On Sat, 5 Sep 1998, Mahesh Shah wrote:
> Can this be answered by epidemiological studies? Protein consumption around
> the word versus the incidence of kidney disease?
For a start, here is a clip from a message on the lowcarb list
that discusses some scientific evidence.
Dr. Marian Blum laid to rest the myth that higher-protein
diets damage the kidneys in a classic paper published in the
Archives of Internal Medicine in 1987. Her research team
identified adult subjects who currently ate and had eaten a
high-protein diet - including meat of all kinds - for most of
their lives and matched them by age and sex to a second group
of adults who were long-term vegetarians. The second group
...consumed very little protein, and what they did eat was
entirely of vegetable origin. The team then measured the
natural "age-related decline" in kidney function ..and found
that there was absolutely no difference between the two groups
across the entire spectrum of ages. This study shows that
eating meat or eating a diet of high protein carries with it
no risk of damage to normal, healthy kidneys. A much more
recent study by the German research team of Remer and Mantz,
published in the Journal of Nutritional Biochemistry in 1995,
showed that weightlifters who consumed excessive amounts of
protein actually experienced IMPROVED kidney function.
Here's an animal study:
Hammond KA, Janes DN "The effects of increased protein intake
on kidney size and function." J Exp Biol 1998 Jul;201( Pt
13):2081-2090
In endothermic vertebrates, long-term increases in metabolic
energy demand are often associated with increases in food
intake and accompanied by increases in organ mass. Wide-scale
increases in organ mass have often been attributed to a
metabolic response to increased energy intake and utilization.
On a constant diet, however, increased food intake is also
associated with increased protein intake. We hypothesized
that, while increased food intake itself may be responsible
for increases in digestive tract mass, the consequent
increased protein intake would be the factor responsible for
increased kidney mass and function. Thus, we exposed male and
female mice to diets differing in protein level (7 %, 15 % or
46 % casein by mass) at different acclimation temperatures (5
degreesC or 23 degreesC). Within an acclimation temperature,
food intake rate remained constant over the entire range of
dietary protein level, and protein intake rate increased as
dietary content increased. The mice in the cold-acclimation
group increased food intake rate by 48-120 % over those in the
warm-acclimation group. Liver, kidney and stomach mass
increased with protein intake rate, while digestive tract and
other vital organ masses increased only in response to
increased energy intake rate. Blood urea nitrogen levels
increased with protein intake rate. Glomerular filtration
rates increased with increases in dietary protein level in
male mice but not female mice. Finally nitrogen filtration
rate increased with protein intake rate for mice on the
high-protein diet. We suggest that it is primarily the
increased protein intake rate rather than the increased food
intake rate that results in the changes in kidney and liver
mass and kidney function observed to occur in situations of
high energy demand.
Todd Moody
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