From: dyer@spdcc.com (Steve Dyer)
Subject: Re: Protein intake and kidney disease
Organization: S.P. Dyer Computer Consulting, Cambridge MA
Distribution: na
Date: Sat, 10 Oct 1992 18:45:41 GMT

In article <1992Oct9.173554.9327@u.washington.edu> rbradbur@hardy.u.washington.edu (Robert Bradbury) writes:
>>>The evidence for excessive protein intake causing premature kidney failure
>>>is fairly strong.
>>Snort.  Protein restriction is one component in the treatment of
>>chronic renal failure.  I've never seen any evidence that someone
>>with healthy kidneys needs to be worried about "premature kidney failure".
>
>Steve, you will find that my comments are rarely based on currently accepted
>medical treatments.

Tell me about it. :-)

>They are based on a careful review of the literature
>and some hard thought about what goes on in our bodies as we age.

That's not hard thought, that's speculation.  There's nothing wrong
with speculation, but it should be labelled as such.  One of the big
problems with the media and science today is that many people have
trouble understanding the difference between ongoing research and
recommendations synthesized from what's known coming from (presumably)
reputable people.  I'm not saying that you have this problem--you've
made the logical leap of your own volition.

>I would suggest you go down to the library and read some of the recent
>studies comparing calorie & protein restricted diets and ad-lib fed diets
>in rodents.  Kidney failure is a major cause of death among elderly rodent
>populations, this "disease" disappears as a significant cause of death
>when the rodents are protein/calorie restricted.

Which says that caloric restriction makes rats live longer.  No argument there.

>Kidney failure is also
>a significant factor in disease and death among human elderly.

Among _some_ elderly.  It's not a major factor by a long shot.
Kidney function decreases as you age, but most older people
still have an adequate reserve.  To some extent any such
putative contribution to premature mortality is obscured by more
pressing risk factors such as heart disease.

"Premature kidney failure" as I interpret Robert to use that phrase
means a decline in kidney function to the point of morbidity and
thereby leading to "premature" mortality earlier than our 100+ years of
age of so, or whatever the longevitists are aiming for these days.
That is, if we learn enough to remove obstancles to an increased life
span significantly in other areas, is there something we can do to
reduce the aging-associated decline in kidney function which then
peskily gets in our way?

You can see that "premature" means different things to different people.
Not that I think about this that much, but I do think that the aim of
increasing longevity is an admirable one, though certainly not one without
extra-medical issues to discuss.  However, when someone says:

>>>The evidence for excessive protein intake causing premature kidney failure
>>>is fairly strong.

it's important to understand the context in which it's made.

>You can
>make lots of arguments that rodent studies should not be extended to human
>conditions but that would throw out most of our current knowledge about cancer.

???  This is a non-sequitur and completely irrelevant to this discussion.
There are lots of cross-species studies on cancer, including a lot of
work on human cells.  And a lot of that work involves cellular mechanisms
which are broadly similar across species.  

>I am willing to accept information from rodent studies can be applied to
>humans except in situations where the physiology/biochemistry is known
>to be different.

Well, rats don't live very long in the first place, do they?  I'm not
quite as ready as you to embrace these starved rats as our brethren on
the leading edge.  You're willing to make broad extrapolations which
may or may not be at all relevant.  More conservative individuals would
not presume to claim as much.  What you're doing (personally) is
betting that this is a reasonable hypothesis and (presumably?) acting
on that.  Again, that's fine, as long as you label it as such.

>The basic argument runs as follows, kidney cells are non-replicative and die
>at some rate over your lifetime so that as an elderly individual you may
>only have 30% of the cells left that you started with.  The rate at which
>these cells die is determined by a number of factors (plaque buildup
>causing a blood shortage, having to filter toxic metals/carcinogenic
>substances and damage (presumably from free radicals) associated with
>the high oxygen/energy consumption of the kidneys.  Excretion of nitrogen
>associated with excessive protein intake increases these energy requirements
>and is expected to accelerate the rate of cell death.

>The only reason that animals survive as long as they do is that kidneys have
>a large reserve capacity.  If you place excess stress on your kidneys so that
>they decline at a more rapid rate you will be looking at renal failure as
>an elderly person.  There is one caveat to all of this and that may be the
>genetic component.  A study of kidney function of individuals in the Baltimore
>longitudinal aging study indicated that some individuals (20-30%) showed no
>decline in function with age.  Perhaps some people have genes which preserve
>kidney function over their lifetimes.

Is there a known association, say, with lifelong protein intake and a
decline in kidney function?  News to me.

-- 
Steve Dyer
dyer@ursa-major.spdcc.com aka {ima,harvard,rayssd,linus,m2c}!spdcc!dyer