Healthy Life Extension

Did You Ever Question the Sense of Living?

posted on March 01, 2011

Reason is full of longevity information wisdom. I suggest you bookmark www.FightAging.org. Here ore some of his recent thoughts with my comments following each thought:

“It is fairly easy to slide from the question 'why live longer?' to the question 'why live?' If you're not so sold on being alive at the present time, it may follow that you're also not so much in favor of being alive for longer in the future. Sadly, many people are on the fence when it comes to their continued existence as thinking, conscious entities: ambivalent until threatened with impending death, at which point deep-seated survival instincts take over, but ultimately vaguely looking forward to their end.”

If life sucks, why would you want your problems to continue? Sadly, many don’t see their way out of their problems, so they give in to aging and death. Ironically, many of the technologies which will solve aging will also reverse most of the world’s social ills and personal problems as well. For example, nanotechology will obsolete most illness, aging, food shortages, pollution, poverty and energy shortages. If more understood this, they would not be so willing to go silently into the night.

Reason goes on to say: “Others call into question the morality of creating new people when they are doomed to inevitable suffering and death, and this cheerful topic leads us to a brace of posts at Depressed Metabolism."

Well, what can I say? Deeply ingrained deathist attitudes are almost impossible to reverse, especially on a grand scale. My aim is to cast a wide net, hoping to catch the attention of those optimistic towards longevity. With success, the messages will get viral. When enough people embrace the expectations of more youth, more energy and longevity, it will be easier to reverse some of the attitudes of others that kill millions prematurely.

“Aging kills people, just as cars do. There are only two things that distinguish aging from other killers: it kills people very slowly, only after gradually and progressively debilitating them over many years, and it only kills people who were born quite a long time ago.”

That’s the point. Death from aging is largely preventable, just as automobile accidents are. And just as we can build safer cars which help you survive accidents, we can build, and are building, technologies that protect you from aging.

“The combination of these features seems to be the only available explanation for why we so meekly and calmly accept the deaths of so vast a number of people from aging, while feeling much more intense anger and despair at the comparatively rare deaths that occur in the industrialized world at younger ages. Is it somehow OK, or at least only a little bit sad, when someone dies of 'natural causes' after 'good innings'? I would suggest that it is not OK.”

Amen Reason. In fact, 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 have. What a horrific loss to society every time we lose a productive life, especially a more mature one!

“Ageism permeates our societies, and our descendants will look back in disgust and horror at the way in which we allowed our historical legacy of prejudice to suppress and slow down progress towards the biotechnologies of rejuvenation. We younger folk write off the old in so many ways, and in doing so each of us is only sticking the knife into the person we'll be a few decades down the line—and teaching our children to do exactly the same. Every death is a tragedy, but so many people work so hard to pretend otherwise."

Yep. Every life is a treasure. Turning a blind eye toward the tragedy of dying from aging sets the stage for unintentional suicide… and even murder if you help set the stage for others to follow in your footsteps. Look, times are changing so rapidly now that our ancestors’ destinies no longer have to be repeated. We have reached a turning point in humanity, and you are lucky enough to be alive to have the opportunity to join the first generation to survive aging. What glorious possibilities!

Don’t get left behind.

Long Life,
David Kekich
____________________________

LATEST HEADLINES FROM FIGHT AGING!
 
IMPROVED MANIPULATION OF THE IMMUNE SYSTEM Friday, February 25, 2011 http://www.fightaging.org/archives/2011/02/improved-manipulation-of-the-immune-system.php
Can improving the technologies of vaccination lead to gains in the capacity of the age-damaged immune system? Progress in the ability to manipulate the immune system may pay off in unexpected ways when further technologies are built atop a new platform: "Vaccine scientists say their 'Holy Grail' is to stimulate immunity that lasts for a lifetime. Live viral vaccines such as the smallpox or yellow fever vaccines provide immune protection that lasts several decades, but despite their success, scientists have remained in the dark as to how they induce such long lasting immunity. Scientists [have] designed tiny nanoparticles that resemble viruses in size and immunological composition and that induce lifelong immunity in mice. They designed the particles to mimic the immune stimulating effects of one of the most successful vaccines ever developed - the yellow fever vaccine. The particles, made of biodegradable polymers, have components that activate two different parts of the innate immune system and can be used interchangeably with material from many different bacteria or viruses.

The yellow fever vaccine stimulated multiple Toll-like receptors (TLRs) in the innate immune system. TLRs [are] molecules expressed by cells that can sense bits of viruses, bacteria and parasites. The immune system sensed the yellow fever vaccine via multiple TLRs, and that this was required for the immunity induced by the vaccine. We found that to get the best immune response, you need to hit more than one kind of Toll-like receptor. Our aim was to create a synthetic particle that accomplishes this task. In experiments with monkeys, nanoparticles with viral protein could induce robust responses greater than five times the response induced by a dose of the same viral protein given by itself, without the nanoparticles."
 
AN EXAMPLE OF YOUTHFUL REGENERATION Friday, February 25, 2011 http://www.fightaging.org/archives/2011/02/an-example-of-youthful-regeneration.php
Young mammals are capable of feats of regeneration: even in humans, it has been known for young children to regenerate lost fingertips. That capacity fades with age, however. Researchers are investigating the biochemistry of this behavior for much the same reasons as they look at regenerating species such as salamanders - if the capacity is there, perhaps it can be restored in adults. "Researchers, working with mice, found that a portion of the heart removed during the first week after birth grew back wholly and correctly - as if nothing had happened. This is an important step in our search for a cure for heart disease, the No. 1 killer in the developed world. We found that the heart of newborn mammals can fix itself; it just forgets how as it gets older. The challenge now is to find a way to remind the adult heart how to fix itself again. Previous research has demonstrated that the lower organisms, like some fish and amphibians, that can regrow fins and tails, can also regrow portions of their hearts after injury. In contrast, the hearts of adult mammals lack the ability to regrow lost or damaged tissue, and as a result, when the heart is injured, for example after a heart attack, it gets weaker, which eventually leads to heart failure. The researchers found that within three weeks of removing 15 percent of the newborn mouse heart, the heart was able to completely grow back the lost tissue, and as a result looked and functioned just like a normal heart. The researchers believe that uninjured beating heart cells, called cardiomyocytes, are a major source of the new cells. They stop beating long enough to divide and provide the heart with fresh cardiomyocytes."

EXERCISE VERSUS ACCELERATED MITOCHONDRIAL DYSFUNCTION Wednesday, February 23, 2011 http://www.fightaging.org/archives/2011/02/exercise-versus-accelerated-mitochondrial-dysfunction.php
Researchers demonstrate that exercise can counter some of the effects of an engineered acceleration of mitochondrial dysfunction: "researchers [found] that signs of premature aging were halted - and even reversed - in virtually every tissue and organ in the bodies of exercised mice. Mice genetically altered to age faster were forced to run on treadmills for 45 minutes, three times a week. Five months later, the mice looked as young, healthy and active as wild-type mice
- mice that didn't have the genetic mutation - while their sedentary and same-aged siblings were balding, greying and shrinking. .. The mice were genetically manipulated to age twice as fast as normal because of a defect in the repair system of their mitochondria, the powerhouses or furnaces inside each cell that give our body energy. Evidence has been mounting for decades that the older we get, the more mutations we accumulate in mitochondrial DNA. The furnaces start to break down, resulting in a steady decline in tissue and organ function. In our study, we saw huge recovery in mitochondrial function [in] the exercised mice." We might expect this result, given that exercise is known to have an impact on longevity, as well as on many of the biological mechanisms that are associated with aging. Given the importance of mitochondria in aging, it is interesting to see more work on the links between exercise and their function - but we must always be careful when evaluating work based on engineered dysfunction or accelerated aging. It is often the case that the putative end result has little relevance to "normal" aging.
 
TOWARDS RAPID PRINTING OF HUMAN SKIN Tuesday, February 22, 2011 http://www.fightaging.org/archives/2011/02/towards-rapid-printing-of-human-skin.php
From CNN: "We started out by taking a typical desktop inkjet cartridge. Instead of ink we use cells, which are placed in the cartridge. The device could be used to rebuild damaged or burned skin. The project is in pre-clinical phases and may take another five years of development before it is ready to be used on human burn victims. Researchers say organs - not just skin - could be printed using similar techniques. The skin-printing process involves several steps. First, a small piece of skin is taken from the patient. The sample is about half the size of a postage stamp, and it is taken from the patient by using a chemical solution. Those cells are then separated and replicated on their own in a specialized environment that catalyzes this cell development. We expand the cells in large quantities. Once we make those new cells, the next step is to put the cells in the printer, on a cartridge, and print on the patient. The printer is then placed over the wound at a distance so that it doesn't touch the burn victim. It's like a flat-bed scanner that moves back and forth and put cells on you. The device can fabricate healthy skin in anywhere from minutes to a few hours, depending on the size and type of burn. Researchers said they're pleased with results of preliminary laboratory testing with the skin printer [and] already have been able to [make] healthy skin."
 
COGNITIVE AGING AS A DISEASE Monday, February 21, 2011 http://www.fightaging.org/archives/2011/02/cognitive-aging-as-a-disease.php
There is a debate over whether aging is a disease, and here is some insight into where the aging of the brain and neurodegenerative diseases fit into that larger argument: the "question of whether 'aging itself' is or is not a 'disease' has long been mooted in biogerontological circles, with a long-held rhetorical preference for asserting that it is not, but rather, that it is a risk factor for the specific diseases of aging. By contrast, the same fundamental semantic dispute was initially resolved in the opposite direction with regard to age-related cognitive decline and dementia, beginning in the early decades after Alois Alzheimer and Emil Kraepelin first identified the pathological basis of the Alzheimer's disease (AD) until the early 1970s. For most of the twentieth century, it was held that dementia occurring in younger people should be classified as a disease, whereas dementia should be expected and accepted when it occurred in people at more advanced ages, despite the knowledge that the lesions linked to Alzheimer's dementia accumulated throughout the course of "normal" aging in middle age and onward, and that the pathological basis of the disorder was the same in both cases.

But beginning in the 1960s, a loose alliance led by social gerontologists but quickly coming to include biogerontologists, geriatricians, and patient advocacy groups successfully campaigned for a new understanding: that while some level of minor cognitive decline was  indeed a 'normal' and inevitable part of aging, the newly-rediscovered clinicopathological entity, 'Alzheimer's disease,' was exactly that: a disease, against which the full force of public and private biomedical research should be mobilized in the pursuit of a cure." These debates are almost entirely driven by the state of regulation in medical development; in particular that the FDA does not approve treatments that are not aimed at a defined and accepted disease - and aging is not a disease to the regulators, so no-one can try to treat it legally. This is an abysmally stupid situation, but sadly par for the course wherever government becomes involved.
 
THE SHAPE OF AGING Monday, February 21, 2011 http://www.fightaging.org/archives/2011/02/the-shape-of-aging.php
An interesting piece on the comparison of aging between species: "The 'shape' of aging describes how much mortality, the risk of dying, changes with age. One way of measuring the shape of aging is the 'aging factor' across species. For example, the common swift has an aging factor of 2, meaning mortality doubles during its adult life, compared with modern humans, who have an aging factor that exceeds 2000. Some organisms live a short time, others live a long time.
This is the pace of aging. Short-lived species have a fast pace of aging, and long-lived species have a slow pace of aging. Pace describes how quickly the clock of life ticks away. For humans it ticks slowly, for small songbirds like the robin it ticks very fast.

At the age of 15, only 2 out of 100,000 girls in Sweden die, but one out of every two women aged 110 will die. This large difference in mortality at the beginning and end of adult life means that for humans the shape of ageing is steep, whereas in other species like the common swift it is shallow. And in some species the risk of death can even fall with age, with older individuals having the least risk of dying. This seems to be the case for the desert tortoise, and for alligators or crocodiles. Comparing robins with Swedish women, humans have a slow pace of aging whereas the robin's is fast, so in terms of length of life the humans are doing best. But if we look at the impact aging has on death rate the robin wins. Its shape of aging is fairly flat whereas the humans' is steep, indicating that death rates increase markedly with age. Not all species with short lives live fast and die young. Robins do, but mountain sheep do things differently. They also live pretty fast but die older. From the data I have, it seems that live fast die young is only one option; you can also live fast and die older, or live slower and die young, or live slow and die old. There might be every combination in nature. That's something we need to find out in the future with better data."

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