$54,000
$1,097

Fight Aging! Newsletter, June 25th 2012

FIGHT AGING! NEWSLETTER
June 25th 2012

The Fight Aging! Newsletter is a weekly email containing news, opinions, and happenings for people interested in aging science and engineered longevity: making use of diet, lifestyle choices, technology, and proven medical advances to live healthy, longer lives. This newsletter is published under the Creative Commons Attribution 3.0 license. In short, this means that you are encouraged to republish and rewrite it in any way you see fit, the only requirements being that you provide attribution and a link to Fight Aging!

______________________________

CONTENT

- The Future Awaits its Makers
- Robin Hanson Donates $5,000 to the Brain Preservation Prize
- It Isn't That Easy to Just Kickstart Funding for Science
- Looking at Changes in Mortality in the Past Century
- Discussion
- Latest Headlines from Fight Aging!
    - Longevity Science and the Social Justice Viewpoint
    - Work on Preparing Xenotransplants With Decellularization
    - DLK and Nerve Regeneration
    - A Resveratrol Meta-Analysis
    - Mitochondrial Membrane Resistance to Explain Clam Longevity
    - Arguing Against the Role of Cytomegalovirus in Immune System Aging
    - Human Optic Cup Grown From Stem Cells
    - Arguing a Mechanism for DNA Damage to Drive Aging
    - CCR2 and the Immune System Versus Alzheimer's Disease
    - Apologism for Aging is Unproductive

THE FUTURE AWAITS ITS MAKERS

With a rapid enough pace of change, the near future looks ever more like today's science fiction:

https://www.fightaging.org/archives/2012/06/the-future-awaits-its-makers.php

"A fellow that you met today will, forty years from now, have an entirely artificial immune system. It is an early model, a prosthetic replacement that is a mix of synthetic cells and less organic medical nanomachines, and requires frequent work and an open data channel to keep in line. Obtaining it wasn't a choice - it is a new treatment for a small class of acquired autoimmune conditions that somehow manage to persist through complete removal and replacement of immune cell populations. It works; he doesn't get sick, at all. Ever.

"Nonetheless, you shook this man's hand today. That future lies in waiting.

"Earlier you passed by a kid who will outlive you, your plans, your memory, your immediate descendants, and the first phase of terraforming to take place on Mars. The young have it good these days: a solid eighty years of probable-worst-case life expectancy at birth that will take them well into the first age of radical life extension - and that even if the next twenty years take us through a miserable economic depression coupled with a spread of repressive regulatory regimes that effectively stifle life science research and its application. Many of the youngest children of today will live for centuries, and many of those will go on to live for thousands of years.

"You walked right by that kid. In fairness, he doesn't know either, of course.

"Then there's that new face at the office, fresh out of college: by the 2070s she'll be a shell of the person she was. A happy shell, however, the original exterior polished up by gene, cell, and enzyme therapies to minimize the changes of aging in skin and musculature, but all of the interior organs below the neck new from labs in Thailand and Vietnam over the years, grown from her own genetic material. That took money, even though it's second string organ biotechnology by that time - but the sharp average worker you can save enough to afford that sort of thing over a lifetime. It's not as though she'll be retiring any time soon, and better low on funds than living like a 80-year old from a century past.

"That probably didn't cross your mind today when the two of you happened to be in the same meeting."

ROBIN HANSON DONATES $5,000 TO THE BRAIN PRESERVATION PRIZE

The Brain Preservation Foundation continues to attract support for its initiatives, one of which is a technology prize for the team that can demonstrate preservation of fine structure in the brain for the long term:

https://www.fightaging.org/archives/2012/06/robin-hanson-donates-5000-to-the-brain-preservation-prize.php

"Cryonics is one existing way of preserving a human brain sufficiently well to enable a future resuscitation with more advanced technologies than are available today. Plastination is another possibility, but one that was never developed into a commercial service such as that offered by cryonics providers - arguably for no reason other than historical accident and the specialties of those who founded the cryonics movement. Interestingly there are currently a pair of teams competing in the Brain Preservation Prize, and they are employing quite different methods from cryonics and plastination. I see that economist Robin Hanson of Overcoming Bias is in favor of this initiative, as one might expect from his views on cryonics."

"An anonymous donor has actually funded a $100K Brain Preservation Prize, paid to the first team(s) to pass this test on a human brain, with a quarter of the prize going to those that first pass the test on a mouse brain. Cryonics and plastination teams have already submitted whole mouse brains to be tested. The only hitch is that the prize organization needs money (~25-50K$) to actually do the tests! This is the exceptionally worthy cause to which I am donating $5K, and to which I encourage others to donate. ... We seem close to having a feasible plastination technique, where for a few 10K$ or less one could fill a brain with plastic, saving its key brain info for future revival in an easily stored form. We may only lack donations of a similar amount to actually test that it does save this key brain info."

IT ISN'T THAT EASY TO JUST KICKSTART FUNDING FOR SCIENCE

There are fundamental differences between crowdfunding success for commercial products and crowdfunding success for research projects:

https://www.fightaging.org/archives/2012/06/you-cant-just-kickstart-a-science-project-it-isnt-that-easy.php

"Crowdfunding of commercial products is having a lengthy day in the sun at the moment. It has emerged from years of great success in small markets, such as the pen and paper gaming and indie publishing industries, and people are now applying the same models to fields where much more money is involved. ... If you have a dedicated community, then you want to turn that dedication into professional organizations and the funds to run them. This is always going to be a messy, organic process of development, but which perhaps may be open to improvement through the spread of a more formalized crowdfunding culture. But in any case, I wanted to expand on the point made in the quote above - that crowdfunding for scientific research is a radically different undertaking from crowdfunding for development of a commercial product. This seems worth emphasizing, given that a whole range of startups and new ventures seem to be trying to port over crowdfunding into the sciences pretty much as-is, or with just a few embellishments.

"The basic point of divergence between crowdfunding a product versus crowdfunding research is that in the former case the funders are definitively buying something concrete: that is their motivation and incentive. They are putting down money in expectation that what they are doing is submitting a preorder. Variations on the preorder theme are legion, but they all boil down to paying for a definitive item, a which will usually have fairly solid delivery date. Scientific research is notoriously bad when it comes to delivering on both those points, however. The work that is most amenable to crowdfunding consists of small projects that only incrementally add value to their fields - and which may not even do that, given the necessarily high failure rate for research.

"The challenge facing science crowdfunding is the same challenge faced by scientific advocates at all times: they do their part to grow communities of supporters and encourage those supporters to pay for research work. That work will give no immediate result, the eventual result may be hard for supporters to understand, it will likely not benefit them for some time, if ever, and in addition to all of that the undertaking will quite likely fail. Science is a high risk endeavor, with few short-term payoffs that people find rewarding - and thus it is a hard sell when held up against the allure of immediate gratification, candy, and shiny objects."

LOOKING AT CHANGES IN MORTALITY IN THE PAST CENTURY

Science and technology are, at root, a collection of endeavors and methods that aim to eliminate death and suffering, one cause at a time. Thus the principal focus tends to be on whatever is causing the most death and suffering - and with success in research and development, that focus shifts:

https://www.fightaging.org/archives/2012/06/a-look-at-the-changes-in-mortality-in-the-past-century.php

"The first thing to notice here is how much our mortality rate has dropped over the course of a century, largely due to big reductions in infectious diseases like tuberculosis and influenza. ... On the large scale, medicine chases the priorities of the now - and in wealthier regions of the world that has become cancer and heart disease. The size of the cancer and heart disease research communities reflects the present degree to which the two groups of conditions contribute to human mortality. What it does not yet reflect is the new and more meaningful unified way of looking at the conditions that kill the most people: that they are all caused by aging, and stem at root from a limited range of mechanisms and changes that happen over the years as a byproduct of our normal metabolism. We rust, and that rust blossoms into a thousand different failure modes. Yet medical science is still largely focused on end states, and patching over catastrophic damage rather than preventing its origins.

"To keep reducing the human mortality rate, the research community has to start in on prevention in the form of repair biotechnologies - ways to halt and reverse the earliest development of the age-related conditions that kill most people. It is as much a cultural change in the life sciences as it is a technical challenge, as the path ahead is fairly clear. This is why organizations like the SENS Foundation, mixing aggressive advocacy with targeted research work where few others are making progress, are so important. It is not so much that they will get the work done by themselves, but that they will spawn a sea change in the research community, such that many, many groups will tomorrow be performing similar work with similar end goals: to to be able to treat and reverse the course of aging.

"You might think of a focus on aging and its causes as the germ theory of today's medical community: a unifying set of ideas and resulting research strategies that will bring the bulk of the medical community onto a better path forward, one that will lead to a more rapid improvement in the human condition, and longer, healthier lives for all."

DISCUSSION

The highlights and headlines from the past week follow below. Remember - if you like this newsletter, the chances are that your friends will find it useful too. Forward it on, or post a copy to your favorite online communities. Encourage the people you know to pitch in and make a difference to the future of health and longevity!

______________________________

LATEST HEADLINES FROM FIGHT AGING!

LONGEVITY SCIENCE AND THE SOCIAL JUSTICE VIEWPOINT
Friday, June 22, 2012
https://www.fightaging.org/archives/2012/06/longevity-science-and-the-social-justice-viewpoint.php
It is always a good idea to learn more about how the other half of the world thinks. Most people are closer to the values of social justice than the values of libertarianism, for all that that sort of "justice" (i.e. forced redistribution and mob envy) is just as destructive of wealth and progress as communism or fascism when put into earnest practice. It becomes a tyranny of egalitarianism, a leveling down, a tearing down of the high points of society, the groups that produce advances in technology. One of the values of reading In Search of Enlightenment is seeing the thinking that leads someone enmeshed in the culture of social justice - whose members characteristically belittle or reject scientific progress and the markets that drive it - come to advocate for longevity science and the defeat of aging: "Over the past decade I have worked at the intersection of issues in political philosophy/theory and the medical sciences. I have tried to help bridge what I take to be a troublesome divide between the field most concerned with ideals of justice and equality, and scientific advances (especially in the field of biogerontology) which could profoundly improve human health and prosperity. These two things are linked in important ways, but there is very little actually written by theorists on these kinds of topics. Bridging this gap is an up-hill struggle for a variety of reasons. The theoretical concepts and normative theories developed in political philosophy over the past 4 decades either ignored the realities of morbidity (e.g. like the fact that aging is a major risk factor for disease) or just assumed people went through their complete lives as 'healthy and productive members of society'. This meant the (almost exclusive) focus of theories of distributive justice was on the distribution of wealth and income. A fair society could be measured, so went the reasoning, to a large extent by the pattern of the distribution of a society's wealth. And the extent to which theories of justice have expanded, in the last 2 decades, to tackle topics like global justice and health, they are still constrained by the original assumptions and limited perspectives/concepts with which the dominant normative theories were originally devised. In other words, taking a theory of domestic justice designed to apply to a healthy and affluent society and then trying to make a few modifications once you take disease and debt seriously is not, imho, a recipe for success."

WORK ON PREPARING XENOTRANSPLANTS WITH DECELLULARIZATION
Friday, June 22, 2012
https://www.fightaging.org/archives/2012/06/work-on-preparing-xenotransplants-with-decellularization.php
Decellularization involves stripping out the original cells from a donor organ and then repopulating it with cells grown from the recipient's tissue - thereby removing the possibility of immune rejection. One implication of this approach is that the donor doesn't necessarily have to be human: "In proof-of-concept research [a] team successfully used pig kidneys to make 'scaffolds' or support structures that could potentially one day be used to build new kidneys for human patients. The idea is to remove all animal cells - leaving only the organ structure or 'skeleton.' A patient's own cells would then be placed on the scaffold, making an organ that the patient theoretically would not reject. ... this is one of the first studies to assess the possibility of using whole pig kidneys to engineer replacement organs ... For the research, pig kidneys were soaked in a detergent to remove all cells, leaving behind the organ's 'skeleton,' including its system of blood vessels. In addition, the structure of the nephron - the kidney's functional unit - was maintained. The scaffolds were implanted in animals, where they were re-filled with blood and were able to maintain normal blood pressure, proving that the process of removing cells doesn't affect the mechanical strength of the vessels. ... It is important to identify new sources of transplantable organs because of the critical shortage of donor organs. These kidneys maintain their innate three-dimensional architecture, as well as their vascular system, and may represent the ideal platform for kidney engineering."

DLK AND NERVE REGENERATION
Thursday, June 21, 2012
https://www.fightaging.org/archives/2012/06/dlk-and-nerve-regeneration.php
To go along with a recent post on cell therapies for nerve regeneration, here researchers investigate a different set of mechanisms: "A protein required to regrow injured peripheral nerves has been identified by researchers. ... The finding, in mice, has implications for improving recovery after nerve injury in the extremities. It also opens new avenues of investigation toward triggering nerve regeneration in the central nervous system, notorious for its inability to heal. ... scientists show that a protein called dual leucine zipper kinase (DLK) regulates signals that tell the nerve cell it has been injured - often communicating over distances of several feet. The protein governs whether the neuron turns on its regeneration program. ... How does an injured nerve know that it is injured? How does it take that information and turn on a regenerative program and regrow connections? And why does only the peripheral nervous system respond this way, while the central nervous system does not? We think DLK is part of the answer. ... If an axon is severed somewhere between the cell body in the spinal cord and the muscle, the piece of axon that is no longer connected to the cell body begins to disintegrate. Earlier work showed that DLK helps regulate this axonal degeneration. And in worms and flies, DLK also is known to govern the formation of an axon's growth cone, the structure responsible for extending the tip of a growing axon whether after injury or during development. The formation of the growth cone is an important part of the early, local response of a nerve to injury. But a later response, traveling over greater distances, proves vital for relaying the signals that activate genes promoting regeneration. This late response can happen hours or even days after injury. But in mice, unlike worms and flies, [DLK] is not involved in an axon's early response to injury. Even without DLK, the growth cone forms. But a lack of DLK means the nerve cell body, nestled in the spinal cord far from the injury, doesn't get the message that it's injured. Without the signals relaying the injury message, the cell body doesn't turn on its regeneration program and the growth cone's progress in extending the axon stalls. ... A neuron that has seen a previous injury now has a different regenerative program than one that has never been damaged. We hope to be able to identify what is different between these two neurons - specifically what factors lead to the improved regeneration after a second injury. We have found that activated DLK is one such factor. We would like to activate DLK in a newly injured neuron to see if it has improved regeneration."

A RESVERATROL META-ANALYSIS
Thursday, June 21, 2012
https://www.fightaging.org/archives/2012/06/a-resveratrol-meta-analysis.php
Here is another paper suggesting that resveratrol isn't necessarily a great place to be spending hundreds of millions of dollars on research and development, given the poor results in studies that evaluate its effects. In an ideal world this money that would go towards improving biotechnology rather than the old-school approach of mining the natural world for compounds that maybe do more good than harm: "Resveratrol has shown evidence of decreasing cancer incidence, heart disease, metabolic syndrome and neural degeneration in animal studies. However, the effects on longevity are mixed. We aimed to quantify the current knowledge of life extension from resveratrol. We used meta-analytic techniques to assess the effect resveratrol has on survival, using data from 19 published papers, including six species: yeast, nematodes, mice, fruitflies, Mexican fruitflies and turquoise killifish. Overall, our results indicate that resveratrol acts as a life-extending agent. The effect is most potent in yeast and nematodes, with diminished reliability in most higher-order species. Turquoise killifish were especially sensitive to life-extending effects of resveratrol but showed much variation. Much of the considerable heterogeneity in our analysis was owing to unexplained variation between studies. In summary, we can report that few species conclusively show life extension in response to resveratrol. As such, we question the practice of the substance being marketed as a life-extending health supplement for humans."

MITOCHONDRIAL MEMBRANE RESISTANCE TO EXPLAIN CLAM LONGEVITY
Wednesday, June 20, 2012
https://www.fightaging.org/archives/2012/06/mitochondrial-membrane-resistance-to-explain-clam-longevity.php
You might recall the species of clam that can live for at least four centuries. Similarly, you might also recall the membrane pacemaker hypothesis that explains differences in longevity between species in terms of the resistance of cell membranes - and especially mitochondrial membranes - to damage. Here, the two topics are linked: "The deleterious reactive carbonyls released upon oxidation of polyunsaturated fatty acids in biological membranes are believed to foster cellular aging. Comparative studies in mammals and birds have shown that the susceptibility to peroxidation of membrane lipids (peroxidation index, PI) is negatively correlated to longevity. Long-living marine molluscs are increasingly studied as longevity models, and the presence of different types of lipids in the membranes of these organisms raises questions on the existence of a PI-longevity relationship. We address this question by comparing the longest-living metazoan species, the mud clam Arctica islandica (maximum reported longevity = 507 y) to four other sympatric bivalve molluscs greatly differing in longevity (28, 37, 92, and 106 y). We contrasted the acyl and alkenyl chain composition of phospholipids from the mitochondrial membranes of these species. The analysis was reproduced in parallel for a mix of other cell membranes to investigate if a different PI-longevity relationship would be found. The mitochondrial membrane PI was found to have an exponential decrease with increasing longevity among species and is significantly lower for A. islandica. The PI of other cell membranes showed a linear decrease with increasing longevity among species and was also significantly lower for A. islandica. These results clearly demonstrate that the PI also decreases with increasing longevity in marine bivalves and that it decreases faster in the mitochondrial membrane than in other membranes in general. Furthermore, the particularly low PI values for A. islandica can partly explain this species' extreme longevity." This emphasizes the importance of mitochondrial damage in aging and longevity, and thus the importance of research into mitochondrial repair biotechnologies for humans.

ARGUING AGAINST THE ROLE OF CYTOMEGALOVIRUS IN IMMUNE SYSTEM AGING
Wednesday, June 20, 2012
https://www.fightaging.org/archives/2012/06/arguing-against-the-role-of-cytomegalovirus-in-immune-system-aging.php
There's a fair amount of evidence implicating cytomegalovirus (CMV) in immune system decline, rhe theory here being that the immune system devotes ever more of its fixed resources to dealing with the largely harmless variants of this virus that it cannot clear. Here researchers argue against that view: "Aging is accompanied by the development of low grade systemic inflammation, termed 'inflammaging', characterised by raised serum C-reactive protein (CRP) and pro-inflammatory cytokines. Importantly, inflammaging is implicated in the pathogenesis of several of the major age-related diseases including cardiovascular disease, type 2 diabetes and dementia and is associated with increased mortality. The incidence of infection with the persistent herpes virus cytomegalovirus (CMV) also increases with age. Cross-sectional studies have proposed CMV infection as a significant driver of inflammaging, but a definitive case for CMV as a causative agent in inflammaging has not yet been made. We studied longitudinally 249 subjects (153 men, 96 women) who participated in the Hertfordshire Ageing Study at baseline (1993/5, mean age 67·5 years) and at 10 year follow up. At both times [subjects] provided blood samples for analysis of inflammatory status and CMV seropositivity. In the cohort as a whole, serum CRP and pro-inflammatory cytokines [were] increased between baseline and follow up ... These changes to cytokine status over time occurred equally in the 60% of subjects who were seropositive for CMV at baseline and follow up, the 8% who were CMV negative at baseline but who became CMV positive by the 10 year follow up, and also in the 32% who were CMV seronegative throughout. We conclude that CMV infection is not a primary causative factor in the age-related increase in systemic inflammation."

HUMAN OPTIC CUP GROWN FROM STEM CELLS
Tuesday, June 19, 2012
https://www.fightaging.org/archives/2012/06/human-optic-cup-grown-from-stem-cells.php
From Nature: researchers have "grown the precursor of a human eye in the lab. The structure, called an optic cup, is 550 micrometres in diameter and contains multiple layers of retinal cells including photoreceptors. The achievement has raised hopes that doctors may one day be able to repair damaged eyes in the clinic. ... the most exciting thing is that the optic cup developed its structure without guidance from [the] team. ... Until recently, stem-cell biologists had been able to grow embryonic stem-cells only into two-dimensional sheets. But over the past four years, [this group] has used mouse embryonic stem cells to grow well-organized, three-dimensional cerebral-cortex, pituitary-gland and optic-cup tissue. His latest result marks the first time that anyone has managed a similar feat using human cells. ... The various parts of the human optic cup grew in mostly the same order as those in the mouse optic cup. This reconfirms a biological lesson: the cues for this complex formation come from inside the cell, rather than relying on external triggers. ... retinal precursor cells spontaneously formed a ball of epithelial tissue cells and then bulged outwards to form a bubble called an eye vesicle. That pliable structure then folded back on itself to form a pouch, creating the optic cup with an outer wall (the retinal epithelium) and an inner wall comprising layers of retinal cells including photoreceptors, bipolar cells and ganglion cells. ... This resolves a long debate [over] whether the development of the optic cup is driven by internal or external cues."

ARGUING A MECHANISM FOR DNA DAMAGE TO DRIVE AGING
Tuesday, June 19, 2012
https://www.fightaging.org/archives/2012/06/arguing-a-mechanism-for-dna-damage-to-drive-aging.php
There is some debate over the degree to which accumulated nuclear DNA damage contributes to aging. Here researchers propose a class of mechanisms: "Aging is characterized by the inability of tissues to maintain homeostasis. This leads to an impaired response to stress and, as a consequence, an increased risk of morbidity and mortality. ... Aging is thought to be driven, at least in part, by the accumulation of stochastic damage in cells. ... However, the mechanism by which cellular damage drives aging is not known. The simplest model is that damage causes attrition of functional cells. But this is inadequate in light of emerging evidence that aging-related degenerative changes in old and damaged organisms can be delayed or reversed by circulating factors. These observations point instead toward the cellular response to damage being the key driver of aging. The transcription factor NF-κB is a central component of the cellular response to damage, stress, and inflammation ... Numerous studies report increased NF-κB activity with aging. ... Genetic depletion of NF-κB in the skin of transgenic mice reversed age-related gene expression and histologic changes, providing support for NF-κB activation playing a causal role in skin aging. ... it remains to be determined whether NF-κB activation drives systemic aging and whether NF-κB is a therapeutic target for attenuating and/or delaying aging-related degenerative changes. ... We found that NF-κB is stochastically activated in a variety of cell types with normal and accelerated aging and that genetic or pharmacologic inhibition of NF-κB activation delays the onset of numerous aging-related symptoms and pathologies. Inhibition of IKK/NF-κB activity reduced cellular senescence and oxidative damage, including DNA and protein damage, revealing that cellular stress responses promote further cellular damage. Our findings strongly suggest that inhibitors of the IKK/NF-κB pathway may delay damage and extend healthspan in patients with accelerated aging and chronic degenerative diseases of old age."

CCR2 AND THE IMMUNE SYSTEM VERSUS ALZHEIMER'S DISEASE
Monday, June 18, 2012
https://www.fightaging.org/archives/2012/06/ccr2-and-the-immune-system-versus-alzheimers-disease.php
One portion of the Alzheimer's research field is focused on immune therapies - training the immune system to attack and break down amyloid beta plagues characteristic of Alzheimer's disease. It is important to note that the buildup of signs of Alzheimer's, such as amyloid beta, occurs in most people to a lesser degree, whether or not they go on to develop the condition, and that the level of this sort of damage is associated with level of mental decline with aging. Here researchers show that this may all have something to do with how effective the immune system is in clearing out unwanted junk from the brain: "Recent work in mice suggested that the immune system is involved in removing beta-amyloid, the main Alzheimer's-causing substance in the brain. Researchers have now shown for the first time that this may apply in humans. [Researchers] screened the expression levels of thousands of genes in blood samples from nearly 700 people. The telltale marker of immune system activity against beta-amyloid, a gene called CCR2, emerged as the top marker associated with memory in people. The team used a common clinical measure called the Mini Mental State Examination to measure memory and other cognitive functions. The previous work in mice showed that augmenting the CCR2-activated part of the immune system in the blood stream resulted in improved memory and functioning in mice susceptible to Alzheimer's disease. ... This is a very exciting result. It may be that CCR2-associated immunity could be strengthened in humans to slow Alzheimer's disease, but much more work will be needed to ensure that this approach is safe and effective."

APOLOGISM FOR AGING IS UNPRODUCTIVE
Monday, June 18, 2012
https://www.fightaging.org/archives/2012/06/apologism-for-aging-is-unproductive.php
Via the IEET: "Louis Begley vividly describes the last years of his mother's life, who had been a widow for the previous 40 years before her death. Begley lets us feel the pain in her joints and in her heart. He obviously sees aging as nothing but misery and loneliness. But I think he misses the point - he believes his mother's solitude is the reason of her woes, but it actually is aging, her declined health, pain and suffering - these are the real reasons of her tragedy. If she had been young she would have had no diseases, but only good looks and the opportunity to start over, but alas! she rots alive. Louis Begley caught the very overwhelming in its inevitability, horrifying feeling that it's all over, no need to buy new costumes. They will not be worn for a long time and they're not worth spending time and money. Mr. Begley was widely criticized - and by whom? Who do you think justified aging? The Executive Director and chief scientific officer of the Alzheimer's Drug Discovery Foundation wrote: 'Mr. Begley's bitter portrayal of aging is neither universal nor inevitable... Old age should never be measured by the metrics of youth. An adaptive rather than a maladaptive response to old age and even frailty is possible.' This is unbelievable. So wrong. In reality it's exactly the opposite - aging is universally debilitating and inevitable. While this type of words are coming out of the mouths of people who are the advocates for aging research, nothing good will happen. There will be no money for research to live longer in a younger body. And the reason is the faulty idea that aging can be healthy, productive, or enjoyable. It can't by definition."

______________________________

Comments

Post a comment; thoughtful, considered opinions are valued. Comments incorporating ad hominem attacks, advertising, and other forms of inappropriate behavior are likely to be deleted.

Note that there is a comment feed for those who like to keep up with conversations.