A Users Guide To Immortality

A Users Guide To Immortality

Enquiry into the evolution of aging aims to explain why almost all living things weaken and die with age. There is not yet agreement in the scientific community on a single answer. The evolutionary origin of senescence remains a fundamental unsolved problem in biology.

Historically, aging was first likened to "wear and tear": living bodies get weaker just as with use a knife's edge becomes dulled or with exposure to air and moisture iron objects rust.
How to Keep Your Muscles Strong as You Age

Experts Are Looking Into Promising Treatments for Muscle Decline. But There Are Things You Can Do About It Now

Muscle strength is one of the keys to healthy aging, yet after we achieve peak mass in our early 40s, it's pretty much downhill from there. Most people begin to lose modest amounts of muscle at that point and experience progressive deterioration as the years go by, especially if they are sedentary.

Now, with a growing population of aging baby boomers, experts are turning their attention to interventions to help stem the loss of muscle mass, quality and strength, known as sarcopenia. It is caused by a number of complex factors that are not entirely understood, including decreasing amounts of testosterone in men. Muscle decline often goes hand in hand with frailty, a decline of physical function that leads to falls, hospitalization and the need for nursing-home care.

Researchers are looking at promising treatments including inhibiting a naturally occurring protein called myostatin that curbs muscle growth. Pharmaceutical companies already have drugs in the pipeline that act by blocking myostatin or blocking the sites where it is detected in the body, potentially rebuilding muscle.

For now, however, the best medicine available to maintain muscle mass and strength is less complicated and costly—namely, exercise and a healthy diet. Yet about 60% of people over 65 are insufficiently active or overtly inactive, and many have poor nutrition, says Nathan LeBrasseur, a researcher who directs the Muscle Performance and Physical Function Laboratory and the Healthy Aging and Independent Living Initiative at Mayo Clinic in Rochester, Minn. Dr. LeBrasseur estimates that most people will lose approximately 30% of muscle mass over their lifetime, and as much as 50% by the time they reach their 80s or 90s.

Keep Your Motor Running

Muscle is also central to metabolism, or the rate at which fat and calories are burned, and can help improve resiliency to the stressors of aging, Dr. LeBrasseur says. By simply stepping up activity like walking, gardening and household tasks, "we can slow the loss and prevent crossing that critical threshold that leads to functional limitations and metabolic issues."


Chronic diseases such as diabetes, which inhibits the metabolism of nutrients in the body, are believed to contribute to age-related muscle loss, and older obese individuals with decreased muscle mass or strength are at special risk for adverse outcomes, according to research funded by the National institute on Aging. Related conditions include cachexia, a state of general physical decline and malnutrition associated with chronic disease and cancer, and wasting disorders that can be associated with nerve disease or injury.

There is still debate about how best to define and measure sarcopenia, and doctors caring for the elderly may not even be aware of the term, which was derived from Greek words for poverty of the flesh and was introduced in the late 1980s. Researchers have a better handle on frailty, a syndrome of decreased strength reserves, reduced resistance to physical and psychological stressors, and cumulative decline across multiple systems of the body, including the brain. A number of frailty scales are available to help doctors evaluate patients.

Jeremy Walston, a professor of geriatric medicine and co-director of the Biology of Healthy Aging program at Johns Hopkins University's Center on Aging and Health, says a major goal of research is to understand the complex interplay of molecular and physiological declines in multiple systems of the body with advancing age—a mix that may increase general vulnerability in frail, older adults. His team is studying changes in mitochondria, the energy-generating components of cells, and the impact of chronic inflammation in the body.

The Johns Hopkins researchers are also studying whether the drug losartan, commonly used to treat high blood pressure, can slow muscle decline in adults 70 and older, after promising results in mice.

More Protein

In addition to the mounting evidence of the benefits of physical activity in stemming decline, Dr. Walston says there is an emerging body of research that suggests older people should eat more protein, with a focus on leaner sources.

According to guidelines published in 2010 by the Society on Sarcopenia, Cachexia and Wasting Disorders, a nonprofit group, as many as 41% of women and 35% of men age 50-plus ingest less than the recommended daily allowance of 0.8 grams of protein per kilogram of body weight (0.36 grams per pound). The group recommends that total protein should be higher in that age range, or 1 to 1.5 grams per kilogram per day (0.45 to 0.68 grams per pound), spread equally through three meals.

The group also says low vitamin D levels are associated with low muscle strength, and supplementing it in those cases has been shown to increase strength and function and reduce falls. But it's best to talk to a physician before starting any supplements such as protein or vitamin D.

As for exercise, the group notes that resistance exercises can improve strength, while aerobic exercise can improve overall health and quality of life. The group recommends a combination of the two for 20 to 30 minutes three times a week.

Building Up Reserves

Evidence continues to show the benefits of exercise at any age. Last month, a study in the Journal of the American Medical Association found that an exercise program reduced the onset of major disability for at-risk older adults by 18% over about 2½ years. The study, the largest of its kind, was conducted by a consortium of major aging research centers and funded by the federal government.

Known as the LIFE study—for Lifestyle Interventions and Independence for Elders—it compared a supervised, moderate-intensity physical activity program with a health education program on aging in 1,600 sedentary older adults. The activity portion included aerobic, strength, flexibility and balance training, based on individual levels of fitness, while the education arm had only limited focus on physical activity.

The study defined major mobility disability as the inability to walk 400 meters within 15 minutes without sitting, leaning against a wall, or getting assistance from another person or walker. Roger Fielding, a co-author of the study and director of the Nutrition, Exercise Physiology and Sarcopenia Laboratory at Tufts University, says the study shows that "even as we advance into very old age, physical activity can help preserve independence." The study group hopes to follow the subjects for three more years to gauge longer-term benefits.


There is some inevitability to declining strength and muscles in aging, "but whatever we can do to mitigate that by building up the health reserve can pay off in dividends later," says Karen Bandeen-Roche, another researcher at the Johns Hopkins aging center. "We can't say frailty can be prevented in all people, but we can compress it to a smaller proportion of the end of life."


Prospects For Extending Healthy Life - A Lot
 

But this idea was discredited in the 19th century when the second law of thermodynamics was formalized. Entropy (disorder) must increase inevitably within a closed system, but living beings are not closed systems. It is a defining feature of life that it takes in free energy from the environment and unloads its entropy as waste.




Living systems can even build themselves up from seed, and routinely repair themselves. There is no thermodynamic necessity for senescence. In addition, generic damage or "wear and tear" theories could not explain why biologically similar organisms (e.g. mammals) exhibited such dramatically different life spans.
Furthermore, this initial theory failed to explain why most organisms maintain themselves so efficiently until adulthood and then, after reproductive maturity, begin to succumb to age-related damage.

THE IMMORTALISTS - A Short Film By Jason Silva

Aging has been slowed and healthy lifespan prolonged in many disparate animal models (C. elegans, Drosophila, Ames dwarf mice, etc.). Thus, assuming there are common fundamental mechanisms, it should also be possible to slow aging in humans. 



Greater knowledge about aging should bring better management of the debilitating pathologies associated with aging, such as cancer, cardiovascular disease, type II diabetes, and

Alzheimer's. Therapies targeted at the fundamental mechanisms of aging will be instrumental in counteracting these age-related pathologies.






Seniors Hound Doctors For A Chance To Participate In New Anti-aging Study

What if there were a way to stave off the creaks and calamities of old age? Nir Barzilai, director of the Institute for Aging Research at the Albert Einstein College of Medicine, is working on it.

With word leaking out, seniors from all over the globe have been hounding Dr. Barzilai and his colleagues to get in on the action—with many writing to prove their worthiness. Never mind that formal patient recruitment is still perhaps a year away.

One 71-year-old sent a photo of himself along with a note: “still do 100 push ups every day!” A retired engineer disclosed his schedule: “Completing 2 crosswords a day; walking for 30-45 minutes daily; playing the piano for one hour a day; consuming 1000 mg of turmeric.”

“I constantly worry, how long will I be able to work; will I ever be able to retire and will I be able to care for myself when I’m older?” another prospective volunteer wrote.

“All humankind is waiting and watching,” wrote a 76-year-old who teaches “Introduction to Twitter” at a senior center in Las Vegas.

Would-be participants—from Cherry Hill, N.J., the Four Corners area of New Mexico, the Netherlands and beyond—have inundated Dr. Barzilai with calls and letters. Other researchers in the project have been swamped as well.

Behind the mania is a widely used, inexpensive generic pill for Type 2 diabetes called metformin. Scientists are planning a clinical trial to see if the drug can delay or prevent some of the most devastating diseases of advanced age, from heart ailments to cognitive decline to cancer. To test the pill, gerontologists at 14 aging centers around the U.S. will follow 3,000 seniors for six years. Half the seniors involved would get the drug, while the others would receive a placebo.

“Clearly we have tapped into something that is fundamental to humanity,” said S. Jay Olshansky, a professor at the school of public health at the University of Illinois at Chicago who is also involved in the project.

Dr. Olshanksy hasn’t seen this kind of patient interest in a medical study. “You are never contacted by the public, ever,” he said.

Medical researchers often practically have to beg for volunteers, and sometimes offer them big money. A plea for subjects for a National Institute on Aging-funded sleep study, for instance, makes participation sound fun. “37-day Sleep Research Study! Needs Healthy Participants Ages 55-70!” Participants “receive up to $10,125,” the notice says.

The metformin study has a more natural appeal, acknowledges Dr. Olshansky. “We’re talking about the most valuable commodity on earth: life itself.”

Senior sleuths have dug up his cellphone number and called it repeatedly. “What’s your story?” the doctor asked a California man who kept phoning. The caller, a 70-year-old entrepreneur, told the doctor he is enjoying life and doesn’t want it to end.

A few people said they craved significant life extensions—complete with retirement benefits. “The thought of living on until 120 years old fills me with great excitement, and also the thought of drawing my pensions until then would be an amazing gift,” a 71-year-old British man wrote.

Others seem motivated by their dread of an emotionally and financially challenging decline. “It’s not so much a fear of dying, it’s a fear of living in pain and agony and being a burden to everyone else and my wife and so forth,” said Bill Thygerson, 70, a retired missile-systems engineer.

Many who raised hands, including Mr. Thygerson, of Huntsville, Ala., already live carefully. He has cut way down on sugar and red meat. He’s a gym regular. A few years ago, he got back to his college weight. (“I did have three vegan cupcakes for my daughter’s birthday,” he confessed.)

While life expectancy has increased dramatically in the last century, aging also boosts one’s chance of developing cancer, Alzheimer’s, heart disease and more.

Gerontologists’ interest in metformin dovetails with research by the U.S. National Institutes of Health, which is also testing ways to postpone or prevent debilitating and costly conditions. The idea behind the effort is to target pathways in the body, at the molecular level, that when defective can trigger chronic disease or death, said Rafael de Cabo, chief of the agency’s Translational Gerontology Branch.

In the past dozen years, his lab and others identified multiple compounds, including metformin, that affect these pathways and have led to a healthier old age, and in some cases longer life, in mice.

Researchers consider metformin the best choice of the bunch to try first on humans because of its history of causing little to no side effects.

Also encouraging the researchers: A large British study, published in 2014, reported that older diabetics on metformin on average lived longer than their healthier peers.

The team planning the U.S. study is working to raise about $64 million. No pharmaceutical company is involved, and none of the doctors have a financial stake in the pill.

“I just think we need to think out of the box,” said Vicki Hayes, a 61-year-old retired school principal in Wilmington, N.C., who asked to volunteer for the clinical trial. She may be out of luck: researchers are planning to select subjects between the ages of 65 and 79.

Some prospective participants have already had brushes with an illness. “You don’t think about mortality until something like that hits you straight in the face,” Randolph von Gans, of Marbella, Spain, said by phone. The 72-year-old semi-retiree relishes the outdoors and socializing, and recalled feeling somewhat “shattered” during a setback from a blocked coronary artery.

Even Dr. Olshansky’s older sister is nudging him to get her into the study. (He instructed her to write a letter, same as the other wannabes.)

The sister, 64-year-old Arlene Schultz, did just that. She shared her concerns during a phone call, during which she was simultaneously walking on a treadmill.


“I don’t want to look old. I don’t want to feel old,” said Ms. Schultz, a retired skin care technician who lives in Farmington Hills, Mich. “I’m trying my darndest to fight it.”

Eliminating Cancer With Nanotechnology

Therefore, this blog is a call to action for greater funding and research into both the underlying mechanisms of aging and methods for its postponement. Such research may yield dividends far greater than equal efforts to combat the age-related diseases themselves. 


Personalized Medicine

Drugs Tailored to your Genetic Makeup 

Personalized Medicine: Using an individual’s own genetic information to guide better treatment and prevention of diseases—is one of the most talked-about areas in healthcare. To understand how personalized medicine may play out in real life, consider a frequent traveler whose business takes him or her to Asia, South America or Africa. In all of those places, mosquitoes spread dengue fever—a rapidly-growing, infectious tropical disease for which there is no vaccine.

People who contract dengue fever can have a wide range of reactions. A fortunate few develop no symptoms at all. Others experience a week of flu-like symptoms—high fever, vomiting, headaches, muscle pain or a measles-like rash. However, a small number of people develop a life-threatening variety known as dengue hemorrhagic fever. Diagnosing and treating the disease quickly, especially the more severe variety, has always been challenging for doctors.

How does this relate to personalized medicine? Allan Brasier, director of the Institute for Translational Sciences at the University of Texas Medical Branch (UTMB), led a team that identified protein markers that may be able to predict a predisposition toward developing dengue fever and dengue hemorrhagic fever. In the future, these markers could guide physicians to take earlier steps with those who show symptoms and are at high risk for the more serious strain of the disease. They could receive transfusions and other early intervention strategies that could save more lives.

This has been the goal of personalized medicine since the human genome was first sequenced in 1993. “Personalized medicine could eliminate the trial-and-error approach of giving every patient with the same disease the identical drugs or treatment,” Brasier says. “We can identify subgroups that have the same disease and can be targeted for different treatments based on their genetic information.” The goal is to avoid wasting time and money on potentially ineffective treatments, which expose many patients to harmful side effects.

Collaborations Provide Major Advance in Cancer Treatment

Researchers may have solved a puzzle about which patients will
benefit from immunotherapy

A collaboration between an immunologist helping his stepmother fight cancer and the oncologist who treated her led to a discovery that could help many more patients benefit from a transformative new therapy.

A new class of drugs called checkpoint inhibitors works by releasing a molecular brake that stops the immune system from attacking tumors. So-called immunotherapy has been approved for several types of cancers and found to extend lives of patients with advanced disease for many years. The problem is that for most patients immunotherapy
doesn't work.

The researchers, from University of California, San Francisco, said
they identified a unique type of immune-system cell that "robustly"
predicts whether patients will respond to one of the medicines-an
achievement has the potential to significantly expand the number of
cancer patients who benefit from checkpoint inhibitors.

The new discovery is based on a high-tech analysis of melanoma tissue from 40 patients treated with a checkpoint inhibitor from Merck And Co. called Keytruda, which targets an immune-system brake called PD-1. Although researchers say it will take further research to determine its value in treating patients, the finding offers fresh insight into the complex relationship between the immune system and tumor cells.

"This tells us a lot of important biology," said Jedd Wolchok, chief
of the melanoma and immunotherapies service at Memorial Sloan
Kettering Cancer Center, New York, who wasn't involved with the
research. "It fits with many hypotheses many of us have had about who these treatments work best in." A report on the finding was published online August 15 in the Journal of Clinical Investigation.

The discovery might not have occurred at all had two researchers not met. In 2012, Michael Rosenblum, a physician-scientist who runs a basic-science immunology lab at UCSF, learned his stepmother, Jackie Rosenblum, now 65, had been diagnosed with a rare form of advanced melanoma in her lung, a recurrence of cancer that originally appeared as a skin lesion and had been removed a few years earlier. She was given six months to live.

Dr. Rosenblum had heard about Adil Daud, another UCSF clinical
researcher who was treating patients with skin cancer, and the
exciting results Dr. Daud was seeing in clinical trials with
checkpoint inhibitors. "I cold-called him," Dr. Rosenblum says. The
two men were both in UCSF's dermatology department, although Dr. Rosenblum interest is in inflammatory skin diseases, not cancer.

After initial conversations between the two researchers, Ms.
Rosenblum flew in from her home in North Carolina to see Dr. Daud. He treated her initially with Yervoy, a checkpoint inhibitor marketed by Bristol-Myers Squibb Co. that targets an immune-system brake called CTLA-4. She stopped taking it after developing colitis, one of that drug's potential serious side effects.

In June 2013, Dr. Daud enrolled her in a clinical dose-escalation
trial in which she would be treated with Merck's Keytruda, then known as pembrolizumab.

The two scientists' collaborated on research that focuses on PD-1, a
protein that appears on the surface of immune cells and the target of
the two most popular checkpoint drugs, Keytruda and Bristol-Myers's Opdivo. A biomarker for PD-1 already exists but it has limitations: Patients whose tumors have high levels of a PD-1 related protein called PD-L1 appear to have a better response to therapies targeting PD-1. But some patients with low PD-L1 levels also benefit-meaning that it can help guide some treatment decisions but isn't useful for ruling out anti-PD-1 therapy.

Dr. Rosenblum's lab had developed a technique for analyzing immune cells in tumors and other tissue that he says is more comprehensive than conventional methods. At the beginning of their collaboration he invited Dr. Daud to "send me some samples."

The prevailing theory of how checkpoint inhibitors work is based on evidence that immune-system fighters called CD8 cells, which are normally primed to kill enemy cells, initially see and infiltrate
tumors but can end up in a state of chronic activation, too exhausted to mount an effective attack.

Using the lab's laser-based flow cytometry technology, Dr. Rosenblum and his colleagues identified a candidate CD8 cell that had infiltrated tumors marked by levels of not only PD-1 but also of a second immune-system brake called CTLA-4.

The researchers analyzed results of a study involving Keytruda before it was approved. They looked at the CD8 cells that had infiltrated the melanoma tumors of 20 patients treated with the drug and found that if at least 30% of those cells were marked by PD-1 and CTLA-4, the patient responded to treatment. When fewer than 20% of the infiltrated cells had those markers, not one patient responded.

They did a second similar study on 20 more patients and got the same result. Results varied for patients whose CD8 cells fell between 20% and 30%, making them prime candidates, Dr. Daud suggested, for a combination immunotherapy regimen to potentially increase their chances of a response.

Further analysis showed that the anti-PD1 drug reactivated the
exhausted CD8 cells, and when they were in sufficient numbers, they were able to mount an effective attack on the tumor.

Memorial Sloan Kettering's Dr. Wolchok called the study "a really
important piece of work," but cautioned that among other things, it
needs to be further validated in more patients. Dr. Rosenblum
acknowledged that few hospitals or labs are equipped to perform the analysis, suggesting further work is necessary for it to be easily
adapted to patient care.

But the findings did show that the particular CD8 cells identified
"are the guys that are doing all the work to kill the tumor," Dr.
Rosenblum noted. Researchers are already exploring whether it's
possible to retrieve such cells from the tumor, expand them into huge quantities outside the body and infuse them back into
patients-possibly using a PD-1 inhibitor-to increase the number of
patients who respond.

As for Ms. Rosenblum, 12 weeks after she began treatment with
Keytruda, a CT scan showed that her tumors had shrunk by 70%. She recalls Dr. Daud delivering the news to her by phone while she was on a train. He told her she was "a golden child"; she burst into tears. Her tumors ultimately disappeared. She stopped treatment in June of 2014, about a year after she started, and remains free of any
evidence of disease.

Genomics and Disease

Clay Marsh, M.D., executive director of the Center for Personalized Health Care at The Ohio State University Medical Center, explains the leading uses for personalized medicine so far have been treatments for cancer and infectious diseases, along with better targeting of pharmaceuticals.

“Cancer is the most clinically applicable domain of genomics in medicine today. A cancer cell is clearly identifiable as the problematic cause of the disease and genetic profiling has identified key cellular pathways to target with specific drugs. Similarly, infectious disease cells can also be genetically fingerprinted for a specific disease, and this is the next exciting application of genomics. Other diseases are proving to be more complex to fingerprint.”

Currently, there are an estimated 300 Phase II or higher oncology drugs that are being developed which have the potential for testing against a genetic biomarker. Right now, molecular testing is helping identify which patients with breast cancer and colon cancer are likely to benefit from different treatments.

For example, a gene expression test has been developed that can help determine which patients with breast cancer might benefit from chemotherapy. Joseph Sparano, M.D., associate chairman of the department of oncology at Montefiore Einstein Center for Cancer Care in New York, says the test measures the activity level of a panel of genes within the tumor sample, and the result correlates with the likelihood of having breast cancer recurrence.

Because of this information, doctors can identify a subset of patients who are likely to be cured with surgery and hormonal therapy alone, sparing them the need to undergo chemotherapy after surgery. Clinical trials are underway to help guide treatment of the 25 to 50 percent of patients who fall into the “gray” area—the intermediate risk category—for which the best course of action is unclear.

Personalized Prescriptions

Pharmacogenomics, the science of how a person’s genetics affects how they respond to certain medications, is another key area of personalized medicine. Variations in DNA affect how an individual’s body absorbs, metabolizes and uses drugs.

Michael Christman, Ph.D., president and chief executive officer of the Coriell Institute for Medical Research, a nonprofit biomedical research institution in Camden, N.J., points to clopidogrel, a medication that is prescribed after someone has a heart attack or stent placement.

“Up to 30 percent of people prescribed the medication do not activate the drug, and may as well take sugar pills,” he says. “However, there is an alternative FDA-approved drug, and if genetic testing were performed for the patient prior to dosing, the best drug could be selected first.”

This is hardly an isolated example. Personalized medicine has the potential to assist the large number of people who are prescribed medication that provides them no benefit because of their individual genetic response.

“Right now, we know that one-third of the people who receive a drug get a positive response, one-third get no response, and one-third get a toxic response,” says Jonathan S. Dordick, Ph.D., director of the Center for Biotechnology and Interdisciplinary Studies at the Rensselaer Polytechnic Institute. “By tailoring drugs to the physiologic of the person, we can change the number of people who get a beneficial response from one-third to two-thirds. And we can reduce the negative reaction from one-third to one-sixth.”

That means fewer trial-and-error prescriptions and a steep drop in the number of adverse drug reactions, which cause more than 770,000 injuries and deaths a year in the U.S.

Faster Time to Market

Genetic information could also provide benefits in how new drugs are developed. Dordick points out that pharmaceutical companies now focus on developing drugs that have a large enough potential to generate $1.5 billion to $2 billion in revenues. That’s primarily because the complex drug approval and clinical trial process is so costly.

The promise of personalized medicine is that instead of developing, say, one drug for asthma, a pharmaceutical company could develop five different versions of the drug designed for different populations based on their genetics.

However, one issue is that each of these five versions, under the current drug development framework, would need to undergo the expensive drug approval and testing process. That may not be cost effective since the testing costs would increase fivefold, but the amount of revenue the five drugs generate in total would not be five times that of a single version of the drug.

Dordick envisions new testing techniques that would make it more viable to develop a series of drugs for genetic subgroups of patients. For one thing, he suggests eliminating the initial step of testing a drug’s efficacy on rats or dogs—the idea is that if human genetics are so dissimilar that not every drug will work with every human, there is no reason to spend time and money testing the drugs on biologically dissimilar creatures.

Instead, researchers could leverage new technologies that test the toxicity and effectiveness of new drug molecules using individual human cell cultures. In essence, at some point, a doctor could test how effectively a drug would work for you by testing your own cells. If such tools were integrated into the drug approval process, Dordick says they could speed the process, reduce the costs, and weed out unsafe or ineffective drugs early in the process.

“If you are giving a drug to a specific set of the patient population, you can get very high quality candidates for testing and shave a tremendous number of years off the development,” he says. “Because the limited number of patients can be more easily classified, you will be able to use hundreds of patients in the clinical trials rather than thousands of patients.”

Inventing the Rules

At the same time, medical practitioners say that safeguards need to be put in place for how to use the evolving information about genetics in treatment. The Coriell Institute uses a scientific advisory panel composed of physicians, scientists and ethicists called the Informed Cohort Oversight Board (ICOB) to help determine what genetic variants will be used in guiding treatment for different diseases.

“We generate and present risk information to the ICOB panel that independently judges its validity. We abide by the panel’s expert decisions, even when they disagree with our recommendations,” Christman says. For example, research done by the Institute identified a genetic risk variant for breast cancer. The researchers thought the variant could be useful in determining which women should receive a mammogram at an early age. However, an oncologist on the advisory panel noted the increased radiation risk from the earlier mammograms outweighed the predictive value of the genetic information.

As all this suggests, there are many questions about how to best integrate genetic information into the treatment of patients. Personalized medicine has huge promise, but it also brings up issues such as healthcare, payer and physician incentives, medical record privacy, and the ethics of clinical trials that will need to be worked through.

“This has happened so quickly,” says Brenda Finucane, a certified genetic counselor and president of the National Society of Genetic Counselors (NSGC). “We have the genetic technology before we have evidence-based models on how to use the technology. This is very different than other developments in medicine, where you had time to think about it for a while and developed evidence-based medicine. We don’t have time, so we are developing practice guidelines on the fly. Patients and healthcare providers will all be learning together as this gets rolled out.”

As the mechanisms of aging are increasingly understood, increasingly effective interventions can be developed that will help prolong the healthy and productive lifespans of a great many people.

Transending Human Capabilities

Transhumanism is an international intellectual and cultural movement that affirms the possibility and desirability of fundamentally transforming the human condition by developing and making widely available technologies to eliminate aging and to greatly enhance human intellectual, physical, and psychological capacities. Transhumanist thinkers study the potential benefits and dangers of emerging technologies that could overcome fundamental human limitations, as well as study the ethical matters involved in developing and using such technologies. They predict that human beings may eventually be able to transform themselves into beings with such greatly expanded abilities as to merit the label "posthuman". 

Bone Marrow Stem Cells

You have within you a powerful set of tools to repair your body and keep you healthy. The future of medicine is NOT better drugs but better use and application of your body’s own stem cells. As of now stem cell-rich tissue can be extracted from your hip with virtually no discomfort and used to help restore your body. This opens up an exciting new horizon in terms of preventing and treating disease and tackling the symptoms of aging – if not aging itself. Already, patients are returning to Dr. Steenblock for additional bone marrow treatments because they are seeing that their gray or white hair is turning back to its original color. Their skin not infrequently looks younger too and they report having more energy and less arthritic aches and pains! 

In regard to its anti-aging effects, the bone marrow contains primitive progenitor cells that are associated with the early development of the fetus. These primitive cells reside dormant deep inside your bones and sport a genetic profile from your early development. When these primitive cells are released into your system, there can be a revitalization of your body that physiologically “sets the clock back” in-a-way. Several patients have reported that the bone marrow transplants have also improved their sexual performance. This side effect is thought to be the result of stem and progenitor cells repairing sex organs as well as other tissues.

What does this mean for you? Your bone marrow stem cells have the potential to repair damaged tissues and organs. Whether you want an “anti-aging” treatment or you need the procedure to repair damage in your joints, liver, kidneys, heart or brain, a bone marrow transplant is an efficient and sure way to flood your body with stem cells.

Simple Tests Determine How Long You'll Live

The Power of Knowing

Telomere length is one of the best biomarkers of overall health status. It is a major "integrator" of current and lifelong factors that impact health, including genetics, diet, fitness, toxins, and chronic stress. Knowing your telomere length (and monitoring changes over time) can provide valuable information on your disease risk – or even the rate at which you are aging. With this information, you have the knowledge to change the quality of your life and health status at a cellular level. 

The Power of Change

Telomeres are the only "changeable" part of the genome, and positive lifestyle choices can increase telomere length and promote individual wellness. Your Cells are Your Guide to Personalized Solutions for Optimal Health Monitoring your telomere length over time can provide insights about potential disease risk and your rate of physiological aging. This knowledge can help to inform your lifestyle and, eventually, as research reveals more specific applications, it may also help inform therapeutic or prophylactic drug choices and decisions. 

"Knowing whether our telomeres are a normal length or not for a given chronological age will give us an indication of our health status and of our physiological 'age' even before diseases appear," says Maria A. Blasco, who heads the Telomeres and Telomerase Group at the Spanish National Cancer Research Center and who co-founded the company Life Length.

Telomere research pioneer Calvin B. Harley, who co-founded Telome Health last spring with Nobel laureate Elizabeth H. Blackburn, considers telomere length "probably the best single measure of our integrated genetics, previous lifestyle and environmental exposures." 

Soon the companies will offer telomere-measurement tests to research centers and companies studying the role of telomeres in aging and disease; the general public may have access soon after through doctors and laboratories, perhaps even directly.

When Human Brain Cells Meet Silicon Chips

Direct interfaces between small networks of nerve cells and synthetic devices promise to advance our understanding of neuronal function and may yield a new generation of hybrid devices that exploit the computational capacities of biological neural networks. There are several research teams in the U.S. and Europe that are currently working on so-called neural-silicon hybrid chips.

One of the most celebrated researchers in the field is Ted Berger at the Center for Neural Engineering at University of Southern California in Los Angeles. Berger is also a key player in the newly established National Science Foundation Engineering Research Center devoted to biomimetic microelectronics.

Berger has set his sights on building artificial neural cells, initially to act as a cortical prosthesis for individuals who have lost brain cells to neurological diseases such as Alzheimer’s. But eventually, his lab’s efforts may usher in a new era in biologically inspired computing and information processing.

Berger’s strategy in building artificial neurons has been an empirical one. Rather than attempt to determine every aspect of how neurons communicate, he’s chosen to emulate their behavior, bombarding live neurons from rat hippocampus tissue with every conceivable type of electrical input, and observe what output emerges from the cell. His team at USC then built a silicon microcircuit that behaves accordingly, at least in terms of spatio-temporal patterns of electrical inputs and outputs. The USC team has built circuits that model 100 neurons; their goal is to construct a 10,000-neuron chip model for implantation in primate hippocampus.

The Max Planck Institute in Germany is another center of research on neural-silicon hybrids. Recently, RA Kaul and P. Fromhertz from the Institute and NI Syed from the University of Calgary reported in Physical Review Letters on direct interfacing between a silicon chip and a biological excitatory synapse. The team constructed a silicon-neuron hybrid circuit by culturing a presynaptic nerve cell atop a capacitor and transistor gate and a postsynaptic nerve cell atop a second transistor gate.

They applied a voltage to the capacitor, which excited the presynaptic neuron, and this activity was recorded with the first transistor. When the presynaptic neuron fired, it generated excitation of the postsynaptic neuron, presumably via an excitatory synapses, and the activity in the postsynaptic neuron was recorded with the second transistor. Further, short trains of activity in the presynaptic neuron appeared to increase the strength of the excitatory synapse between the cells, creating a memory trace within the circuit.

These results demonstrate the ability to use integrated capacitors and transistors to stimulate and record from cultured neurons. The neuron-silicon hybrid provides a tool to study formation and plasticity within small neural circuits and may lead to novel computational devices.


The Keys of Life and Death (Thoth, The Atlantean)


"List ye, O man, whilst I give the secret so that ye, too, shalt taste not of change. 

One hour each day shalt thou lie with thine head pointed to the place of the positive pole (north). 

One hour each day shalt thy head be pointed to the place of the negative pole (south). 

Whilst thy head is placed to the northward, hold thou thy consciousness from the chest to the head. 


And when thy head is placed southward, hold thou thy thought from chest to the feet. 

Hold thou in balance once in each seven, and thy balance will retain the whole of its strength. 

Aye, if thou be old, thy body will freshen and thy strength will become as a youth's. 

This is the secret known to the Masters by which they hold off the fingers of Death. 

Neglect not to follow the path I have shown, for when thou hast passed beyond years to a hundred to neglect it will mean the coming of Death."

Leading Aging Researchers

www.DPL-Surveillance-Equipment.com

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NOW, look in on your home, second home, lake house or office anytime, anywhere from any internet connected PC/Lap-top or Internet active cell phone, including iphone or PDA: http://www.dpl-surveillance-equipment.com/wireless_hidden_cameras.html

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FACT SHEET:  HIDDEN NANNY-SPY (VIEW VIA THE INTERNET) CAMERAS

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Note: Simply Choose e-Lay-Away as a "Payment Option" in The Shopping Cart

DPL-Surveillance-Equipment.com is a world leader in providing surveillance and security products and services to Government, Law Enforcement, Private Investigators, small and large companies worldwide. We have one of the largest varieties of state-of-the-art surveillance and counter-surveillance equipment including Personal Protection and Bug Detection Products.

Buy, rent or lease the same state-of-the-art surveillance and security equipment Detectives, PI's, the CIA and FBI use. Take back control!

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