Longevity Meme Newsletter, April 30 2007

April 30 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.



- An Interesting Discussion on "The Way We Age"
- Never Too Late To Start Calorie Restriction
- Discussion
- Latest Healthy Life Extension Headlines


You'll find an interesting discussion underway in the comments for the following Fight Aging! post, using a recent popular science article on aging and aging research as a starting point:


"I would argue that wear-and-tear model is gross oversimplification. If the simple wear-and-tear model was true for complex biological organisms then one would not expect wild differences in lifespan of equally complex organisms such a mouse (2 years), human (100 years), Bowhead whales and turtles (200 years), or some plants/trees (1000s of years).

"While the engineering analogies made by some appear intuitive or attractive, they forget the biological systems are autonomous in that they have built in repair and control mechanisms and far more flexibility then material systems. When a gear of a car breaks down or rusts, that car can not repair itself or install a new gear, whereas our bodies perform these operations every day both on the cellular and organismal level. This is a fundamental distinction."

This sort of debate, repeated at various scales throughout the aging research and funding communities, is far from academic. The direction of debate determines the direction of longevity research - and the degree to which that direction succeeds will mean the difference between life and death for each and every one of us, one day in the future.

It's in our interest to understand these debates, just as it's in the interest of a cancer patient to understand the cut and thrust of cancer research. We all suffer from aging, and we all benefit when medical technology advances to the point of repairing the underlying damage that causes aging:



As I mention here and there, the present consensus appears to be that it's never too late to start practicing calorie restriction (with optimal nutrition, of course). You might have missed out on the benefits that accumulate over years, but there are still benefits that appear fairly rapidly in later life.


In essence calorie restriction appears to encourage increased turnover in cellular components at any age, which rapidly reduces some levels of damage and damage-causing components through a variety of related mechanisms. Expect a beneficial impact on the chances of suffering cancer, for example.

As always, you should involve your physician, reading around the subject and your common sense in changes you make regarding your health. Those parties know more than I do, and calorie restriction, much like exercise, isn't good for everyone or under absolutely all circumstances - very beneficial for most folk, by the look of the human research, but not for everyone.



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/

Exercise Versus Parkinson's (April 29 2007)
Health 24 reports that an analysis of the data from a large cancer study suggests that exercise helps lower the risk of Parkinson's disease: "The researchers looked at exercise levels and tried to determine if they affected the rate of Parkinson's disease after adjusting the numbers to reflect the possible influence of factors such as age, gender and smoking. People who exercised more than 75 percent of their fellow study participants were 20 percent less likely to develop Parkinson's, compared to those who didn't exercise. The risk of the disease was 40 percent lower in those who took part in the highest levels of moderate to vigorous activity, defined as exercise such as jogging, lap swimming, tennis and bicycling, the study found." This sort of analysis is never as robust as the results of a study specifically designed to produce the data you're after, so treat with caution. We already know that exercise is strongly correlated with resistance to most common age-related conditions, however. It's almost as good as calorie restriction! Even if Parkinson's isn't one of these conditions, that's no reason to skimp on keeping up with the health basics.

Changing Cancer Cells Back Into Normal Cells (April 29 2007)
One logical outgrowth of the quest to control cell state as a part of regenerative medicine is an initiative to control the state of cancerous cells. From EurekAlert!: researchers "discovered that aggressive melanoma cells (but not normal skin cells nor less aggressive melanoma cells) contain specific proteins similar to those found in embryonic stem cells. This groundbreaking work led to the first molecular classification of malignant melanoma and may help to explain how, by becoming more like unspecialized stem cells, the aggressive melanoma cell gained enhanced abilities to migrate, invade and metastasize while virtually undetected by the immune system. ... Embryonic stem cells are pluripotent, meaning they are able to differentiate into any of the more than 200 cell types in the adult body. Which type of cell they become depends on the signals they receive from their microenvironment. Similarly, during cancer progression, malignant cells receive and release signals from their own microenvironment, cues that promote tumor growth and metastasis. ... scientists can change human metastatic melanoma cells back to normal-like skin cells - by exposing the tumor cells to the embryonic microenvironment of human embryonic stem cells."

Common Sense on Extending Healthy Longevity (April 28 2007)
A dose of common sense from calorie restriction (CR) practioner April Smith: "First, no one I know thinks that true immortality is a possibility. There will always be accidents ... However, there are some very reasonable people who believe that it is possible that technology will advance enough to defeat many of the mechanisms that cause aging. If we could repair the damage of aging, then we could dramatically extend life and health. I believe that would be a very good thing. ... Before I got involved in the CR Society, I wasn't aware that these perspectives existed. I was hopeful that CR could help me look forty at fifty-five, or at least help me not feel like total crap at 29, but I didn't even think about radical life-extending biomedicine. ... but there are quite a few who hope that by pursuing vigorous CR, we might live and be in good health at a time when more advanced medical technologies are available to extend healthy life further. For those who dismiss this as childish fantasy, I ask on what basis they make that determination. ... I can attest that I was quite unaware of the real progress that has been made in recent years, and when I found out more, my perspective changed."

What Happened To the Point of the Exercise? (April 28 2007)
An interesting position paper from Aubrey de Grey via the Annals of the NYAS: "The early days of biogerontology were blessed with an undiluted forthrightness concerning the field's ultimate goals, epitomized by its leaders. Luminaries from Pearl to Comfort to Strehler declared the desirability of eliminating aging with no more diffidence than that with which today's oncologists aver that they seek a cure for cancer. The field's subsequent retreat from this position garnered a modicum of political acceptability and public financial support, but all biogerontologists agree that this fell, and continues to fall, vastly short of the funding that the prospect of even a modest postponement of aging would logically justify. The past 20 years' discoveries of life-extending genetic manipulations in model organisms have weakened the argument that a policy of appeasement of the public's ambivalence about defeating aging is our only option; some of the biogerontologists responsible for these advances have espoused views of which our intellectual forefathers would be proud, without noticeably harming their own careers. With the recent emergence of a detailed, ambitious, but practical roadmap for the comprehensive defeat of aging, this process has moved further: our natural and most persuasive public stance is, more than ever, to reembrace the same unassailable logic that served pioneering biogerontologists perfectly well."

Israeli Parkinson's Research (April 27 2007)
A glance at some of the Parkinson's research from young Israeli concerns via Globes Online: "The damaged neurons of patients suffering from Parkinson's can no longer create dopamine in the brain, thus causing the muscle tremors, rigidity and twitches that make life a nightmare for them. When given synthetically, dopamine relieves the patient's symptoms but its effect is temporal and is associated with significant side effects. Reubinoff hopes to successfully transplant these converted dopamine producing neurons into the human body, enabling the body to resume producing its own dopamine. ... While Parkinson's patients show an inflammation of the central nervous system, anti-inflammatory medication has not helped. Proneuron's research has shown that boosting the right immune system response can successfully modulate the immune activity to become beneficial for neuronal survival and renewal. This approach has the potential not only to attenuate or stop disease progression, but also to restore lost function."

The Cost of Just One Age-Related Condition (April 27 2007)
Age-related degeneration is an ongoing corrosion of all our resources - for all resources spring from human action, which requires health and life. Aging costs us greatly in every way; here, EurekAlert! catalogues just one fraction of the whole: "Arthritis and other rheumatic conditions exact a large and growing economic toll on the nation as a result of the increase in numbers of persons affected, rather than an increase in mean expenditures and earnings losses ... In 2003, employed adults with arthritis earned an average of $3,613 less than healthy working adults between the ages of 18 and 64. Nationwide, raw earnings losses due to arthritis totalled $108 billion, up from $99 billion in 1997. ... Since the number arthritis sufferers is projected to increase steadily to nearly 67 million by 2030, [the] economic toll threatens to continue to escalate. He calls urgent attention to the need for cost-effective efforts to decrease medical expenses and increase the earning power of people with arthritis." This projection is a future in which we fail to support and advance medical research. The solutions proposed in the article are, as ever, second-rate, given that we're in the midst of a biotechnology revolution. The real solution to age-related disease is to push hard for cures, preventions, and real anti-aging research like SENS.

The Consensus on Sirtuins (April 26 2007)
From Michen and Sinclair, a look at the present consensus on sirtuins: "Sirtuins are a conserved family of proteins found in all domains of life. The first known sirtuin, Sir2 (silent information regulator 2) of Saccharomyces cerevisiae, from which the family derives its name, regulates ribosomal DNA recombination, gene silencing, DNA repair, chromosomal stability and longevity. Sir2 homologues also modulate lifespan in worms and flies, and may underlie the beneficial effects of caloric restriction, the only regimen that slows aging and extends lifespan of most classes of organism, including mammals. Sirtuins have gained considerable attention for their impact on mammalian physiology, since they may provide novel targets for treating diseases associated with aging and perhaps extend human lifespan. In this review we describe our current understanding of the biological function of the seven mammalian sirtuins, SIRT1-7, and we will also discuss their potential as mediators of caloric restriction and as pharmacological targets to delay and treat human age-related diseases."

The Wrong Perspective (April 26 2007)
A good example of absolutely the wrong way to look at what is happening in longevity and medicine can be found at Newslink: increasing longevity is "happening" and we must marshall our resources to "address" it. This is nonsense - we humans are making our own longevity, creating additional years of healthy life through investment in medical research and development. We don't need to run around babbling about society and organization and coping. Instead we should recognize that people are dying of aging in vast numbers each and every day, and that it is well within our power to make the present slow inroads into fighting aging proceed a great deal more rapidly. "While life expectancy continues to increase at its current rate, we must wake up to the fact that we are living a 29-hour day. have 24 hours to use now, and we are putting by five hours away for later." This is nothing compared to what we know to be possible in the decades ahead - but we won't get there by thinking that longevity just happens, and that longer lives must be "addressed."

More Melatonin Research (April 25 2007)
People - within and without the scientific community - spend far more time than is warranted in the study of compounds and lifestyle that are never going to have a large effect on aging. Yet a ferocious attention is given to the slightest rumor and every study involving food and supplements - while practical methods of moving far beyond the world of pills and diet are neglected. From ScienceDaily: researchers concluded "that the consumption of melatonin - a natural substance produced in small amounts by human beings and present in many types of food - delays the oxidative damage and inflammatory processes typical of the old age. ... not only did this substance neutralize the oxidative stress and the inflammatory process caused by aging, but it also delayed its effects, thus increasing longevity." The further conclusions from the researcher seem overstated - until you realize that melatonin is illegal to use in his country, and dealing with that meddling injustice is partially why this research release exists in the first place. Melatonin may be nothing compared to the prospects of SENS and other future medicine, but people should stand up for the right to ingest whatever they see fit to ingest.

Alzheimer's, Gamma-Secretase and Tau (April 25 2007)
I should point your attention to another good NYAS presentation summary from recent days: "No consensus emerged on the single best way to tackle Alzheimer's disease. But in a symposium such as this, designed to stimulate discussion and debate, that's probably a good sign: the diversity of opinions and approaches indicates that neurodegenerative disease research is a vibrant and healthy field. Looking toward the near future for new therapies, [gamma-secretase] modulators are probably furthest ahead; some candidates are well into clinical trials. Amyloid immunotherapy - inducing the brain to attack aggregated pathogenic [amyoid-beta] species - is potentially effective, but the first subjects treated with this approach showed serious side effects. Drugs that work upon synaptic transmission also show promise. The wide range of approaches and ideas is encouraging. While the gradual progress of Alzheimer's disease may be painful to watch, its slow time course has a silver lining: the promise of interrupting the disease before it's too late."

Don't Bet Against Longevity (April 24 2007)
(From News.com.au). The world has a way of presenting us with tiny and fleeting replicas of the vast, slow and complex dances that take place behind the scenes of everyday life. Actuarial concerns are engaged in a years-long process of education and change in response to a future of increasing longevity. Billions of dollars are moving with the times - but you'll find that same advance wherever money changes hands over the length of healthy life. "A man who bet £100 ($240) a decade ago that he would live to be 100 is preparing to pick up his £25,000 ($60,000) winnings. So confident was bookmaker William Hill in 1997 that it gladly offered Alec Holden odds of 250/1. ... When we started taking these bets, 100 years old seemed to be an almost mythical landmark and we were prepared to offer massive odds. But these age wagers are starting to cost us a fortune and from now on we are going to push out the age to 110. I am sure that Alec will get more pleasure from our letter than he will from the Queen's."

Organ Printing in a Nutshell (April 24 2007)
RSC Publishing provides a compact overview of the application of bioprinting technologies: "In order to build an organ, you need four components: cells (the bio-ink), a biomaterial (the biopaper), a device to make three-dimensional structures (the bioprinter), and a method to aid tissue assembly and maturation (the bioreactor). In addition to this shopping list, you need the expertise to put the components together, and you need funding. Enter the hydrogel chemists, the cell and developmental biologists, the physicists, the computational modellers, and a company that builds rapid prototyping devices. ... in many ways, the biomaterial is the easy part. Shaping an artificial 'neo-organ', developing the printing tools and a computer model for layer-by-layer construction, and devising a strategy to mature the neo-organ before transplantation are among the main challenges." If you can build organs from a patient's cells - or even meaningful amounts of undamaged tissue for transplant - that will make an enormous difference to the future of health and longevity.

The Way We Age (April 23 2007)
The New Yorker looks at medicine and aging; folk on the Gerontology Research Group list have been disputing some of the presented information, but it's a decent article overall: "Nonetheless, as the defects in a complex system increase, the time comes when just one more defect is enough to impair the whole, resulting in the condition known as frailty. It happens to power plants, cars, and large organizations. And it happens to us: eventually, one too many joints are damaged, one too many arteries calcify. There are no more backups. We wear down until we can't wear down anymore. ... Hair grows gray, for instance, simply because we run out of the pigment cells that give hair its color. ... We rely on stem cells under the surface to migrate in and replace them. Gradually, however, the stem-cell reservoir is used up. ... Inside skin cells, the mechanisms that clear out waste products slowly break down and the muck coalesces into a clot of gooey yellow-brown pigment known as lipofuscin. ... The eyes go for different reasons. ... Even without cataracts [the] amount of light reaching the retina of a healthy sixty-year-old is one-third that of a twenty-year-old. ... There is [no] single, common cellular mechanism to the aging process. Our bodies accumulate lipofuscin and oxygen free-radical damage and random DNA mutations and numerous other microcellular problems. The process is gradual and unrelenting. ... We just fall apart."

All the More Reason For AGE Breakers (April 23 2007)
A research team recently demonstrated that a diet lower in advanced glycation endproducts (AGEs) extended life in mice: "Aging is accompanied by increased oxidative stress (OS) and accumulation of [AGEs]. AGE formation in food is temperature-regulated, and ingestion of nutrients prepared with excess heat promotes AGE formation, OS, and cardiovascular disease in mice. We hypothesized that sustained exposure to the high levels of pro-oxidant AGEs in normal diets (RegAGE) contributes to aging via an increased AGE load [and a same-calorie] AGE-restricted (by 50%) diet (LowAGE) would decrease these abnormalities. ... This was associated with a reduction in systemic AGE accumulation and amelioration of insulin resistance, albuminuria, and glomerulosclerosis. Moreover, lifespan was extended in LowAGE mice, compared with RegAGE mice. Thus, OS-dependent metabolic and end organ dysfunction of aging may result from life-long exposure to high levels of glycoxidants ... A reduced AGE diet preserved these innate defenses, resulting in decreased tissue damage and a longer lifespan in mice." More attention should be given to developing AGE breaker drugs. Diet is just one source - your body also creates AGEs itself as a byproduct of metabolic processes.



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