Ed McMahon, Farah Fawcett, Michael Jackson and Billy Mays: Wake Up Call!

Life Extension Wake Up Call!

Funding Aging Research

Ed McMahon, Farah Fawcett, Michael Jackson and Billy Mays: Wake Up Call!

posted on July 07, 2009

Two weeks ago, Ed McMahon passed away at the age of 86.

I grew up watching Ed on the Tonight Show with Johnny Carson. But that's not the reason his death hit me hard.

A few years ago, Ed interviewed me on his radio show. I didn't think about him very much recently, until he passed away. Then I listened to the interview again and was reminded of his zest for life, his positive reaction to the possibility of open-ended youth... and of his dwindling chances over the past few years.

It's very sad.

Granted, someone aged 86 has slim chance for extreme life extension, but they're not zero. After all, they'd probably have to live to about 106 to have a chance - at least. Even then, it's far from a shoe in. But it's possible. And of course, you can always fall back on cryonics.

Unfortunately, Ed and Johnny missed the boat. After tens of thousands of years, they may have been part of the last generation to die from aging-related causes. But you should be luckier.

Click on https://www.maxlife.org/audio/McmahonKekich.mp3 to hear our interview.

About the same time, Farah Fawcett died after a long fight with cancer, and Michael Jackson shocked the world again, this time tragically and with finality. Then, on June 28th, we lost Billy Mays, one of TV's most popular pitchmen of all time.

Ed's death may have been avoided if we were 20-30 years in the future. But the cancer and heart disease that did in Farah, Michael and Billy might have been dodged had they taken advantage of the lifestyle habits I write about in Life Extension Express. Granted, cancer is tricky, but you can cut your odds way back. Heart disease is another matter. It's very avoidable if you know what what to do... and then do it.


Boosting Repair Mechanisms Beneficial in Alzheimer's (July 03 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4275
One might expect that improving repair and maintenance systems in the brain would provide some benefit irrespective of how present damage came about, and this may be the case: "The granulocyte-colony stimulating factor (GCSF) significantly reduced levels of the brain-clogging protein beta amyloid deposited in excess in the brains of the Alzheimer's mice. The growth factor prodded bone-marrow derived microglia outside the brain to join forces with the brain's already-activated microglia in eliminating the Alzheimer's protein from the brain. Microglia are brain cells that act as the central nervous system's main form of immune defense. Like molecular 'Pac-men,' they rush to the defense of damaged or inflamed areas to gobble up toxic substances." This is still a rearguard action against end-stage consequences, however - the underlying chain of causes is not addressed. Repair of final consequences isn't a viable long-term strategy for dealing with an ever-worsening root cause, as those consequences will rapidly exceed the ability to repair them. At some point you have to address the origin of the problem in order to prevent it from spiraling out of control.

Collecting Cellular Junk (July 02 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4273
Newer longevity science blog Green Light Go here looks at the harmful accumulation of metabolic byproducts and other junk such as lipofuscin in our cells with age: "I just finished an entry for the SOA timeline on the 1970s discovery that nematodes collect inactive enzymes and molecules as they grow older. The main idea being that the body is unable to clear out the junk inside cells and that the energy cost of carrying this junk leads to senescence, or aging. The theory reminded me of a similar finding by Coleen Murphy who found that long lived daf-16 elegans mutants lived longer in part because they encoded antimicrobial lysosomes, that helped to clear out microbes that would get "packed" inside the nematodes precipiating senescence and eventually their death. As far as I know, the reason for the slow decline in enzyme activity and for the collection of intracellular junk is still unknown. Why i sn't our body clearing this stuff out and selling it on ebay? The SENS foundation, which is perhaps the biggest player in anti-aging research, is pushing forward with a solution anyway. Their strategy is to find enzymes manufactured by soil bacteria and fungi that can then be applied therapeutically to help clear junk out of cells. It is going to be interesting in the future to see what result comes of this. Both for understanding the chemical mechanism of the collection of junk, and the therapeutic solutions which can get rid of it."

Regenerating Salamanders and Their Blastemas (July 02 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4272
Progress in understanding the mechanisms by which salamaders regenerate lost limbs from The Scientist: "The cells responsible for the salamander's famed ability to regenerate amputated limbs aren't pluripotent, as scientists have thought. They're retaining their memory of the tissues they came from, and they go on to form cells of that same type. That's not what most people thought was going on. That's good news for regenerative medicine: If the mechanism salamander cells use for regrowing body parts doesn't depend on pluripotent stem cells, it may be easier than researchers have assumed to mimic that organism's regenerative strategy in potential therapies. Salamanders' regenerative abilities were thought to rely on the dedifferentiation of cells near the damaged limb to a pluripotent state, a feat that mammalian cells are normally incapable of. Instead of trying to generate multipotent or pluripotent cells, [researchers] should try to understand how these cells get the appropriate signals to make a new limb in terms of organizing the different tissue types."

The Compression of Morbidity School of Thought (July 01 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4270
This interview with Leonard Hayflick is illustrative of the thinking of gerontologists who aim not to extend human life (in this case because he thinks it's an implausible goal) but to shorten the period of age-related disability. It's a view very much at odds with reliability theory, which suggests that any reduction in ongoing damage will extend healthy life, and with the many demonstrated extensions of lifespan in animals. "The facts are these. There are four aspects to the finitude of life: aging, longevity determination, age-associated diseases, and death. Aging is what we call a catabolic process - the breakdown of molecules.
Longevity determination is the reverse - the repair or maintenance of molecules. Aging gets confused with longevity determination. The aging process increases vulnerability to age-associated diseases. These concepts are distinguishable from each other and fundamentally different. You cannot learn about the fundamental biology of aging by studying disease processes. Resolving age-associated diseases tells us nothing about the fundamental biology of aging, just as the resolution of childhood diseases, such as polio and childhood anemia, did not tell us one iota about childhood development."

Exercise and Neurogenesis (June 30 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4268
Another benefit of regular exercise is proposed in this recent research: scientists "have, for the first time, been able to demonstrate that moderate exercise significantly increases the number of neural stem cells in the ageing brain. Neuroscientists have known for some time that, in healthy brains, the creation of new neurons is an ongoing and lifelong mechanism. However, it has also been known for more than a decade that the number of new neurons we produce slowly declines with age. Investigating the mechanism by which neural stem cell numbers are altered will undoubtedly increase our understanding of how the brain responds to its environment. Ultimately, this should allow us to discover how to harness the brain's regenerative capacity, and to bring about new and effective treatments for conditions caused by trauma, disease, or even normal ageing. The brain's ability, even at an advanced age, to respond in a positive manner is very exciting as it extends the time-frame in which manipulation is possible."

"Minicells" as Targeting Mechanism (June 29 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4266

Effective per-cell-type targeting of therapies is a fundamental and very important technology platform for the future of medicine. Here's another way of doing it, distinct from methods using viruses or nanoparticles: "The minicells are generated from mutant bacteria which, each time they divide, pinch off small bubbles of cell membrane. The minicells can be loaded with chemicals and coated with antibodies that direct them toward tumor cells. No tumor cell, so far as is known, produces a specific surface molecule for toxins to act on. But 80 percent of solid tumors have their cell surfaces studded with extra-large amounts of the receptor for a particular hormone, known as epidermal growth factor. The minicells can be coated with an antibody that recognizes this receptor, so they are more likely to attach themselves to tumors than to the normal cells of the body. The tumor cells engulf and destroy the minicel ls, a standard defense against bacteria, and in doing so are exposed to whatever cargo the minicells carry. Treatment arrested tumor growth in mice implanted with either human colon or human breast tumors, and enabled mice with drug-resistant human uterine tumors to eliminate the tumors altogether."

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