RE: Mechanism by which CR Retards Ageing

[Guest guest]

While I am not up on the very latest theories, I believe

the " rate of living " theory is not widely embraced.

AFAIK the current thinking is that CR induces an

up regulation of cellular level repair/maintenance in

response to a " starving " stress. There is debate over

the precise mechanism or chain of related mechanisms

that accomplish this.

The pot of gold for longevity researchers is to be able

to mimic CR without having to actually restrict. A

billion dollar pill for sure.

I'm not smart enough to know who's right or wrong but

it seems to me that moderate restriction with good nutrition

is a very healthy place to be while waiting for the experts

to figure it out.

JR

-----Original Message-----

From:

[mailto: ]On Behalf Of Rodney

Sent: Sunday, June 19, 2005 11:06 AM

Subject: [ ] Mechanism by which CR Retards Ageing

Hi folks:

Well at the risk of repeating myself once too often, I predict that

when the mechanism by which CR extends maximum lifespan is finally

determined, it will be found to be the following:

I suspect the lifespan expansion effects of CR will be shown to

result from a postponement in reaching the Hayflick limit. And that

this delay is enabled by an expansion of the time period between

successive cell replications. And the expansion of the time between

one cell replication and the next will be found to be caused, very

very simply, by insufficient resources (nutrients) available to

complete the next cell replication.

I speculate therefore that cell replication occurs only when enough

of the necessary resources become available for it to be performed

successfully. Under CR conditions these resources are in short

supply, so replication must be delayed. Or, perhaps more likely,

replication, rather than being done fairly liberally throughout the

body, is done only when and where it is absolutely most urgently

needed, and postponed elsewhere, with the necessary resources being

carefully rationed out.

[There is an analogy here with economics, where competition and

prices ration resources to the places they are most needed and

thereby living standards are maximized.]

So, what are the most essential resources needed for cell

replication? I certainly have no expertise in this, but I speculate

that a shortage of either fat or protein could prompt a delay in

replication. Energy is also necessary, so a severe restiction of

carbohydrates would also somewhat delay replication, as seems to have

been shown in the latest Partridge study, on fruit flies. But since

energy can be generated from any of the macronutrients it makes sense

that carbohydrates might be less important than fat or protein.

But also, protein can be converted to fat, but perhaps not to the

types of fat critical for cell replication? But fat cannot (????)

I believe, readily be converted to protein. So if fat restriction

turns out to be important it is likely to be only restriction of the

types of fat needed for cell replication that the body cannot produce

from other energy sources.

As for protein shortages, restriction of those of the eight essential

amino acids that are the most important for cell replication would be

those the restriction of which would have the greatest effect on

extension of the time between successive replications and therefore

maximum lifespan.

Please do not ask me for evidence of this! It is simply my attempt

to fit the pieces of the puzzle I am aware of, together in a pattern

that seems to fit.

fwiw, wmnbm ; ^ )))

Rodney.

>

> > Rodney,

> >

> > You are right that different body tissues have different metabolic

> > requirements. As we lose our fat on CR, we are left with a

greater

> > proportion of lean tissue which has greater caloric

requirements. So

> > as we get leaner, our caloric requirement per unit of body weight

> > should increase, just like the CR mice. This will give the

appearance

> > of " increasing " our metabolism.

> >

> > I think this " increased " metabolism is what is associated with

> > longevity in CR mice.

> >

> > Tony

>

> Al Pater, PhD; email: old542000@y...

>

> __________________________________________________

>