In article <2kk5ussv4mi7qf19u78chpa8cmsik54is5 at 4ax.com>,
et_al at my-deja.com wrote:
> 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
> >discussion
> >> group,
> >> I relize that the studies invovle SAM and not SAM-e, but again they
> >are
> >> linking the neural damage to elevated SAM and elevated methylation.
> >> Also, im fairly sure that ive heard of people reporting parkinsons
> >symptoms
> >> 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.
> >
> >Regards,
> >Larry
>> 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.
I'd dispute that, but for the purposes of this discussion, it may be a
moot point.
> 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.
I think that an error was made in the assignation of serotonin as "the"
cause, rather than simply a factor. For some people, tryptophan acts as
a powerful antidepressant. That this is not a universal response is
more likely due to the heterogeneity of the disorder, suggesting that
the inappropriateness of the hypothesis is one of restricted
generalizability from a limited sample. In a more restricted context,
the hypothesis may very well hold true, if there were some way to
identify those individuals whose depressions involved tryptophan
absorption/conversion problems.
> 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.
Again, I would invoke the specter of heterogeneity. It worked for some
people. We just don't have any way of determining, a priori, which ones
would actually benefit.
> 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.
For some people. I hope I'm not being too redundant. In rough terms,
30% of people with major depression obtain no benefit from any receptor-
active medication. I am one such unfortunate.
> 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 fact, if the early literature on the subject is correct (check
medline, as I did), SAMe was first tried as an antidepressant nutritive
supplement for the very reason that depressed people were significantly
more likely to have lower levels of SAMe in their blood than were
normal controls. SAMe is involved in a number of biochemical pathways,
not restricted to those which involve the formation of
neurotransmitters. Chronic stress, for example, invoking activation of
the HPA axis, would deplete SAMe. The outcome, in susceptible
individuals, could be depression.
Please note that nothing I have expressed yet raises the issue of
genetic factors. There is a clear heritability of mood disorders,
perhaps stronger than nearly all other disorders yet identified which
have a genetic component. What if a single enzyme in the pathway
involving SAMe were involved? Would those individuals not benefit from
supplements? What if a sub-acute malabsorption syndrome limited full
utilization of dietary factors? Megadoses might be necessary to simply
normalize blood levels. We don't criticize people who lack intrinsic
factor (required for absorption of B-12) when they take megadoses of a
nutrient that is readily found in a good diet. Why couldn't a dietary
factor be involved in SOME peoples' depressions? Statistically, it has
been estimated that each person has between 120 and 180 genetic flaws.
Which ones do you have? Which do I?
> In this case its to be hoped that the dose required is less than
> that which sets in train the Parkinson like side effects.
Indeed. But more than that which leads to the alternative: suicide.
Let's not forget that depression is a fatal disease.
Regards,
Larry
Sent via Deja.com http://www.deja.com/
Before you buy.
