Fight Aging! Newsletter, May 7th 2012
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May 7th 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!



- Video: "this house wants to defeat aging entirely"
- Radical Life Extension at the Melbourne Humanity+ Conference
- Plausible, Possible, Expensive, Prohibited
- Cryonics Magazine, March-April 2012
- Discussion
- Latest Headlines from Fight Aging!


Video has been posted of the recent Oxford University Science Society public debate between Aubrey de Grey of the SENS Foundation and Colin Blakemore, former head of the Medical Research Council.

"Formal debates in science and medicine, sponsored by academic societies, are a long-standing tradition in England: in the history of the sciences many of the important inflection points and transitions between eras of knowledge were marked by public debates held between the worthies of the time. The debates do not in and of themselves determine anything: they are a reflection of ongoing matters of interest and the clash of strategies or theories that currently engage the scientific community. Thus it should be taken as a promising sign that awareness of SENS-style rejuvenation biotechnology is at a level at which such debates are held and well-attended.

"Rejuvenation through medical technology is in our future, and factions within the scientific and medical development communities are forming and polarizing around opinions on plausibility, how to construct therapies for aging, and just how urgent it is to take action on this issue. Much of the ongoing debate within the scientific community is invisible to the world at large - but make no mistake, it is taking place, and has been for the better part of a decade. When it comes to aging and what to do about it, the research community of today is a radically different place from the research community of the first years of this century."


And here is Aubrey de Grey in the news again, getting good press in Australia on the occasion of the 2012 Humanity+ conference in Melbourne held this past weekend:

"When British gerontologist Aubrey de Grey talks about radical life extension for humans - decades, even centuries more of existence - he is not imagining us slogging by with brain plaque, loose dentures and walking frames. Rather, we would be in rude health, with all the hallmarks of age in abeyance, even retreat. No wrinkles, fraying organs, leaky bladders or aching joints. And not much need for aged care or pensions. ... In a world where life expectancy has already dramatically increased over the past century or two, we now face the likelihood of being able to custom-order fresh organs and body parts on 3D-printers, and to treating the basic causes of ageing with the likes of stem-cell therapy and nanotechnology.

"De Grey and [Natasha] Vita-More, in Melbourne for this weekend's Humanity+ conference, are in the vanguard of futurists who believe that looking great or designing our bodies to suit (blue skin and magenta eyes anyone?) will be fringe benefits. That is because, in a fast-approaching era of living longer, healthier lives, it is expected we will have time to enjoy the wisdom and opportunities of getting older - we won't be so focused on all the medical appointments, decrepitude and fragility associated with old age. ... de Grey, who once said some of today's infants might live to 1000 years old, and who not so long ago was viewed sceptically by other scientists for his insistence that ageing is a preventable, treatable medical condition, now sees much broader acceptance of his ideas among scientists.

'"'Attitudes have changed enormously,' he says. 'The feasibility of what I have been proposing is now generally accepted. It took a long time, because essentially ... people who were expert in regenerative medicine didn't know about ageing; and people expert in ageing didn't know about regenerative medicine.'

"A bigger battle has been with the attitudes of the general population, who view ageing as natural and inevitable and who, asked if they would like to have much longer lifespans, deliver predictable objections, often saying they would get bored (so much for the human imagination). De Grey says these responses are because people don't think of ageing in the same category as other diseases: if they understood they could live much longer without medical problems or signs of ageing, they would be enthusiastic. 'They just don't think of [ageing] as a plausible target for medicine.'"


What could you choose to do today, if you had enough money for a major medical procedure, and the legion of medical regulators didn't exist? If you were free to choose your own risks in medicine, and doctors and researchers were free to be paid to help you? Here are a few examples, with varying degrees of risk, reward, and unknown factors:

"Have your aging immune system wiped out with chemotherapy and replaced from your stem cells. Your wager here would be that undergoing chemotherapy (not a wonderful experience under the best of circumstances) will cause you less harm in the long term than keeping your original, increasingly misconfigured immune system. Alternately, you could wait a decade for targeted cell-killer therapies demonstrated in mice to become a practical concern in humans.

"Undergo any one of a number of potential enhancing gene therapies. For example, why not pay your way into possessing a myostatin mutation? That boosts muscle mass, increases resistance to a range of age-related conditions, and otherwise seems to be beneficial all-round in mammals.

"Purchase stem cell infusions of the sort that seem to be at least modestly helpful for any number of degenerative conditions - a better option than traditional pharmaceutical medicines. But of course you can't do that in the US, just like you can't benefit from near all of the most recent advances, locked away in trials for years yet. You'd have to head overseas as a medical tourist to become a customer of the more reliable clinics in Asia or the Middle East.

"Decide in your healthy old age that the possible benefits outweigh the risks for infusion-based biphosphonate therapy [which was unexpectedly shown to extend life expectancy by years in the elderly]. Of course you can't obtain that legally as a healthy person - those regulators again, deciding that they know better and anyone who disagrees with them will ultimately wind up in jail.

"Choose to end your own long-lived life in a safe and painless way at the time of your choosing, while attended by cryonics professionals who can provide an immediate and expert preservation - offering absolutely the best chance of later restoration with minimal damage, while keeping the cost to a sensible minimum thanks to scheduling.

"I could go on - that just scratches the surface. But of course any group that gathered in the US to try these things, or offer services, or make the process as safe and transparent as possible would quickly find themselves prosecuted and jailed. The land of the free long ago ceased to have much to do with liberty or personal freedom. Freedom is the freedom to take your own risks and pay the costs if you pull a bad card from the deck - and that freedom is exactly what drives progress. Take it away and what results is the regulatory stagnation you see in medicine today."


The March-April issue of Cryonics is available online:

"The main topic of the issue ties into the ongoing discussion on maintaining Alcor's reserve of funds at a sufficient level for the long term - which is essentially a battle against the predatory inflation produced by the self-serving actions of politicians and political appointees. The political class can be expected to create ever more money from nothing, continually reducing the value of money in circulation and savings accounts, because it is the most effective way to tax the masses - all other forms of taxation generate far more unrest, resistance, and non-compliance, and are thus much more self-limiting in the revenue they can generate.The battle against the inflation resulting from depreciation of the currency is fought by all entities that must tie contracts inked today to outlays required years from now:

"As evidenced by recent exchanges on the Alcor Member Forums, our members have a wide variety of suggestions for how to close the substantial funding gap that has been produced by Alcor's practice to date of not raising cryopreservation minimums for existing members. If there is one area of strong agreement, however, it is that all members who are underfunded for today's cryopreservation minimums and who can afford to change or upgrade their life insurance, should do so. This will not just reduce Alcor's funding shortfall but it will also allow the member to secure new cryopreservation and storage technologies that cannot be offered without charging an additional amount. Surplus funding can also be allocated to a personal revival trust or to Alcor's hardship fund to help members with poor funding and/or challenges to pay annual dues.

"The March-April issue of Cryonics magazine features an extensive review of life insurance options by Alcor member and life insurance agent Rudi Hoffman. Rudi introduces the topic by presenting the disturbing long-term effects of (medical) inflation. Not all of Alcor's services may be subject to the kind of cost increases we see in medicine but it is prudent to plan using conservative assumptions. After this sobering introduction, Rudi runs us through the various forms of life insurance, their pros and cons, and how to read those long, intimidating policy illustrations. We at Alcor hope that many of you will make efforts to update your cryonics funding to make it easier to solve the underfunding problem and to assist with the really hard cases."


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!



Friday, May 4, 2012
More rejuvenation of stem cell function demonstrated in mice: "Researchers have rejuvenated aged hematopoietic stem cells to be functionally younger, offering intriguing clues into how medicine might one day fend off some ailments of old age. ... The paper brings new perspective to what has been a life science controversy - countering what used to be broad consensus that the aging of hematopoietic stem cells (HSCs) was locked in by nature and not reversible by therapeutic intervention. HSCs are stem cells that originate in the bone marrow and generate all of the body's red and white blood cells and platelets. They are an essential support mechanism of blood cells and the immune system. As humans and other species age, HSCs become more numerous but less effective at regenerating blood cells and immune cells. ... Researchers in the current study determined a protein that regulates cell signaling - Cdc42 - also controls a molecular process that causes HSCs from mice to age. Pharmacologic inhibition of Cdc42 reversed HSC aging and restored function similar to that of younger stem cells. ... We know the aging of HSCs reduces in part the response of the immune system response in older people, which contributes to diseases such as anemia, and may be the cause of tissue attrition in certain systems of the body. ... One reason the research team focused on Cdc42 is that previous studies have reported elevated activity of the protein in various tissue types of older mice - which have a natural life span of around two years. Also, elevated expression of Cdc42 has been found in immune system white blood cells in older humans. In the current study, researchers found elevated activity of Cdc42 in the HSCs of older mice. They also were able to induce premature aging of HSCs in mice by genetically increasing Cdc42 activity in the cells. ... To test the rejuvenated cells, the researchers used a process known as serial competitive transplantation. This included extracting HSCs from young (2-4 months) and aged (20-26 months) mice and processing them in laboratory cultures. Young and rejuvenated cells were then engrafted into recipient mice. This allowed scientists to compare how well young and rejuvenated aged HSCs started to repopulate and transform into different types of blood cells. It also confirmed that HSCs rejuvenated by targeting Cdc42 do function similarly to young stem cells."

Friday, May 4, 2012
An example of ongoing work to make targeted cell-killing technologies economically practical: "For more than a decade, researchers have been trying to develop nanoparticles that would deliver drugs more effectively and safely. The idea is that a nanoparticle containing a drug compound could selectively target tumor cells or otherwise diseased cells, and avoid healthy ones. Antibodies or other molecules can be attached to the nanoparticle and used to precisely identify target cells. ... [Researchers] devised a method by which the building blocks of the nanoparticle and the drug self-assemble into a final product. Two types of polymer combine to form the tangled mesh of [a] drug-laden spherical nanoparticle. One of these polymers has two chemically and structurally distinct regions, or 'blocks': a water-insoluble block that forms part of the mesh that encapsulates the drug, and a water-soluble block that gives the final product a stealthy corona to evade the immune system. The other type of polymer has three blocks: the same two as the first, as well as a third region that contains a targeting molecule - the signal that will ensure the final particles attach to the desired cell types. The drug-carrying nanoparticles are formed by simply mixing these polymers together with the drug in the appropriate conditions. The self-assembling polymers can be produced in a repeatable and scalable fashion. But the method has an additional benefit ... The method by which the nanoparticles are built - from individual preparations of the two-block and three-block polymers - would also let researchers use high-throughput screening approaches, akin to how medicinal chemists design and test new drug compounds. Each block could be tweaked - extend one block, change the charge on another - and the relative amounts of each polymer could be varied. With so many parameters for tinkering, [scientists] can screen many combinations."

Thursday, May 3, 2012
It has been a number of years since researchers started to investigate the role of DJ-1 in Parkinson's disease. Here, the work has made it to the stage of a possible therapy: "As we age, we naturally lose dopamine-producing neurons. Parkinson's patients experience a rapid loss of these neurons from the onset of the disease, leading to much more drastic deficiencies in dopamine than the average person. ... Mutations in the gene known as DJ-1 lead to accelerated loss of dopaminergic neurons and result in the onset of Parkinson's symptoms at a young age. The ability to modify the activity of DJ-1 could change the progress of the disease. [Researchers have] now developed a peptide which mimics DJ-1's normal function, thereby protecting dopamine- producing neurons. What's more, the peptide can be easily delivered by daily injections or absorbed into the skin through an adhesive patch. Based on a short protein derived from DJ-1 itself, the peptide has been shown to freeze neurodegeneration in its tracks, reducing problems with mobility and leading to greater protection of neurons and higher dopamine levels in the brain. ... We attached the DJ-1-related peptide to another peptide that would allow it to enter the cells, and be carried to the brain. ... In pre-clinical trials, the treatment was tested on mice ... From both a behavioral and biochemical standpoint, the mice that received the peptide treatment showed remarkable improvement. Symptoms such as mobility dysfunctions were reduced significantly, and researchers noted the preservation of dopamine-producing neurons and higher dopamine levels in the brain. Preliminary tests indicate that the peptide is a viable treatment option. Though many peptides have a short life span and degrade quickly, this peptide does not."

Thursday, May 3, 2012
Moderate exercise improves life expectancy: "Undertaking regular jogging increases the life expectancy of men by 6.2 years and women by 5.6 years, reveals the latest data from the Copenhagen City Heart study ... the study's most recent analysis (unpublished) shows that between one and two-and-a-half hours of jogging per week at a 'slow or average' pace delivers optimum benefits for longevity. ... SThe study, which started 1976, is a prospective cardiovascular population study of around 20,000 men and women aged between 20 to 93 years. The study, which made use of the Copenhagen Population Register, set out to increase knowledge about prevention of cardiovascular disease and stroke. Since then the study, which has resulted in publication of over 750 papers, has expanded to include other diseases ... The investigators have explored the associations for longevity with different forms of exercise and other factors. For the jogging sub study, the mortality of 1,116 male joggers and 762 female joggers was compared to the non joggers in the main study population. All participants were asked to answer questions about the amount of time they spent jogging each week, and to rate their own perceptions of pace (defined as slow, average, and fast). ... The first data was collected between 1976 to 1978, the second from 1981 to 1983, the third from 1991 to 1994, and the fourth from 2001 to 2003. For the analysis participants from all the different data collections were followed using a unique personal identification number in the Danish Central Person Register. ... These numbers have been key to the success of the study since they've allowed us to trace participants wherever they go. ... Results show that in the follow-up period involving a maximum of 35 years, [risk] of death was reduced by 44%."

Wednesday, May 2, 2012
Chronic inflammation is a bad thing - it greatly increases your risk of suffering age-related disease, and may be one of the more important mechanisms linking excess fat tissue to risk of disease and lowered life expectancy. Here is more evidence to show that being overweight exposes a person to greater inflammation: "Postmenopausal women who were overweight or obese and lost at least 5 percent of their body weight had a measurable reduction in markers of inflammation. ... Both obesity and inflammation have been shown to be related to several types of cancer, and this study shows that if you reduce weight, you can reduce inflammation as well. ... Women in the trial who were assigned to a weight loss intervention had a goal of 10 percent weight reduction during the course of one year achieved through a diet intervention with or without aerobic exercise. ... The researchers measured levels of C-reactive protein, serum amyloid A, interleukin-6, leukocyte and neutrophil in 439 women. At the end of one year, C-reactive protein reduced by 36.1 percent in the diet-alone group and by 41.7 percent in the diet and exercise group. Interleukin-6 decreased by 23.1 percent in the diet group and 24.3 percent in the diet and exercise group. ... there were greater reductions in these measures among women who lost at least 5 percent of their body weight. They also found that exercise alone, without a dietary weight loss component, had little effect on inflammation markers."

Wednesday, May 2, 2012
An introduction to what is known of telomeres can be found at the Scientist: "The ends of linear chromosomes have attracted serious scientific study - and Nobel Prizes - since the early 20th century. Called telomeres, these ends serve to protect the coding DNA of the genome. When a cell's telomeres shorten to critical lengths, the cell senesces. Thus, telomeres dictate a cell's life span - unless something goes wrong. Work over the past several decades has revealed an active, though limited, mechanism for the normal enzymatic repair of telomere loss in certain proliferative cells. ... Telomeres shorten as we age. By analogy to the cellular mitotic clock, telomeres have been postulated as a marker of 'genetic age,' and telomere length has been marketed as a simple predictor of longevity. Assays of telomere length have been bundled with recommendations for lifestyle modification and for drug therapy, neither based on appropriate clinical studies. Simple but appealing arguments relating telomeres and aging are currently controversial, likely simplistic, and potentially harmful. Telomere length does indeed reflect a cell's past proliferative history and future propensity for apoptosis, senescence, and transformation. Cellular aging, however, is not equivalent to organ or organismal aging. ... Studies in humans have attempted to relate telomere length to life span. In the provocative initial publication from the University of Utah in 2003, individuals around 60 years of age who had the longest telomeres lived longer than did subjects with the shortest telomeres, but the main cause of death in the latter group was, inexplicably, infectious disease; the persons with shorter telomeres did not have a higher rate of cancer deaths. Moreover, these findings have not been confirmed in other studies of older subjects. In another study evaluating a different population, telomere length failed to predict survival, but interestingly it correlated with years of healthy life. In a Danish study of people aged 73 to 101 years, telomeres correlated with life expectancy in a simple univariate analysis, but only before the researchers corrected for age, suggesting that the correlation was driven simply by the fact that younger subjects had longer telomeres. And a Dutch study of 78-year-old men found that while telomere lengths eroded with age, they failed to correlate with mortality."

Tuesday, May 1, 2012
Following on from a recent interview with Michael Batin, one of the organizers of the 2nd International Conference on the Genetics of Aging and Longevity, here is a machine translation of his speech to the attendees: "We hope that the conference will identify the most promising points of growth, will contribute to international scientific and research funding [from] international and national foundations, private investors. Let me ask the main question [in biogerontology]. Why [is] aging research funded by the minimum amount? How to change the situation? How to change the attitudes of society and government to seek scientific methods of prolonging life? The first thing that prevents us [is that] aging itself is not considered a disease. Although the aging process fully complies with all common signs of the disease. Aging - a cause of illness and disease. Failure to understand this - [a] deadly mistake. The price of this confusion is very real - [100,000] people die every day from diseases related to aging. Another misconception - aging can be successful and healthy. No, [it] can not! Aging can flow more smoothly. Aging can be slowed down. But you can not make a destructive process or healthy, or successful. As it is impossible to make a decent poverty [or toothache enjoyable]. [This is] the amazing paradox. Nobody disputes the fact that there is nothing more important than human life. All agree that there is nothing more terrible than death. Many suspect that the main cause of death in people [is] aging. But few people make this a logical conclusion. What is the most useful and meaningful activity that has ever engaged [mankind? It is the] struggle with aging. And in particular [the study of] fundamental mechanisms of aging and genetics of longevity. That's what [the scientists in this room do].. And I believe [that they are the] most helpful people on the planet."

Tuesday, May 1, 2012
There are numerous high-level hypotheses that seek to explain why different people suffer neurodegeneration to different levels. Some people remain sharp in old age, whilst others descend into dementia. At the fine-grained level of measuring different types of mental capacity, there are also large variations across an aging population: "Episodic memory and working memory decline with advancing age. Nevertheless, large-scale population-based studies document well-preserved memory functioning in some older individuals. The influential 'reserve' notion holds that individual differences in brain characteristics or in the manner people process tasks allow some individuals to cope better than others with brain pathology and hence show preserved memory performance. Here, we discuss a complementary concept, that of brain maintenance (or relative lack of brain pathology), and argue that it constitutes the primary determinant of successful memory aging. We discuss evidence for brain maintenance at different levels: cellular, neurochemical, gray- and white-matter integrity, and systems-level activation patterns. Various genetic and lifestyle factors support brain maintenance in aging and interventions may be designed to promote maintenance of brain structure and function in late life." It makes more sense for neurodegeneration to be more greatly affected by the impact of regular exercise on long-term tissue health than by the genetics of having a cognitive research.

Monday, April 30, 2012
An interview with a researcher in the field: "the reality is that our brains age throughout life and, in fact, the science tells us that at age 45 we can measure cognitive and memory decline in the average person. There's a steady gradual decline that continues. ... Age is the greatest risk factor. By age 65 or older, your risk is about 10 per cent for Alzheimer's dementia. By 85, it's 40 per cent or more. The implications are that we have a lot more people who have dementia and a lot more people concerned about developing it. ... The studies of successful aging tell us that, when it comes to cognitive success or avoiding dementia or developing it, for the average person only a third of what determines that cognitive outcome results from genetics, from what we inherit. Rarely there are families, less than 2 per cent of cases, with very strong genetic components; they have mutations that cause the disease very early in life. For the vast majority, the genetics are not as strong. They are a factor. About 20 per cent of the population has this risk. It increases the likelihood of getting the disease and the likelihood of getting it at an earlier age but it's not 100 per cent. That means that two-thirds of the formula comes from non-genetic factors: the lifestyle choices we make every day have a major impact on how well our brains age. ... Physical exercise, mental exercise, nutrition, stress management and other behaviours, like avoiding head trauma, not smoking and so forth. ... Exercise seems obvious [but] it may not be completely obvious for people. They know there is a connection between exercise and physical health, exercise and avoiding heart disease. But not everybody is aware of the strong connection between physical exercise and brain health."

Monday, April 30, 2012
Researchers are trying to create new lymph nodes in the body, but tailored to specific needs: "Designer lymph nodes are built with specialized gene-modified cells that are injected into patients and produce a pre-planned immunologic response for cancer patients locally and then throughout their bodies. The researchers are examining a cancer vaccine 'boosting' effect of the manufactured lymph nodes in patients with advanced melanoma. ... Patients with cancer have a dysfunctional immune system either because of the tumor's presence in the body or as a side effect of drugs or radiation used to treat the tumor. The designer lymph nodes, aimed at rebuilding their immune systems, may overcome this dysfunction. ... the researchers are using antigen-presenting cells made from the patient's blood, which are then genetically manipulated to express certain genes before injection into patients. They can inject gene-modified cells at multiple, independent sites throughout the body to create independent lymph nodes that work together. In the trial, the researchers have found early formation of lymph nodes at the vaccine injection sites and are subsequently testing the nature and anti-tumor function of them. [The team] anticipate partnering with [other institutions] to create designer lymph nodes for diseases other than cancer and expand their designer gene immunity boosting research into fighting infectious diseases and even improving the function of immune systems in the elderly."


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