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From: ((Steven B. Harris))
Subject: Re: *Practical* Immortality: An how to do it?
Date: 24 May 1995

In <3p7ncr$> (Angelo
Schouten) writes:

>In article <3os1ap$>, says...
>>Practically immortality is a statistical impossibility. at least until
>>we are able to transform ourselves into coherent patterns of light. at
>>this stage of the game nonsenescence makes much more sense. practically
>>speaking i would suggest nutritional sense and supplementation, hormone
>>replacement and/or manipulation and exercise, weight training and some
>>low impact aerobics. this 3 pronged approach should provide some
>>symptomatic relief from the ravages of senescence. die we must, but die
>>decrepit and senile, i think not.

Comment: then what are you going to die OF?  I keep trying to tell the
NIA that their stated goal of dying healthy in old age is not realistic,
because healthy people don't DIE.  The only thing that gives us the
impression that they do are people who are healthy except for one thing
that you cannot see (their heart, say, or a brain artery), and who
succumb rapidly from that.  But that's not what was specified in the
rules, remember?  At some point, rectangularizing the life curve
*requires* that we *deliberately* allow for one weakest part, which we
leave in to be the pre-failure mode, to save us from the senescent
period where nothing works very well for some years, which is the end
of the line in ANY scenario where death by aging is permitted.  THe NIA
folks haven't admitted this to themselves, even yet.  Duh.

                                            Steve Harris, M.D.

From: B. Harris)
Subject: Re: What is the oldest lived species on the planet?
Date: 30 Dec 1996
in Message-ID: <>


>>One question that I have that if answered should shed some
light on the aging process is what species is the longest lived
species on the planet?-I heard that the creosote bush can live
for up to 10,000 years in the desert, and that some trees on
mountain tops live 3,000 years plus, I think California redwoods
also live a long time. What is different about these plants as
compared to their shorter lived cousins that could account
for the longevity?<<

    Comment:   The longest lived plants are those that grow in
colonies, like creosotes and aspens and huckleberries.  They are,
for all intents and purposes, functionally immortal (they can be
killed, but don't age).  In such colonies, all the trees and
bushes are just offshoots of a single organism.  What makes this
different from all other plants, is obviously that with colonial
plants you can loose a lot of differentiated tissue (a tree can
rot and fall, say) without killing the entire organism.  This is
characteristic of ageless creatures: they don't have brains, or
any other differentiated tissue or non-repairable structure that
they cannot afford to lose.  A redwood, by contrast, can live a
long time, but "ages" as its heartwood rots.  Eventually, it's
going to fall, and that's the end of it. (NB, I for one do not
believe that some fish claimed to be "ageless," really are.  I
think we just haven't followed them long enough).

   >>Also, I have heard that the Galapagos tortise is the oldest
living animal at 150 years maximum life span-why is this?<<

    See below.

    >>And finally that a study shows that in general the higher
the metabolic rate of an animal the shorter its lifespan. Now
this is true and there is a constant function across species
except for one...Birds-which have a very high metabolism yet many
can live as long as much larger land animals with slow
metabolisms-why is this?<<

   First of all, it's not true across species except for "one."
There are several outstanding classes of organisms that get a lot
more metabolic time (lifespan) than they should for their size.
The standard explanation for this, is that nature will postpone
aging, and give an animal more metabolic time to reproduce, *if*
the animal is less subject to death by misadventure, or
predation (there's no point in spending the food energy to repair
an animal that is just going to get eaten-- better to divert food
energy in such animals to reproduction).  Thus, animals with a
particularly good mechanism for avoiding death by misadventure or
predation, will age more slowly (all other things metabolically
being equal).

   Birds age more slowly than mammals of their size, and far more
slowly than mammals of their metabolic rate.  Why?  Birds have
wings, a neat trick to avoid predation.  This is illustrated by
the fact that among mammals, bats live as long as birds.  Even
bats which don't undergo torpor, may live ten times as long as
mice in their metabolic class.  That's what wings do for you.

   Among the rest of the mammals, primates stand out-- presumably
because big brains are almost as good as wings for keeping you
alive.  The little capuchin (organ-grinder) monkey gets almost as
much metabolic time as humans do.  Being a good and fast climber
is probably almost as good as being a ground-hugger and tool

    Finally, reptiles live longer than mammals of their size,
because of their slow metabolic rate.  Within reptiles, turtles
live the longest for their size, because of the neat trick of
having a shell.  The largest turtle known thus takes the prize in
both categories, and that's the explanation for the Galapagos
tortoise.  These animals (until the recent coming of man, which
evolution hasn't taken into account) also had an especially low
predation rate because of their isolated and oceanic
environment.  Isolated islands are a good place to avoid big
predators, because big predators aren't often carried over vast
stretches of ocean alive.

    Now, I have to confess that some of this sounds to me like a
"just so" story, and there are still a few things to explain.
Like: why don't killer whales and elephants live longer?  Here's
my first thought: elephants basically die in the wild when their
last set of teeth wear out (after molars are replaced 5 times, in
sets of 4, rather than replaced once in a set of 12, as in
humans).  The mammal design only allows for 24 total molars in a
life time, it seems, and perhaps there is a fundamental physical
limit as to how hard these molars can be, if constructed of the
usual materials.  I dunno.  As for killer whales, I'm at a loss,
but perhaps a similar tooth problem operates.

   Evolution can postpone aging if there is an advantage to it,
you see, but evolution cannot totally redesign, wholesale,
systems which are already in place, for this purpose.  So perhaps
some large animals with a tooth-unfriendly life style, get nailed
that way, needing the kind of upkeep that evolution simply cannot
do (it's rather amazing that evolution has done as much with
elephants' teeth as it has).  In such animals, cellular aging
might in theory be capable of letting them go on for a longer
time, but their teeth aren't up to it.  And of course, evolution
isn't going to repair the rest of a body of a mammal to a
standard any better than is set by the fatal wear and tear on its
teeth (that is, if the animal is one which can't adapt to losing
all of its teeth, which is the case for all animals with the
possible exception of humans).  It's the same deal as with
predation: if one part of an animal is weak and can't be fixed,
why should mother nature waste the energy on repairing any of the
rest of its body to a better standard?  So elephant teeth "age"
prematurely, and the rest of the elephant, in consequence, ages
just as fast (i.e., don't expect zoo elephants to exceed the
species lifespan by much, even if fed soft foods).  Insectivores
and fruitivores like bats and birds might luck out in this
regard, but top herbivores that have to eat tough plants, and top
carnivores that have to bite bone for a living, perhaps have a
real problem.

                         Your Faithful Just-So-Storyteller

                         Steve Harris

From: B. Harris)
Subject: Re: Cloning dead vs live cells
Date: 09 Mar 1997
Newsgroups: sci.cryonics

In <5fnjno$>
(RHA) writes:

>   I don't agree, Mr. Wowk. The hurdle was not the cloning itself,
>   it was the proof that the genetic clock can be reset. After
>   all, how much sense would it make to, if suspended as a sixty
>   terminal cancer patient, to come back as a healthy sixty year
>   old? This was an enormous stride.

    Look, we already knew the genetic clock could be reset--- sperm
come from somatic cells that have already been aging and dividing for a
generation in the father.  If THAT DNA is repaired (and there is
evidence for a blast of DNA repair in early embryogenesis), then there
is good reason to hope that in the period following fertilization, ANY
DNA could be repaired (heh-- I say this in the light of present
knowledge, of course).  Still, there's not MUCH more reason to be
astonished that this lamb from a 6 year old ewe looks good as new, than
there is that a baby fathered by a 70 year old man looks good as new.

   The germ line does not age, please note-- it's been dividing for
billions of years, and it's still fine.  Even just looking at a single
species (such as humans), we can see that if the germ line was aged by
cell divisions, that even the couple of months of cell division (and
thus, aging) that happens in each generation from fertilized ovum to
new embryonic ova, would long ago have added up to several lifetimes of
aging, and doomed us as a species.  But here we are.  Obviously, every
generation the clock is re-set.

    The problem of aging is not (in my humble opinion) to be sought in
the cumulative damage done as cells divide (for this is completely and
eternally fixable in principle, and sometimes even in practise), but
more in the damage that is done by time to cells which cannot by nature
of their function divide.  Nerve and muscle tissue foremost.  We age
because long ago Nature was given, in some simple multicellular
organisms, a choice between making cells specialized, and making them
immortal.  She chose specialization, which is how we can be sitting
here thinking this problem, using ridiculously specialized and
nonrepairable cells that are 10 microns wide and many centimeters long.

    And the irony is that this same mental ability tells us that we are
naturally doomed as individual organisms, because of that basic
engineering trade-off.  Not that Nature cares, of course.  If the
immortal germ line gets to ride on better (more specialized, faster,
stronger, smarter) carriers, that's one way things will go.

                                        Steve Harris

From: B. Harris)
Subject: Re: Cloning dead vs live cells
Date: 09 Mar 1997
Newsgroups: sci.cryonics

In <> Chris Benatar
<> writes:

>>    The problem of aging is not (in my humble opinion) to be sought in
>>the cumulative damage done as cells divide (for this is completely and
>>eternally fixable in principle, and sometimes even in practise), but
>>more in the damage that is done by time to cells which cannot by nature
>>of their function divide. Nerve and muscle tissue foremost. We age
>>because long ago Nature was given, in some simple multicellular
>>organisms, a choice between making cells specialized, and making them
>>immortal. She chose specialization, which is how we can be sitting here
>>thinking this problem, using ridiculously specialized and nonrepairable
>>cells that are 10 microns wide and many centimeters long.
>>And the irony is that this same mental ability tells us that we are
>>naturally doomed as individual organisms, because of that basic
>>engineering trade-off. Not that Nature cares, of course. If the immortal
>>germ line gets to ride on better (more specialized, faster, stronger,
>>smarter) carriers, that's one way things will go.
>This seems to be a good arguement in support of the importance of
>MNT to prevent ageing. MNT should be able to repair even specialised
>cells repeatedly so we may still yet put two fingers up to nature.
>>                                        Steve Harris
>Chris Benatar

    If "MNT" is abbreviation for "mature nanotechnology" aka the
Millennium, then I must agree.  It won't take anything less to prevent
aging completely, since adequate repair systems for specialized
non-dividing and fairly large structures like neural networks, have
never even been invented by evolution.  And they are HARD.  Repairing a
complicated object is always a more difficult proposition than making a
new one, which is why only a minor amount of damage is necessary to
"total" (the English would say "write off") an automobile.  The same
principle applies to organisms.  Making a new organism (or a new cell
in "restorative" cell division) requires only a dumb assembly line (we
almost have totally automated assembly lines for cars NOW).  Repairing
a car, OTOH, requires a mechanic with very complex diagnostic skills,
if certain brainless "pull and replace" opperations are forbidden
(which is the case with repair of our brains, note-- you can't just fix
that part of us by pulling the motherboard and putting in another one).
 We're a long, long, way from automated car restoration, in the way
that a loving antique auto restorer does it, which is the way it will
have to be done one our brains.  But that's what it will take in
biology to stop brain aging.  As for the rest of our bodies, "plug and
replace" stategies (the way less knowledgeable mechanics repair things)
will do fine.  As recent advances in xonografts and cloning show, we're
probably not that far from this level of sophistication.

                                         Steve Harris

From: B. Harris)
Subject: Re: If Doctors are so bad, Stay away from them
Date: Sun, 21 Sep 1997

In <601ovd$> "Cheryl A. Snider"
<> writes:

>YES, menopause is a normal physiologic event! How do you arrive at any
>other conclusion??? Or are you still thinking it is a syndrome leading to
>death and decay?

   Comment: it's not that easy.  Decay and death are normal
physiological events, also.  Sometimes they are programmed by Mother
Nature, who doesn't care about individuals, but only their genes.

   I've mentioned the salmon.  In some species, Mother Nature in her
infinate wisdom gives the salmon enough steroids to make it up a river
without any inflammation or pain.  Sort of like doping a race horse
with butazoladine-- and with the same result: injury and side effects.
The steroid overdose gives the salmon osteoporosis and fungal diseases
and deforms its face.  But no problem, the salmon gets to reproduce and
Mother Nature doesn't really care what the hormonal manipulations do to
the individual fish so long as the line is propagated.

   Ma Nature doesn't really care what the hormone changes do to the
individual woman at menopause, either.  So long as she becomes
infertile at the proper time, Mother Nature will do whatever it takes,
so long as it's not immediately fatal.   But make no mistake, Mother
Nature does not have a woman's best interests at heart in doing this,
but rather those of her children.  Natural isn't always nicer.

                                    Steve Harris, M.D.

From: B. Harris)
Subject: Re: HRT questions
Date: Sun, 21 Sep 1997

In <601m90$> "Cheryl A. Snider"
<> writes:

>Did they teach you in medical school that menopause is a syndrome?
Doesn't this word imply a disorder or disease which requires treatment?
It is my understanding from the above definitions that menopause is a
natural, normal expected occurance in the female body.  Why do you call
it a disorder?<

    Regarding my other message on this topic, would you regard what
happens to a salmon at the end of its life, a "disorder"?   It's normal
and natural.  It also kills the salmon.  There are many species of
salmon and octopi, which, if you remove their hypothalamus or otherwise
prevent the hormone surges that accompany the ends of their lives, will
live years longer (this experiment has been done).  If you were an
octopus or salmon, what would YOU do?  Would you be an octopus or
salmon conservative, and argue that if mother nature wanted you alive,
she'd have provided for you to stay alive naturally?    Just curious.

                                   Steve Harris, M.D

From: B. Harris)
Subject: Re: Aging (was "telomerase")
Date: 15 Apr 1998 05:16:16 GMT

In <01bd683f$e8c513a0$> "Kate"
<> writes:

>  If you are Pacific salmon, with few mating opportunities, you may
>decide to go for broke and throw all your resources into reproduction,
>churn out lethal ammounts of hormones to promote spawning and
>then succumb to entropy in a few days.

    Yeah, salmon die from an overdose of corticosteroids in order to
get through the world's toughest game, and mate.  They remind me very
much of an "all drug" olympics, where anything is permitted.  So in
order to play injured, look good for the ladies, whatever, the young
player will take damaging anabolic steroids or glucocorticoids for the
short term benefit, knowing that in the long term, he'll pay. But so
what?  Humans do exactly this, knowing the costs.  Lyle Alzado did it
with steroids, but many do the same thing with tanning salons.  You can
SEE the kinds of choices "blind" evolution makes automatically, in the
kinds of choices that humans make, by trading off important values.
And you can see WHERE we get our important values.  From evolutionary
pressure also.  Sex!  The right mate!   Now! It's just like Freud said.
Antagonistic pleiotropy, thy name is Faustus.

                                        Steve Harris, M.D.

From: B. Harris)
Subject: Re: Aging (was "telomerase")
Date: 20 Apr 1998 09:45:45 GMT

In <6hb8i1$dnq$> (RHA)

>>   Both assumptions have problems.  The idea of no outbreeding
>>doesn't hold for most familiar species, and this screws up all
>>kin selection giving slow-aging a kin-selective disadvantage.
>>For while high inbreeding due to a terrific reproductive advantage
>>of one individual (due to a an advantageous trait like no aging) may be
>>bad for a population in the long term, in the short term that trait is
>>going to spread to other groups anyway because of short term
>>advantages, and there will just not be enough chance for the
>>long term disadvantages to wipe it out.  That was what
>>killed off the Weismann theory of the origin of aging which
>>you here advocate (and which is more than a century old).
>   I don't follow your above argument.

    Imaging 10 populations of rats in a territory.  They can
interbreed, but don't (distance, or natural barriers, or something).
In some of them an individual develops antiaging genes, and by virtue
of not getting old, manages to father or mother a lot more offspring.
Those genes spread throughout the population and make it a lot more
inbred.  Short term advantage of the ageless gene has led to long term
disadvantage for the population, which is now inbred.  Climatic
conditions change, and the inbred populations don't survive, which the
more diverse rapid agers do. That's the Weissman theory of why
agelessness is disadvantageous-- it's short term advantage to an
individual is more than compensated for by kin selection disadvantages
to populations that have the trait.

   Population modeling shows this ONLY works if there is no
interbreeding.  If there is, the ageless trait is so advantageous it
takes over all populations before the kin selection factor has a chance
to select against it.  Indeed, there's no way to select against it, if
every population has it, because the trait's only advantage is a KIN
selection one (population vs population).  For that to work, you can't
have any outbreeding, and populations have to stay pure.  The problem
is that mammals are not that pure, and outbreed too much for this to
happen.  Only one outbreeding per generation is enough to totally screw
up any disadvantage that an ageless gene has, which works by kin
selection and on a population basis.  So that's NOT why we don't see
more ageless animals.

   Indeed, there are populations of ageless plants-- clones of aspen or
huckleberry or what have you.  Even animals like coral or other polyps.
They seem to do okay-- neither being wiped out nor taking over because
of the trait.  And there are populations of parthenogenically
reproducing lizards (they're all female, and all the same identical
"critter"--- just not physically connnected).  They are, in a sense,
ageless (you would say they were if they were connected-- so what's the
difference?).  And here they are.  They exist.  Nature doesn't forbid
this kind of thing.  It just isn't very crazy about it.  Nature prefers
sexual reproduction, and for some reason is stingy on repair of animals
of most kinds.  Not all.  Just most.  All mammals.  And us.

>>There are other problems in the idea that slow aging has no cost.
>>Medawar says that agelessness would not be an advantage because of high
>>accidental mortality which is age *in*dependent, but ultimately that's
>>NOT a good argument against why slow-aging doesn't spread, because ANY
>>reproductive advantage of slow aging will give it at least a LITTLE
>>relative advantage, and it will eventually spread to take over the gene
>>pool (or at least to get to high Hardy-Weinberg equalibrium values). So
>>Medawar still has problems explaining why this doesn't happen, even if
>>the Makeham term does far outweigh the Gompertz term,if you will.
>>The answer to Medawar is provided by Kirkwood, who points out that the
>>natural thing for machines to so is fall apart, and it takes active
>>energy to keep them in repair and good order. That energy comes directly
>>out of the reproductive budget. And there you have it. It makes no sense
>>to make a mouse that doesn't age, if that only increases the mouse's
>>chance of living another year by some small number like 10%, which is
>>what you can calculate it does, in the first year (by looking at
>>mortality in the wild at 12 months vs 3). Not if the energy cost of
>>agelessness is very high at all.


>    I think that's a conclusion not driven by the facts. One must
>    look at what optimizes a species' opportunities and what optimizes
>    an individual's opportunities. For example, how many litters
>    and number of offspring per litter does a mouse have per lifetime
>    versus a human? Why is there a difference. I do not argue that
>    all the DNA of a species gather and debate their possible
>    strategies but that the environment deletes organisms which do
>    not have more optimal behaviors. Extremely short life expectancies
>    for mice must confer some environmental advantage. If it
>    can be explained by energy budgets so be it, but that isn't
>    an implacable rule. Consider a chickadee versus a mouse. Fairly
>    the same in size, what differences are there in life style?
>    (Personally, I don't know, but I'll bet significant. Maybe I'll
>    invest the time and read up.)

    The difference is the chance of getting eaten.  Things with wings
and shells and large brains get more metabolic time for their size,
because of lower predation rates.  It's worth while for nature to
invest in better repair if non-aging mortality is expected to be less.
There are some bats that have mouse metabolic rates, but live 20 years.

>    Oddly've just argued my case. So "they 'know' a
>    bad gamble" huh? Mayhaps the linkage to the "energy budget" is
>    the mechanism genes use to select against immortality.
>    Think about what you've argued...Imagine a world of (a finite)
>    number of immortal organisms. Where would they get energy from,
>    assuming they're not plants. After a bit, there'd be only one.

    I don't follow you.  They'd get the energy the same place they
would if they aged.  Again, please remember that ageless does not mean
immortal.  It just means ageless.  You're just as mortal, just as
subject to accident and wounding and disease and being eaten, as if you
were perpetually at the age of puberty (when your intrinsic rate of
non-accidental mortality is least).

>    To bring energy into the discussion is valid, but not to think it
>    through is not. Even a mouse, as an individual, could profit from
>    immortality if, along with immortality, came the ability to fend
>    off predators and disease, and control a larger territory to
>    provide a larger energy budget. The more ergs you have, the more
>    you can do with them. But what happens when you're the only
>    mouse in a larger territory? Ya kin'a stick out!

    You'll have to try again, because this time *I* don't get what YOU
are driving at.  If anti-aging took a lot more food energy, you would
need a larger territory, and it would be harder.  Models that looked
just like you but were cheaply made and short lived, and needed less
food, would have some advantages, dispite a shorter breeding life.  But
that's the Kirkwood disposable soma model.  That's where aging theory
is today.

                                             Steve Harris, M.D.

Pardon typos: it's the lateness of the hour.

From: B. Harris)
Subject: Re: Cause of aging
Date: 16 Aug 1998 08:22:00 GMT

In <> gtwolke <>

>Still, I would like Dr. Harris to clarify some of his statements in
>fairness to Skrecky's article. For example, Dr. Harris says that many
>organisms have mitochondria but don't age (a hyperbole of his own!)
>Skrecky says that there is a robust relationship between the amount of
>hydrogen peroxide produced in the mitochondria and the aging potential of
>a species. (I have also heard much the same thing about SOD.)

    All this is true, but there's a robust relationship between rate of
metabolism and aging rate, as Pearl noted long ago.  There are many
evolutionary reasons why that might be so, and most have to do with
time between generations (why should nature keep down your aging once
your genes have jumped ship).  And further, there are a lot of animals
way off that curve (all of them have survival tricks for staying alive
to produce many more young).   SOD and would be expected to correlate
with metaboblic rate and animal size and generation time.  It could be
no more than a marker.

>Dr. Harris says that the mitochondria take a beating in the aging process
>but so does the rest of us. What rest of us? If mitochondria are present
>in every living cell, where is the rest of us?

   Red blood cells age in many interesting ways, without mitochrondria.
 And you can culture cells without oxygen, which stops mitochondrial
free radical production.  This has no effect on Hayflick limit, and not
that much effect on lipofuscin and membrane changes and anything else
you can reasonably call aging in vitro.  Nor does it stop mitochondria
from degenerating.

> If Skrecky is right, the free radical generated by
>the mitochondria and their effect on cellular metabolism could be
>sufficient to do the damage.

    They could, or they could not.  The evidence just isn't in.  If
some plants (aspen) and animals (corals) repair all damage from their
mitochonidria, then what philsophical reason is there to locate "aging"
in the mitochrondria.  Rather, it seems obvious that it would be
located in whatever makes us repair such damage less well than coral
and aspen.  I personally think it's because we have CNS systems, and
nature just hasn't ever figured out how to repair non-dividing cells
from free radicals.  But don't blame mitochondria for that.  They make
the nasty things, but the nasty things are perfectly easy to deal with,
if nature just would.  She doesn't' because she's lazy and or simply
hasn't happened onto a scheme for animals with non-dividing cells.

>I am interested in what attempts have been made to influence aging by
>fooling with the mitochondria. I recall reading about such things but
>perhaps he could come up with some examples that disprove Skrecky's

    I'll look, but the entire series of Tappel's vitamin E
supplementation experiments on mammals pretty much lays the issue to
rest.  Mitochondria are protected, but aging isn't slowed.

>Empirically, Strecky suggests that substances which inhibit hydroxyl
>radicals in the mitochondria make test subjects live longer, more
>youthful lives.

    What, fruit flys?

From: B. Harris)
Subject: Re: Re Duesberg Delurks (Part two)
Date: 13 Oct 1998 12:02:04 GMT

In <6vkf1h$rq0$> "Bennett" <>

>Ahh, now this I agree with totally. As far as evolution goes humans have
>to be the black sheep. As far as offensive weapons, defensive barriers,
>speed, camoflage (sp?) etc goes, we're crap. Our only real assest is our

   Don't sell our basic non-brain equipment short!  We're not opossums,
but instead finely designed machines.  Humans are corsairial hunters
with longterm running endurance to outmatch any other animal, except
members of the canidae (which are the undisputed champs).  Due to our
excellent sweat glands and lack of body hair we tolerate extremes of
heat, and work load under heat, which no other mammal can. We have arm
muscles and articulation which allow us to throw and catch-- not
something other animals can do.  We have not only opposible thumbs, but
impressive fine motor skills.  This is not just due to our brain.  You
cannot teach chimps to do many things with their hands, simply because
they cannot feel their fingers any better than humans can their toes.
This has to do with those huge collections of nerve cells in our finger

   And I should add that last, and not least, we humans live a LONG
time-- far longer than an animal our size ought to.  Most mammals, from
elephants to mice, don't get more than about a billion heartbeats in a
lifetime.  Maybe a billion and a half if lucky.  Bats, birds, and
primates, including humans, can go out past 3 billion. There are lots
of advantages in the extra time and experience this gives.


From: B. Harris)
Subject: Re: Re Duesberg Delurks (Part two)
Date: 22 Oct 1998 07:16:54 GMT

In <707tm2$5v$> "Bennett" <>

>>   And I should add that last, and not least, we humans live a LONG
>>time-- far longer than an animal our size ought to. Most mammals, from
>>elephants to mice, don't get more than about a billion heartbeats in a
>>lifetime. Maybe a billion and a half if lucky. Bats, birds, and
>>primates, including humans, can go out past 3 billion. There are lots of
>>advantages in the extra time and experience this gives.
>>                                    SBH
>Yeah, like chronic diseases ;-) Take away infectious deaths and what so
>you get? Cancer, heart disease (elephants get that too), diabetes,
>rheumatoid arthritis...
>Just thought the other side needed pointing out. Keeps us Docs in clover
>though ;o)

   Animals get chronic diseases.  I used to see all kinds of them in my
aging lab mice.  Zoo keepers see all kinds of them in their older
mammals, from lions to wolves.  Pet dogs and cats are not unique in
this department, as I sometimes hear.  About the only animals that
really do get to old age without chronic diseases are birds.  And old
bird looks pretty much like a young bird.  In extreme old age they just
lose weight for a very short time, and die.  No fuss, no muss.  Has to
do with the tremendous evolutionary pressure to keep all of a bird's
systems opperating in top shape, I imagine, since anything less would
be instantly fatal.

   The difference in various animals in not presense of chronic
disease, but WHEN they get these diseases.  A mouse gets arthritis and
goes gray and cannot clean itself well at about a billion heartbeats.
That's about how much a human has gotten by age 30.

                                   Steve Harris, M.D.

From: B. Harris)
Subject: Re: can anyone refute the Paliolithic Diet?
Date: 14 Dec 1998 08:20:34 GMT

In <7528pi$eu7$> "Kate" <> writes:

>>   The argument of what we're evolutionarily adapted for, BTW, is
>>irrelevent to what we should eat for longevity, anyway.  Remember,
>>evolution does not care very much about longevity.  Evolution cares
>>about reproduction.  In most mammals, diets that allow fastest growth
>>and earliest and most successful reproduction, are also those which
>>cause more rapid aging and greatest cancer incidence in older ages.
>>And in humans, such diets tend to be the most atherogenic.  Thus, you
>>can't trust your tastebuds or your instincts.  Nor can you trust
>>history or Mother Nature.  None of them have your long and happy
>>retirement in mind.  They have survival of your GENES in mind, but
>>that's hardly the same thing.  Not at all.
>>                                      Steve Harris, M.D.
>  Evolution does seem to promote longevity in species, like birds of
>  prey, that are not subject to predation.( the payoff for longevity is
>  poor if you're going to be killed by a sabertooth, anyway ). Can't
>  remember the source, but I read somewhere that in species where the
>  males "duel" over women, longevity tends to be poor for the same
>  reason.
>			 Kate

     Quite so, but this has nothing to do with what evolution wants you
to eat.  Evolution lets species not subject to predation live longer by
giving them genes for slow aging.  It doesn't do it by giving them a
craving for some longevity food.  Cells from such animals even show
better health in glass dishes.  Food has nothing to do with it.

    Humans (like other primates) probably live longer than most mammals
in terms of our metabolic rate, because our large brains give us a
predation advantage, so evolution kindly slows our aging process some.
That advantage is apparently not as good as that conferred by wings,
but it's pretty good.   The only reason we outlive birds and bats is
that they are a lot smaller.  But birds and bats shockingly outlive
animals of similar size.  20 years for canaries and bats, which have
mouse-sized bodies and even faster metabolisms, is not unheard of.  But
lab mice live 3 years (or 4.5 if starved).  Even the champion longevous
mouse species (Peromyscus) don't go longer than about 7 years.  That's
about as well as humans do in terms of calories per pound per lifetime.
It doesn't hold a candle to most warm blooded critters that fly.

From: B. Harris)
Subject: Re: Backlash against HMOs: a declaration of war (was Doctor-bashing)
Date: 12 Apr 1999 10:31:15 GMT

In <> Bret Wood
<> writes:

>"Steven B. Harris" wrote:
>>     Biology is tough.  Nature didn't design us to be entirely
>> self-repairing, and your teeth are but a simple example of the stuff
>> that's missing. It'll be a while before we solve it.
>I dunno.  As far as this article says, there hasn't been much progress.

   That's basically correct.  Once you get to the point that death rate
is determined by aging (things wearing out because there is no
mechanism for them to be repaired), you're in trouble.   Progress then
requires you to develop devices for repair, that nature never did.  And
that are as much more difficult to implement is it is to repair a very
old or chashed car, vs. manufacture a new one.   And for the same
reason.  The reason it takes so little damage to "total" your car, is
that we're close to having nearly completely automated auto
manufacturing facilities, since making a car is easy (from the
intellectual standpoint) compared with identifying and fixing
everything that can go wrong with one, forever.  A computer can make
one.  A computer is about as far from repairing one as it is from
recognizing faces.  Farther-- since visual recognition would be only a
tiny part of car repair.

From: B. Harris)
Subject: Re: Smell of old people
Date: 13 Apr 1999 04:09:28 GMT

In <> (GFHH)

>Old folks seem to have a certain, similar, unpleasant "smell" to them.
>Any idea what this might be?

   Some of it is the critters that grow on dentures and bridgework,
which get more common the older you get.  And there is the increasing
incidence of urine odor from small amounts of urge and stress
incontinence.  (The Depends smell).  You're not smelling "oldness" per
se.  Toothless elderly, or those with very good teeth, if not
incontinent of urine, smell pretty much the same as anyone else.

From: "Steve Harris" <>
Subject: Re: Does Prevention Work?
Date: Tue, 9 Jul 2002 18:18:26 -0700
Message-ID: <agg29u$8gq$>

Andrei Prokopiw wrote in message ...
>On 5/21/02 8:51 AM, in article,
>"John 'the Man'" <DeMan[62]> wrote:
>> It is a very well known fact that only about 30% of all death risk
>> factors are due to genetics.
>Could you be so kind as to direct me to the source of this claim?
>    -Andrei Prokopiw

COMMENT:  it's not too far off to say that the the variance in differences
in longevity between individuals is 30-50% genetic. This can be estimated in
twin studies, in which you find that the mean difference between identical
twin longevity after 40 due to "natural causes" is somewhere around 6.5
years (surprisingly high, I thought when first hearing about it), whereas
for siblings it's more like 8.5. And for the rest of us, with cohort and sex
matched, it's more like 10 or 12  years for any random pair of persons.

For genetically identical mouse strains, the standard error in life span for
natural causes of death is something like 10% of the mean life span as well,
so I shouldn't have been TOO shocked. Identical mice don't all die of the
same thing, but wildly different kinds of cancers, and non-cancerous causes.
And that's even when they eat identically, are caged identically, and so on,
in the same lab facilities.   There's a LOT of randomness in what "natural
causes" kill you in old age, even if you do everything "right" and have the
"right" genes.

Psychol Aging 1990 Mar;5(1):25-30

Genetic influence on life events during the last half of the life span.
Plomin R, Lichtenstein P, Pedersen NL, McClearn GE, Nesselroade JR.
Center for Developmental and Health Genetics, College of Health and Human
Development, Pennsylvania State University, University Park 16802.
Genetic influence on perceptions of major events later in life was
assessed with a combination of twin and adoption designs as part of the
Swedish Adoption/Twin Study of Aging (SATSA). The SATSA design includes 4
groups totaling 399 pairs of same-sex twins: identical and fraternal
twins reared apart and matched twins reared together. The average age of
the twins was 59 years. The results demonstrate significant genetic
influence on reports of the occurrence of life events, especially for
controllable events in which the individual can play an active role.
Maximum likelihood model-fitting estimates of genetic influence indicate
that 40% of the variance of the total life events score is due to genetic
differences among individuals.  How genetic factors can affect life
experiences and directions for future research are discussed.  PMID:
2317298 [PubMed - indexed for MEDLINE]

I welcome email from any being clever enough to fix my address. It's open
book.  A prize to the first spambot that passes my Turing test.

From: "Steve Harris" <>
Subject: Re: Medical Scientism is at a Standstill
Date: Fri, 16 May 2003 13:21:04 -0700
Message-ID: <ba3hja$s46$>

"N-H-P" <> wrote in
> >From: "Steve Harris"
> Besides, my primary interest is Jack LaLanne.  The fact that both
> exercised a lot and both lived to a ripe old age makes Bragg icing on
> the cake.

You can have Jack LaLanne. The French lady Jeanne Calment
was riding her bike through the streets of Paris at age 100,
and I'll be impressed if Jack makes it that far doing
anything. Call us then.

Calmentt lived to 122 years of
age( dying in 1997,
without doing anything particularly special except giving up
smoking later in her life. There's a photo of her as a fully
adult woman in 1875 at the age of 20, and lots of records,
so unlike a few of these health gurus, she's totally
authentic and fully documented.

She ate lots of chocolate and wine and the French diet
(probably good things), but did no juicing, no iron pumping,
and no more excercise than the average Parisian got (which
is more the the average urban American gets today, but it's
nothing like athletic training). No rowboat pulling with her
teeth. Genes count. LaLanne probably has reasonably good
ones. So what?

Whatever genes you have, you can shorten your life 10 or 15
years by really stupid living (smoking, gross obesity), and
you can maybe get 5 or 10 extra ones if you do some
prevention, and maybe a few more if you really work at
prevention. But it's a very steep tradeoff at the upper end
of the prevention work curve, for the average person.
Statistically so what if every hour spent juicing or jogging
or pumping iron gives you an extra hour of life, and it
really does become a full time job, as for LaLanne?  I feel
sorry for the man if it is, unless he enjoys it for its own
sake (which is possible for him, but not for most people) An
extra year or two in my mind is NOT worth it, if composed of
full time training and food obscession.


From: "Steve Harris" <>
Subject: Re: Medical Scientism is at a Standstill
Date: Fri, 16 May 2003 17:43:58 -0700
Message-ID: <ba40kd$9ua$>

Wups. Yes, of course.

Imagine having a picture of yourself at age 20 and being
able to say "boy that seems like a hundred years ago.." and

"MARK D...." <> wrote in message
> "Steve Harris" <>
wrote in message news:
> >
> > The French lady Jeanne Calment
> > was riding her bike through the streets of Paris at age 100,
> I once saw a splendid interview with her - in which she described the
> time she met *van Gogh* (d.1890)!
> > There's a photo of her as a fully adult woman in 1875 at the age of 20
> Typo? I suspect you meant *1895*...
> Regards,
> M.

From: Steve Harris <>
Subject: Re: Low fat, low protein diet boosts longevity
Date: 3 Jun 2005 10:44:11 -0700
Message-ID: <>

>>model: drosophila
meaning for homo sapiens: nil. <<


Exactly right. Especially since these studies have been done also
extensively in rodents. THERE, it makes NO difference in life span or
cancer risk what the composition of the diet is, insofar as
macronutrients like fat or protein. Only total calories are predictive.

It's unbelievable that a dumb insect study could get this much press
when the much more difficult and relevent rat and mouse studies never
did. Insects don't even GET cancer. They are largely post-mitotic
organisms. They don't even heal, really. Bust a part off or hurt them,
and they gum it up and live with a permanent scab.  If you've seen the
movie "Death Becomes Her" you have a pretty good idea of the kind of
"aging" the average adult insect does. Why anybody would want to infer
anything from this when it comes to human aging, is beyond me.


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