Patrick wrote:
>> On Mon, 6 May 1996, Richard Kondo wrote:
>> > One repeated criticism regarding the ascorbic acid
> > hypothesis is that ascorbic acid (AA) is water soluble, which means
> > that absorption of AA would probably occur via a transport
> > mechanism. Such a mechanism would be saturable, and therefore, the
> [...]
>> It is my understanding that the RDA is the amount of whatever nutrient is
> required to avoid health problems associated with a deficiency...hence,
> they are the minimum required.
The RDA levels are set to amounts required to avoid nutritional
deficiency diseases such as scurvy.
However, when one eats something, it must be absorbed into the
body via the lining in the small intestine. If it is water soluble,
then usually it will not traverse the membranes of the cells of the gut
unless there is a transport mechanism. Transport mechanisms are
saturable, which means there is a maximum amount of substrate
(scientific jargon for stuff) which can be moved across the membrane in
an unit of time (consider an elevator - there is a maximum number of
people that can be transported upwards, irrespective of the number of
people waiting at the bottom).
Similarly, all the ascorbate in a nutritional supplement, may
not be able to be absorbed into the body prior to it being excreted from
the body (via the colon and feces).
> > not absorbed and that some of its beneficial impact is achieved in
> > the colon.
> [...]
>> Perhaps it is acting as a free radical scavenger?
>> patrick
Ascorbate is an anti-oxidant (oxygen free radical scavenger),
and its putative protective effect may function in this fashion.
It may reduce the oxidation of LDL, a process which promotes the
development of atherosclerotic lesions, for example, and thus protect
people from myocardial infarction. But, again, it needs to be absorbed
into the body. The AHFS (American Hospital Formulary Service) drug
information book states that diarrhea may occur at oral doses of 1g/day.
It, moreover, quotes an unnamed study which observed 50% absorption of a
single 1.5g oral dose in normal subjects.
Richard Kondo
Cardiovascular Research Lab
UCLA