Anti-Aging Research, according to Tom Mahoney

Excelife excelife at earthlink.net
Wed Sep 30 00:06:02 EST 1998

In article <3611468C.672E3870 at notarealaddr.ess>, bmdelaney at notarealaddr.ess 

>Rather, my point is -- especially now, after reading more of
>your recent responses -- to get you to see that you are
>ultimately relying on a definition of maximum life span such
>that only a genetic (perhaps even genomic) change can extend
>it. That is to say, you don't agree with the
>researcher-intervention definition, but rather only with
>"Maximum life span is that achievable without the
>intervention of a genetic-tinkerer."

There are at least two other and probably more non-genetic methods of 
possibly extending human life span. One is to maintain cellular viability and 
length between replications.

Given the Hayflick limit on reproductions of replicating cells the number of 
replications is fixed.  But the time between those replications can be 
extended and this could result in a lengthening of life span.

It's a distinct possibility that this is what we are seeing in CR.  If we are 
able to identify the cause of this delay in replication, it may be able to be 
enhanced. This further lengthening of the period between replications may 
extend life span beyond that which we have seen so far.

I believe this is much of the theory behind oxidative stress and some other 
aging theories; that by identifying the causes of aging in individual cells, 
mitigating those factors and allowing the cell to live for a longer period, 
this would result in a longer life span.

This is exactly what was demonstrated in Drosophila melanogaster, where 
oxidative stress was reduced and the flys cells survived for a period beyond 
that which is normally seen in these flys.  (note; here I would agree that 
life span was increased since the intervention to reduce free radical damage 
was not something Drosophila melanogaster would normally encounter).

Another non-genetic intervention to increase life span may include cellular 
replacement of tissue lost to aging or other causes.  This could include the 
use of various growth factors and/or stem cells.

If functioning lost due to aging could be restored by these cellular 
replacement therapies then life span may be extended.

To determine if these strategies are successful we need to have a reliable 
yardstick in our definition of life span.  As you suggested on your web 
pages, any research into life span needs to control for the effects of CR or 
they may be getting false results.  I suggest this also has to be taken into 
consideration when evaluating the results of CR itself.

>> If some substance were found in nature that had
>> an effect on the genetic  code, it would be
>> considered a mutation and the resulting animal
>> would be a  "different" breed or species.
>My example didn't stipulate that there was a substance that
>changed the genetic code, rather that we were such,
>naturally, that telomeres could be lengthened by means of a
>substance found in nature. (I'm assuming you don't mean that
>lengthening telomeres would amount to changing the genetic

Your assumption is in error.  Telomeres are an integral part of the genome.  
The research often refer to them as Telomere DNA, consisting of TTAGGG 
repeats. Un-natural changes in the telomeres would and are considered to be 
genetic mutations.

>> More to the point, however, is that since the
>> substance has not yet been  encountered it's
>> effects would not be an "adaptive" response.
>I specified only that it hadn't been known about until
>recent times. The example assumes that it HAD been
>encountered -- that's why we evolved a way to utilize it. I
>specified specifically that we had evolved a mechanism to
>utilize it.

And when we find that person who ingested this substance and lived to 140 we 
can then say that the natural human life span is 140 years.  Until we find 
him it's still 120 years.

>>> One last thing:
>>> Please don't say things that are false, or very misleading,
>>> when you almost certainly know better, like this:
>>> > The beneficial effects of CR, including the
>>> > suppression of mitotic  activities, is related
>>> > to a decrease in body temperature in both mice
>>> > and  Rhesus monkeys.
>I took the statement out of a context that more strongly
>suggested that you meant that the "relation" was at least
>partly causative. But you didn't directly say that it was
>causative, to be sure. Sorry if I was reading in more than
>was there. Still, it seems like the most natural
>interpretation of "is related to" is "is at least partially
>caused by". When scientists mean "is correlated with,"
>that's usually precisely what they say.

Actually I was using the phrase "related" as it was used in the cited 
research; "The anti-aging effects of CR are believed to relate, at least in 
part, to changes in energy metabolism."  

If I had included their phrase, "at least in part", much of our 
mis-understandings may have been avoided.

>No matter. I now know what you meant.


>(For the record, I actually think it's more likely than not
>that lowered body temperature IS actually partly responsible
>for some of CR's benefits. But we don't know yet.)

It would appear that the reduction in temperature is a "result of the 
induction of an energy conservation mechanism during CR".  Thus body 
temperature would be a marker and a means of measuring this energy 
conservation and that this energy conservation would be a potential cause of 
CRs benefits, at least in part:-)

Thomas Mahoney, Pres.
Lifeline Laboratories, Inc.

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