LONGEVITY MEME NEWSLETTER
March 27 2006
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.
- A Thank You to the Three Hundred
- The Tithonus Error at Large
A THANK YOU TO THE THREE HUNDRED
Eighty-seven people have so far chosen to join The Three Hundred, generous supporters of the Methuselah Foundation and mostly folk of quite modest means. As taxes come and go in the US again, I think it's worth pointing out that The Three Hundred help to keep the foundation within the arcane boundaries of 501(c)3 nonprofit status as the larger donations mount.
While we all have our varying opinions on taxes and regulation - and I'm sure you know mine by now - I think that any excuse is a good excuse to point out just how much the Three Hundred are contributing to the future of meaningful anti-aging research and healthy life extension advocacy. I strongly suggest that you consider joining: where else can you leverage so much positive change for the future of health and longevity from a couple of dollars a day?
THE TITHONUS ERROR AT LARGE
Will advocates ever manage to move the Tithonus error into obscurity and the past? Will the public at large continue to hold the half-formed belief that healthy life extension means to be old and frail for longer, even while attempts to raise large-scale funding for meaningful anti-aging research are proceeding?
It seems we still have a long way to go if we seek to keep an aging Tithonus healthy in the mind's eye, although there is certainly no consensus as to the necessity of general public support amongst healthy life extension advocates. There is a school of thought that has public discussion and education as consequences following the results of large scale funding; in this viewpoint, the prospective world-changer only needs to convince those in charge of the purse strings. I don't see that as correct. While capital investment in progress clearly makes the world go round, a more subtle feedback loop is at work. Those who control funding organizations are largely very conservative, and are greatly influenced by the present consensus - as expressed by public opinion and discussion. Investment may influence opinion, but opinion determines investment.
Hence, I see efforts to lay to rest the Tithonus error - and other hoary old excuses for aging, suffering, death and inaction - as an important form of advocacy. It helps to ease the way for those attempting to raise research funding to intervene in the aging process and extend our healthy life spans.
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
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/
The Potamkin Prize (March 26 2006)
Since it's been a week of Alzheimer's research news, I should point to this Senior Journal article: "Three scientists are to be awarded the $100,000 Potamkin Prize [for] their work in helping advance the understanding of Alzheimer's disease and related disorders. ... Using a new technology called multiphoton microscopy we are able to [watch] plaques and tangles in the living brain and directly observe the effects of therapeutic interventions ... Our findings show that the clumps of amyloid-beta and tau proteins in plaques and tangles are not the main culprits of memory loss ... Her recent work has shown that a class of drugs known as kinase inhibitors that target an abnormal form of tau may be useful in treating tangles in Alzheimer's disease and other dementias." Until we're talking about underlying mechanisms and age-related biochemical damage at the root of it all, it's still early days - cleaning up the end results is not the way to go.
Plain Common Sense (March 26 2006)
A dose of common sense via the Life Extension Foundation News: "The life span of human beings is partially influenced by genetic factors, but outcomes of aging are profoundly influenced by lifestyle and other environmental factors. Age-related modifications of the cardiovascular system are preserved by anti-aging lifestyle interventions such as physical activity and caloric restriction. ... Accordingly, physical activity and low body mass index reduce mortality in older men with cardiovascular diseases. ... Thus, older persons can implement lifestyle practices that minimize their risk of death from cardiovascular diseases." It works over the long term for younger people too: you can choose not to damage your healthy life span, and thus have a better chance of living to benefit from real anti-aging technologies of the future.
Comparing the Pathways (March 25 2006)
Now that scientists have a handful of different ways to extend healthy life span in a range of lower species - largely through manipulation of metabolism - there is much to be learned through experiments that combine and contrast: "Many gene products known to affect lifespan are intimately involved in the control of energy metabolism, including the fuel sensor AMP-activated protein kinase (AMPK). We have shown previously that over-expression of an AMPK [alpha] subunit in Caenorhabditis elegans, designated aak-2, increases lifespan. Here we show the interaction of aak-2 with other pathways known to control aging in worms. Lifespan extension caused by daf-2/insulin-like signaling mutations was highly dependent on aak-2, as was the lifespan extension caused by over-expression of the deacetylase, sir-2.1. ... These results show that aging is controlled by overlapping but distinct pathways." Next up: the same in mice.
Cartilage Without Scaffolds (March 25 2006)
The Houston Chronicle is running an article on the tissue engineering of new cartilage as a brute force therapy for the age-related damage of arthritis: "I have been researching this area of cartilage since 1984, and this is the most excited I have ever been about the work ... Athanasiou's group describes the first successful method of growing and molding cartilage into natural forms without requiring scaffolds, trellis-like arrangements upon which cells are seeded and grown. ... Using nothing but cartilage donor cells, Athanasiou's group grew dime-sized disks of cartilage nearly identical to that in the body. ... We're no longer talking about repairing a small lesion. Potentially, we're talking about effectively treating osteoarthritis by resurfacing the entire joint. I'm not saying we're there yet, but we're beginning to see that it's doable."
Ever More Multipotency (March 24 2006)
Via ABC News, news of yet another population of multipotent adult stem cells: "In the report Hasenfuss and his team described how they isolated the sperm-producing stem cells from mice testes. The cells, which they call multipotent adult germline stem cells (maGSCs), under certain conditions, acted like embryonic stem cells. When the researchers injected the cells into early embryos they found the cells contributed to the development of different organs. ... However, much more research is required before the similarities and differences between these testes cells and embryonic stem cells are understood, and before their potential for use in therapy can be properly assessed."
Pin1 Enzyme and Alzheimer's (March 24 2006)
The Alzheimer's research has been rolling in of late; more progress can be found at Medical News Today: "These new findings, shown in an animal study, provide further evidence that Pin1 (prolyl isomerase) is essential to protect individuals from age-related neurodegeneration and for the first time establish a direct link between amyloid plaques and tau tangles, the two abnormal structures that are considered the pathological hallmarks of this devastating disease. ... when Pin1 was missing, neurons in the regions of the brain responsible for memory would collapse under the weight of the tau protein tangles, ultimately leading to age-dependent neurodegeneration. ... As was earlier shown with tau proteins, it appears that Pin1 acts to restore misshapen amyloid precursor proteins to their original healthy shape, possibly preventing the onset of neurodegeneration."
Virus-Armed Immune Cells Versus Cancer (March 23 2006)
(From Forbes). The weight of funding in the field of cancer research is driving promising technology demonstrations in this age of rapidly advancing biotechnology: "The technique -- which uses targeted viruses hidden in immune cells to destroy tumors -- has only succeeded in mice so far, and it's not known if it will work in humans. ... some viruses hone in on cancer cells, and they know that the immune system often swings into action whenever it detects a tumor. Blending these two potential weapons, researchers at Stanford University have taken immune cells, 'supercharged' them with a cancer-killing virus, and sent them on a mission to destroy tumors. ... the study's authors say the approach appeared to kill off tumors in mice infected with human ovarian cancer cells." The reliable prevention and cure of all cancer is vital to healthy life extension; cancer is in many ways the most threatening and pervasive age-related condition.
More On Alzheimer's as Type 3 Diabetes (March 23 2006)
EurekAlert follows up on the team that argues Alzheimer's could be classified as a form of diabetes: "By depleting insulin and its related proteins in the brain, [researchers] have replicated the progression of Alzheimer's disease - including plaque deposits, neurofibrillary tangles, impaired cognitive functioning, cell loss and overall brain deterioration - in an experimental animal model ... In the study, brain deterioration was not related to the pancreas, which regulates insulin for the body. When pancreatic insulin is deficient or the body fails to respond to it, the result is Type 1 or Type 2 diabetes. ... postmortem brain tissue of Alzheimer's patients showed a strong link between insulin depletion in the brain and Alzheimer's disease, raising the possibility that Alzheimer's is a neuroendocrine disorder, or a Type 3 diabetes. ... We now know that if you specifically target insulin and its actions in the brain, you could develop new treatments for this disease."
How to Read Studies, How to Read Science (March 22 2006)
This is a nice introduction to critical thinking in the face of claims made in the "anti-aging" marketplace - as well as in reputable branches of aging and longevity research: "Although there are myriad ways to undermine a research study, [readers] should be on the lookout for issues that frequent the Longevity and Aging literature. A common issue is the extrapolation of animal (or even yeast or bacteria!) longevity data to humans. Beware studies that avoid mentioning the study species in their abstract or conclusions. They may want you to over-estimate the import of their work. ... beware of surrogate markers or intermediate endpoints. Have the investigators 'cherry picked' only the markers that prove their bias? ... Look for adequate numbers of study subjects. In general one needs over 20 individuals per study arm to approach adequate approximation of a general population."
Ghandi Stage 3 (March 22 2006)
If you haven't yet read Aubrey de Grey's thoughts on recent history for the Strategies for Engineered Negligible Senescence (SENS), then you should do so now: "SENS is a radical departure from the approaches that biogerontologists have traditionally explored for combating aging ... Thus, it is no surprise that SENS is extremely controversial within the field. ... I am attempting to bring about a change in thinking about aging and how to combat it that is bigger than the field has ever undergone before ... there is a good deal of knee-jerk resistance from those with a large intellectual investment in the prevailing orthodoxy. Gandhi's famous description of campaigns to change people's thinking goes something like this: 'First they ignore you, then they laugh at you, then they oppose you, then they say they were with you all along.' By that measure, 2005 was the year in which SENS emphatically progressed to 'Gandhi stage 3'."
Alzheimer's and the Choroid Plexus (March 21 2006)
A most interesting article from the Purdue University News Service: "an organ in the brain called the choroid plexus apparently plays a critical role in preventing the accumulation of a protein associated with Alzheimer's disease. The researchers found that the choroid plexus acts as a sort of 'fishnet' that captures the protein, called beta-amyloid, and prevents it from building up in the cerebrospinal fluid, which surrounds and bathes the brain and spinal cord. Moreover, tissue in the organ is able to soak up large amounts of the protein and may contain enzymes capable of digesting beta-amyloid. ... Future research may focus on efforts to isolate possible enzymes. ... the findings suggest that aging may degrade the organ's performance."
Biochemistry of Neurodegeneration (March 21 2006)
Scientists are striving to understand the biochemical processes fundamental to neurodegenerative diseases: "There is tremendous urgency right now to determine which processes cause the destructive mechanisms that we see in neurodegenerative diseases ... oxidative stress, whatever its origin, is capable of causing the cytoskeleton of this artificial system to collapse in the same way that it does in diseased or aging brains. ... One of the future experiments planned by the team is to induce oxidative stress in the presence of key proteins thought to be involved in the underlying causes of the brain pathologies associated with Alzheimer's and Parkinson's diseases to see whether these proteins accelerate the damaging effects." This is interesting in light of recent research into the biochemistry of cell death in Alzheimer's.
More Multipotent Adult Stem Cells (March 20 2006)
This sort of press release should be taken with a grain of salt while waiting for confirmation of the science, but it's a good measure of where the state of the art is seen to be at the present time: "Moraga Biotechnology Corporation [announces] the discovery in adult tissues of a very primitive stem cell with properties that are similar to embryonic cells. The Company's scientists found that these adult stem cells were able to differentiate into most tissues and organs of the body ... Moraga's scientists have also discovered that their stem cells normally reside in large numbers throughout the body. More importantly, the Company has developed a simple and cost-effective method for isolating and purifying millions of its stem cells from adult tissues without the need to expand them outside the body." A number of groups are claiming easily accessed multipotent adult stem cells, but we'll see how it all shakes out in a year or two.
How Fat Causes Inflammation (March 20 2006)
Inflammation is a form of ongoing biochemical damage; more inflammation means a shorter, less healthy life as the damage builds up and age-related conditions set in. Via Life Extension Foundation News, a look at how fat causes inflammation: "Greenberg and his colleagues found that as fat cells reach their maximum size, they eventually break down and die. ... more than 90 percent of the macrophages in adipose tissue of obese mice and humans are located around dead fat cells. ... these immune cells now appear to be rushing to fat cells after their death to mop them up. When this happens, the macrophages may emit potentially dangerous amounts of inflammatory chemicals. ... In a case of molecular rescue gone awry, the findings may explain how enlarged fat cells, as found in obesity, promote obesity-related complications such as arthritis, insulin resistance, diabetes, or heart disease."