Why Do We Resist a Brighter Future?

Healthy Life Extension

Funding Aging Research

Why Do We Resist a Brighter Future?


posted on December 13th, 2011

Dear Future Centenarian,

It continues to amaze me how often, in fact, how regularly a recurring objection to life extension comes up.

Reason addressed this issue in one of his recent editorials, and I hear it all the time.

The default assumption by a majority of people is that extending life through medical technology will result in being physically old for longer - an extended period of ever greater disability, and nothing to look forward to. Historically, this is a legitimate assumption. After all, modern medicine treats diseases, keeping people alive longer, but it rarely finds cures. To expect more might be hanging on to false hope.

But the direction research is taking, and the accelerating speed at which it is growing, gives us real hope. We finally have a legitimate goal in sight to not only cure age-related diseases once and for all, but to ultimately reach the point where we enjoy open-ended youthfulness and vitality.

Meanwhile, you might be interested in the following article which explains the psychology of clinging to past beliefs, in lacking imagination when it comes to healthy longevity and why radically extended youth will be a reality:

http://www.fightaging.org/archives/2011/09/depressing-and-not-rocket-science-some-roots-of-the-tithonus-error.php

"The Tithonus Error is one the learned patterns by which people reject life extension out of hand: from roots in childhood and education and stories, a majority of people come to believe that extending life means making people older for longer.

Most people have an entirely justified horror of the later stages of degenerative aging, and so the idea of more of that just isn't on the table. The rejection of more life under those terms is instinctive and visceral. This rejection is based on a false premise, however, and all that rational fear of aging is piled atop a single irrational misunderstanding. The goal of all medicine, and especially longevity science, is to enable people to be younger for longer, not older for longer.

Aging is nothing but damage, and longevity therapies will be no more than ways to slow, or for preference repair, the accumulation of that damage. A machine with less damage is a machine that works better for longer, not a machine that lingers on its dying gasp for longer. That rational fear of aging is big and powerful, however, and it's been somewhat hard to fight one's way past it to point out that 'older for longer' just isn't going to happen."

Long Life,
David Kekich
____________________________

LATEST HEADLINES FROM FIGHT AGING!

MORE ARGUMENTS FOR PROGRAMMED AGING Friday, December  9, 2011 http://www.fightaging.org/archives/2011/12/more-arguments-for-programmed-aging.php
A viewpoint from Vladimir Skulachev, whose research group works on mitochondrially targeted antioxidant compounds: "'It is recognized that in exceptional circumstances the possibility exists for selection to favor limiting survival. In acknowledging that at least in theory, aging might occasionally be adaptive, however, the high barriers to validating actual instances of adaptive ageing are made clear' ... A few years ago it was hardly possible to find the latter statement in an article written by the most famous proponents of non-programmed aging. Certainly, this conclusion is accompanied by some reservations.

Nevertheless, the balance between concepts of programmed and non-programmed aging seems to be really shifted to the programmed one. The idea that programmed death was invented by biological evolution was introduced in the end of nineteenth century by August Weismann, who suggested that such a death is useful for evolution as a mechanism which (i) purifies the population from weak individuals and (ii) promotes succession of generations. For sure, both these roles may be inherent in aging. However, they failed to explain why aging represents slow and concerted decline of many physiological functions (slow phenoptosis) rather than simple fast switching off of a single function of vital importance (acute phenoptosis). There is, it must be acknowledged, an instinctive attraction to the idea that aging is programmed. Aging is widespread across species and applies universally to all individuals within a species in which it is observed. There is also reproducibility about changes that occur with aging.

I may only add that, if aging is programmed, it can be retarded, prevented, and perhaps even reversed by treatments interrupting execution of this program, just as we already can interrupt programs of cell death. In other words, programmed aging can be cured like a disease. As for the concept of non-programmed aging, assuming occasional accumulation of stochastic injuries as its reason, it is quite pessimistic for finding any way of successful treatment. Here we simply observe and describe such a process without the possibility of improving the situation." This last viewpoint is exactly the wrong way around - repair of damage is likely to be far easier through SENS and similar programs than safely altering the exceedingly complex systems of metabolism to change the way in which aging happens. We should hope that genetic programs are of limited and narrow influence as a driver of aging - that they are merely reactions to underlying accumulations of damage where they exist at all. Because otherwise we're in for a long, slow road when it comes to extending healthy life.

COMMENTARY ON RAPAMYCIN Friday, December  9, 2011 http://www.fightaging.org/archives/2011/12/commentary-on-rapamycin.php
A commentary on recent research into the effects of rapamycin on longevity: "Aging is a complex process associated with accumulation of damage, loss of function and increased vulnerability to disease, leading ultimately to death. Despite the complicated etiology of aging, an important discovery of recent years has been that simple genetic alterations can cause a substantial increase in healthy lifespan in laboratory model organisms. Many of these longevity-extending mutations down-regulate the activity of the mTOR/S6K pathway suggesting that reduced Tor/S6K signaling promotes entry into alternative phases normally entered during periods of starvation. In fact, dietary restriction (DR), a reduction in food intake without malnutrition, lowers Tor/S6K signaling and extends the average and maximum life span of a variety of organisms including yeast, flies, worms, fish, and rodents.

Recently, it has been demonstrated that supplementation with rapamycin (an inhibitor of mTOR) started both at 9 and 20 months of life determines a small but significant extension of average and maximal life span in genetically heterogeneous male and female mice. More studies are needed to understand benefits and side-effects of rapamycin supplementation in different strains of mice and in monkeys as a candidate cancer-preventive and life-extension pharmacological agent. However, the efficacy of intermittent rapamycin treatment in cancer prevention and life span extension [is] very promising since it is likely to reduce the side effects associated with chronic treatment."

RESTORING SYNAPTIC PLASTICITY IN OLD RATS Thursday, December  8, 2011 http://www.fightaging.org/archives/2011/12/restoring-synaptic-plasticity-in-old-rats.php
In the next few years were going to see a lot of technology demonstrations in which one very narrow biochemical aspect of aging is reversed in laboratory animals - these are the first few pebbles in what will become an avalanche of rejuvenation biotechnology. You might recall the reversal of lysosomal functional decline in the livers of mice in 2008 as an example of the type. Here is one for the brain: "Drugs that affect the levels of an important brain protein involved in learning and memory reverse cellular changes in the brain seen during aging, according to an animal study.

[Aging] affects brain cells' ability to alter the strength and structure of their connections for information storage, a process known as synaptic plasticity, which is a cellular signature of memory. Compared with younger rats, hippocampi from older rats have less brain-derived neurotrophic factor (BDNF) - a protein that promotes synaptic plasticity - and less histone acetylation of the Bdnf gene. By treating the hippocampal tissue from older animals with a drug that increased histone acetylation, they were able to restore BDNF production and synaptic plasticity to levels found in younger animals. The researchers also found that treating the hippocampal tissue from older animals with a different drug that activates a BDNF receptor also reversed the synaptic plasticity deficit in the older rats."

CONSIDERING THE ODDS OF CANCER Wednesday, December  7, 2011 http://www.fightaging.org/archives/2011/12/considering-the-odds-of-cancer.php
To what degree can you swing the odds of suffering cancer in your favor? A fair amount, if this article is to be taken at face value, as much or more as other common age-related conditions: "Nearly half of cancers diagnosed in the UK each year - over 130,000 in total - are caused by avoidable life choices including smoking, drinking and eating the wrong things, a review reveals. Tobacco is the biggest culprit, causing 23% of cases in men and 15.6% in women, says the Cancer Research UK report. Next comes a lack of fresh fruit and vegetables in men's diets, while for women it is being overweight.

Many people believe cancer is down to fate or 'in the genes' and that it is the luck of the draw whether they get it. Looking at all the evidence, it's clear that around 40% of all cancers are caused by things we mostly have the power to change. We didn't expect to find that eating fruit and vegetables would prove to be so important in protecting men against cancer. And among women we didn't expect being overweight to be more of a risk factor than alcohol. About 100,000 (34%) of the cancers are linked to smoking, diet, alcohol and excess weight. The researchers base their calculations on predicted numbers of cases for 18 different types of cancer in 2010, using UK incidence figures for the 15-year period from 1993 to 2007." As usual, excess fat and smoking show up as undesirables - they are there as prominent risk factors for most of the unpleasant things that aging inflicts upon us.

GROWING EYES, GLANDS, AND BRAIN TISSUE Monday, December  5, 2011 http://www.fightaging.org/archives/2011/12/growing-eyes-glands-and-brain-tissue.php
The Guardian looks at the activities of one Japanese research group: "In the latest of a series of remarkable studies, researchers from the RIKEN Center for Developmental Biology in Kobe, Japan report that embryonic stem cells grown under special conditions can spontaneously organize themselves into a partial pituitary gland that is fully functional when transplanted into mice. Over the past four years, Yoshiki Sasai and his colleagues of RIKEN's Organogenesis and Neurogenesis Group have developed a novel cell culture technique for growing embryonic stem (ES) cells in floating three-dimensional aggregates.

In 2008, Sasai's group showed that ES cells grown in 3D cultures can recapitulate the earliest stages of neural development to self-organize into functional brain tissue, which integrated into existing neural circuits when transplanted into the brains of newborn mice. And earlier this year, they reported ES cells can also generate embryonic eyes with retinas. Growing complete, fully functional organs for transplantation is the holy grail of regenerative medicine, one which is being pursued by many groups of researchers around the world. Sasai's group is at the forefront of these efforts. Their work shows that ES cells can spontaneously form complex three-dimensional structures when grown under the right conditions, in the absence of a scaffold. With each new study, they demonstrate the generation of increasingly complex structures, and the pituitary gland is the most complex one yet."

Back to Top