Latest Article

Calorie Restriction, Metabolic Rate, and Longevity

One of the pieces of evidence that points to our mitochondria as a prime point of interest for engineered longevity is the correlation between maximum life span and resting metabolic rate (RMR) across species. In that light, this research on calorie restriction and metabolic rate is interesting even though it’s an insect study: “Caloric restriction (CR) extends lifespan in most animals, but the mechanisms underlying this phenomenon are the subject of much debate. We investigated the association between longevity and resting metabolic rate (RMR) in Indian stick insects (Carausius morosus) [by] quantifying the response of RMR to diet history … Over a range of body sizes, [RMR] decreased in response to CR, particularly when food was restricted during juvenile stages. With one exception, RMR of insects in different life-history stages matched current feeding level and was not substantially affected by intake history. Total lifespan was affected by intake, with insects that experienced CR early in development living longer than insects that were fed ad libitum. … CR and decreased RMR were associated with slower progression through pre-reproductive life-history stages.”

View the Article Under Discussion: http://pmid.us/19328225

Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

Continue reading

Recent articles

The Misrepair Accumulation Theory of Aging

Here is a twist on the "aging is biochemical damage" viewpoint that theorizes bad repairs to be the important form of damage: "It is now increasingly realized that the underlying mechanisms which govern aging (ageing) are a complex interplay of genetic regulation and damage accumulation. Aging as a result of accumulation of 'faults' on cellular and molecular levels, has been proposed in the damage (fault)-accumulation theory by Kirkwood. However, this theory fails to explain some aging phenotypes such as fibrosis and premature aging, since terms such as 'damage' and 'fault' are not specified. Therefore we introduce here a specification of the underlying mechanism of aging and arrive at a novel theory: aging of the body is a result of the accumulation of Misrepair of tissue. It emphasizes: a) it is Misrepair, not the original damage, that accumulates and leads to aging; and b) aging can occur at different levels, however aging of the body takes place at least on the tissue level, but not necessarily on cellular/molecular level. The novel concept of Misrepair introduced here unifies the understanding of the roles of environmental damage, repair, gene regulation, and multicellular structure in the aging process. The Misrepair-accumulation theory introduced in the present paper gives explanations for the aging phenotypes, premature aging, and the difference of longevity in different species, and is consistent with the point of view of physical theory of complex systems."


View the Article Under Discussion: http://arxiv.org/abs/0904.0575
Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

Update on Induced Pluripotency Research

It is impressive to see how rapidly researchers are moving forward with induced pluripotency. Here's another step forward via EurekAlert!: scientists have "used tiny molecules called microRNAs to help turn adult mouse cells back to their embryonic state. These reprogrammed cells are pluripotent, meaning that, like embryonic stem cells, they have the capacity to become any cell type in the body. The findings suggest that scientists will soon be able to replace retroviruses and even genes currently used in laboratory experiments to induce pluripotency in adult cells. This would make potential stem cell-based therapies safer by eliminating the risks posed to humans by these DNA-based methods, including alteration of the genome and risk of cancer. ... [MicroRNAs] are transient, non-coding molecules that do not incorporate into the genome, but promote self-replication and have the potential to induce pluripotency. They do their thing -- turn a somatic cell into an embryonic stem cell-like one -- and then they're gone ... The goal now is to ensure the safety of induced pluripotent stem cells and to differentiate them into cells that can be used to repair damaged tissue and treat disease."


View the Article Under Discussion: http://www.eurekalert.org/pub_releases/2009-04/uoc--utc040809.php
Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

More Thoughts on Cryonics

From Existence is Wonderful: "If you can manage to scrape away enough of the subcultural detritus and personality artifacts that have glommed onto cryonics over the years, what you're left with is: (a) an experiment in tissue preservation, (b) the idea that future technology may someday be able to repair injury and illness not addressable by today's medicine, and (c) a view of death as a process rather than a discrete event. None of these things seem to me particularly irrational or farfetched in and of themselves. Of course in reality you can't actually ignore the cultural connotations and fringe entanglements of something like cryonics. These things must be acknowledged and addressed if one wants to actually have a clear view of the subject, and that's part of what I am trying to do here. E.g., I think the notion of cryonics has been harmed by assertions that it's a means to (even potentially) 'buy immortality'. Immortality, after all, is incoherent - nobody knows how long they or anyone else is going to live, and it might end up being a pretty long time, but it sure as heck isn't going to be forever, any more than having a job gives you a shot at making Infinity Zillion Dollars."

View the Article Under Discussion: http://www.existenceiswonderful.com/2009/04/cryonics-redux.html
Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

On Preparing For the Future

From In Search of Enlightenment: "In the year 2048 the children from my grade 2 class will be the age of many of those in nursing homes today. Globally there will be 2 billion humans alive over the age of 60. And this will bring unprecedented levels of chronic disease (cancer, heart disease, stroke, [Alzheimer's disease], etc.). If there was something we could do to alter this possible future of unprecedented human suffering and disease from becoming a reality, shouldn't we try to avoid it? ... Instead of feeding the next generation of inquisitive thinkers useless platitudes about the importance of switching off lights to save the world we should encourage them to harness the great potential of [our present knowledge of biology to slow or reverse aging itself] ... Given the certainty and severity of the harm of aging you might expect that vast amounts of public funding are being invested in aging research. You might think that the brightest and most talented scientists who long to make the world a better place are being lured into the field. Unfortunately it is very hard to get people to rally behind aging research. This must change. A deceleration of the aging process might make nursing homes a thing of the past. And that would be an enormous achievement that all future generations of humans could enjoy."

View the Article Under Discussion: http://colinfarrelly.blogspot.com/2009/03/appreciating-impact-natural-selection.html
Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

SIRT1 and Cancer

This research suggests a way in which calorie restriction (which upregulates sirtuins) might be effective in resisting cancer: "The yeast and nematode equivalents of SIRT1 are fountains of youth that stretch lifespan. Whether SIRT1 slows aging in mammals isn't certain, but it's beneficial in other ways. The protein tunes up metabolism, reducing blood levels of glucose and insulin, and might forestall neurodegenerative illnesses such as Alzheimer's disease and ALS. Given its pro-life credentials, you might expect SIRT1 to inhibit cancer. And several studies suggest that it does. But other work indicates that the protein aids tumors. For example, SIRT1 chops off acetyl groups, which can inactivate the tumor suppressor p53. [Researchers] determined SIRT1's effect on the transcription factor c-Myc, whose expression surges in many breast, colon, and liver cancers. The two proteins are tangled in a regulatory loop, the team found. c-Myc latched onto SIRT1's promoter, spurring cells to manufacture more SIRT1. In turn, SIRT1 detached acetyl groups from c-Myc, hastening its breakdown. To test SIRT1's effects on tumor growth, the researchers implanted cancerous cells expressing c-Myc into nude mice that lack immune defenses. Boosting production of SIRT1 blocked tumor formation."

View the Article Under Discussion: http://www.sciencedaily.com/releases/2009/04/090413083311.htm
Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/