Healthy Life Extension

In Memory of a Giant

posted on March 08, 2011

I hate writing this week’s letter more than you can imagine.

Last fall, I wrote about suddenly and unexpectedly losing Mickey Miller, a friend and treasured associate. His brother, whom I did not know, called and broke the sad news to me.

Last Wednesday, I got a similar call from another stranger, Phil Bradbury. It was almost an identical version of the first call, except this time, Robert Bradbury vanished from my life… and from yours. Robert was a genius who had the potential to rescue millions from premature death from aging. Tragically, the world will never know of him and his now invisible innovations that should have been. Many will die unnecessarily because of the sudden passing of one relatively unknown individual.

Coincidently, Mickey Miller was doing important patent research for Robert when Mickey died.

Prophetically, last week, I wrote about how when people die, they take with them the knowledge and wisdom of a lifetime. Here’s what I said:

“I find it even more sad when elders die. I don't buy into the rationalization that "they had full lives." Life can never be full with an infinite universe of possibilities lying before us. When they die, the elderly take with them much more wisdom, knowledge, social networks and skills than the younger generations can ever amass. What a horrific loss to society every time we lose a productive life, especially a more mature one!”

Robert’s was unique. He was one of a handful who had the background to accomplish the “impossible”. Robert integrated information technology and biotechnology to give us the capability to re-engineer the human genome. By doing so, we would eventually be impervious to disease and aging.

He was also on the threshold of developing a stem cell technology that would turbocharge virtually every adult stem cell treatment in the world. Not only did it offer the promise of young replacement parts in aged patients, but it also held the possibility of complete skin rejuvenation ability by 2014 or sooner.

If funding were available a year or two ago, the stem cell enterprise would be well under development, and the genome re-engineering possibilities would have been well underway and well cataloged. As it is, these life-giving technologies will need to be largely recreated, while millions suffer and die due to the delay.

Robert will be almost impossible to replace as a scientist and impossible to replace as a friend. He amassed a wider and deeper knowledge and understanding of all the aspects of aging than maybe anyone in the world. His ability to step back and connect the dots gave him insights that I rarely see. Then when you add his specialties, you realize what a treasure resided between his ears.

He was a world class thinker, researcher, and entrepreneur. His interests ranged from the problems of the real limits to personal longevity and intelligence, the processes that govern the long term evolution of technological civilizations, as well as current unresolved problems in astronomy, such as the nature of the missing mass and dark matter in the Universe. His current primary focus was developing "whole genome engineering" to not only treat aging, but to address problems ranging from energy to food production. He had a deep comprehension of a unique information set that included computer science, molecular biology and nanotechnology.

I’ll really miss Robert, the stimulating discussions we had, the plans we made to develop his ideas and the anticipation of seeing his concepts blossom into realities. We lost the ability to fast track some of the research with his passing, and saddest of all, he won’t be alive to profit from his efforts.

Robert was wealthy once, and he died a pauper. He amassed his wealth by cashing in his Oracle stock. He was one of Oracle’s first seven or eight employees and left the company as a multimillionaire determined to solve aging. He was too far ahead of his time. The technology was not yet developed to incorporate his ideas. His quest took him to Russia where he established a lab and a team of scientists. Over the years, Robert’s fortune dissipated, but never his resolve and enthusiasm. He would have unquestionably rebuilt his estate… and more. But now at the age of 54, he is gone.

Sadly, Robert’s back-up plan did not kick in either. He understood how viable cryonics is and made it well-known he wanted to be cryonically suspended (frozen) in the event he died before age-reversal became a reality. Unfortunately, he never made arrangements, most likely due to his lack of resources. He knew there was a good chance cryonics could rescue him, with his memory intact. But because of his devotion to life and life extension, he could not afford the modest amount of funds to secure it for himself. How ironic and how tragic!

I’m still reeling from Robert’s death. He suffered a massive stroke, without warning.

If you had advance notice of your expiration date, wouldn’t you plan more aggressively? Wouldn’t you, in fact, do everything in your power to postpone that date? And wouldn’t you consider at least becoming informed about cryonics as the ultimate life insurance policy?

If so, you can get a free information pack at www.Alcor.org. Or call 877-462-5267.

It’s time to quit grieving and to get back to our mission. As one of our colleagues put it, “We’re all going to have to work harder now.”

Long Life,
David Kekich
____________________________

WORK ON BUILDING NEW NEURONS Friday, March  4, 2011 http://www.fightaging.org/archives/2011/03/work-on-building-new-neurons.php
One strand of stem cell research is learning how to construct exactly the type of cell needed: "researchers for the first time have transformed a human embryonic stem cell into a critical type of neuron that dies early in Alzheimer's disease and is a major cause of memory loss. This new ability to reprogram stem cells and grow a limitless supply of the human neurons will enable a rapid wave of drug testing for Alzheimer's disease, allow researchers to study why the neurons die and could potentially lead to transplanting the new neurons into people with Alzheimer's. These critical neurons, called basal forebrain cholinergic neurons, help the hippocampus retrieve memories in the brain. In early Alzheimer's, the ability to retrieve memories is lost, not the memories themselves. There is a relatively small population of these neurons in the brain, and their loss has a swift and devastating effect on the ability to remember. Now that we have learned how to make these cells, we can study them in a tissue culture dish and figure out what we can do to prevent them from dying.

This technique to produce the neurons allows for an almost infinite number of these cells to be grown in labs, allowing other scientists the ability to study why this one population of cells selectively dies in Alzheimer's disease. The ability to make the cells also means researchers can quickly test thousands of different drugs to see which ones may keep the cells alive when they are in a challenging environment. [Researchers] demonstrated the newly produced neurons work just like the originals. They transplanted the new neurons into the hippocampus of mice and showed the neurons functioned normally. The neurons produced axons, or connecting fibers, to the hippocampus and pumped out acetylcholine, a chemical needed by the hippocampus to retrieve memories from other parts of the brain."

ALZHEIMER'S PLAQUE AND THE LIVER Friday, March  4, 2011 http://www.fightaging.org/archives/2011/03/alzheimers-plaque-and-the-liver.php
Interesting research reported via ScienceDaily: "Unexpected results from a [recent study] could completely alter scientists' ideas about Alzheimer's disease - pointing to the liver instead of the brain as the source of the 'amyloid' that deposits as brain plaques associated with this devastating condition. The findings could offer a relatively simple approach for Alzheimer's prevention and treatment. The product of [the mouse gene corresponding to a gene known to predispose humans carrying particular variations of it to develop early-onset Alzheimer's disease], called Presenilin2, is [involved] in the generation of pathogenic beta amyloid. Unexpectedly, heritable expression of Presenilin2 was found in the liver but not in the brain. Higher expression of Presenilin2 in the liver correlated with greater accumulation of beta amyloid in the brain and development of Alzheimer's-like pathology.

This finding suggested that significant concentrations of beta amyloid might originate in the liver, circulate in the blood, and enter the brain. If true, blocking production of beta amyloid in the liver should protect the brain. Mice were administered imatinib [which] has poor penetration of the blood-brain barrier in both mice and humans. Because it doesn't penetrate the blood-brain barrier, we were able to focus on the production of amyloid outside of the brain and how that production might contribute to amyloid that accumulates in the brain, where it is associated with disease. The drug dramatically reduced beta amyloid not only in the blood, but also in the brain where the drug cannot penetrate. Thus, an appreciable portion of brain amyloid must originate outside of the brain, and imatinib represents a candidate for preventing and treating Alzheimer's."

MORE ON HDL LEVELS AND HUMAN LONGEVITY Thursday, March  3, 2011 http://www.fightaging.org/archives/2011/03/more-on-hdl-levels-and-human-longevity.php
You might recall that studies of centenarians turned up an association between reaching that age and levels of HDL, high density lipoprotein, a form of cholesterol transport mechanism. Here is another study demonstrating the same correlation for younger old people: "No previous researchers have sought to determine whether high-density lipoprotein (HDL) cholesterol levels are associated with survival to 85 years of age in a prospective cohort of aging men. We selected 652 men (mean age 65 years) enrolled in the VA Normative Aging Study who had [at least one] HDL cholesterol level documented during the study and who were old enough on the date of HDL cholesterol measurement to reach 85 years of age by [2008].  We used proportional hazards to determine hazard ratios (HRs) for mortality before age 85 years for each category of initial HDL cholesterol compared to the reference adjusting for co-morbidities, calculated low-density lipoprotein cholesterol, medications, smoking, body mass index, and alcohol consumption. Treating HDL cholesterol as a continuous predictor, we also determined the HR for each 10-mg/dl increment in HDL cholesterol. Each 10-mg/dl increment in HDL cholesterol was associated with a 14% [decrease] in risk of mortality before 85 years of age. In conclusion, after adjusting for other factors associated with longevity, higher HDL cholesterol levels were significantly associated with survival to 85 years of age." Which leads to the thought that if HDL is so good, why not test to see if artificially creating more of it in the body is beneficial?

THE FLIP SIDE OF STUDIES ON STRESS Wednesday, March  2, 2011 http://www.fightaging.org/archives/2011/03/the-flip-side-of-studies-on-stress.php
Stress appears to affect long-term health and biochemistry in some fundamental ways, some of which are connected to the aging process - such as telomere length, chronic inflammation, and immune system function. So what happens when a person is the opposite of stressed? There is reason to believe that being happy over the long term has just as much of a beneficial effect as stress does a negative effect: "A review of more than 160 studies of human and animal subjects has found 'clear and compelling evidence' that - all else being equal - happy people tend to live longer and experience better health than their unhappy peers. Its lead author [analyzed] long-term studies of human subjects, experimental human and animal trials, and studies that evaluate the health status of people stressed by natural events.

We reviewed eight different types of studies, and the general conclusion from each type of study is that your subjective well-being - that is, feeling positive about your life, not stressed out, not depressed - contributes to both longevity and better health among healthy populations. A study that followed nearly 5,000 university students for more than 40 years, for example, found that those who were most pessimistic as students tended to die younger than their peers. An even longer-term study that followed 180 Catholic nuns from early adulthood to old age found that those who wrote positive autobiographies in their early 20s tended to outlive those who wrote more negative accounts of their young lives. There were a few exceptions, but most of the long-term studies the researchers reviewed found that anxiety, depression, a lack of enjoyment of daily activities and pessimism all are associated with higher rates of disease and a shorter lifespan."

LEARNING FROM THE AGELESS ANIMALS Wednesday, March  2, 2011 http://www.fightaging.org/archives/2011/03/learning-from-the-ageless-animals.php
Some species do not age in any easily detected way - lobsters, for example. Others are just far more resilient to the passage of years than we humans, living longer or losing little of their vitality over the course of their lives. What can be learned from a study of their biochemistry? "The first photo is from 1973, when a dark-haired and spry Nisbet was banding chicks of the small sea bird off the rocky Cape Cod coast. The second photo was taken 33 years later and shows a grizzled, silver-haired Nisbet holding a 29 year old tern, one of the oldest on record. Nisbet's body shows common signs of wear and tear - gray hair, wrinkles, achy joints. The tern, however, shows none of these outward signs, despite being the equivalent of a human centenarian. Terns don't even demonstrate diminished physical abilities as they age. They aren't the only animals that have combined a long lifespan with minimal signs of aging; other seabirds, alligators, crocodiles, and some tortoises also seem to sip from the Fountain of Youth. Although medical advances have extended the human lifespan, these same advances haven't been able to prevent the inimical onslaught of old age. Scientists hope that by studying the secrets of ageless critters, humans will one day be able to pause the hands of time. The main difference between humans and organisms like common terns is how growing older affects the risk of dying. In some animals, like freshwater hydras, risk of death remains pretty constant during life. For other animals, like the tern, the risk of death actually decreases with age. It seems almost counter-intuitive: an older tern is less likely to die than a younger one. 'My 29-year-old tern was still breeding,' Nisbet said. The oldest terns produced the healthiest offspring and were actually more likely to survive the year than younger terns."

A SURGEON'S PERSPECTIVE ON MEDICAL NANOTECHNOLOGY Tuesday, March  1, 2011 http://www.fightaging.org/archives/2011/03/a-surgeons-perspective-on-medical-nanotechnology.php
From h+ Magazine: "A [trend] towards nanotechnology is evident in the miniaturization of surgical tools. Experimental microrobots are already available, and being tested in live tissues. It seems likely that in one or two decades, microrobots will be in common use in surgery, before their eventual replacement by nanorobots. Microrobots will resemble minute machines from the macroscale. But what will nanorobots look like? They won't be akin to artistic representations of miniature submarines placed beside erythrocytes.

Most likely, they will bear some resemblance to the body's existing nanomachines, such as mitochondria. Nanorobots will be scavengers for atherosclerotic plaque, just like artistic representations you may find online, but not with exactly the same mechanics. We will witness a gradual transition from surgical repair, to prevention. Atherosclerosis, which is in fact the gradual stenosis of the arteries due to plaque formation, will be solved at the genomic and proteomic level, and this will lead to a great enhancement of the human life span. Minimally invasive microrobots will be used instead of stents inside arteries, for repairs that are currently being performed laparoscopically. Last but not least, one of the greatest achievements of nanotechnology in surgery will be what we call the 'ideal graft'; that is, biocompatible and durable 'repairs' of parts of the body like arteries, joints or even organs. At first, these repairs will be used for healing, but soon afterwards, they will be used for transcendence: to enhance current human abilities.

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