Monday, January 08, 2007

ANTIAGEING SCIENCES

"We are on the verge of a revolution in medicine: understanding, treating, and ultimately preventing the causes of degenerative aging. But medical revolutions only happen if we all stand up in support of funding and research. We did it for cancer. We're doing it for Alzheimer's. We can do it for aging - and create an era of longer, healthier lives!"




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What is Anti-Aging?



On the Causes of Aging

Accumulating AGEs
Aging Immune System
Junk in the Lysosome
Mitochondrial Free Radicals
Other Causes of Aging




Recent Entries


Echoes of SENS
Medical Tourism Means Medical Competition
Eating Mitochondria
Deckchairs on the Titanic: The Present Study of Aging
Encapsulating the World of Knee-Jerk Reactions to Calorie Restriction
Site Updates at Fight Aging! and the Longevity Meme
Speculation on Solar Radiation and Longevity
Being Aged is a Torment No-One Should Be Forced to Bear
Read the Popular Science Press With a Careful Eye
Computation as the Root of Physical Immortality
If You Want the Job Done, Then Help to Get the Job Done
Take the Money and Run?
Magical Thinking Abounds in the "Anti-Aging" Marketplace
Death (By Degenerative Aging) and Taxes
A Look At Incremental Progress In Alzheimer's Research
Of the Aging Body, What Might Be Easiest To Rejuvenate?
Let the Engineers Have At the Biotechnology
From Around the Healthy Life Extension Blogosphere
"Raging Against Aging" Transcript
The Costs and Consequences of Medical Socialism
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Accelerating Future
Alcor News
April's CR Diary
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Anti-Aging Medicine & Science
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Friday, January 5, 2007


Echoes of SENS

As Chris Patil of Ouroboros points out, the latest issue of the Journal of Pathology focuses on the pathology of aging - accumulated molecular damage leads to failure of organs and processes, named diseases of aging, and then suffering and death. Against that backdrop, I am pleased to more often see echos of the intent and thinking behind SENS, the Strategies for Engineered Negligible Senescence, out in the scientific community these days. Strong ideas don't exist in a sealed realm; rather they are diffuse at the edges, spreading to cause change. The active efforts of SENS supporters help that process along - and so we can hope to see ever more scientists declaring that something can be done about aging:

The mechanisms of cellular ageing at a genetic, protein and organelle level are becoming clearer, as are some of the more complex associations between environment and ageing. System ageing is also becoming better understood, and the potential biological advantages of ageing are being explored. Many of the advances in these fields are opening up the prospect of targeted therapeutic intervention for ageing and age related disease.
As Chris Patil notes, "The devotion of an entire issue to this subject is just the latest example of the increasing mainstream attention being paid to the biology of aging." There's a lot of good stuff in there, but this caught my eye:

Autophagy, organelles and ageing:

As a result of insufficient digestion of oxidatively damaged macromolecules and organelles by autophagy and other degradative systems, long-lived postmitotic cells, such as cardiac myocytes, neurons and retinal pigment epithelial cells, progressively accumulate biological garbage (waste materials). The latter include lipofuscin (a non-degradable intralysosomal polymeric substance), defective mitochondria and other organelles, and aberrant proteins, often forming aggregates (aggresomes). An interaction between senescent lipofuscin-loaded lysosomes and mitochondria seems to play a pivotal role in the progress of cellular ageing. Lipofuscin deposition hampers autophagic mitochondrial turnover, promoting the accumulation of senescent mitochondria, which are deficient in ATP production but produce increased amounts of reactive oxygen species. Increased oxidative stress, in turn, further enhances damage to both mitochondria and lysosomes, thus diminishing adaptability, triggering mitochondrial and lysosomal pro-apoptotic pathways, and culminating in cell death.
In other words, you need well-functioning lysosomes (the little recycling plants inside your cells that digest failing components and damaging chemicals) to keep your mitochondria (the power plants inside your cells) in good shape. Mitochondria need to be replaced when they are damaged, or else they can start to damage the cell that hosts them - and that damage is a cause of aging. But simply living across the decades generates an ever-increasing load of biochemical junk that lysosomes can't deal with; eventually they become bloated and inefficient.

Long-time readers of this blog will find this an interesting link between past posts on the mitochondrial free radical theory of aging, methods to tackle lipofuscin buildup, and the lysoSENS project - the latter being a search for bacterial enzymes that can degrade and remove this buildup of "biological garbage" in lysosomes and elsewhere in your cells.

The paper above is a good reminder that many classes of age-related cellular damage feed off one another; damage accelerates damage in all failing machinery. This is all the more reason to accelerate the search for ways and means to fix these problems before they kill us!

Technorati tags: aging, gerontology, medical+research








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Thursday, January 4, 2007


Medical Tourism Means Medical Competition

Medical tourism is accelerating, as well it should. Advancing biotechnology, computing power and materials science means that (a) the practice of good medicine is coming down to pretty much the cost of regulation plus the cost of the people running the show, and (b) many more regions of the world have the technology base, medical community and level of economic success to do the job well.

A Filipino doctor has partnered with a Hong Kong-based company to give his countrymen hope in experiencing renewed health and strength with autologous stem cell transplants. There is so much controversy surrounding stem-cell research because of cloning issues but plastic and cosmetic surgeon Dr. Florencio Lucero believes that autologous transplants will not only help Filipinos but also enhance medical tourism in the Philippines. In fact, he said less than a fourth of his over 20 stem cell patients are Filipinos.
This sort of thing is "eat your lunch out from under you" competition for the biotechnology and medical industries of over-regulated US and Europe. Here, competition is relatively muted, squashed beneath the regulatory burden of patents, trials, compliance with a thousand inane laws. Those comparative few who source enough capital make it past the regulatory costs move into the realm of protectionist policies and short term gain - the barrier now behind them is the fence against competition, and it is in their interest to keep that fence high. A high fence means high profits and less of a need to try anything new and better to keep the money coming in.

Let me say this: human beings are damn lazy when there isn't a spear prodding them in the back. It's our nature. Competition is that spear, the serious threat of your profits and edges vanishing elsewhere, forcing you to inventively accomplish more and better for less. Competition is the alchemical weapon that transforms all the worst aspects of human nature into tools to bring progress to all as rapidly and cheaply as possible. The more aggressive, open and unrestricted the competition, the better the resulting service is for the customers - folk like you and I.

So we should all be very pleased to see Asian biotech and medical entrepreneurs eating the very lunch out from underneath late-stage researchers and new businesses in the US and Europe. It's the only way that those insulated folk inside the regulatory fence are going to feel any meaningful pressure to help tear it down - and thus better serve us over the long term.

Technorati tags: competition, economics, medical tourism








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Wednesday, January 3, 2007


Eating Mitochondria

This is the age of barnstorming and invention in biotechnology - an age wherein one can speculate about much more complex variations of inserting tab A into slot B without too much fear of proposing an impossibility. Thinking in that vein, I should mention an article I noticed on the topic of bacteria that feed upon mitochondria:

"We'd never seen anything like this before," Lo says, as he opens the image files on his laptop on a rainy afternoon in Sydney. "They seem to get in between the inner and outer mitochondrial membranes and eat the mitochondria up. In the end you've just got this empty sack."
"It's a very novel observation," says Scott O'Neill, a specialist in invertebrate endosymbionts and head of the School of Integrative Science at the University of Queensland, who wasn't involved in the research. O'Neill, whose recent work has focused on the bacterium Wolbachia, says he wasn't aware of any other bacteria that live inside mitochondria. "It's pretty surprising to see a bacterial species living inside the mitochondrion, which itself was a bacterium," he says. "I think it is significant." Bill Ballard, a mitochondrial specialist from the University of New South Wales, agrees. "This is, as far as I know, the first [bacterium] that actually infects within the mitochondria," he says. "It's a pretty cool paper."

Lo's newly found organism doesn't seem to have any negative effects on the ticks. "About half the mitochondria don't get infected," he says, "so perhaps they are only destroying old ones. We don't really know what's going on."


Perhaps distracted by the Star Wars references, I didn't stop to link this to our mammalian problem of accumulating mitochondrial damage - one of the roots of age-related degeneration and disease. Damaged mitochondria take over a fraction of your cells over the decades, turning them into mass exporters of damaging free radicals into the body at large. A regular at the Immortality Institute forums did sit up and take notice, however:

So I'm wondering if these hungry bacteria (mito-phages?) could be reprogrammed to kill defective mitochondria in particular.
Considering all the other things that bacteria have been engineered into doing for us to date, it doesn't seem outside the realm of the possible - although it could certainly be in the realm of "too hard and expensive this decade or next." After all, there has to be some identifiable biochemical methodology already present for our cell to recognize damaged mitochondria - how would one engineer a bacteria to do as much, or to otherwise prefer consuming the damaged mitochondria that lead to aging?

More practical and immediate methods of dealing with damaged mitochondria appear to be in the pipeline - such as protofection - but that's no reason to refrain from speculating on novel or more distant approaches. The more the merrier.

Technorati tags: aging, biotechnology, science








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Tuesday, January 2, 2007


Deckchairs on the Titanic: The Present Study of Aging

I look at a great deal of the popular press on aging and see articles informed by the strange, deep-seated belief that nothing will change - that the only action of merit is rearranging or understanding the minutiae. In a world in which we are quite possibly a couple of decades away from adding those couple of decades back on to healthy life spans, articles that treat a year of difference in life expectancy for one racial group over another as an issue of vital importance seem to drift in from some different, dream-ridden reality.

For example, a recent analysis by Irma T. Elo, a demographer at the University of Pennsylvania, indicates that a 65-year-old white woman will live, on average, an additional 18.9 years. But a 65-year-old Hispanic woman who immigrated to the United States will live an additional 19.8 years, a significant difference.
The longevity difference persists even though Hispanic immigrants tend to be like Mrs. Lara, poor and poorly educated and lacking health care. It persists even though, like Mrs. Lara, they get chronic diseases like arthritis and high blood pressure and are often overweight.

“Everyone,” said Kyriakos S. Markides, who directs the Division of Sociomedical Sciences at the University of Texas in Galveston, “is trying to figure out what the hell is going on.”


It's not a reality I'd like to live in - one of a narrow fascination with the color of pebbles at the site of construction of a mighty dam. The pebbles will be there tomorrow, and tens of millions are dying of aging now. Yet pebbles it is, a focus here on researchers who turn the tools of modern science to trivial pursuits in the face of an ongoing avalanche of death and suffering. We could be doing far more to halt the death and suffer of aging - but not a word here on those working to make a difference.

This next article isn't much better:

“The idea was, when a state changed compulsory schooling from, say, six years to seven years, would the people who were forced to go to school for six years live as long as the people the next year who had to go for seven years,” Dr. Lleras-Muney asked.
All she would have to do was to go back and find the laws in the different states and then use data from the census to find out how long people lived before and after the law in each state was changed.

“I was very excited for about three seconds,” she says. Then she realized how onerous it could be to comb through the state archives.

But when her analysis was finished, Dr. Lleras-Muney says, “I was surprised, I was really surprised.” It turned out that life expectancy at age 35 was extended by as much as one and a half years simply by going to school for one extra year.


So much effort going into filling in the dots, to picking at the grains of what is, and narry a mention of what could be done today (not to mention what is being done today) to work towards a real difference - not a year for a few, but decades for all. What a hole we have dug for ourselves in our present culture and its attitudes towards aging, towards change! The passive life is little better than death, and the popular press is ever the mirror held up to a passive life; the rejection of change; the numbing of the mind to the new; the discarding of individual responsibility for a better future.

So it's deckchairs on the titanic, from here until your allotted part is spent. Hah! I would hope that we can all sense there is more than that to a life well-lived. What of building, what of creating the new? We humans can change the rules of the game - and here in modern biotechnology we have the chance to change some of the oldest rules of all, to bring about the defeat of aging, an end to suffering, frailty and death for billions in the decades ahead.

Technorati tags: aging, life extension, media








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Monday, January 1, 2007


Encapsulating the World of Knee-Jerk Reactions to Calorie Restriction

The sensible practice of calorie restriction (CR) - for health and the aim of greater healthy longevity - tends to inspire some merged set of knee-jerk responses drawn from (a) the pool of poorly thought-out objections to enhanced longevity, and (b) the motley collection of ridiculous objections to healthy eating. Human beings - smart creatures, but basically built out of ape - are very normalized; so long as everyone is doing it, any damaging behavior will have its legion of defenders and justifications pulled from thin air. Not to mention the fake array of moral judgements; you'll find every variety of condemnation in the sordid history of "you're not the same as us." It is a pity that we humans haven't moved past that point yet.

So - smoking, empire-building, and so forth; these are norms, and so too with eating more than is good for you in the long term - which is to say, eating ad libitum. Veer from the norm on a better path, and you'll soon be hearing the squawks of outrage. April Smith recently gave a good response to one set of complaints regarding the practice of CR:

Third, you write:
"As far as I can tell, none of these people have children, and they all are fairly well off."

As a union organizer, I am very sensitive to the class implications of most everything. ... I find that my food budget is actually less now than it was before I started CR because while I still enjoy the occasional meal out at one of our fabulous Philly restaurants, I eat out much less, and I never grab fast food takeout. By packing my food for work (often both lunch and dinner, as I work a whole lot of 12 and 16 hour days) and enjoying homecooked meals with my partner, I save a whole lot of money.

...

If we are to conquer the obesity epidemic that is robbing the majority of our citizens of their health, we need to develop attitudes towards food that don't involve moral judgement.


I find class judgements heaped upon people who are making the effort to better manage their health equally annoying, though possibly for different reasons. It is sheer laziness, self-protective delusion, that leads a person to build a construct around skin color, health, lifestyle choices - and then extend it to the alleged cost of goods. It is a vindictive, unpleasant view of the world, as are most such viewpoints when allowed to thrive independent of any factual input.

Ignore people who exhibit a disdain for facts as guidance; they won't know what they're talking about. Instead learn how to productively listen to what the scientists have to say when it comes to health and longevity. You'll do well by that choice.

Technorati tags: calorie restriction, health








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Sunday, December 31, 2006


Site Updates at Fight Aging! and the Longevity Meme

As you might have noticed, I have enacted a number of updates - obvious and not so obvious - here at Fight Aging! and over at the Longevity Meme over the past week or so. The intent is to both to focus more clearly on the purpose and use of these websites as they stand today, and to clean up the laundry list of minor improvements, factual updates and bugfixes that have been languishing untouched or unnoticed for quite some time.

As I see matters, the Longevity Meme is a combination of news tracker and introductory reference library for healthy life extension and its activism, while Fight Aging! is equal part bullhorn at large and conversational market maker for the healthy life extension community. This is how matters have shaken out over the years, in any case. I'm happy to keep it this way and focus my attention to working on education and awareness by growing the audience.

Of note here at Fight Aging! is that I have finally set foot upon the link sharing enablement bandwagon. Better late than never; I am, as ever, the cautious late adopter. You'll see that posts here now come equipped with links to ease submission to the various aggregation and link sharing communities (StumbleUpon, Reddit Science, and so forth) that have helped discussion of healthy life extension reach a wider audience in the past. Feel free to use them if you feel a post is worthy of more attention.

As always, if you see anything untoward or outright broken as a result of recent changes, please do let me know.








Posted by Reason at 3:13 PM
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Saturday, December 30, 2006


Speculation on Solar Radiation and Longevity

Speculation indeed:

The reasons for the link are not fully understood, but it has been suggested that the amount of solar radiation we are exposed to in the womb is a key influence. The amount of radiation varies according to where you are in the world, what time of year it is and cyclic changes in the sun’s behaviour. The Equator generally gets the most radiation, and in the northern hemisphere, the usual radiation peaks will be in June and July, but there will be variations from year to year according to “solar cycles”. Every 11 years the Sun goes through a cycle when the magnetic field changes and the number of sunspots grows and dwindles. This affects the amounts of radiation produced.
The Maine researchers suggest that high radiation levels either stress the immune system of embryos and foetuses or cause small mutations in their DNA, which can either predispose or protect from disease, mould brain characteristics and influence length of life.

So the reason that people born in December might live longer could be that they were conceived in March, possibly avoiding the most harmful affects of radiation early on, when the embryo is at its most vulnerable, but also avoiding very low levels of UVR that might predispose people to certain conditions.


The assumed general mechanism in biology is good, whatever you might think of the rest of the theory; it's essentially covered by the reliability theory of aging - biochemical damage, caused by radiation or otherwise, lowers remaining life expectancy by reducing or destroying the functionality of component parts in the machine that is you.

The reliability-engineering approach to understanding aging is based on ideas, methods, and models borrowed from reliability theory. Developed in the late 1950s to describe the failure and aging of complex electrical and electronic equipment, reliability theory has been greatly improved over the last several decades. It allows researchers to predict how a system with a specified architecture and level of reliability of the constituent parts will fail over time. But the theory is so general in scope that it can be applied to understanding aging in living organisms as well. ...
In reliability theory, aging is defined through the increased risk of failure. More precisely, something ages if it is more likely to fall apart, or die, tomorrow than today. If the risk of failure does not increase as time passes, then there is no aging.


Some interesting studies are quoted in the article on solar radiation, but it looks very much like a case of having a hammer and seeing nails in everything. It is logical to suppose that demonstrated variations in human longevity and disease by location of birth date in solar and seasonal cycles have something to do with the sun at root - but that certainly doesn't mean that the sun is the direct cause of the biochemical damage that leads to such variations. It might be solar radiation, or it might be one or more differences in other systems caused by variations in solar radiation - diet, weather, hormonal changes, behaviors ... just to rattle off a few. There are certainly many more.

Once the article starts in on the distribution of mathematical or creative ability by latitude, with an eye on solar radiation as a root cause, I think it's completely lost in the sea of secondary, cultural and population-level genetic effects. There really is nothing of use to be said about that; more hammers in search of nails.

But back to aging: the interesting part of reliability theory as applied to aging is that is suggests we are born with a certain level of damage already present. The Strategies for Negligible Senescence outline a list of classes of biomolecular damage that can be demonstrated to contribute to age-related degeneration, much of which falls into the camp of accumulated biochemical products of metabolism - which one would not expect to see to any meaningful degree in the newborn. That doesn't leave too many types of damage that might be present in infants, either as a result of developmental errors or some process with the sun at it's ultimate root - missing or malfunctioning cells in important populations (such as stem cells, for example), and genetic mutations, essentially.

Once we can repair these forms of damage in adults - as a part of the effort to develop working rejuvenation technologies - reliability theory suggests that humans would gain some modest benefit in the longevity (or at least life expectancy) stakes by applying the very same rejuvenation techniques to the newborn as well. Science is interesting, is it not?

Technorati tags: aging, longevity, radiation








Posted by Reason at 6:46 PM
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