On Mon, 09 Oct 2000 14:05:16 GMT, larryhoover at my-deja.com wrote:
>In article <8rr6me$iuq$1 at bob.news.rcn.net>,
> "eric" <errock at rcn.com> wrote:
>> ok, i stumbled accross the first one when reading a neurology
>> I relize that the studies invovle SAM and not SAM-e, but again they
>> linking the neural damage to elevated SAM and elevated methylation.
>> Also, im fairly sure that ive heard of people reporting parkinsons
>> from sam-e which im looking for evidence of on deja.
>>Eric, concerning this and subsequent postings, I would first be
>concerned about the assumptions which underlie your conclusions. If
>SAMe is used for antidepressant purposes, the hypothesis is that it is
>correcting an imbalance in biochemistry, i.e. the deficiency of SAMe
>that is associated statistically with the symptoms of depression. The
>studies you quote reflect purposeful imbalance in the opposite
>direction. The fact that increasing SAMe levels from normal levels may
>cause neurological damage does not in any way support the conclusion
>that raising SAMe levels to normal levels from a deficient state must
>also cause similar damage. The dose makes the posin, and the subject
>pool differs as well.
I'm not sure that the concept that depression, or most other psych
disorders, is the result of biochemical deficiency/imbalance is
still considered valid.
Low levels of Serotonin or it's precursor L-Tryptophan was long
promoted as the cause of depression. It turned out to be much more
complicated than that, although 'health' food stores still make big
bucks out of that misconception.
Nor is anxiety now regarded as being due to low GABA levels. And
while phenylalanine is still registered as a treatment for some
psych disorders, it wasn't all that effective for most patients and
is not much used now.
In most of these chemicals, its been the receptors for them, or some
other aspect of neuronal 'machinery,' not the levels of the
chemicals themselves that have been the causative factor.
I'd be very surprised if low levels of SAM actually occurred in
anyone eating a normal diet, so of itself, its unlikely that any
positive effect from SAM-e on depression is due to the correction of
a lack of SAM. As with most of these neurotransmitter precursors it
is probable that larger than normal brain levels of SAM/SAM-e forces
some change in specific neurons.
In this case its to be hoped that the dose required is less than
that which sets in train the Parkinson like side effects.