Nutrasweet - problem and a solution (?)
Alan J. Robinson
robin073 at maroon.tc.umn.edu
Thu Nov 30 08:38:45 EST 1995
I picked up some of the basic references on aspartame and brain
monoamines at the med school library because the whole subject of
aspartame safety appears to tie in with some other important recent
developments in medicine.
Just a couple of minutes of thumbing through these books was enough to
convince me that the problem is so simple and straightforward it
is a wonder it wasn't resolved a long time ago. In fact aspartame is
a very good demonstration of the problems associated with
administering a single psychotropic agent by itself.
Many neurotransmitters are derived, directly or indirectly, from the
amino acids in food proteins. It's a wonder we don't go crazy each
time we have a meal because of the sudden changes in plasma levels
of neurotrasnmitter precursors, but apparently the body can handle a
simultaneous increase of the 20 different amino acids in food. What
it can't handle is an increase in just one - evolution never had to
deal with the problem of an animal consuming massive quantities of
just one of the amino acids.
In any case, it only appears to cause problems in certain humans who
have a genetic susceptibility. (This would include both type I and
II diabetics.) It doesn't show up in laboratory mice or rats, for the
same reason that these animals don't get diseases like manic
depression or Tourette's Syndrome - they don't have the genetic
variation and sophistication of the human brain.
Evidence has been building for some time that it is much more
effective and causes fewer problems to increase both dopamine and
serotonin simultaneously when treating various medical and psychiatric
conditions. This has been vividly demonstrated with the phentermine +
fenfluramine combination, but this is only just one
possibility.
Because aspartame causes an increase in brain dopamine, there is a
strong possibility of an idiosyncratic reaction in tbose with a
genetic susceptibility. It is interesting that Hans Fisher at Rutgers
has recently shown by reverse microdialysis in rats that ethanol
withdrawal seizures are accompanied by an increase in striatal
dopamine and a reduction in serotonin.
The (obvious) solution to the aspartame problem is to combine it
with L-tryptophan or 5-HTP. Moreover, this combination would
probably be mildy stimulating and refreshing for many people, like an
OTC form of the phentermine + fenfluramine treatment. It may indeed
be just what the world is looking for, to take its place alongside the
universal stimulants caffeine and nicotine! I believe that the
Japanese put great store in "brain cocktails" - I wonder what is in
them. Not to get too far ahead of ourselves, but this combination
might even be protective against certain diseases, like nicotine is
supposed to be for Alzheimer's.
But speculation aside, it should be fairly easy to test the
L-tryptophan augmentation, at least outside the U.S., where the drug
companies appear to be putting great pressure on the FDA and the
meidcal establishment not to give their blessing to unpatented
simple chemical compounds and foodstuffs. But phentermine and
fenfluramine are probably going to decimate the market for drugs like
Prozac and Valium anyway.
Incidentally, as I discussed in a previous post, this is not to rule
out the possibility of other toxic reactions, but in the spirit of
Ockam's razor the above mechanism largely suffices. This might be
worth a letter to the FDA and G. D. Searle, Monsanto, and Nutrasweet,
or whoever is the current manufacturer.
Alan Robinson
robin073 at maroon.tc.umn.edu
More information about the Neur-sci
mailing list