Scientists find path to fountain of youth

From Yahoo!:

WASHINGTON (AFP) – The fountain of youth may exist after all, as a study showed that scientists have discovered means to extend the lifespan of mice and primates. The key to eternal -- or at least prolonged -- youth lies in genetic manipulation that mimics the health benefits of reducing calorie intake, suggesting that aging and age-related diseases can be treated. Scientists from the Institute of Healthy Ageing at University College London (UCL) extended the lifespan of mice by up to a fifth and reduced the number of age-related diseases affecting the animals after they genetically manipulated them to block production of the S6 Kinase 1 (S6K1) protein. Scientists have shown since the 1930s that reducing the calorie intake by 30 percent for rats, mice and -- in a more recent finding -- primates can extend their lifespan by 40 percent and have health benefits.

Booyah, I'm looking forward to living forever! Maybe...

The Good die young, but pricks live forever! What's that say about our civilization?

Wow this is a really good find! Imagine what we could do if we could live for another 200 or 300 years? Life wouldn't be so much of a hurry anymore.

I have a question, is there any way i could offer my body for some of these studies :| i much rather not wait 50 years before these are actually approved then another 50 years for it to come onto the market for a high price.

reply to post by Shamrock87


Maybe that will finally induce us to stop looking only at the short term.

To give you an idea, the protien(S6K1) increases protein synthesis and cell proliferation. This is very similar to the effects of IGF(Insulin like Growth Factor) and insulin.

It wouldn't surprise me if insulin and IGF have an influence on S6K1 and protein synthesis.

As the article stated, these results have been achieved in labs since the 1930's with caloric restriction. Here's a little information on Insulin's role in Calorie restriction: Insulin Signaling

Lowering of the concentration of insulin and substances which are related to insulin, e.g Insulin-like growth factor 1 and Growth hormone has been shown to upregulate autophagy, the repair mechanism of the cell [6]

Early work in C. elegans (see Cynthia Kenyon) and more recent research in mice has suggested (see Matthias Bluher, C. Ronald Kahn, Barbara B. Kahn, et al.) that it is not only reduced calorie intake which influences longevity. This was done by studying animals which have their metabolism changed to reduce activity of the hormone insulin or downstream elements in its signal transduction, consequently retaining the leanness of animals in the earlier studies. It was observed that these animals can have a normal dietary intake, but have a similarly increased lifespan. This suggests that lifespan is increased for an organism if it can remain lean and if it can avoid any excess accumulation of adipose tissue: if this can be done while not diminishing dietary intake (as in some minority eating patterns, see e.g. Living foods diet or Joel Fuhrman) then the 'starvation diet' anticipated as an impossible requirement by earlier researchers is no longer a precondition of increased longevity.[citation needed]

The extent to which these findings may apply to human nutrition and longevity is as noted above under investigation. A paper in the Proceedings of the National Academy of Sciences, U.S.A. in 2003 showed that practitioners of a CR diet had significantly better cardiovascular health.[39] Also in progress are the development of CR mimetic interventions.

In other words: Less insulin and/or decreased insulin signaling = less fat and longer life.

The article makes the mistake of assuming that mice lived longer due to increased adipose tissue(body fat)-a side effect of low insulin levels-instead of attributing it directly to insulin.

Calorie restricted diets typically yield a lower insulin response. It's possible to have this same response without restricting calories. Seeing as how most data have suggested insulin, and not energy reduction, as the driving factor, it might be safe to assume that insulin affects the production of S6K1, especially considering insulin's effects on metabolism and endocrinological stimuli.

-Dev