Date: Sat, 12 Aug 2000 14:15:18 -0400
To: <Mission-Possible-USA@altavista.net>
From: Betty Martini <Mission-Possible-USA@altavista.net>
Subject: Aspartame and Depression

Here are a few comments on:  Aspartame and Depression:

Depression is obviously a highly complex phenomenon, but
over the past several years there has been overwhelming
evidence that one factor in the development of major
depressive illness is decreased availability of serotonin.
Serotonin is one of many so called neurotransmitters -
chemical substances released into the synapse, or space,
between brain cells.

Information is transmitted from one cell to the other both
chemically, via neurotransmitters such as serotonin, and
electrically.  Antidepressants such as Prozac work by
increasing the availability of serotonin in the synapse.
The synthesis, or manufacture of serotonin in the brain is
very much dependent on the availability of an amino acid
building block, L-tryptophan.  Multiple studies demonstrate
that tryptophan depletion is associated with the development
of depressive symptoms.  Work done in Richard Wurtman's
laboratory has demonstrated that aspartame decreases the
availability of L-tryptophan to the brain.

The neurochemical impact of aspartame on the brain is fairly
complicated.  Not only does it decrease the availability of
the building block for serotonin (L- tryptophan), but one of
the two amino acids that comprise aspartame, phenylalanine,
is a precursor for another very important neurotransmitter,
norepinephrine.  Papers which I published in 1986 and 1993
discuss what I believe is the clinical impact (accentuating
depressive illness) of altering the balance between these 2
neurotransmitters (norepinephrine and serotonin).

There is evidence that the therapeutic effect of
antidepressants can be blocked by parachlorophenylalanine -
a form of phenylalanine- one of the major constituents of
aspartame.  Administration of this substance has also been
associated with aggression and binging.

Aspartame and Weight Gain

Food seeking behavior and satiety are driven by an area of
the brain known as the hypothalamus.  Stimulation of the
medial hypothalamus in a laboratory rat leads to eating.
Stimulation of the lateral hypothalamus leads to satiety and
cessation of eating.  Placing a lesion in the lateral
hypothalamus produces an obese rat.  The lateral
hypothalamus is driven by serotonin.  There are many papers
in the current literature demonstrating that antidepressants
which increase serotonin (but not antidepressants which act
on other neurotransmitters) are useful in treating binge
eating disorders.  I believe that consuming large amounts of
aspartame decreases the availability of serotonin and is
thus analogous to placing a lesion in the lateral
hypothalamus.  Although much of this work is recent,
clinical suggestions that aspartame can lead to a
paradoxical increased appetite date back to Blunder's work
of 1986.

An evolving view in modern psychiatry is that although
depression, obsessive compulsive disorder, panic disorder,
impulse control disorders and eating disorders have
historically been viewed as separate entities, in fact they
should be viewed as a continuum of disorders all involving
some degree of dysregulation of serotonin.  I believe that
at this time there is overwhelming evidence that aspartame
contributes to this dysregulation.

(By Ralph Walton, M.D.)