From: Robert J. Bradbury (bradbury@aeiveos.com)
Date: Thu Feb 07 2002 - 10:58:52 MST
On Thu, 7 Feb 2002, Robert Coyote wrote:
> The amplitude of growth-hormone secretory pulses decreases with age in ad
> lib-fed animals, and short-term caloric restriction in young animals also
> results in a decline in the amplitude of growth hormone.
The reason for this needs to be determined. I've always thought
there might be a number of possibilities.
1) A loss of cells producing GH (neurons die with age).
2) A decrease in protein production efficiency with age, say
due to the accumulation of junk like lipofuscin in the cells.
3) A decrease in the energy available for protein production with age,
due to an increase in mitochondria with damaged DNA.
4) A decrease in protein manufacturing capability due to homologous
recombination repair between ribosomal-RNA "repeats" in the genome
causing a physical loss of raw ribosomal blueprints from which
ribosomes can be produced.
5) Explicit downregulation of GH production.
Obviously there can be complex interactions between 2-4, perhaps
promoting 1. This can also be "systemic". If GH declines and
causes liver production of albumin to decline and albumin is
required for the adequate production of GH, then you get locked
into a downward spiral (note that I don't *know* this is the case,
I'm speculating here). Rafal might comment on the degree to
which various parts of the brain depend on circulating levelsFrom owner-extropians@tick.javien.com Thu Feb 7 11:18:45 2002
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From: CurtAdams@aol.com
Message-ID: <107.c8e2878.29941eef@aol.com>
Date: Thu, 7 Feb 2002 13:18:23 EST
Subject: Re: HGH and CR
To: extropians@extropy.org
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In a message dated 2/7/02 10:01:57 AM, bradbury@aeiveos.com writes:
>The reason for this needs to be determined. I've always thought
>there might be a number of possibilities.
>1) A loss of cells producing GH (neurons die with age).
>2) A decrease in protein production efficiency with age, say
> due to the accumulation of junk like lipofuscin in the cells.
>3) A decrease in the energy available for protein production with age,
> due to an increase in mitochondria with damaged DNA.
>4) A decrease in protein manufacturing capability due to homologous
> recombination repair between ribosomal-RNA "repeats" in the genome
> causing a physical loss of raw ribosomal blueprints from which
> ribosomes can be produced.
>5) Explicit downregulation of GH production.
IIRC, GH spikes start falling off quite early - around 30. That would argue
against most of 1-4. I wasn't aware 4 happened. What's the timeframe on
that?
>Also, if I recall some presentations at the A4M meetings a few
>years ago correctly, it isn't GH per se that is the source
>of the problem, its GHRH that is the primary player.
As in, response to GHRH holds up, it's the GHRH spikes which fall off?
>I also seem to recall a presentation at the AGE conference
>last year where there was a PharmaCo that had a drug that
>mimiced GHRH but it was shelved because one can't apply for
>drug approvals to treat aging because aging isn't a disease.
Goofy on one level, but then even if aging were recognized
as a disease, how do you measure it? Better to test and
market these things as preventing loss of muscle strength,
osteoporosis, atherosclerosis, memory loss, etc. Something
with a significant effect on aging in general (to the extent that
that means something) will show up on some of those nice
crisp markers. We won't lose anything useful.
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