LONGEVITY MEME NEWSLETTER
August 22 2005
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.
- Cart But No Produce - How The Past Generation Failed
- Complexity and Calibrating Kurzweil's Predictions
- Latest Healthy Life Extension Headlines
CART BUT NO PRODUCE - HOW THE PAST GENERATION FAILED
I recently penned a Fight Aging! post in which I asked whether it was harsh to accuse the past generation of healthy life extension advocates of having failed. Think about it this way: look at what patient advocates for cancer, AIDS and diabetes have wrought over the past three decades, and compare it with longevity and aging science today. Where are the research and funding communities for healthy life extension capable of matching cancer science dollar for dollar? Where is the vocal public support for this research?
A little while after writing the post linked above, it occurred to me that a cart was built under the assumption that the produce to take to market was on the way. The cart is an active distribution, commercialization and marketing community for any product or medical technology that might actually extend healthy life span. It exists today. The most prominent organizations within this community - A4M, Kronos, the Life Extension Foundation, and so forth - are the outgrowths of early healthy life extension advocacy. Whatever you might think of their present activities - and many people are less than happy at how the cart earns its keep - these organizations would jump at the opportunity to commercialize actual, working anti-aging medicine and deliver it to the public. The cart is ready to carry produce ... but we have no produce, no technologies capable of meaningful healthy life extension, let alone radical life extension, nor the ready infrastructure to research and build these technologies.
To my eyes, the wrong infrastructure - the comparatively easy infrastructure - came into being, while the harder, more necessary task failed. Why did efforts to build the cart succeed and prosper, while efforts to build a sufficient research infrastructure failed? Or to put it another way, why were sufficient efforts not undertaken? The cancer research advocates kept at it until they won. AIDS patient advocates put cancer research advocates to shame with their success. But healthy life extension is still negligibly funded and poorly publicized.
Present day advocates for healthy life extension face much the same set of tasks as existed twenty or thirty years ago: how to direct funding and engage public support to make best speed in developing working anti-aging medicine. Understanding the failures of the past will, one would hope, let us avoid repeating them in our present day efforts.
COMPLEXITY AND CALIBRATING KURZWEIL'S PREDICTIONS
But enough pessimism - let's shift into a more optimistic mood. As I'm sure you've noticed by now, Ray Kurzweil - a futurist with a good track record, as these things go - has a very positive view of the future of healthy life extension, medical technology and the human experience as a whole. You can get a feel for his ideas from the "Fantastic Voyage" except at the Longevity Meme:
With that in mind, I think you'll find this Fight Aging! post and referred articles on Kurzweil's latest book an interesting read: when critiquing a futurist's timescales and predictions for greatly extended healthy life spans, it's all about the complexity. Read on by following the links below:
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!
Founder, Longevity Meme
LATEST HEALTHY LIFE EXTENSION HEADLINES
On Double-Strand Breaks In DNA (August 21 2005)
From details of the recent Fanconi anemia research and insight into DNA repair, it is interesting to note that "We have known for decades that patients with Fanconi anemia have chromosomes that break easily ... we can now suggest that DNA double-strand breaks are the lesions that underlie the pathology of this disease." Digging into past material at Fight Aging!, we find "DNA double strand breaks are regarded as one of the primary causes of cancer." If you're of a scientific mindset, you should find the first and second parts of a conversation on aging theories between Robert Bradbury, Aubrey de Grey and Joao Magalhaes to be relevant and interesting: "DNA double strand breaks are bad."
Shedding Light On DNA Repair (August 21 2005)
If we fully understand how our cells repair damaged DNA, then we should be able to find ways to improve on the process in order to prevent age-related degeneration caused by accumulated DNA damage. Here, EurekAlert reports on another step forward towards this understanding: "researchers have discovered a new gene, FANCM, which sheds light on an important pathway involved in the repair of damaged DNA. Specifically, mutation in this gene is responsible for one of the forms of Fanconi anemia (FA) ... understanding this gene's role in the development of FA provides insights into other medical problems - in this case, age-related conditions ... We believe that this new gene, FANCM, may be a potent cog in the DNA repair machinery. It is possible that we could learn how to promote the function of DNA repair complexes and thereby prevent the age-related accumulation of DNA damage."
Read Up On SENS This Weekend (August 20 2005)
Make some time this weekend to read up on biomedical gerontologist Aubrey de Grey's Strategies for Engineered Negligible Senescence - proposals for a practical approach to developing real anti-aging medicine. If you would like a more gentle introduction, start with the introduction to SENS here at the Longevity Meme, but I think you owe it to yourself to find out more about what the future of healthy life extension could look like. If the science can be discussed in this level of detail, then we are certainly close enough to begin funding research and development - that funding depends on widespread public support. When it comes down to it, we are responsible for building the future we would like to see, and that includes speaking out in favor of real anti-aging medicine and longer, healthier lives.
A New Class Of Stem Cell (August 19 2005)
A number of research groups have been working on extracting and using stem cells from the umbilical cord. As Medical News Today reports, scientists are making progress: "They have been using [bioreactors enabling] them to produce stem cells sharing many of the same characteristics as cells found in embryos. Research has so far relied on so-called adult cells found in blood and bone marrow from birth onwards or cells grown from embryos. The new type detected by the team harnesses the benefits of both. 'We have found a unique group of cells that bring together the essential qualities of both types of stem cells for the first time' ... The team has taken its first steps towards proving its claims by growing defined liver tissue using the new cell type."
More On Fetal Stem Cells (August 19 2005)
In light of recent work demonstrating the capacity of fetal stem cells to induce healing, it's worth revisiting some of the other research that has been taking place in this area. From the New Scientist: "Stray stem cells from a growing fetus can colonise the brains of mothers during pregnancy, at least in mice. If the finding is repeated in humans, the medical implications could be profound. Initial results suggest that the fetal cells are summoned to repair damage to the mother's brain. If this is confirmed, it could open up new, safer avenues of treatment for brain damage caused by strokes and Alzheimer's disease, for example. This is a long way off, but there are good reasons for thinking that fetal stem cells could one day act as a bespoke brain repair kit." It may even turn out that we don't need the cells - we just need to replicate the signals they produce.
Mitochondrial Decline And Diabetes (August 18 2005)
The age-related decline of mitochondria due to an accumulation of mutations in their DNA is thought to be one primary cause of aging. Here, Medical News Today reports on a better understanding of the link between mitochondrial decline and the onset of type 2 (age-related) diabetes: "A detectable decline in energy production by mitochondria - the organelles that are the cell's furnace for energy production - seems to be a key problem leading to insulin resistance, and thus to type 2 diabetes ... a decreased ability to burn sugars and fats efficiently is an early and central part of the diabetes problem. Their new data also suggest the basic defect lies within the mitochondria." Efforts to develop the tools required to repair or replace damaged mitochondria are currently underway.
Activating Stem Cells For Regeneration? (August 18 2005)
SFGate reports on telomerase, stem cells and long-haired mice: "a key component of the enzyme, known as telomerase, can switch on stem cells resting in mouse hair follicles. The otherwise ordinary-looking mice promptly became as shaggy as '70s rock stars. ... In ancient Egypt, men smeared their pates with hippopotamus fat in a desperate bid to stave off baldness. Is telomerase the new hippopotamus fat? Probably not ... Stem cells, found in virtually all organs of the body, are the wellsprings of tissue regeneration. Specialized stem cells in the hair follicles cycle between a quiescent and active state. The timing of these cycles helps to regulate hair growth. In the mouse studies, researchers found that [one component of telomerase known as telomerase reverse transcriptase] 'can kick these resting stem cells into action.'"
Looking More Closely At Sirt1 (August 17 2005)
Scientists are making progress in understanding connections between the Sirt1 protein, metabolic regulation and life span: "Sirt1 is referred to as Sir2 in lower organisms where it has previously proven to be a key to aging and longevity: Increasing the amount of Sir2 dramatically extends life spans in experimental yeast, worms and flies. ... In mammals, scientists have shown that restricting calories can extend life span and also leads to an increase in Sirt1, the mammalian version of Sir2. ... Sirt1 is probably a very important regulator that integrates cellular response to different types of nutrients, such as glucose, amino acids, and fatty acids." We can hope that a full understanding of the mechanisms of calorie restriction will lead to therapies that can improve on gains in healthy life span obtained via this method.
Another New Aging Gene (August 17 2005)
EurekAlert reports on another gene newly connected to the aging process: "Researchers have discovered that the loss of a gene called p63 accelerates aging in mice. ... Aging and cancer are two sides of the same coin. In one case, cells stop dividing and in the other, they can't stop dividing. We suspect that having the right amount of the p63 protein in the right cells at the right time creates a balance that enables organisms to live relatively cancer-free for a reasonably long time." A lack of p63 accelerates aging in tissue - but then so do a large number of other things. There's no such thing as useless information in the biochemistry and genetics of aging, but it remains to be seen how important this new discovery turns out to be.
A Reminder About Fat (August 16 2005)
The PakTribune reports that researchers "found that the more people weigh, the older their cells appear on a molecular level, with obesity adding the equivalent of nearly nine years of age to a person's body. The findings suggest that many health problems associated with being overweight - heart disease, cancer, diabetes, arthritis - may result from fat cells hastening the natural aging process." Correlation is not causation, but "the results are consistent with recent findings that, contrary to the long-held belief that fat cells are inert blobs, they churn out a host of substances that can be toxic to the body ... So it may be the body has to repair itself much faster and that accelerates the aging process." Poor diet and lack of exercise that accompany obesity could also be to blame - it's clearly a good idea to maintain a healthy lifestyle and keep the weight off.
Nerve Stem Cells Made (August 16 2005)
The BBC reports on progress in control of embryonic stem cell differentiation: "The world's first pure nerve stem cells made from human embryonic stem cells have been created ... "This is incredibly exciting in terms of curing disease. We may be able to create the disease in a dish. If we do that, we'll be able to better understand the disease and also to test drugs. ... the long-term aim of the Edinburgh research is for cells to be used to build replacement neural tissue for Alzheimer's and Parkinson's sufferers. But he said the more immediate use for the artificially-created cells is to test out the effectiveness of new drugs. ... Hopefully that will come to pass within two to three years. In terms of the possibility of using the cells for transplantation, that's a much more difficult and longer term thing and I think there we're talking more of the five to ten year range."
How Adult Stem Cell Therapies Work (August 15 2005)
An adult stem cell therapy for acute renal failure (ARF) provides insight into how these first generation therapies work. EurekAlert reports that transplanted stem cells are only present briefly, but administer a swift, positive kick to the local environment: "Administered stem cells don't stay in the kidney that has ARF long enough to differentiate into kidney cells, but rather appear to alter the course of ARF by a number of identifiable and some still unexplored paracrine mechanisms. The former include the induction of organ-protective and repair-supporting genes in surviving renal cells, robust suppression of proinflammatory cytokines in the ARF kidney and upregulation of anti-inflammatory genes, as well as the delivery and release at the site of injury of organ-protective and other beneficial gene products by the stem cells."
A Path To Technological Immortality (August 15 2005)
A Tech Central Station author provides a good overview of the prospects for forms of physical immortality in 2050 that have much more to do with nanotechnology and computational science than with medical biotechnology - a merging of man and his machines that produces immortality almost as a side-effect along the way to far greater things. Good, well-studied predictions of the technological singularity to come have at least a decade-long history, and it is hard to argue against the fact that progress in core convergent technologies and sciences is accelerating rapidly. Still, for most of us, standard old-fashioned human-sourced hard work on first-generation healthy life extension medicines will be needed if we are to be healthy and alive in 2050. First things first.