Longevity Meme Newsletter, May 31 2010

May 31 2010

The Longevity Meme Newsletter is a weekly email containing news, opinions, and happenings for people interested in aging science and engineered longevity: making use of diet, lifestyle choices, technology, and proven medical advances to live healthy, longer lives. This newsletter is published under the Creative Commons Attribution 3.0 license. In short, this means that you are encouraged to republish and rewrite it in any way you see fit, the only requirements being that you provide attribution and a link to the Longevity Meme.



- Video of Aubrey de Grey at TEDMED 2009
- Mitochondrial Antioxidants Now in Canine Trials
- A New Longevity Mechanism in Nematode Worms
- Discussion
- Latest Healthy Life Extension Headlines


A little late, but worth it: follow the link below to see biomedical gerontologist Aubrey de Grey presenting at last year's TEDMED conference:


"His mantra is that aging is metabolism caused cellular damage that leads to organism pathology, and the human body, just like cars, can be made to run longer with adequate maintenance and repair. He views age related problems as belonging to seven types and in order to tackle aging, all seven cellular and molecular problems need to be cured. Aubrey also coined the idea of a Longevity Escape Velocity (LEV), which is the point of life span where progress in aging science is occurring faster than the degradation of the body itself. He believes that if someone is able to live to 150 years old, then by that point the progress in the ability to keep them alive will be faster than their rate of death, thus they will live into their 1000s."

You can read more on the science behind these views at the SENS Foundation:


Or in great detail in the book Ending Aging:



In recent years, researchers have demonstrated that ingested antioxidants have little to no effect on life span. But antioxidants engineered to target the mitochondria, the free-floating power plants within our cells, can extend healthy life in mice by 20-30%. Just don't expect to find them in a store any time soon:


"Per the mitochondrial free radical theory of aging, it may be supposed that these antioxidants are slowing the rate at which mitochondria damage themselves; that damage is the first step in a chain of consequences that leads to age-related degeneration and the failure of cells and bodily systems. ... Amongst the researchers working on mitochondrial targeting of antioxidants are Rabinovitch, who used gene-engineering to boost mitochondrial levels of a natural antioxidant, and Skulachev, who has engineered an ingested antioxidant compound called SKQ1 that is taken up by the mitochondria - unlike any other form of ingested antioxidant. A fellow emailed me today to let me know that SKQ1 is moving ahead in animal studies, now using dogs rather than mice. ... trials of the mitochondrially targeted antioxidant, SKQ1, are now underway in the canine model in both Moscow State Veterinary School and the St George Animal Hospital in Sydney. Early results have proven positive in a number of age related conditions."

You can find out more about why mitochondria are important in aging from the Fight Aging! archives:



Researchers have discovered what may be a new biological mechanism of longevity in nematode worms, which so far looks to be distinct from the well known effects on life span of manipulating calorie restriction and insulin metabolism. Discoveries in nematodes have a good track record of carrying through to work similarly in mouse studies:


"In the present atmosphere of enthusiasm for manipulating metabolism to slow aging, I'm sure that the funding will be raised for further investigation. Now if we could just transfer some of that enthusiasm to the more productive and promising lines of research based upon periodic repair of the damage generated by metabolism rather than changing metabolism to slow down the rate at which damage is caused..."


The highlights and headlines from the past week follow below.

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A lot of work has taken place in recent years on killing cancer cells by heating targeted nanoparticles. Here is an example of the present state of the art: "When irradiated with light, gold nanoparticles become hot quickly, hot enough to generate explosive microbubbles that will kill nearby cancer cells ... To boost this approach, researchers [have] developed a method for creating supramolecular assemblies of gold nanoparticles that function as highly efficient photothermal agents of a size designed to optimize their delivery to tumors. ... They first took gold nanoparticles, 2 nanometers in diameter, and decorated the nanoparticles' surface with adamantane. They then added two other constructs: cyclodextrin attached to a biocompatible polymer known as polyethylenimine, and adamantane linked to polyethylene glycol, another biocompatible polymer. When combined in various ratios, these three constructs quickly assemble into nanoparticles with well defined sizes ranging from 40 to 118 nanometers in diameter. Once the complexes were purified, the researchers then attached a tumor targeting molecule to the surface of the resulting supramolecular complexes. ... when irradiated with a laser beam, the temperature of the assemblies rapidly soared above 374 C, the temperature at which explosive microbubbles form."

Another step forward for tissue engineers: "scientists have created an eight-layer, early stage retina from human embryonic stem cells, the first step toward the development of transplant-ready retinas to treat eye disorders such as retinitis pigmentosa and macular degeneration that affect millions. ... The retina is the inside back layer of the eye that records the images a person sees and sends them via the optic nerve from the eye to the brain. Retinal diseases are particularly damaging to sight. More than 10 million Americans suffer from macular degeneration, the leading cause of blindness in people over 55. About 100,000 have retinitis pigmentosa, a progressive, genetic disorder that usually manifests in childhood. ... To mimic early stage retinal development, the researchers needed to build microscopic gradients for solutions in which to bathe the stem cells to initiate specific differentiation paths. ... creating transplantable retinas from stem cells could help millions of people, and we are well on the way. ... researchers are testing the early-stage retinas in animal models to learn how much they improve vision. Positive results would lead to human clinical trials."

CNN Money is running a longer piece on calorie restriction mimetic research and the goal of slowing down aging to extend healthy life: "In early 1934, Depression-weary Americans were beginning to see tendrils of hope poking out of the bleak landscape. ... But one of the new year's most promising developments passed almost unnoticed. ... researcher Clive McCay was nearing the end of a four-year study that showed that rats' life spans were greatly extended when they were put on near-starvation diets. To many of his scientific peers, McCay's data made no sense at all. A glorious new chapter in nutrition science had been opened not long before by the discovery of dietary deficiencies behind scourges such as rickets, pellagra, and beriberi. In the wake of such progress, it seemed almost subversive to suggest that a bunch of rodent Oliver Twists, raised on such short rations that their growth was stunted, could live radically longer than well-fed ones. ... Over the next several decades, his discovery was all but forgotten outside of the back halls of science - a laboratory curiosity that didn't actually spark much curiosity. Most scientists were reluctant to risk wasting time probing an anomaly that seemed as baffling as aging itself. Calorie restriction (CR), as it's now called, eventually was shown to extend many species' life spans by a third or more. Now that anti-aging research is hot, it seems bizarre that CR spent decades on science's back shelf."

A review paper: "The definition of sarcopenia continues to evolve, from an observational phenomenon to a differential diagnostic approach. Clinical relevance for sarcopenia is defined by a loss in lean muscle mass and impairment of functional status. A therapeutic approach to the loss of skeletal muscle mass and strength in older persons depends on correct classification. The term sarcopenia is reserved for age-related decline in muscle mass not attributable to the presence of proinflammatory cytokines. For persons with sarcopenia, the primary intervention should include resistance exercise. An improvement in muscle mass and strength has been demonstrated with resistance exercise, even in the very old. Targeting the hormonal changes with aging is an attractive intervention. However, testosterone replacement in elderly hypogonadal men has demonstrated only modest increases in muscle mass and strength. Administration of growth hormone in pharmacologic doses increases muscle mass but not muscle strength. Nutritional therapy is promising, but the effects in clinical trials have been small."

A brace of popular science books on gerontology and engineered longevity have been written in past years - one of the many signs that the field is growing in profile in the public eye, an important step on the way to obtaining funding for more rapid progress. Here the Village Voice notes an irreverent forthcoming addition to the portfolio. Per the article, we probably shouldn't take it seriously as anything but a sign of the times: "Along with the origin of life and the nature of consciousness, why and how we age is one of the weightiest questions out there. It's one Weiner tackles in his new book Long for This World, a brilliant and improbably funny look inside the mind-bending science of immortality ... These people are asking what makes us mortal. It's something everyone's curious about, whether they're scientists or not. ... Human life expectancy has doubled over the past 200 years, Weiner writes, thanks primarily to advancements in medicine. And while prominent gerontologists argue that we can expect another seven years fairly soon, the most fervent members of the field are gunning for the total eradication of death. Chief among the latter is Aubrey David Nicholas Jasper de Grey, Weiner's arch protagonist."

From Impact Aging earlier this year, an open access paper on some of the mechanics of hormesis: a little stress on your system improves longevity. "Oxidative stress constitutes the basis of physio-pathological situations such as neurodegenerative diseases and aging. However, sublethal exposure to toxic molecules such as reactive oxygen species can induce cellular responses that result in stress fitness. Studies in Schizosaccharomyces pombe have recently showed that the Sty1 MAP kinase, known to be activated by hydrogen peroxide and other cellular stressors, plays a pivotal role in promoting fitness and longevity when it becomes activated by calorie restriction, a situation which induces oxidative metabolism and reactive oxygen species production. Activation of the MAP kinase by calorie restriction during logarithmic growth induces a transcriptional anti-stress response including genes essential to promote lifespan extension. Importantly enough, the lifespan promotion exerted by deletion of the pka1 or sck2 genes, inactivating the two main nutrient-responsive pathways, is dependent on the presence of a functional Sty1 stress pathway, since double mutants also lacking Sty1 or its main substrate Atf1 do not display extended viability. ... We propose that moderate stress levels that are not harmful for cells can make them stronger."

Some people do have better genes than others when it comes to a long life, though lifestyle choices do still seem to play a greater role. Here, researchers were looking to "determine whether offspring of parents with exceptional longevity (OPEL) have a lower rate of dementia than offspring of parents with usual survival (OPUS). ... [Participants were a] volunteer sample of 424 community-residing older adults without dementia aged 75 to 85 recruited from Bronx County starting in 1980 and followed for up to 23 years. ... Epidemiological, clinical, and neuropsychological assessments were completed every 12 to 18 months. OPEL were defined as having at least one parent who reached the age of at least 85. OPUS were those for whom neither parent reached the age of 85. ... The OPEL group had a lower incidence of Alzheimer's disease. After adjusting for sex, education, race, hypertension, myocardial infarction, diabetes mellitus, and stroke, results were essentially unchanged. OPEL also had a significantly lower rate of memory decline on the Selective Reminding Test (SRT) than OPUS. ... OPEL develop dementia and Alzheimer's disease at a significantly lower rate than OPUS. Demographic and medical confounders do not explain this result. Factors associated with longevity may protect against dementia and Alzheimer's disease."

Raised levels of heat shock proteins can protect against sarcopenia, age-related loss of muscle mass and strength: "HSP10 (Heat Shock Protein), helps monitor and organise protein interactions in the body, and responds to environmental stresses, such as exercise and infection, by increasing its production inside cells. Researchers [found] that excessive amounts of HSP10 inside mitochondria - 'organs' that act as energy generators in cells - can [preserve] muscle strength. ... We studied the role of HSP10 inside mitochondria, as it is here that unstable chemicals are produced which can harm parts of the cell. The damage caused by this is thought to play an important part in the ageing process, in which skeletal muscle becomes smaller and weaker and more susceptible to stress damage. In response to these stresses HSP10 increases its levels and helps cells resist damage and recover more effectively. Our research is the first to demonstrate that age-related loss of skeletal muscle mass is not inevitable." The article is sadly sensationalist, overhyping a slowing of muscle loss as "halting the aging process" when it is of course no such thing. It is unfortunate that university publicists feel the need to do this - it only makes them and the researchers they promote look foolish.

Via EurekAlert!: "Cancer and diabetes – are risk factors the same for these two diseases? Or does diabetes cause processes in the body which promote the onset or growth of cancer? It is still unclear why diabetics have a higher rate of cancer than people who are not affected by this metabolic disorder. In order to precisely identify the types of cancer in which diabetes plays a role, [researchers carried out] the largest study ever on cancer risks of people with type 2 diabetes. The study included 125,126 Swedish citizens who had been hospitalized due to problems associated with type 2 diabetes. The epidemiologists compared the cancer incidence in these patients with that of the general population in Sweden. ... The researchers discovered that people with type 2 diabetes have an increased risk of developing 24 of the types of cancer studied. The most significant risk elevation was established for pancreatic and liver cell cancers. The rate of these cancers in people with type 2 diabetes is elevated by factor six and 4.25 respectively compared to the general population. The epidemiologists also found the risk of cancers of the kidneys, thyroid, esophagus, small intestine and nervous system to be more than twice as high." Diabetes is a very preventable condition - do the work, and you'll most likely avoid both it and the increased cancer risk that comes with it.

Artificial hearts have come a long way in recent years, but still have a long way to go to match the potential offered by tissue engineered organs: "For nearly two years, 43-year-old Charles Okeke has tried to live a normal life in the hospital tethered to a 400-lb. machine ... Okeke now has what is called a 'total artificial heart.' Both ventricles were removed along with four valves. Connector tubes were sewn in. It pumps blood just like a human heart. ... The FDA has just approved this backpack-sized device that runs on batteries and weighs just 13 lbs. It's the first portable technology to support the entire artificial heart. ... Sensors that used to be the size of a can of soup are now about the size of a quarter. That leap has enabled us to downsize the entire console. ... Charles will have to work hard to maintain his health as he awaits a new heart, but if the right match is not found, doctors say he could live indefinitely on this device. The Syncardia total artificial heart costs about $125,000 and about $18,000 a year to maintain."



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