My Best Friend Died

Healthy Life Extension

Funding Aging Research

My Best Friend Died

posted on November 22nd, 2011

Dear Future Centenarian,

Who was your best friend growing up? Mine was Bob. We moved into his neighborhood when I was in second grade, two homes away. He died at 12:57 AM Eastern from metasticized kidney cancer.

Bob had a few things going against him. Both of his parents died from cancer, so he may have been more susceptible than most. Then there was lifestyle.

He did exercise mildly. He didn™t smoke, and he took supplements. But his diet was typical of most Americans™, even worse when you factor in the massive amounts of soda he consumed most of his life. He also drank more beer than average.  We discussed his diet for many years, and he did finally improve it and quit drinking soda and most beer¦ but only after being diagnosed with diabetes.

Bob™s death is very tough for me. Here was someone I loved, and he did follow some of my basic advice, but I couldn™t influence him to override his cravings. That is the reason I wrote Life Extension Express. If I can™t influence most of the people close to me to manage their health more effectively, maybe I could spread my message to people I don™t know, but to lots more of them.

The sad fact is, people have to be in tune to the message before it resonates with them. So hopefully, many will read my book, and the new improved version, Smart, Strong and Sexy at 100?, which is due for publication at the beginning of the year. One-on-one presentations are generally a waste of time and are extremely draining. With enough distribution, I may be able to improve a smaller percentage of lives but a much larger number. And other better-known authors, with their own advice and wider distribution, can do the same.

The bottom line is, we™re not immune, no matter what we do right¦ at least for now. That includes you, me and even every multi-billionaire in the world. Until we see the day when researchers put these killer diseases and aging behind us once and for all, the best we can do is improve our odds. And we can improve them dramatically by managing what we eat, how we move and our other lifestyle habits.

Billionaires can do one thing that most of us can™t though. They have the resources to fast-track aging research and maybe ultimately their own immunity. Until then, we™re all at risk.

Our researchers tell us they know how to cure aging. We have the scientific roadmap, and it™s delayed because of a lack of surprisingly modest funding. Sad.

For the sake of those who love you, those who will grieve and suffer if you leave them behind, and for the sake of your own wellness and longevity, please take care of yourself.

Long Life,
David Kekich


An open access commentary: "Aging is now viewed as a plastic phenotype that can be altered by nutritional, pharmacological and genetic manipulations. However, most pro-longevity mutations are discovered by systematic gene deletion or RNA interference screens, which mainly reveal abolished or diminished gene functions. In our recent publications, we used global acetylation proteome screens to study aging in yeast, and showed that enhancing the function of certain genes through specific acetylation can promote longevity. It is well known that acetylation of histone proteins in cultured human fibroblasts decreases during aging, which is believed to be directly related to decreased metabolic rate and reproductive capacity associated with aging. However, histone deacetylation is not likely to be a universal driving force of aging because histone acetylation and deacetylation mimetics similarly shortened life span, which could simply reflect nonspecific fitness decreases in both instances.

Extension of lifespan promoted by certain genetic and/or pharmacological perturbations will more likely lead to identification of bona fide regulatory factors of aging. Aging is conventionally thought to be characterized by accumulation of molecular, cellular, and organ damage, leading to increased vulnerability to disease and death. Our data, on the contrary, support the idea that the gradual loss of a crucial component promoting 'healthy young status' might underlie an intrinsic aging process. Many of the mutations that extend life span decrease the activity of external nutrient signaling, such as the IGF (insulin-like growth factor)/insulin and the TOR (target of rapamycin) pathways, suggesting that they may induce a metabolic state similar to that resulting from periods of food shortage."

If you can build new living tissue to be implanted in patients, then why not also give it the capacity to perform additional useful tasks? This is a technology platform with some potential: "combining gene therapy with tissue engineering could avoid the need for frequent injections of recombinant drugs. Patients who rely on recombinant, protein-based drugs must often endure frequent injections, often several times a week, or intravenous therapy. Researchers [have demonstrated] the possibility that blood vessels, made from genetically engineered cells, could secrete the drug on demand directly into the bloodstream.

Such drugs are currently made in bioreactors by engineered cells, and are very expensive to make in large amounts. The paradigm shift here is, 'why don't we instruct your own cells to be the factory?' [Researchers] provide proof-of-concept, reversing anemia in mice with engineered vessels secreting erythropoietin (EPO). The researchers created the drug-secreting vessels by isolating endothelial colony-forming cells from human blood and inserting a gene instructing the cells to produce EPO. They then added mesenchymal stem cells, suspended the cells in a gel, and injected this mixture into the mice, just under the skin. The cells spontaneously formed networks of blood vessels, lined with the engineered endothelial cells. Within a week, the vessels hooked up with the animals' own vessels, releasing EPO into the bloodstream. Tests showed that the drug circulated throughout the body and reversed anemia in the mice."

THE END OF TOOTH DECAY LOOMS LARGE Thursday, November 17, 2011
Teeth are one of the first parts of our body to become seriously damaged as the years go by, thanks to bacterial agents, but that will soon enough be a thing of the past. On the one hand enamel regeneration is close to realization, and on the other hand so are ways of eliminating the agents of tooth decay: "A new mouthwash developed by a microbiologist at the UCLA School of Dentistry is highly successful in targeting the harmful Streptococcus mutans bacteria that is the principal cause tooth decay and cavities.

In a recent clinical study, 12 subjects who rinsed just one time with the experimental mouthwash experienced a nearly complete elimination of the S. mutans bacteria over the entire four-day testing period. This new mouthwash is the product of nearly a decade of research conducted by Wenyuan Shi. Shi developed a new antimicrobial technology called STAMP (specifically targeted anti-microbial peptides) [which] acts as a sort of 'smart bomb,' eliminating only the harmful bacteria and remaining effective for an extended period. With this new antimicrobial technology, we have the prospect of actually wiping out tooth decay in our lifetime."

As knowledge of cellular programming and signaling systems increases, the future of cell therapies will most likely move away from transplants and towards controlling existing populations of cells in the body: "In order to regenerate damaged heart muscle as caused by a heart attack [simpler] vertebrates like the salamander adopt a strategy whereby surviving healthy heart muscle cells regress into an embryonic state. This process, which is known as dedifferentiation, produces cells which contain a series of stem cell markers and re-attain their cell division activity. Thus, new cells are produced which convert, in turn, into heart muscle cells. The cardiac function is then restored through the remodeling of the muscle tissue. An optimized repair mechanism of this kind does not exist in humans.

Although heart stem cells were discovered some time ago, exactly how and to what extent they play a role in cardiac repair is a matter of dispute. It has only been known for a few years that processes comparable to those found in the salamander even exist in mammals. [Researchers have] now discovered the molecule responsible for controlling this dedifferentiation of heart muscle cells in mammals.

The scientists initially noticed the high concentration of oncostatin M in tissue samples from the hearts of patients suffering from myocardial infarction. It was already known that this protein is responsible for the dedifferentiation of different cell types, among other things. Using a mouse infarct model, the [researchers] succeeded in demonstrating that oncostatin M actually does stimulate the repair of damaged heart muscle tissue as presumed. One of the two test groups had been modified genetically in advance to ensure that the oncostatin M could not have any effect in these animals. The difference between the two groups was astonishing. Whereas in the group in which oncostatin M could take effect almost all animals were still alive after four weeks, 40 percent of the genetically modified mice had died from the effects of the infarction."

STEM CELLS REVERSE HEART DAMAGE Tuesday, November 15, 2011
More evidence for the utility of early stage stem cell therapies of the sort that have been available overseas through medical tourism for a number of years, and which would also be available in the US if not for the FDA: "16 patients with severe heart failure received a purified batch of cardiac stem cells. Within a year, their heart function markedly improved. The heart's pumping ability can be quantified through the "Left Ventricle Ejection Fraction," a measure of how much blood the heart pumps with each contraction. A patient with an LVEF of less than 40% is considered to suffer severe heart failure. When the study began, Bolli's patients had an average LVEF of 30.3%. Four months after receiving stem cells, it was 38.5%. Among seven patients who were followed for a full year, it improved to an astounding 42.5%.

A control group of seven patients, given nothing but standard maintenance medications, showed no improvement at all. We were surprised by the magnitude of improvement. [Elsewhere] 17 patients [were] given stem cells approximately six weeks after suffering a moderate to major heart attack. All had lost enough tissue to put them 'at big risk' of future heart failure. The results were striking. Not only did scar tissue retreat - shrinking [between] 30% and 47% - [but] the patients actually generated new heart tissue. On average, the stem cell recipients grew the equivalent of 600 million new heart cells. By way of perspective, a major heart attack might kill off a billion cells. The heart contains a type of stem cell that can develop into either heart muscle or blood vessel components - in essence, whatever the heart requires at a particular point in time. The problem for patients [is] that there simply aren't enough of these repair cells waiting around. The experimental treatments involve removing stem cells through a biopsy, and making millions of copies in a laboratory."

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