation to recent changes drops drastically as we age.

 Most of the seven habits I describe in Life Extension Express can be fairly easy to implement once you grasp the incredible benefits. In fact, they can even be fun, especially once you experience the results. I thought this one would take lots of will power though, at least for me.

 I enjoy a cup of chocolate ice cream every month or so, and I do like cheese. There are fairly good healthy alternatives, even though they’re not quite the same. And although I seldom touch bread, I thought it would be tough to figure out how to replace my oatmeal and whole grain cereals. Well, I was wrong. I even found grainless alternatives to both bread and cereals. For example, you can get ones made from sunflower seeds. See www.LydiasOrganic.com for some tasty substitutes.

 The web is full of recipes for grain-free breads, cereals and pancakes as well as sources and recipes for non-dairy cheeses. And who needs dairy when you can enjoy delicious and nutritious almond milk?

 Sure, a hunter/gatherer diet is not as convenient, especially when you dine out. And it does take some trial and error and more creative grocery shopping. So the question you might ask yourself is, “Is it worth it”?

 The answer is a no-brainer for me. “Yes”! Why? Because it positions you and me better to take advantage of the emerging age-reversal and repair technologies described in Part I of Life Extension Express by extending our average lifespans now. In fact, this may be the greatest life-extender of them all. And yummies like honey, cacao, and avocado, or plants like them, have probably been in our diet for millions of years, so we are not talking total self-denial.

 There’s an additional benefit too, if weight loss is your goal. It’s next to impossible to be overweight if you adopt a hunter/gatherer lifestyle for a protracted period of time.

 Long Life,

David Kekich

____________________________

REGENERATIVE HEALING OF CAVITIES IN TEETH

The dental application of regenerative medicine is one of the more advanced areas in this field of research. Whole teeth have been grown from stem cells in animal studies, and here scientists demonstrate healing of cavities by regrowth of tooth enamel. After about one month, the cavities had disappeared.

 http://www.fightaging.org/archives/2010/06/regeneration-of-tooth-enamel-cavities-healed-in-mice.php

______________________________

 LATEST HEALTHY LIFE EXTENSION HEADLINES

INDUCED PLURIPOTENT STEM CELLS FROM BLOOD (July 02 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4795

From Wired: “Blood drawn with a simple needle stick can be coaxed into producing stem cells that may have the ability to form any type of tissue in the body, three independent papers report. The new technique will allow scientists to tap a large, readily available source of personalized stem cells. Because taking blood is safe, fast and efficient compared to current stem cell harvesting methods, some of which include biopsies and pretreatments with drugs, researchers hope that blood-derived stem cells could one day be used to study and treat diseases. Three research groups used similar methods to prod certain immune cells in human blood to become induced pluripotent stem cells. Because they are reprogrammed adult cells, these stem cells share many of the same regenerative abilities as true embryonic stem cells but may not have as much versatility. Scientists’ manipulations turned the stem cells in the new studies into several types of mature blood cells, including infection-fighting T cells. What’s more, all the groups showed that a batch of the stem cells implanted into mice developed into the three main types of progenitor cells found in human embryos.”

 

IMPROVED ASSOCIATION OF LONGEVITY GENES WITH LONGEVITY (July 02 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4794

Via ScienceNews: “In the new study, researchers looked at genetic markers called single nucleotide polymorphisms, or SNPs, in 1,055 centenarians and 1,267 younger people, all of European descent. The scientists found 150 genetic SNP variants linked to extreme longevity. Initially, the team identified only 33 SNPs found more often in people aged 90 to 114 years but not in a control group made up of people who will presumably live an average lifespan. Biostatistician Paola Sebastiani [devised] a different statistical method to identify additional SNPs that would improve the team’s ability to predict longevity. The team tested their predictions on a separate group of centenarians and controls. With the 150 SNPs, the researchers could correctly predict who was a centenarian 77 percent of the time. Now on one side, 77 percent is a very high accuracy for a genetic model, which means that the traits that we are looking at have a very strong genetic base. On the other hand, the 150 SNPs can’t explain why the remaining 23 percent of centenarians in the study have reached such ripe old ages. It could mean that those people have other, rare genetic variants or lifestyles responsible for their longevity or some combination of the two.”

ORGANS MADE TO ORDER (July 01 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4793

As the Smithsonian notes, “It won’t be long before surgeons routinely install replacement body parts created in the laboratory. Anthony Atala works in the body shop of the future. He and his colleagues use human cells to grow muscles, blood vessels, skin and even a complete urinary bladder. Much of the work is experimental and hasn’t yet been tested in human patients, but Atala has implanted laboratory-grown bladders into more than two dozen children and young adults born with defective bladders that don’t empty properly, a condition that can cause kidney damage. The bladders were the first lab-generated human organs implanted in people. If they continue to perform well in clinical tests, the treatment may become standard not only for birth defects of the bladder but also for bladder cancer and other conditions. Regenerative medicine’s once-wild ideas are fast becoming reality. Late last year, Organovo, a biotech company in San Diego, began distributing the first commercially available body-part printer. Yes, you read correctly: a printer for body parts. Using the same idea as an ink-jet printer, it jets laser-guided droplets of cells and scaffold material onto a movable platform. With each pass of the printer head, the platform sinks, and the deposited material gradually builds up a 3-D piece of tissue. Regenerative medicine laboratories around the world have relied on the printer to generate pieces of skin, muscle and blood vessels. Atala’s lab has used the technology to construct a two-chambered mouse-size heart in about 40 minutes.”

ARE OLD STEM CELLS LESS USEFUL? (June 30 2010)

http://www.longevitymeme.org/news/vnl.cfm?id=4791

Researchers are gathering evidence to suggest that stem cells from the old are less useful when transplanted – which means that some form of repair or other manipulations may need to be included in future stem cell therapies for the degenerative conditions of aging: “Clinical trials of cardiac cell therapy have indicated limited benefits in aging patients, even though preclinical studies using young animals consistently reported significant improvements. Animal studies have demonstrated reduced efficacy of donor cells isolated from older individuals. Here, we evaluated the effects of donor age on the function of human mesenchymal stem cells (hMSCs) in the context of cell therapy for ischemic cardiomyopathy. The regenerative capacity of hMSCs was significantly influenced by age. Transplanting young hMSCs improved functional outcomes after an MI by preventing matrix degradation and promoting angiogenesis. The clinical implication is that aged patients require an optimized source of stem cells for treatment.”

NOTE: There may be a solution on the horizon.

PROGRESS TOWARDS UNDERSTANDING MEMORY (June 29 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4789

Understanding the physical basis of human memory will enable therapies to both enhance youthful memory and reverse its decline with age. From ScienceDaily, an example of present investigations into the biology of memory: “We found one of the key proteins involved in the process of memory and learning. This protein is present in the part of the brain in which memories are stored. We have found that in order for any memory to be laid down this protein, called the M3-muscarinic receptor, has to be activated. We have also determined that this protein undergoes a very specific change during the formation of a memory – and that this change is an essential part of memory formation. In this regard our study reveals at least one of the molecular mechanisms that are operating in the brain when we form a memory and as such this represents a major break through in our understanding of how we lay down memories. This finding is not only interesting in its own right but has important clinical implications. One of the major symptoms of Alzheimer’s disease is memory loss. Our study identifies one of the key processes involved in memory and learning and we state in the paper that drugs designed to target the protein identified in our study would be of benefit in treating Alzheimer’s disease.”

MORE ON OVARIES AND LONGEVITY IN MICE (June 29 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4788

Another study to show that transplanting young ovaries into old mice extends life quite significantly: “successful ovarian transplants increased the lifespan of the mice by more than 40%. All the mice in both experiments that had received transplants resumed the normal reproductive behavior of young mice. They showed interest in male mice, mated and some had pups. Normally, old mice stay in the corner of the cage and don’t move much, but the activity of mice that had had ovarian transplants was transformed into that of younger mice and they resumed quick movements. Furthermore, the lifespan of the mice who received young ovaries was much longer than that of the control mice: the mice that had received two ovaries lived for an average of 915 days, and the mice that had received one ovary, for an average of 877 days. The newest of our data show the life span of mice that received transplants of young ovaries was increased by more than 40%. The average normal lifespan for this particular breed of mice [is] 548 days. It was not known why the ovarian transplant increased the lifespan of the mice, but it might be because the transplants were prompting the continuation of normal hormonal functions.”

MORE DECELLULARIZED LUNGS DEMONSTRATED (June 28 2010) http://www.longevitymeme.org/news/vnl.cfm?id=4787

Following on from a demonstration of decellularized rat lungs, another team has produced similar work: “Researchers have been able to create tiny mouse lungs in the lab that are able to breathe. The lungs were created with stem cells and attached to a ventilator. They used a technique called decellularization, similar to the method used to create a beating mouse heart in a different lab at the University of Minnesota in 2008. In the cancer center, they took a mouse lung and stripped away all its cells. Then, injected the natural framework with stem cells. At first they used fetal mouse lung cells, but this year they had another breakthrough using adult stem cells called ‘induced pluriopotent stem cells.’ That’s basically a cell that we can take from anybody and re-program to act like an embryonic stem cell. The hope is one day human lungs could be re-created for transplant with a greater chance of success. Right now, there is no tissue matching for lung transplants. The beauty of that is that you can then create a tissue for an organ that’s transplantable that is derived from the patient and therefore would not be recognized as foreign by the immune system and not rejected. By adding the ventilator to make the lungs breathe, the stem cells are further trained to act like lung cells. It’s a huge success considering lungs are such complicated organs with some 60 different kinds of cells.”

______________________________

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/.

David A. Kekich

Maximum Life Foundation

www.MaxLife.org

“Where Biotech, Infotech and Nanotech

     Meet to Reverse Aging by 2029”





Genes That Let You Live Beyond 100

30 06 2010

Dear Future Centenarian, 

Bill Andrews sent me an interesting article about life extension. Bill is CEO of Sierra Sciences, where they screen compounds for their effect on activating telomerase. You might remember that telomerase is the enzyme that regulates telomere length, and telomeres are the protective tips of your chromosomes that gradually shorten as your cells divide. Lengthening shortened telomeres appears to reestablish your youth and potentially let you live a lot longer. 

Doing that is a bit tricky, but Sierra Sciences is making progress. A big part of the solution to aging is understanding our genes and influencing their activity. First, it’s necessary to identify the ones which affect aging. 

This month, the New York Post and The Times of London published the article “Found: genes that let you live to 100,” detailing longevity research at Leiden University.

 Leiden University had previously published research on the physiological differences between centenarians and the rest of the population, finding that centenarians metabolize fats and glucose differently than the general population; that their skin ages more slowly; and that they have a lower prevalence of heart disease, diabetes, and hypertension. They also appear to have genetic protection against the effects of smoking and poor diet habits.

 Now, the group has analyzed the genomes of these centenarians and found a suite of genes that are statistically much more common in centenarians than in the general population. The hope is that these genes can be used as drug discovery targets, and that one or more drugs can be developed that will afford us all the same protection against disease and environmental damage that centenarians enjoy. The research itself is due to be published later this year.                        

Many other researchers are identifying aging-related genes as well. Michael Rose at the University of California at Irvine, for example, has already discovered what could be hundreds of them, with more on the way. Next step is developing drugs that tweak them. This step is underway as you read this.

Donate to the Maximum Life Foundation to do your part to advance the field anti aging research.

 Long Life,

David Kekich





A Manhattan Project to “Cure” Aging

26 08 2009

On June 24th and 25th, 2000, Maximum Life Foundation sponsored its first international anti-aging scientific conference in Manhattan Beach, California.

 

Its purpose was to brainstorm ideas that could lead to breakthroughs in extreme life extension medicine. It held conferences the next two years and worked with the dozen participants and other scientists since to develop a scientific roadmap to reverse the aging process. This all-out assault on aging was dubbed the “Manhattan Beach Project”.

 

We now know what needs to be developed to deliver open-ended youth to you and to your loved ones. And we know how to eventually rescue many of the 100,000 people who die every day from aging. We even have an idea as to what it will cost and about how long it might take once we raise the funds.

 

On November 13th-15th, we are going to launch the Manhattan Beach Project.

 

The Project will marshal the best forces of the capitalistic system to not only conquer aging, but it will also lead to full age-reversal. That means, transforming the elderly into twenty-something versions of themselves.

 

Recent breakthroughs tell us this is real—we will reverse the aging process, and researchers have proven the concept with several new scientific approaches.

 

Radically increased lifespans depend mostly on how soon real anti-aging medicine is developed and commercialized.

 

Fourteen of the leading life extension scientists will meet in Manhattan Beach to put the finishing touches on the scientific roadmap to conquer aging. It will not only showcase all the various technologies that need to be developed, but we will fine tune real timelines and real budgets to do it, mostly within the private sector.

 

But that’s just the beginning.

 

The last day of the session will be closed to all except the movers and the shakers of the world.

 

At that private session, successful entrepreneurs; business management experts; ultra wealthy individuals; publicists; marketing gurus; prominent members of the entertainment industry, including athletes; venture capitalists; money managers; politicians and industry leaders will participate in a Longevity Summit master mind session to successfully launch what promises to be one of the most influential events in medical history. We already have a good lineup and are looking for more fabulously successful creative participants. Please let me know right away if you have any candidates. Send an email to info@maxlife.org with your recommendations.

 

I can prove to them that the last nine years of research have shown we are on the verge of either being part of the last generation to suffer and die from aging… or part of the first to enjoy open-ended youth and vitality.

 

Launching this project will mean tomorrow’s age-reversing medical miracles could mature in your lifetime.

_________________________________________

 

LATEST HEALTHY LIFE EXTENSION HEADLINES

 

THE END OF AGING: AN EVENING WITH AUBREY DE GREY (August 21 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4345

Here is something for those of you who will be in the New York area this time next month: “The Singularity Institute for Artificial Intelligence is co-sponsoring a program on ending aging with gerontology researcher Aubrey de Grey and the New York Academy of Sciences, on the evening of Tuesday, September 22nd in New York City. Could it be possible for humans to live hundreds of years in the very near future? Is aging a curable disease? Iconoclast Aubrey de Grey predicts it’s only a matter of decades before regenerative medicine extends human life expectancy indefinitely. This event is one of five events in the 2009 Provocative Thinkers Series presented by Science & the City, a program of the New York Academy of Sciences. Cosponsored by the Singularity Institute.” A large number of de Grey’s past presentations to groups large and small can be found at YouTube – you might want to take a look.

 

NOTE; Aubrey will be one of our key presenters at the November conference.

 

TRENDS IN MINIATURIZATION OF FUNCTIONAL ORGAN REPLACEMENTS (August 21 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4344

A dialysis machine, intended to replace the function of damaged kidneys, might weigh 55kg. Researchers now have that down to 5kg in a wearable form, a machine which does a better job to boot. Looking ahead, we’d expect even more effective implants or bracelets worn over surface veins in the 2020s – essentially viable artificial replacements for the function of an organ. This is an important trend to watch, as I believe it will ultimately contribute to enhanced longevity just as greatly as regenerative medicine: “Our vision of a technological breakthrough has materialized in the form of a Wearable Artificial Kidney, which provides continuous dialysis 24 hours a day, seven days a week. The device – essentially a miniaturized dialysis machine, worn as a belt – weighs about 10 pounds and is powered by two nine-volt batteries. Because patients don’t need to be hooked up to a full-size dialysis machine, they are free to walk, work, or sleep while undergoing continuous, gentle dialysis that more closely approximates normal kidney function. We believe that the Wearable Artificial Kidney will not only reduce the mortality and misery of dialysis patients, but will also result in significant reduction in the cost of providing viable health care.”

 

CATALASE IN THE MITOCHONDRIA VIA VIRUS (August 20 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4343

Mitochondrially-targeted antioxidants – such as catalase – have been shown to extend life span in mice. Here is a method of using catalase that employs a viral vector: “Earlier studies have found that mice would live longer when their genome was altered to carry a gene known as mitochondria-targeted catalase gene, or MCAT. However, such approaches would not be applicable to human. Duan and Dejia Li [took] a different approach and placed the MCAT gene inside a benign virus and injected the virus into the mice. Once injected, Duan and Li tested the mice and found that they could run farther, faster and longer than mice of the same age and sex. Duan attributes this performance enhancement to the MCAT and believes the gene is responsible for removing toxic substances, known as free radicals, from the mitochondria, the powerhouse of the cell. By using this specific gene therapy vector, the virus, to introduce the longevity gene, Duan and Li opened the possibility of human treatment. Our results suggest similar therapy may one day improve the life quality of the elderly. This could have important implications for many diseases, such as muscular dystrophy, heart disease, diabetes and neurodegenerative diseases. These patients typically have too many toxic free radicals in their cells.”

 

LIKE CLOCKWORK (August 20 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4342

Mainstream press articles on increasing life expectancy arrive on a schedule like clockwork: “U.S. life expectancy has risen to a new high, now standing at nearly 78 years. The increase is due mainly to falling death rates in almost all the leading causes of death. The average life expectancy for babies born in 2007 is nearly three months greater than for children born in 2006. Life expectancy is the period a child born in

2007 is expected to live, assuming mortality trends stay constant. U.S. life expectancy has grown nearly one and a half years in the past decade, and is now at an all-time-high. Japan has the longest life expectancy – 83 years for children born in 2007, according to the World Health Organization. The CDC report found that the number of deaths and the overall death rate dropped from 2006 – to about 760 deaths per 100,000 people from about 776. The death rate has been falling for eight straight years, and is half of what it was 60 years ago. Heart disease and cancer together are the cause of nearly half of U.S. fatalities. The death rate from heart disease dropped nearly 5 percent in 2007, and the cancer death rate fell nearly 2 percent, according to the report.” Life expectancy is a statistical construct that looks back into the past to measure trends; it doesn’t actually have anything to say about how long people born today are likely to live. This, after all, is an era of great change and progress in biotechnology.

 

SUPERLONGEVITY, SUPERINTELLIGENCE, SUPERABUNDANCE (August 19 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4341

From Accelerating Future, thoughts on goals: “Superlongevity, superintelligence, and superabundance are a perfect summary of what we want and need. How can we achieve them? Superlongevity can be achieved by uncovering the underlying mechanisms of aging and counteracting them at the molecular level faster than they can cause damage. Huge research project, a long-term effort, but definitely worth the time and money. Leading organization in this area? The SENS Foundation. Superintelligence will be a difficult challenge, creating an intelligent being smarter than humans in every domain. It could take decades, or possibly longer, but it does seem possible. Superabundance can be achieved by creating programmable self-replicating machines powered and supplied by easily available resources and materials. Achieving superlongevity, superintelligence, and superabundance will be incredibly challenging, but seemingly inevitable as long as civilization continues to progress. There is no guarantee that we will achieve these goals in our lifetime – but why not try? Achieving any of these milestones would radically improve quality of life for everyone on Earth. The first step to making technological advancements available to everyone is to make them available for someone.”

 

SEEKING AN APPLICATION OF KLOTHO (August 19 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4340

Researchers are looking for ways to apply knowledge of the longevity gene klotho for medical benefit: “A newly-discovered anti-aging gene could be manipulated to stop or even prevent high blood pressure, a leading contributor to early death. Persistent high blood pressure, also called hypertension, can lead to stroke, heart attacks and kidney failure. About one-third of Americans struggles with the condition. An anti-aging gene called klotho decreases as humans age while hypertension tends to increase. Increasing the expression or output of the gene in lab animals reduced blood pressure and reversed kidney damage from hypertension. Sun said testing on humans is the next step, and it would be years before a therapy could be sold. All of us will be and should be extremely hopeful this can occur. It’s possible the therapy could protect other organs – such as the brain and eyes – from conditions related to aging.” This is all pretty speculative beyond the fact of the animal study results – and for most people lifestyle conditions like hypertension are very avoidable. Lead a fat, sedentary life, and don’t be surprised when your body starts to fail more rapidly than those who kept fit or practiced calorie restriction.

 

GROWING NEW CORONARY ARTERIES (August 18 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4339

Scientists continue to experiment successfully with the use of stem cells to engineer regeneration: “researchers have identified stem cells that are able to grow new coronary arteries, a finding that could lead to new ways to treat atherosclerosis. We have defined this novel class of primitive cells and named them coronary vascular progenitor cells [CVPCs]. These cells possess all of the fundamental properties of stem cells and are distributed within niches located in the vessel wall of the entire human coronary circulation system. To test the activity of these cells, the scientists created a blockage in a coronary artery in dogs and injected human CVPCs in the blocked artery. After one month, the dogs showed improvements in blood flow and heart functioning. The researchers found that the dogs had grown large, intermediate and small human coronary arteries. The findings suggest that the human heart contains a reservoir of CVPCs that can be used to create a biological bypass in patients with chronic coronary artery disease and ischemic cardiomyopathy, which results when arteries that supply blood and oxygen to the heart are blocked.”

 

A VIEW OF LONGEVITY SCIENCE FROM THE MAINSTREAM (August 18 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4338

To the man in the street and mainstream journalism, medical science is nothing more than drug development – an unfortunate and blinkered viewpoint. Here is that viewpoint turned to regard research into metabolic manipulation to slow aging: “It may be the ultimate free lunch – how to reap all the advantages of a calorically restricted diet, including freedom from disease and an extended healthy life span, without eating one fewer calorie. Just take a drug that tricks the body into thinking it’s on such a diet. It sounds too good to be true, and maybe it is. Yet such drugs are now in clinical trials. Even if they should fail, as most candidate drugs do, their development represents a new optimism among research biologists that aging is not immutable, that the body has resources that can be mobilized into resisting disease and averting the adversities of old age. This optimism, however, is not fully shared. Evolutionary biologists, the experts on the theory of aging, have strong reasons to suppose that human life span cannot be altered in any quick and easy way. But they have been confounded by experiments with small laboratory animals, like roundworms, fruit flies and mice. In all these species, the change of single genes has brought noticeable increases in life span.”

 

FOR THOSE WHO WANTED TO KNOW MORE ABOUT GENESCIENT (August 17 2009)

http://www.longevitymeme.org/news/vnl.cfm?id=4336

I notice that Genescient’s newly relaunched website is up and running, and provides much more information as to what the company is up to: “Our focus is to extend healthy human lifespan by using advanced genomics to develop therapeutic substances that attack the diseases of aging.  We are the first company founded to exploit artificial selection of animal models for longevity. Our extremely long-lived animal models (Drosophila melanogaster) have been developed over 700 generations. They are an ideal system for the study of aging and age-related disease because Drosophila metabolic genetic pathways that are highly conserved in humans. Our sophisticated analysis cross-links gene function in Drosophila with their human orthologs, thus revealing the targets for therapeutic substance development.  To date we have discovered over 100 of these genomic targets, all related to the primary diseases of aging. This large library of targets, enables Genescient to effectively select and test therapeutic drug candidates.  To date, Genescient’s ‘proof-of-concept’ testing program has yielded a number of very promising therapeutic substances.”

 

NOTE: Genescient and their underlying science will be represented at the November conference as well.

______________________________

 

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/.

 

David A. Kekich

Maximum Life Foundation

www.MaxLife.org

 

“Where Biotech, Infotech and Nanotech

     Meet to Reverse Aging by 2029”





Your Perfect Cure Is Prevention

2 03 2009

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.
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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.