Fight Aging!

LONGEVITY MEME NEWSLETTER
June 11 2007

The Longevity Meme Newsletter is a weekly e-mail containing news, opinions and happenings for people interested in healthy life extension: making use of diet, lifestyle choices, technology and proven medical advances to live healthy, longer lives.

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CONTENTS

- Notes From a Recent Cryonics Conference
- Discussion
- Latest Healthy Life Extension Headlines

NOTES FROM A RECENT CRYONICS CONFERENCE

One of the attendees of the recent Advances in Human Cryopreservation conference was kind enough to post his notes online. You can find links and a few of the high points here:

https://www.fightaging.org/archives/001234.php

The big announcement of the conference was significant new funding for cryonics research and development: "An anonymous donor has funded a multimillion-dollar grant proposal by Greg Fahy to work toward successful reversible suspended animation. The 3-year project, staffed with half a dozen scientists in a new facility, will extend over 3 phases: Phase 1 will identify an optimal method for vitrifying the body from a physical point of view in rabbits. Phase 2 will verify and extend Phase 1 results in larger mammals and possibly human cadavers donated for non-cryonics medical research. Phase 3 will work toward true suspended animation (biologically reversible whole body vitrification)."

Vitrification is the more modern replacement for straight freezing of tissue, and a number of different groups are presently working on improving the technology. Vitrification has many advantages over other forms of low-temperature storage, and has the potential to become a money-spinning technology used in a variety of fields in medicine. Minimizing the damage of low-temperature tissue storage is a big deal; think of tissue banks and transplants, for example:

https://www.fightaging.org/archives/000794.php

That sort of economic engine could help the cryonics industry grow to provide its services to more of those who would benefit:

https://www.fightaging.org/archives/2002/11/cryonics/

"Cryonics is the only option for life extension open to many older and seriously ill people: those who cannot wait for the promised therapies of the next few decades. It is the science of placing humans and animals into a low-temperature, biologically unchanging state immediately after clinical death, with the expectation that advances in medical technology may eventually enable full restoration to life and health. A small industry of cryonics providers exists to freeze or vitrify your body on death, in the hopes that future scientists (most likely using nanotechnology and nanomedicine) will be able to revive and repair you.

"The practice of cryonics is an ongoing medical experiment with an unknown chance of success. Responsible cryonicists understand that cryonic suspension is an educated gamble. The chances are certainly better than zero, however, and as one wag noted, 'the control group in this experiment isn't doing so well.' By this, he was referring to the vast number of people who are cremated, buried or otherwise interred. The chances of any plausible future science restoring them is zero. Cryonic suspension is, after all, only the second worst thing that can happen to you."

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!

Reason

Founder, Longevity Meme

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LATEST HEALTHY LIFE EXTENSION HEADLINES

To view commentary on the latest news headlines complete with links and references, please visit the daily news section of the Longevity Meme: http://www.longevitymeme.org/news/

Understanding Type 2 Diabetes (June 08 2007)
http://www.uphs.upenn.edu/news/News_Releases/jun07/diabetes-protein-target.html
Progress on the mechanisms of age-related diabetes is noted at the PENN Medicine newsroom: "When a type 2 diabetic eats a meal, insulin cannot stop the manufacture of glucose in the liver, but it can stop the burning of fat stores. This gives the diabetic person a 'double whammy:' fatty acids accumulate from food and from the liver. Consequently, more fat is deposited in tissues and obesity worsens. Until now there was no clear connection between insulin and the control of fat metabolism. This study shows that when insulin is present, as it is after a meal, the protein Akt2/PKB adds a phosphate group to its molecular partner PGC-1a. When this happens, PGC-1a cannot activate the genes needed for fat metabolism. ... if a drug could induce Akt2/PKB to add the phosphate group (phosphorylation) to PGC-1a, then the liver of a diabetic might be 'fooled' into stopping the oxidation of fat stores." This sort of "finger in the growing crack in the dam" approach to medicine is inefficient in comparison to methods of prevention - type 2 diabetes is very avoidable, after all. Relying on the medicine of the future to rescue you from conditions you could have prevented or minimized doesn't strike me as a good strategy - the medicine of the future already has a mountain to climb in the defeat of unavoidable age-related degeneration.

Engineering Fly Longevity (June 08 2007)
http://www.eurekalert.org/pub_releases/2007-06/uosc-sff060707.php
The better the tools, the easier it becomes to precisely alter the operation of complex biochemical systems. From EurekAlert!: "Receptors are proteins that transmit signals across a cell membrane. [Researchers] manufactured short proteins that blocked a receptor involved in fruit fly aging ... Flies with a blocked receptor saw their lives extended by a third, with no apparent side effects. ... [scientist] literally threw trillions of peptides at the receptor and saved the ones that stuck. ... We let the molecules themselves decide if they bind, rather than trying to design them rationally ... After multiple cycles, the researchers had a group of peptides that stuck to the receptor and not to any other protein. Fruit flies genetically altered to produce such peptides lived longer, suggesting that the peptides were interfering with the receptor's normal function. Why these particular peptides work, and why the receptor they target plays such an important role in fruit fly aging, remain the bigger and as yet unanswered questions." Precision of operation doesn't necessarily mean you immediately know what the result is going to be, or why, of course. We'll see where this goes, but it's a long road from flies to humans, littered with techniques that don't work for mammals. The real story here is the new technology platform for blocking receptors - that'll be generating progress across the board for a decade.

Myostatin Versus Sarcopenia (June 07 2007)
http://pmid.us/17551508
Researchers are making progress in developing therapies for sarcopenia based on manipulating myostatin: "A reduction in muscle mass and strength is often observed with aging, and this phenomenon is known as sarcopenia. This age-related atrophy frequently correlates with insufficient levels of muscle regeneration resulting from impairment of satellite cell involvement and myogenesis brought about by the aged environment. Using myostatin-null mice, we recently showed that negative regulators of muscle mass such as myostatin play an active role in the regulation of myogenesis during aging. The present study specifically tests the therapeutic value of a myostatin antagonist in sarcopenia. We report here that a short-term blockade of myostatin, through stage-specific administration of a myostatin antagonist, significantly enhanced muscle regeneration in aged mice after injury and during sarcopenia. ... In addition, the antagonist demonstrated a high degree of efficacy, as only minimal doses during the critical period of regeneration after injury were sufficient to restore the myogenic and inflammatory responses in the aged environment."

Diabetes and Dementia (June 07 2007)
http://pmid.us/17544131
This paper is a good reminder of the merits of taking care of your health: "Recent evidence suggests that the molecular defects associated with the development of diabetes also contribute to an increased risk of all types of dementia, including Alzheimer's disease, vascular dementia and Pick's disease. Indeed, the presence of type II diabetes mellitus results in a two to three fold higher risk of developing dementia ... There are currently 250 million people [worldwide] diagnosed with diabetes, and this number is predicted to double within the next 20 years, therefore the associated risk translates into a potential explosion in the appearance of dementia in the population. This review primarily focuses on the proposed molecular links between insulin action, Diabetes and Alzheimer's disease, while discussing the potential for therapeutic intervention to alleviate these disorders." Diabetes is a lifestyle condition for most - it can be avoided, minimized or reversed to a surprisingly large degree. Little that medical science can do today is better than taking care of your health over the years when it comes to metabolic disorders and their impact on your life span.

On Antagonistic Pleiotropy (June 06 2007)
http://ouroboros.wordpress.com/2007/06/06/conditioned-for-aging/
As noted at Ouroboros, evolution is a harsh designer. Benefits are front-loaded for optimal fitness in early life, with no regard to just how much damage, pain and suffering the underlying biological machinery will go on to cause later. Hence aging: "Oft-quoted examples include the prostate and breast, where robust proliferation improves early-life fitness (via effects on reproduction and child-rearing, respectively) but can increase cancer risk (and thereby mortality rate) in old age. One might, therefore, expect to find that gerontogenes (genes whose wildtype function promotes or accelerates aging) are enriched among what are sometimes referred to as 'housekeeping genes': genes with run-of-the-mill functions in metabolism, whose efficacy is intimately linked with the success of fundamental processes like cell division, protein production, etc. ... Unfortunately for this theory, it's particularly hard to identify mutations in these genes, where loss of function means loss of life. In order to investigate the hypothesis outlined above, one would need to allow these essential genes to function throughout development, and then turn them off at maturity." Which researchers can now accomplish - and are turning up interesting results.

Aging Stem Cells and DNA Damage (June 06 2007)
http://www.eurekalert.org/pub_releases/2007-06/sumc-asc060407.php
It's comparatively easy to produce results that look like premature aging - anything that raises the rate of biochemical damage to your cells should do the job. Diabetes has been used as a model for aging in animal studies for some time, for example. Deliberate changes leading to what appears to be premature aging are not always relevant to "normal" aging. From EurekAlert!: "Normally, a few stem cells are enough to completely replenish the bone marrow of mice and produce normal amounts of blood and immune cells. However, error-filled blood-forming stem cells taken from the mutant mice were much less effective at colonizing the depleted bone marrow than normal stem cells, and became even less effective when taken from older mutant mice. ... these results suggest that mutations accumulating in stem cells as they age were preventing them from doing their normal job of producing new blood and immune system cells. ... young stem cells from normal mice contained [little] or no DNA damage. Older stem cells, on the other hand, showed extensive [DNA damage]. ... blood-forming stem cells do accumulate DNA damage with age even though they rarely divide, and that damage is passed on to the blood and immune system cells they make. Weissman said these findings could explain the origin of blood cancer (leukemia) and immune dysfunctions that occur as people age."

Embryonic Stem Cells Versus AMD (June 05 2007)
http://www.eurekalert.org/pub_releases/2007-06/ucl-uss060507.php
Regenerative strategies for the treatment of age-related macular degeneration (AMD) are proceeding apace: "Around 25 per cent of over-60s in the UK have some degree of visual loss due to AMD, and some 14 million people in Europe currently suffer blindness through the condition, caused by defects in the retinal support cells. There is currently no treatment that prevents the treatment of dry AMD. There has been some success in controlling new blood vessel formation in wet AMD, but these approaches are only suitable for certain patients and are often only temporary. ... The London Project's approach will involve production of a cell replacement therapy from human embryonic stem cells, which are effective in replacing dysfunctional [retinal pigment epithelial cells] and photoreceptors found in AMD, leading to a surgical therapy capable of stabilising and restoring vision in the vast majority of patients. Surgical procedures already developed and trialled in a number of patients using the patients' own cells have illustrated that a cell replacement therapy can work."

Biogerontology: the Mainstream View Of Itself (June 05 2007)
http://ouroboros.wordpress.com/2007/06/05/thou-shalt-not-fear-the-reaper/
Ouroboros looks at a position paper from the mainstream of UK biogerontology: "Ageing is a highly differentiated and malleable process. Therefore, the commitment must be to develop interventions that can affect the ageing process or the experience of ageing in order to extend healthy life expectancy, independence and well-being in old age. ... Investments in ageing research should be significantly increased as they are likely to produce immense gains to both the economy and society, in particular to the quality of life, productivity and self-sufficiency of the rapidly growing older population group." Which is a good start, but after that it lapses into calls for more of the slow path - metabolic manipulation to slow aging rather than medical engineering to repair aging, the phantom goal of compressed morbidity (increased years of health without increased life span), government control over research and unimpressive aims for the magnitude of healthy life extension. Too few years, and too long to attain them; not a good goal when we can plausibly do far better. In that, it mirrors the Longevity Dividend initiative on the other side of the pond.

Commonalities In Cancer Stem Cells (June 04 2007)
http://www.eurekalert.org/pub_releases/2007-06/sumc-srf053107.php
EurekAlert! reports on the discovery of another variety of cancer stem cells. Intriguingly, there are similarities between a number of those types found so far: "Researchers [have] identified the cancer stem cells that propagate tumors in colon and rectal cancer ... We have brought together a team of scientists and clinicians who will help find the weak points in cancer, devise new immune and molecular diagnostics and therapeutics, test them in mice that carry the cancer stem cells and, hopefully, in a few years begin to test them in our patients ... A protein called CD44 that has already been found dotting the surface of both breast and head and neck cancer stem cells also turns up on the colorectal cancer stem cells. ... that finding could simply reflect the fact that all of those tumors arise from similar tissue. It could also mean that a similar therapy could target all three cell types." Similar biomarkers means a lower cost of developing therapies - but it remains an open question as to whether cancer stem cells are the quick path to victory. We can hope, because a highly effective cure for cancer will have its part to play in the longevity medicine toolkit.

Alzheimer's is a Very Gradual Process (June 04 2007)
http://www.eurekalert.org/pub_releases/2007-06/sonm-wca052707.php
The neurodegeneration state we call Alzheimer's is not a sudden onset at all, but rather builds up very slowly over time. This is becoming more clear as scientists more effectively detect biochemical markers early on: "Our findings show that beta-amyloid is associated with brain dysfunction - even in apparently normal elderly individuals ... PET is a highly specialized, noninvasive imaging technique that uses short-lived radioactive substances to produce three-dimensional images of those substances functioning within the body. ... We found that apparently normal elderly subjects with positive PIB PET scans do have mild - but significant - reduction in memory test scores, and this is related to the amount of amyloid present ... Besides providing an accurate diagnosis of early Alzheimer's disease, this research is helpful in providing the possibility of early diagnosis and intervention for individuals who are minimally impaired ... Additionally, 20 percent of the normal volunteers in our study whose average age was 72 had a positive scan. In subjects with mild cognitive impairment (MCI) - a condition that leads to Alzheimer's dementia in about 60 percent of cases - we found positive scans in 60 percent of the subjects. The amount of amyloid present, measured by the PIB scan, related to the severity of memory impairment in these subjects." Much like diabetes, early detection may mean a chance to change course.

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