Longevity Meme Newsletter, December 26 2005

December 26 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.



- A Calorie Restriction Christmas Feast
- Ever Faster, the Aging Genes
- Discussion
- Latest Healthy Life Extension Headlines


Traditional feasts - events that have lost their raw, hard-edged character in these modern times of plenty and insulating technology, and thankfully so - are perhaps a useful time to reflect on the strength of scientific backing given to the large health benefits, resistance to age-related disease and potential for healthy life extension resulting from calorie restriction, the practice of eating fewer calories while still obtaining optimal nutrition.


Let me direct your attention to one rapid and positive result of the recent Methuselah Foundation dinner: an article by Jason Pontin of the Technology Review on Foundation volunteers and calorie restriction advocates April Smith and Michael Rae. What do you eat on Christmas day when you're an experienced practitioner of calorie restriction? Follow the link below to find out:



Is it just my imagination, or are the genes directly connected with the aging process flying thick and fast now? This past week saw the publication of an interesting take on aging and metabolism via the lin-4 gene:


If nothing else, this piece aptly illustrates the hellish nature of trying to make sense of a complex system by trial and error: "worms lacking the lin-4 gene died prematurely. Extra copies of lin-4 led to shorter lives. Worms with mutated, less effective insulin receptors and mutated lin-4 lived a normal lifespan. [Worms] with normal lin-4 and mutated insulin receptors lived twice as long as normal." One can imagine a year of pulling hair out in an attempt to reach a publishable conclusion to experiments in cases such as this.

The chief benefit brought by advancing biotechnology is the ability to largely step over this sort of time-consuming experimentation and arrive directly at the answer - scientists can already move from gene to full understanding of all related biochemistry with stunning rapidity. It is still the case that finding the right genes to use as starting points for any given medical condition - such as aging - is a slow affair, a matter of endless studies and comparisons. In yeast, for example, scientists have taken years to test five thousand different genetically altered strains in their efforts to identify genes affecting aging:


Yet this class of work will become much easier in the years ahead. One biotechnologist today can do the work of one hundred in 1995; one biotechnologist in 2015 will be even further ahead. This is a largely a problem of data: obtaining it, correlating it, understanding it. Like all problems of data, it will be eaten whole by the growth in processing power and automation in the years ahead.


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



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 Neural Regeneration (December 25 2005)
From John Hopkins Medicine, welcome news of continuing progress towards a complete understanding of brain biochemistry: scientists "have discovered the steps required to integrate new neurons into the brain's existing operations. For more than a century, scientists thought the adult brain could only lose nerve cells, not gain them, but in fact, new neurons do form during adulthood in all mammals, including humans, and become a working part of the adult brain in mice at the very least. ... We've shown that [the neurotransmitter] GABA instead excites new neurons and that this is the first step toward their integration into the adult brain. ... their discovery might help efforts to increase neuron regeneration in the brain or to make transplanted stem cells form connections more efficiently." A very effective regenerative toolkit for the brain is a requirement for living far longer than we do now.

On/Off Mechanism For Gene Therapy (December 25 2005)
(Via Betterhumans). Some of the most promising new research into cures for age-related conditions is based on gene therapy; editing cellular behavior by changing genes. So it is good to see that scientists are progressing rapidly towards increasingly sophisticated - and thus safer, and more effective - gene therapy technologies: "A new method has been developed for switching genes on and off that could greatly improve gene therapy. ... Until now, researchers working to develop successful gene therapy for diseases such as Parkinson's have hit roadblocks such as toxic side-effects from over-expression of the therapeutic gene, and adverse events caused by immune system reactions to the viral delivery systems currently used to deliver the therapeutic genes. Now, we've engineered a genetic switch in a novel gene transfer vector that will overcome those barriers and set the stage to allow the next phase of research to occur."

Advancing Scaffold Technology (December 24 2005)
(From Innovations Report). The use of biodegradable, often nanoscale-engineered, scaffolds spreading in tissue engineering circles, and a large future market for this technology seems certain. So it is that materials scientists have a strong incentive - sources of funding - to develop better scaffolds: "Flock technology for example is applied in an industrial scale to the production of the velvety surfaces of spectacle-cases. Now, this method shall help to produce new types of medical implants. In order to create resorbable scaffolds, membranes made of mineralised collagen are covered with a gelatine-based biocompatible glue. In the next step, biologically degradable fibres are flocked on the tapes. ... This way a kind of 'velvet structure' is created on which cells can be seeded with a high density."

A Glance At Private Stem Cell Funding (December 24 2005)
Private and venture funds are flowing for at least some areas of stem cell research; successful hybrids of new stem cell technology and old-style drug development pipelines seem to be doing well: "Osiris Therapeutics, Inc. announced that it has closed a $19 million private equity round. The money will fund the company’s five ongoing clinical trial programs using their proprietary adult stem cell technology platform. The round was arranged by Swiss investment firm Friedli Corporate Finance, Inc. In total, the company has raised $70 million in 2005." Elsewhere, Advanced Cell Technology, long the poster child for the detrimental effects of threatened anti-research legislation on private funding, has emerged from the long dry spell in the past year.

The Dance Of Interacting Processes (December 23 2005)
(From the Bristol Press). A look at early stage research into one gene associated with aging shows what scientists have to go through into order to obtain even the smallest insights: "The gene, called 'lineage defective 4,' or lin-4, encodes a small piece of RNA ... worms lacking the lin-4 gene died prematurely. Extra copies of lin-4 led to shorter lives. Worms with mutated, less effective insulin receptors and mutated lin-4 lived a normal lifespan. C. elegans with normal lin-4 and mutated insulin receptors lived twice as long as normal. This finding suggests that lin-4 influences lifespan through the insulin signaling system ... It also explains why worms, rats and mice placed on low-calorie diets tended to live longer ... Less insulin means less protein synthesis and lower production of damaging chemical by-products ... If humans could somehow gear up their lin-4 genes and make extra [microRNA] to turn down insulin signaling, they might be able to delay aging."

Stem Cell Research In India (December 23 2005)
DNA Mumbai takes a glancing look at stem cell research in India: "There are about 15 laboratories across India in cities like Hyderabad, Pune, Bangalore, Delhi and Mumbai engaged in stem cell research and clinical applications. ... The LV Prasad Eye Institute in Hyderabad has been working with stem cells since 2001. 'We have been using limbal stem cells from the eye to treat damaged corneas and have had 70 per cent success in treating over 250 cases' ... In a recent experiment, the Delhi-based All India Medical Institute of Medical Sciences injected stem cells derived from bone marrow into 35 cardiac patients ... The patients were brought in at a critical stage when they were beyond bypass surgery and could have survived only with a transplant ... Sixty-four per cent showed improvement over 18 months."

Embryonic Stem Cells, As Is (December 22 2005)
Injection of unprepared embryonic stem cells into the body sounds like a good way to generate cancers rather than regeneration, but why not try it in animal models? From Betterhumans: "Injecting embryo stem cells 'straight up' - without changing their cell type first - has fixed damage in an animal model of heart attack. ... the stem cells, when transplanted into damaged mouse hearts, morph into functional forms of cells that compose a healthy heart. The study is considered important because it means that blank-slate embryonic stem cells could be introduced directly to damaged heart tissue to repair heart muscle and blood vessels. ... One intriguing result of the new study is that the implanted cells did not result in tumor formation, one of the primary safety concerns for stem cell therapy."

Researching Telomere Length (December 22 2005)
From EurekAlert, a look at one way in which telomeres, stem cells and long term health and longevity are tied together: "In this family, the affected grandmother developed gray hair in her 20s and lung problems in her early 60s and died at age 65. Her affected children developed signs of the disease about 10 years earlier than she had, and analysis of their cells revealed that 60 percent to 75 percent of their chromosomes had dangerously short telomeres. ... We know it only takes one critically short telomere to make a cell die, so it's clear that the more really short telomeres a person has the faster problems will develop. ... We thought there might be some relationship between telomerase, telomere length and the survival of stem cells, but it was really exciting to see it."

Seen From A Distance, Through A Hedgerow (December 21 2005)
Via the Scripps Howard News Service, another great example of how the healthy life extension movement looks to those unfamiliar with the details - or to lazy journalists who can't be bothered to do a little fact checking with the subjects of their article. Still, it's a mainstream press piece on the prospects for radical life extension, complete with links to the Strategies for Engineered Negligible Senescence and the MPrize for anti-aging research: "The first person to live to age 1,000 probably will turn 60 in 2006. Within 20 years or so, we'll have treatments for aging. Medicine will repair the damage that already has occurred in people who are in their 80s. They'll live on and on with healthy bodies and sharp minds. Medicine also will keep younger people from aging and getting frail and decrepit." These aggressive timelines are dependent on massive funding - something that in and of itself will take a decade or two to create.

Metabolic Rate Or Metabolic Stability? (December 21 2005)
From PubMed, an interesting paper on aging and metabolism: "The modern version of [the 'rate of living'] theory is that duration of life is influenced by the relative speed of a species' resting metabolism. However, empirical evidence does not consistently support this hypothesis. ... For example, if the metabolic rate/oxidative stress theory is correct, efforts to intervene in the aging process should be directed at finding ways to reduce metabolic rate, lessen the production of reactive oxygen species (ROS), improve antioxidant defenses, or increase the quantity of antioxidants. If the metabolic stability hypothesis is correct, efforts to intervene in the aging process should be directed at finding ways to increase the stability of the steady state values of ROS, increase the robustness of metabolic networks, or improve the stability of antioxidant enzymes." Which is all about slowing the rate rather than addressing age-related damage directly, of course.

A Utilitiarian View (December 20 2005)
A pro-government - meaning unrealistic on the true costs of socialism and regulation - but utilitiarian view of the cost of health and value of longevity can be found at the NCPA website: "The reduction in mortality from 1970 to 2000 had an economic value of about $3.2 trillion per year. Over the longer term, the cumulative longevity gains during the twentieth century were worth about $1.3 million per person. ... advances against one disease, like heart disease, raise the value of progress against other age-related ailments, such as cancer ... reductions in mortality since 1970 have raised the value of further health progress by about 18 percent. The authors also suggest that current funding of medical research is too low. A single percent reduction in mortality from cancer or heart disease would be worth nearly $500 billion to current and future Americans."

Investigating Free Radicals (December 20 2005)
Kevin Perrott comments on recent investigations into the free radical theory of aging: "Some focused research using mice who exhibited premature aging was published recently in PNAS where reactive oxygen species [ROS] were suprisingly NOT implicated as a potential cause. Rather than supporting the widespread notion that the damage caused by free radical production in mitochondria leads to spiraling reactive oxygen species and more damage, eventually producing the symptoms of aging, the study upsets it." Needless to say, there is debate and disagreement: "He contends that the researchers didn't observe ROS buildup in the mutators because they checked the wrong cell types. Energy-guzzlers such as the nervous system and muscles incur the most harm from mitochondrial faults, he says, and researchers should scrutinize their cells, not connective tissue cells."

Progress Using Follicle Stem Cells (December 19 2005)
(Via Genetic Engineering News). Scientists discovered a population of multipotent stem cells in adult hair follicles back in 2004, and now these cells are bring put to work in regenerative medicine: researchers "have found that stem cells from hair follicles of mice can be used to rejoin severed nerves in mouse models. Easily accessible hair follicle stem cells, which normally function to form the hair follicle which in turn form the growing hair in all mammals including man, have been shown to have great potential to produce nerve cells and many other types of cells. The hair follicle stem cells were used by the AntiCancer researchers to rejoin nerves in the legs of mice that were experimentally severed. After injection of the hair follicle stem cells, the nerves were rejoined and were able to regain function, enabling the mice to walk normally again."

Microarrys To Genes To Mechanism (December 19 2005)
From EurekAlert, a demonstration of the power of bioinformatics to speed medical research into age-related conditions. We already know that scientists can now move very rapidly to identify biochemical processes that cause disease if they just know which genes to use as a starting point. The hard part is finding those genes - but that is getting easier with the application of nanoscale engineering and computing power: "Microarrays are laboratory chips able to pick out which genes are active when different processes are occurring in the brain. When they analysed brains from people with Parkinson's, they found that out of all 25,000 human genes, regulation of 570 was highly abnormal in Parkinson's brains compared with non-diseased brains. This is the first study on Parkinson's disease where all human genes were studied."



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