LONGEVITY MEME NEWSLETTER
November 1st 2010
The Longevity Meme 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 the Longevity Meme.
- So You Want to be a Biogerontologist
- Coverage of TEDMED 2010
- On Body Temperature and Longevity
- Beneficial Mitochondrial DNA Damage?
- Longevity Meme and Fight Aging! Content Feeds
- Latest Headlines From Fight Aging!
SO YOU WANT TO BE A BIOGERONTOLOGIST
There's something to be said for stepping up and helping to get a job done directly. Over the past few years, a number of folk in the healthy life extension community have steered their careers towards the life sciences and study of the biology of aging - a field known as biogerontology - rather than working to raise funds or advocate for engineered longevity:
"By and large, biogerontologists work at research institutions, typically universities or laboratories, though a few also work in the industry and a few companies research aging. The vast majority of biogerontologists have a PhD (or sometimes an MD or both), so if you want to become a biogerontologist you should be prepared to go to graduate and/or medical school. While it is possible to study aging in a private company or as a staff member of a research institution, the majority of well-known biogerontologists have their own research group, like ours, at a research institution. Again, you can certainly contribute to research on aging in a variety of ways and even without making of it your main job, yet if you are serious about becoming a biogerontologist and doing independent research at the highest level then this usually implies developing an academic career."
Where you wind up in life and the degree to which you enjoy success in your goals is all about the connections you make along the way. If you want to make progress in a particular field, you have to establish relationships within that field. For example, the SENS Foundation runs an academic initiative program - whose chief value to the students involved is the opportunity to make connections within the community of researchers interested in repairing the biochemical damage of aging:
COVERAGE OF TEDMED 2010
The TEDMED 2010 conference was held this past week, and Aubrey de Grey and Anthony Atala were amongst the speakers:
"Next up on stage were aging and life extension scientist Aubrey de Grey and regenerative medicine researcher Anthony Atala. Aubrey is a quirky figure in the world of science, with a long beard and provocative views on aging and immortality. Anthony Atala is, by impression, much more grounded and lives in the world of tissue engineering. The most notable thing about their joint talk was not what they said but rather that their institutions, the SENS Foundation and Wake Forest University, are going to partner together on some projects. They approach the idea of fixing the human body from highly different angles and it will be interesting to see the results from their collaboration."
ON BODY TEMPERATURE AND LONGEVITY
The body temperature of mammals appears to affect longevity in ways that overlap with calorie restriction, but the biochemistry is less well understood:
"Caloric restriction (CR) causes a reduction in body temperature which is suggested to contribute to changes that increase lifespan. Moreover, low [body temperature] has been shown to improve health and longevity independent of CR. ... Based on current evidence, it is concluded that low [body temperature] plays an integral role in mediating the effects of CR on health and longevity, and that low [body temperature] may exert independent biological changes that increase lifespan. Our understanding of the overlap between CR- and [body temperature]-mediated longevity remains incomplete and should be explored in future research."
BENEFICIAL MITOCHONDRIAL DNA DAMAGE?
Just to show that nothing is straightforward in biology:
"As you all know by now, accumulated mitochondrial DNA damage is thought to provide an important contribution to degenerative aging. The process by which the small misplaced, changed, or missing segments of DNA known as mutations create the conditions for failing organs - and ultimately death - is complex and has many steps, but it starts with changes in the operation of crucial mitochondrial machinery. There is some evidence for the existence of beneficial mutations to mitochondrial DNA that accumulate with age in at least some populations. On reflection this doesn't seem unreasonable. We know, for example, that some mitochondrial DNA haplotypes are demonstrably better than others - they are associated with people who, on average, benefit from better health and longevity. Some folk have the luck of the draw and inherit good mitochondrial machinery. But our cells are more than just the straight output of their DNA blueprints, both nuclear DNA and mitochondrial DNA, because cellular processes and mechanisms can conceivably influence the way in which those blueprints become damaged over time.
"So [some] human populations may have evolved to allow certain specific types of damage to readily occur in their mitochondria, because that damage changes mitochondrial operation in ways that provide benefits to survival. Devious, but then that's biology for you."
LONGEVITY MEME AND FIGHT AGING! CONTENT FEEDS
As you may have noticed, the Longevity Meme daily news recently moved over to live at Fight Aging! The various feeds have updated to reflect this fact, and the old feed locations should presently be redirecting users to the new locations. You can find an overview of the new situation in the following post:
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!
FIRST VIDEOS FROM TRANSVISION 2010
Friday, October 29, 2010
The TransVision 2010 conference was held in Milan this past weekend, a chance for European transhumanists to meet and make presentations on topics of interest - such as engineering greater human longevity. Some of the conference video is up at the teleXLR8 blog. You might also look at organizer Giulio Prisco's report: "TransVision 2010 is over! I wish to thank all speakers and participants, those who came to Milan and those who participated remotely via Teleplace. ... This was a very interesting event, with great talks by great speakers. I am happy to have seen again many old friends and made many new ones. In the picture above, some speakers and participants at a dinner after the end of the conference. I was not really able to pay attention to any of the talks including my own, and I look forward to watching the video coverage. We recorded everything on video, both in HD with the cameras on site, and from Teleplace. The videos will be available online and on the conference's DVD proceedings. The videos recorded in Teleplace will be available online in a few days, and those recorded on site in a few weeks."
RESVERATROL DOESN'T EXTEND LIFE, LIMITED BENEFIT TO RAPAMYCIN
Friday, October 29, 2010
At the SENS Foundation, Michael Rae looks at the NIA Interventions Testing Program examination of resveratrol and rapamycin: "Combined with their positive results with rapamycin, the failure of resveratrol to extend life using resveratrol in normal mice over a very wide range of doses should reasonably be taken to put the resveratrol "story" to test. On the other hand, the ability of rapamycin to extend life in these mice has been confirmed, and expanded to a preliminary extent. Naturally, further studies are underway or proposed to elucidate the full nature of these effects. ... At the same time, whatever these studies may reveal, even the most optimistic reading of these results and an assumption of perfect human translatability is still overshadowed by how limited the results are. Interventions such as rapamycin, which only retard the rate at which aging damage accumulates (or, perhaps, allows the organism to carry on functioning for a longer period of time under its accumulating burden), can only temporarily delay the onset of age-related ill-health, not arrest or reverse it - and in the case of rapamycin, the first pharmacological agent to extend the lives of otherwise-healthy mammals, its ability to do even this has been found to be limited." Drugs that slow aging - slow the rate at which damage occurs - are not a desirable end point for the next twenty years of research, when we could instead be working instead to reverse aging by repairing biochemical damage.
THE NEWORGAN PRIZE
Thursday, October 28, 2010
A reminder about the NewOrgan Prize from Sentient Developments: "the Methuselah Foundation recently launched the NewOrgan Prize which will be awarded to the first scientist to produce and successfully transplant an organ using regenerative medicine. The contest is meant to speed up the research process and bring the promise of regenerative medicine to reality. As the US Department of Health & Human Services has stated, 'Regenerative medicine will be the standard of care for replacing organ systems in the body.' The trick is to make it happen. When it comes to reconstructing a new organ, 'new organ engineering' will require the development of all tissues that build the organ including muscle, nerves, arteries and veins. The challenges and limitations of the current system for organ replacement are well documented, including the agony of waiting for a donor to die, lifelong limitations from immunosuppressant drugs, and possible organ rejection. And the sad reality is that many die without receiving a new organ or even qualifying to be considered." As for the Mprize for longevity science, the NewOrgan Prize purse will be formed from philanthropic donations: so if you support the goal, make a donation. Prizes have a multiplying effect: every dollar in the prize purse inspires something like $15 to $50 dollars in research and development funding, based on recent and historical prizes.
FINE-TUNING REGENERATION FOR LONGEVITY
Thursday, October 28, 2010
The evolved balance between cancer resistance and tissue maintenance is an important determinant of longevity - but it can be fine-tuned so as to have your cake and eat it, as researchers have found in recent years. Here is another example, in flies this time: "Somatic stem cells are critical for regeneration of many tissues, thus ensuring long-term maintenance of tissue function. Proliferation of stem and progenitor cells has to be limited, however, to prevent hyperproliferative diseases and cancer in aging animals. This conflict between the need for stem cell proliferative potential and cancer prevention compromises regeneration in many high-turnover tissues of aging animals, including humans. ... In old flies, intestinal stem cells (ISCs) hyperproliferate, causing an accumulation of mis-differentiated daughter cells (a phenotype termed intestinal dysplasia). We show that the balance between regeneration and dysplasia in this tissue significantly influences lifespan. When ISC proliferation rates are reduced, but not completely inhibited, dysplasia is limited and lifespan is increased. This can be achieved by moderately reducing insulin and stress signaling activities, as well as by expressing protective proteins in somatic stem cell lineages. Our results show that optimizing proliferative homeostasis (i.e. limiting dysplasia, but allowing sufficient regeneration) in high-turnover tissues is an efficient strategy to extend lifespan." The more that is known about the fine details of metabolic and cellular processes, the more that might be done to tinker with them to extend life. But this will never be as efficient a path forward as repair technologies - when we strive to identify and repair damage within our biochemistry, we have no need to fully understand every aspect. We know what a young metabolism and cell look like, and we are trying to revert the clearly identified differences between young and old.
STEM CELL THERAPY FOR NEURODEGENERATION IN INDIA
Wednesday, October 27, 2010
An example of early applications of stem cell research forging ahead outside the US: "While stem cells have been making news around the world for their potential, and are even being tried on patients, Dr N K Venkataramana, neurosurgeon, BGS Global Hospital in Bangalore, has successfully used the therapy on patients suffering from Parkinson's disease, Alzheimer's, cerebellar degeneration and cerebral palsy. 'I used adult mesenchymal stem cells derived from the bone marrow. They were transplanted into the brain through keyhole surgery. These stem cells multiply and thereby regenerate the damaged areas of the brain. This leads to reactivation of brain cells, resulting in recovery from the disease.' ... He created a state-of-the-art research facility - Advanced Neuro Science Allies - and began his research into the use of stem cell therapy three years ago. 'I picked out authentic mesenchymal stem cells from bone marrow using a marker. The stem cells were purified and tried on animals for safety. Subsequently, we used the therapy on patients. ... Initially, the findings are that we are on the course to a complete cure. All the patients treated so far have a marked decrease in the need for medication. Their symptoms have reduced drastically. They have an increased feeling of well-being and it is obvious that they are recovering. However, there are still some factors to be addressed and understood.'
DAPSONE AND NEMATODE LONGEVITY
Wednesday, October 27, 2010
From In the Pipeline: "there's a report out in PNAS that the longtime treatment for leprosy (Hansen's disease), diaminodiphenylsulfone (DDS or dapsone), also prolongs life in the nematode C. elegans. ... The treated animals showed a significantly longer lifespan, faster body movements compared to untreated controls, and a delay in accumulating the 'aging pigment' lipofuscin. Now, DDS kills bacteria by inhibiting folate synthesis, but that doesn't seem to have anything to do with lifespan extension. The authors found that one of its key targets might be pyruvate kinase - and this might be the source for the mild anemia that's sometimes seen as a side effect in human patients. Nematodes have two isoforms of the enzyme, one mostly in muscle, and the other mostly in the digestive tract. Further study (with RNAi, etc.) showed that the lifespan extension seems to be working through the former, but not the latter. But it also showed that this probably can't be responsible for the whole lifespan effect, either: mutant nematodes with that isoform deleted live longer than wild type, but treating them with DDS makes them live longer still."
SMOKING AND VASCULAR DEMENTIA
Tuesday, October 26, 2010
Smoking is just a more subtle way of stabbing yourself - causing damage that will shorten your life. One of the impacts of smoking is degraded blood vessel function, and this has a long-term effect on the brain. It is an example of the way in which the state of general health impacts the rate of neurodegeneration: "Heavy smoking in middle age appears to be associated with more than double the risk for Alzheimer's disease and other forms of dementia two decades later. ... [Researchers] analyzed data from 21,123 members of one health care system who participated in a survey between 1978 and 1985, when they were 50 to 60 years old. Diagnoses of dementia, Alzheimer's disease and vascular dementia were tracked from Jan. 1, 1994 (when participants were an average of 71.6 years old), through July 31, 2008. A total of 5,367 participants (25.4 percent) were diagnosed with dementia during an average of 23 years of follow-up, including 1,136 with Alzheimer's disease and 416 with vascular dementia. Those who smoked more than two packs per day in middle age had an elevated risk of dementia overall and also of each subtype, Alzheimer's disease and vascular dementia, compared with non-smokers. ... Smoking is a well-established risk factor for stroke, and may contribute to the risk of vascular dementia through similar mechanisms." As we non-smokers look at this and shake our heads, it is worth recalling that a sedentary lifestyle can be just as damaging to human life expectancy as smoking. Have you looked at the exercise in your life recently?
CONCERNED ABOUT THE BRAIN
Tuesday, October 26, 2010
Developing the means to repair the human brain is essential to engineered longevity - it's the one organ we can't just replace as a last resort. From Sentient Developments: "The human brain degrades quickly with advanced age and, as a result, represents the weakest link in the life extension chain; as far as I'm concerned it's full stop until we can meaningfully fix the cognitive problems associated with aging. Yes, age-associated diseases such as cancer and cardiovascular disease are clearly bad, but the most devastating of these involve the nervous system - diseases like Alzheimer's and Parkinson's. These diseases take a brutal toll on individuals and their families, often virtually killing the person well before they die. That we are facing a looming epidemic of neurological diseases shouldn't really come as a surprise to anyone. But what is surprising is that very few people are actively doing anything about it. And it's not that the writing isn't on the wall - it is. The time to act is now. ... Until we can meaningfully treat age-related cognitive decline, many of these other life extending advances are a moot point; what we're in danger of doing right now is extending lifespan, but not necessarily healthy life span." I disagree with this conclusion on the grounds that I think extending life without extending healthy life would be very hard to accomplish even if we were trying - aging is biological damage, and the outcome flows from the state of damage. Reduce the damage and you extend both life and healthy life. Neurodegeneration is driven in large part by the state of general health, perhaps through the mechanisms of blood vessel health, for example.
THE RADICALISM OF CRYONICS
Monday, October 25, 2010
Why, in a world in which a million people die every week, is cryonics still a fringe activity? Some fairly novel arguments are made in this piece over at Depressed Metabolism: "in the case of cryonics, the idea is so antithetical to the existing order of civilization that it can it only be advanced by insurgent means. This is so because cryonics overturns the Vitalistic view of life, challenges the conventional definition of death, invalidates the core tenets of contemporary medicine, erodes the need for a mystical afterlife, radically redistributes capital (disrupts inheritance, bequests, and mortuary customs), mandates a complete change in reproductive behavior, perturbs generational succession, [requires] profoundly disruptive technologies such as cloning, regenerative medicine, nanotechnology, artificial intelligence ... [thus] the idea that cryonics was just an extension of medicine and is compatible with religion and existing social and political institutions, while superficially satisfying, is both mistaken and bound to fail. ... It is becoming clearer and clearer that demonstrating the technological feasibility of cryonics is not sufficient for the acceptance of cryonics. ... Cryonics advocates often seem to believe that if they refute the common scientific and technical objections to cryonics (which is not that hard to do because the psychological resistance to the idea prevents critics of checking even the most basic facts about the rationale and practice of cryonics) the social and psychological reservations will take care of themselves. This is not just incorrect, such reservations are often the most fundamental."
THE AGED ARE LESS DAMAGED THAN THEY USED TO BE
Monday, October 25, 2010
Aging is the accumulation of damage, and given that life expectancies have increased over time, we'd expect the aged to presently have less biological damage than was the case in the past. This is challenging to measure, however, given the crude state of medical technology in earlier eras. Here is an unusually clear example: "Today's 70-year-olds do far better in intelligence tests than their predecessors. It has also become more difficult to detect dementia in its early stages, though forgetfulness is still an early symptom ... The H70 study provides data on cognitive symptoms that researchers have used to predict the development of dementia, and also to investigate whether the symptoms have changed in recent generations. The study involves a large proportion of 70-year-olds from Gothenburg, Sweden, who have been extensively examined over the years ... Using the test results, we've tried to identify people who are at risk of developing dementia. While this worked well for the group of 70-year-olds born in 1901-02, the same tests didn't offer any clues about who will develop dementia in the later generation of 70-year-olds born in 1930. ... The improvement can partly be explained by better pre- and neonatal care, better nutrition, higher quality of education, better treatment of high blood pressure and other vascular diseases, and not least the higher intellectual requirements of today's society, where access to advanced technology, television and the Internet has become part of everyday life."