Healthy Life Extension

Funding Aging Research

I'm Dying!

posted on August 02, 2011

Dear Future Centenarian,

Are you familiar with hPlus Magazine? If not, you™re missing one of the treasures of the Internet if you have an interest in the future and the betterment of humanity.  Following are some slightly edited excerpts of one of Reason™s articles pertaining to, what else, aging¦ and our head-in-the-sand attitude to what it is doing to us.

We all express the symptoms of a fatal, inherited degenerative condition called aging”or so the joke goes. It™s a dark joke, but there™s truth to be found in it, as is often the case in black humor. Unfortunately, all too few people think of themselves as patients suffering aging, and fewer still would call themselves patient advocates, agitating for research leading towards therapies and cures for aging.

This is a sorry state of affairs: given that our time is limited and ticking away, the tasks upon the table should always include some consideration of aging. What can we do about it? How can we engineer a research community, funding and support to make real progress within our lifetimes? If you don™t spend at least some of your time on this issue, then you™re fiddling while Rome burns. Time is the most precious thing we have, and we live on the cusp of technologies that will allow us to gain more of it”but those advances in medicine won™t happen soon enough unless we work at it.

Working on progress in longevity science doesn™t have to mean working in a lab. Much of what Reason has done to help matters along takes the form of written advocacy at Fight Aging! and elsewhere: sharing events, passing on news, putting scientific publications in context, explaining where we stand in research and development, encouraging fundraising, and so on.

In effect this is a sort of loose documentation of the existence of the community of people interested in engineered longevity, and a way to provide direction and grounding to newcomers: how to become involved, how to benefit from becoming involved, and how to help advance the science of human longevity.

This is also the purpose of Longevity News Digest, along with arming you with the information you need to extend your healthspan with the tools we have available today until radical life-extending technologies will be fully developed.

Most important topics relating to the future of advanced technological development are very complex: engineered human longevity, strong artificial intelligence, molecular manufacturing, and so forth.

Even the general concepts (such as œwhy is this important?, œwhy is this plausible?, or œwhy should I support it?) are made up of many moving parts and conditional arguments that the broader public generally hasn™t heard or thought about yet. Thus we advocates can™t just jump in and start persuading people that life extension is a great idea. Instead, when it comes time to try to explain why this goal is important”and how best to proceed with research and development”we must first walk through a whole squadron of supporting concepts that are unfamiliar to the audience. Each must be explained, and only then can they be assembled into the final persuasive conclusion.

In the area of healthy life extension and biotechnologies to repair aging, an array of foundational ideas might include the following:

  • This is a time of radical progress in biotechnology, far more so than even just a decade ago.
  • Scientists can extend life in a score of different ways in laboratory animals.
  • But you don™t see the results of this work in the clinic, because the FDA is needlessly obstructive.
  • Aging is just damage, and that damage is well enough understood for work on practical repair biotechnologies to proceed.
  • A large-scale research program could plausibly produce decades of life extension by 2029.
  • Any effective longevity therapy will give people more time of life and health to wait for even better new therapies.
  • Overpopulation is a myth, and longer lives won™t greatly increase population in any case.
  • Ethical objections to engineered longevity are all weak in comparison to the massive and ongoing harm caused by aging.

Each of these is no small thing in and of itself, and worthy of longer treatment. So presenting all of the concepts that lead up to thinking about rejuvenation biotechnologies is time-consuming, hard to do well, and requires a willing and interested audience.

Unfortunately few people in the broader public are in fact willing put in the effort to follow you, me, or anyone else with a complicated idea all the way from square one to the end point. That takes time and attention”both of which are precious commodities, hard to obtain at the best of times. Thus the ideas that do gain traction in our culture are those that can be successfully communicated in a short period of time, because they build directly upon what is already known.

Long Life,
David Kekich


Here is a repetition of the sort of research from the last century that initially drew interest to calorie restriction, in which researchers are trying to pin down the point at which beneficial calorie restriction becomes harmful malnutrition: "It has been firmly established that the longevity of 20 to 60 %-calorie-restricted rodents, with malnutrition (essential nutrients deficiency) being avoided, is increased when compared to ad libitum fed rodents. However, the effects on life span of severe dietary restriction (i. e. malnutrition), with limited weight loss, remained unknown. The purpose of this 4-year study was to investigate the effects on longevity of a severe form of dietary restriction, with limited and controlled weight loss. To this end, a group of male Long-Evans rats severely dietary restricted (SDR group), with a weight loss throughout the experiment tryptophan, methionine, and fat, for example)."

The Technology Review looks at the work of researchers attempting to restore youthful function in brain cells associated with memory: "By delivering a certain chemical to the brain, researchers could make neurons in old monkeys behave like those in young monkeys. Clinical trials of a generic drug that mimics this effect are already underway. The findings support the idea that some of the brain changes that occur with aging are very specific - rather than being caused by a general decay throughout the brain - and can potentially be prevented.

[Researchers] recorded electrical activity from neurons in a part of the brain called the prefrontal cortex, a region especially vulnerable to aging in both humans and [other] primates. It is vital for our most high-level cognitive functions, such as working memory and the ability to multitask and inhibit distractions. Neural circuits in this region are organized to create a sustained level of activity that is crucial for working memory. By analyzing activity recorded from young, middle-aged, and old monkeys, the researchers found that the firing rate of the neurons in this area declines with age. They found that other neurons, such as those that respond to cues in the environment, still fired normally even as the monkeys aged. The researchers were able to rein in the problem by treating the cells with a drug that blocks the potassium channels. After treatment, brain cells in old monkeys fired more rapidly - just like those in their younger counterparts. The researchers already knew that giving monkeys this drug systemically, rather than delivering it directly into the brain, could reverse age-related deficits in working memory. A clinical trial of the compound, a generic drug called guanfacine, originally used to treat hypertension, is underway."

VIa EurekAlert!: "Approximately 60 million people across the globe have chronic kidney disease, and many will need dialysis or a transplant. [Research] indicates that patients' own kidney cells can be gathered and reprogrammed. Reprogramming patients' kidney cells could mean that in the future, fewer patients with kidney disease would require complicated, expensive procedures that affect their quality of life. In the first study, [researchers] took cells from an individual's kidney and coaxed them to become progenitor cells, allowing the immature cells to form any type in the kidney.

Specifically, they inserted several key reprogramming genes into the renal cells that made them capable of forming other cells. In a second study, [researchers] found that kidney cells collected from a patient's urine can also be reprogrammed in this way. Using cells from urine allows a technology easy to implement in a clinic setting. Even better, the urine cells could be frozen and later thawed before they were manipulated. If researchers can expand the reprogrammed cells - called induced pluripotent stem cells (iPSCs) - and return them to the patient, these IPSCs may restore the health and vitality of the kidneys. In addition to providing a potentially curative therapy for patients, the breakthroughs might also help investigators to study the causes of kidney disease and to screen new drugs that could be used to treat them."

Another reason to exercise: "Senescent T-cells accumulate with age, lowering the naive T-cell repertoire and increasing host infection risk. As this response is likely to be influenced by certain lifestyle factors, we examined the association between aerobic fitness (VO(2max)) and the age-related accumulation of senescent T-cells. Blood lymphocytes from 102 healthy males (18-61yr) were analyzed for [marker] surface expression on CD4+ and CD8+ T-cells. Advancing age (yr) was positively associated with the proportion (%) of senescent [and] CD8+ T-cells and inversely associated with naive CD4+ and CD8+ T-cells. VO(2max) was inversely associated with senescent CD4+ and CD8+.

Strikingly, age was no longer associated with the proportions of senescent or naive T-cells after adjusting for VO(2max), while the association between VO(2max) and these T-cell subsets withstood adjustment for age, BMI and percentage body fat. Ranking participants by age-adjusted VO(2max) revealed that the highest tertile had had 17% more naive CD8+ T-cells and 57% and 37% less senescent CD4+ and CD8+ T-cells, respectively, compared to the lowest tertile. This is the first study to show that aerobic fitness is associated with a lower age-related accumulation of senescent T-cells, highlighting the beneficial effects of maintaining a physically active lifestyle on the aging immune system."

Via ScienceDaily: "The same artery-clogging process (atherosclerosis) that causes heart disease can also result in age-related vascular cognitive impairments (VCI). Cognitive impairment, also known as dementia, includes difficulty with thinking, reasoning and memory, and can be caused by vascular disease, Alzheimer's disease, a combination of both and other causes. Atherosclerosis is a build- up of plaque in the arteries associated with elevated blood pressure, cholesterol, smoking and other risk factors. When it restricts or blocks blood flow to the brain, it is called cerebrovascular disease, which can result in vascular cognitive impairment.

We have learned that cerebrovascular disease and Alzheimer's disease may work together to cause cognitive impairment and the mixed disorder may be the most common type of dementia in older persons. Treating risk factors for heart disease and stroke with lifestyle changes and medical management may prevent or slow the development of dementia in some people. Physical activity, healthy diet, healthy body weight, tobacco avoidance as well as blood pressure and cholesterol management could significantly help many people maintain their mental abilities as they age." An unhealthy lifestyle corrodes the body and mind faster than would otherwise be the case. As we approach the era of age-reversing biotechnologies, it's worth thinking about how you might maximize your chance of reaching and benefiting from those years yet to come.

The mind decays in characteristic ways, and researchers are making inroads in linking the symptoms to the specific physical causes: "Advanced aging is associated with reduced attentional control and less flexible information processing. Older adults often perform poorly in situations where multiple goals and response rules must be maintained and coordinated. Here, we explored age differences in recruitment of brain systems associated with attentional control and their relationship to behavior and markers of neuropathology.

Examining 2 markers of preclinical pathology in older adults revealed that white matter hyperintensities (WMHs), but not high amyloid burden, were associated with failure to modulate activity in response to changing task demands. In contrast, high amyloid burden was associated with alterations in default network activity. These results, in addition to the rarity of co-occurrence between amyloid and white matter pathology among our sample of clinically normal adults, suggest that age-related cognitive failures may arise from multiple distinct pathologies. Age-related failures of dynamic allocation of attention may be an early consequence of disrupted neural integrity within prefrontal-parietal networks."

From the Washington Post: "Robert C. W. Ettinger, a physics teacher and science fiction writer who believed death is only for the unprepared and unimaginative, died July 23 at his home in Clinton Township, Mich. He was 92 and had suffered declining health in recent weeks, said his son David, who could not specify a cause. 'We're obviously sad,' said the younger Ettinger. But 'we were able to freeze him under optimum conditions, so he's got another chance.' Mr. Ettinger is widely considered the father of the cryonics movement, whose adherents believe they can achieve immortality through quick-freezing their bodies at death in anticipation of future resurrection.

Mr. Ettinger's frozen body is being stored in a vat of liquid nitrogen at a nondescript building outside Detroit, home to more than 100 fellow immortalists - including his mother and two wives - who are awaiting revival. If all goes as Mr. Ettinger envisioned, he will remain in a period of icy stasis for decades - or perhaps centuries - however long it takes for doctors, armed with technology of the future, to defrost him and restore him to good health. Mr. Ettinger was a little-known community college professor in the mid-1960s when he wrote the founding document of cryonics, 'The Prospect of Immortality,' a manifesto that described the practical and moral aspects of deep-freezing the dead. Introducing what he called the Freezer Era, Mr. Ettinger described a world in which people would become nobler and more responsible as they were confronted with the reality of living forever." It is important to note that cryonics nowadays is less about freezing and more about vitrification: ice crystal formation is minimized and thus so is cellular damage.

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