Longevity pill on the horizon?

Jul 10, 2009 by Leila Gray

(PhysOrg.com) -- While applauding findings that an Easter Island compound extends the lives of middle-aged mice, University of Washington longevity researchers caution that healthy people shouldn't start taking the drug in the hopes of extending their own life spans -- at least not yet.

UW scientists Dr. Matt Kaeberlein, assistant professor of pathology, and Dr. Brian Kennedy, associate professor of biochemistry, study factors that control aging. They were asked by Nature to write a commentary on a paper published in the July 9 issue showing that dietary supplementation with rapamycin increases the life span of . They observed that, until recently, compounds that slow the hands of time were in the realm of science fiction, but with this finding may be closer to reality.

"The possibility that such compounds might exist, and might perhaps even be within reach," they wrote, "has gained scientific credibility."

Their News & Views editorial, "Ageing: A Mid-Life Longevity Drug?" noted that the study, co-led by Dr. David Harrison at the Jackson Laboratories in Maine, Dr. Richard Miller at the University of Michigan, and Dr. Randy Strong at the University of Texas Health Sciences Center at San Antonio, used a specially formulated, time-release rapamycin supplement in their laboratory mouse chow. Interestingly, the mice were not exposed to rapamycin in the diet until they were middle-aged, or, as the study reported, "roughly the equivalent of a 60-year-old person." Even so, the drug had a profound effect on lifespan.

Rapamycin was originally discovered in soil samples on Easter Island (Rapa Nui), famous for its towering, long-faced, stone Moai statues. Rapamycin already has a clinical role in reducing rejection of transplanted organs, in treating advanced kidney cancer, and in preventing narrowing of the heart's arteries after corrective surgery.

The study of rapamycin's longevity effects was part of the National Institute on Aging Interventions Testing Program. It accepts nominations for compounds from members of the scientific community, and selects the most promising to undergo parallel testing at three different institutions. Several compounds have been tested, but rapamycin is the first to significantly increase lifespan at all three centers in both male and female mice.

Rapamycin, which Kaeberlein, Kennedy and Dr. Stanley Fields, professor of genome sciences, had previously shown increases in yeast, is know to inhibit an enzyme called TOR. TOR activity is regulated by nutrient availability. Prior work by these UW scientists indicated that reducing TOR activity is central to how slows aging in yeast. Dietary restriction has long been known to slow aging in mice and to protect animals against age-related disorders like cancer, obesity, and heart disease. In the commentary, the authors suggest that the possibility that rapamycin is mimicking the effects of dietary restriction in mice merits further study.

The commentators also warn that healthy people shouldn't take rapamycin to slow aging because it can suppress the immune system. However, they don't rule out the possibility that -- or more sophisticated interventions to reduce TOR activity -- might someday prove useful against age-related diseases. They also speculate that drug strategies might be discovered in the relatively near future to provide similar disease-fighting and longevity benefits without unwanted side effects.

The authors concluded: "Although extending human lifespan with a pill remains the purview of for now, the results of the study by Harrison and his colleagues provide reason for optimism that, even during middle age, there's still time to change the road you're on."

Provided by University of Washington (news : web)

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SkyAbove
not rated yet Jul 10, 2009
Decades back, other compounds also increased animal life span. For example, calcium pantothenate, cysteine, BHT, RNA, L-Dopa, selenium and more recently, blueberries even slowed down some aspects of aging in mice.
NeilFarbstein
2.5 / 5 (2) Jul 10, 2009
They dont work as well as rapamycin of the SIRT inhibiors discovered recently. They are many times more potent. Blueberries do work though.
NickFun
3 / 5 (2) Jul 10, 2009
I was going to comment on this but now I forgot what I was going to say. I must be getting old.
earls
5 / 5 (1) Jul 10, 2009
Where is the exercise pill?
otto1923
2 / 5 (1) Jul 10, 2009
It's our overactive immune systems isn't it? attacking healthy tissue, causing inflammation leading to many age-related diseases. Millenia living in overcrowded conditions in close proximity to our domesticated animals caused our immune systems to overevolve, yes? Do mice have this problem? They carry many human contagions.
superhuman
3 / 5 (3) Jul 11, 2009
No, it's not an overactive immune system, yeast don't have an immune system like ours and rapamycin still works for them.

Death is not a fluke or an accident it's an outcome of a carefully planned and executed program. Our lifespan is carefully optimized and encoded in our genes, it's the price we pay for evolution. The clock uses energy consumption as this is the most reliable measure of lifespan available at the cellular level. We die to make room for future generations.

In the molecular arms race of life immortality means extinction.
Ethelred
5 / 5 (2) Jul 11, 2009
The clock uses energy consumption as this is the most reliable measure of lifespan available at the cellular level. We die to make room for future generations.


So far the only candidate for a clock seems to be telomeres. Which is not energy consumption although I suppose you could say it was related since it IS related to the number of times a cell has divided.

Ethelred
superhuman
not rated yet Jul 11, 2009
So far the only candidate for a clock seems to be telomeres. Which is not energy consumption although I suppose you could say it was related since it IS related to the number of times a cell has divided.

There are other candidates like accumulation of damaged proteins or DNA circles for example but we don't yet know enough to pinpoint the clock at the molecular level.

The statement which you quoted is based on a number of observations: 1. the universal occurrence of calorie restriction based longevity 2. genes associated with longevity which are shared between distant eukaryotic species are often those linking nutrient sensing to protein expression 3. energy consumption is the best way to judge how far a cell is along the "program of life" since the actual time it takes to generate offspring depends strongly on nutrient availability, energetic cost of generating offspring is much less variable.

Telomeres are more likely an additional protection against transformation of somatic cells in mammals (and probably other multicellular organisms) then a true lifespan clock, yeast for example maintain stable telomeres throughout lifetime yet they do also age and die.
Ethelred
5 / 5 (2) Jul 12, 2009
There are other candidates like accumulation of damaged proteins or DNA circles for example but we don't yet know enough to pinpoint the clock at the molecular level.


While these certainly count as damage I don't see that as being a clock.

Where I am coming from on this:

A number of people have claimed(wellover a decade ago)that there was no known clock because the cell lines in animals all age at different rates. For instance the immune system and skin cells appear to begin to fail earlier than other lines.

At that time it had only recently been discovered that human cells, in vitro, could only divide so many times (around fifty)before they began to fail.

Later experiments showed that the older the cell donor the fewer the divisions there would be. For example cells from a 70 year old donor might only divide 20 times.

This showed that, despite the claims of some that there was no overall clock, there might very well be such a clock.

Experiments with cancerous cell lines showed that they did not stop dividing. These experiments were mostly if not entirely done with cancer cells from Henrietta Lacks.

http://en.wikiped...iki/HeLa

Her cancer lives on long after her death.

This line of research lead to the discovery that telomeres get shorter with each division in mammals. Obviously this is not the case for all cell types, stem cells in particular.

This makes telomeres look very much like a cellular clock. Not in this sense of a clock ticking at a regular rate but more as count of the number of the divisions. To many, me included, this looks like the telomeres may do a number of things. For one stopping out of control mutated cells. Almost all cancer cells have telemorase activated which resets the length of the telomeres.

In any case the when the telomeres get very short or at least after the telomer is completely gone cells stop dividing. A good thing with tumors but a bad thing if you want to go on living.

yeast for example maintain stable telomeres throughout lifetime yet they do also age and die.


Well yeast are single celled. It is interesting that they even have telomeres. I wouldn't have expected it although if it started with eukaroytes then it makes sense.

Searching I see that plants, fungi and amoeba all have telomeres. Well maybe its some amoeba. I finding this search interesting now but I keep running into pay to read papers. So much for the Information Wants To Be Free rubbish.

Interesting:
Telomerase is a specialized cellular ribonucleoprotein


Fits my thinking that life started with RNA protein compounds rather than DNA or RNA or proteins. Gosh its nice to find a hypothesis might hold water.

Now this gets to the point or at least where I was wandering off too.

http://delangelab...RMCB.pdf

Most eukaryotes use telomerase to compen-
sate for the loss of chromosome-terminal
sequences1
(reviewed in REFS 2,3). The
reverse-transcriptase component of telom-
erase is conserved and has been identified in
vertebrates, invertebrates, plants, fungi and
many unicellular organisms, including cili-
ates, kinetoplastids and even Giardia.


So it looks to me like most but not all eukaryotes uses telomeres.

Ethelred
thales
not rated yet Jul 14, 2009
In any case the when the telomeres get very short or at least after the telomer is completely gone cells stop dividing. A good thing with tumors but a bad thing if you want to go on living.

If that's true, then any broad-based pill that seeks to extend telomeres or slow their degradation would result in longer life but an increased number of cancerous tumors.

I wonder if they've already discovered such a substance but classified it as a potent carcinogen.
Ethelred
5 / 5 (1) Jul 15, 2009
Anything that could activate telomerase would be quite dangerous unless we can get a considerable level of control of just which cells it targeted. I suspect, but do not know, that each cell line would have different optimum telomere lengths as the length might also affect the differentiation of cells as organisms grow to maturity.

Also there is that matter of tumors. Cells more likely to go out of control would need shorter shorter telomeres to cut down on out of control growth.

This is stuff I have read over the years. It may have a high level of crap as I have never taken a biology class and my last formal classes were in the 70's in any case. I do have a biochemistry textbook laying around here but its from the late 90's and I have only glanced at a few parts. Primarily about the ribosomes as I am interested in how life got going.

Ethelred
iamcrazy
not rated yet Jul 19, 2009
it will be interesting to see research on how this molecule is working, and i can imagine an entire science will come out of the product of it. as for the immune system suppression.. i have heard talk of nano machines that could in theory work much better and faster then our own immune cells.

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