In article <68k8uss238bbr1gs4qnijns6c61d97qt03 at 4ax.com>,
et_al at my-deja.com wrote:
> On Tue, 10 Oct 2000 13:25:33 GMT, larryhoover at my-deja.com wrote:
>> >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:
> snipped
> >
> >> 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.
>> Very few I would suggest. I don't have any figures available, but
> anecdotaly, I and a lot of others took large doses of L-Tryp during
> the 1980s, prior to it being banned. I never met one patient that
> derived any benefit from it other than as a sleep inducer.
I'm surprised that you have declined to anecdote. We can't debate
anecdote, and you know it. Tryptophan is a well-accepted augmentative
agent, and is used as a mood-stabilizer for those who cannot tolerate
the anti-seizure meds used for that purpose (at least in Canada, where
the FDA doesn't decide such things). Anecdotally, tryptophan helped me,
though it was insufficient on its own. I reiterate, tryptophan acts as
a powerful antidepressant for some people. Reference: Clinical Handbook
of Psychotropic Drugs, 8th edition.
Please also note that I expressly denied the "serotonin deficiency is
the cause of depression" hypothesis.
> The placebo effect can trigger remission in 40-70% of those with
> mood disorders, so that it acted as a powerful antidepressant in a
> few is no surprise.
God, give me some of those placebos. A 30% placebo rate is the commonly
accepted figure.
> >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.
> >
> The problem with this is that there is growing evidence that
> antidepressants don't increase brain serotonin levels much beyond
> the initial period.
I am not arguing anything serotogenic per se. I am arguing for
heterogeneity, and nothing more. That serotogenic agonists, reuptake
inhibitors, oxidase inhibitors et al work for a goodly number of people
is not in dispute, is it? And the rest have what kind of problem?
> A further nail in the concept that low serotonin levels contribute
> to depression is the considerable success of the French AD
> Tianeptine, which is a Selective Serotonin Re-Uptake Enhancer. That
> is it increases the ability of serotonin transporters to remove the
> neurotransmitter from synapses.
>> Incidently, it seems to be effective in many cases where
> SSRI/TCA/MAOIs weren't.
Again, for the record, I am not arguing that low serotonin levels are
the cause of depression. I am arguing that nutritional supplements may
be the key to effective treatment for some chronic depressives,
particularly those treatment-resistant individuals like myself. By the
way, isn't that a lovely euphemism, "treatment-resistant". I'm not
treatment-resistant. They just don't have a clue how to help me, that's
all. They're thinking "in the box", when the answer, if there is one,
clearly must lie elsewhere. When one has eliminated all obvious
possibilities, what is left, no matter how improbable, must be the
truth. (Or something like that. Please pardon the paraphrase of
Sherlock Holmes.)
> >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.
> >
> But that does not mean that your depression isn't the result of some
> receptor/neuronal "machinery" dysfunction. It just may be that its
> related to a receptor/process for which we don't yet have a
> mediating chemical. There are over 100 neurotransmitters. We only
> have drugs to alter the states of the affected neurons of a handful
> of them.
At some level, whatever it is that is "wrong" with me affects my
neuronal functioning/receptor processes. I have a gut-level self-
awareness that leads me to consider nutrition/absorption. And I have
begun to find relief using supplements.
> I don't know enough about SAM-e, or the matters you've referred to
> to comment. Nor at the moment do I have the time to study this in
> more detail. However, I'll raise one point. Much of what you've
> written echoes the literature at the time that the significance of
> tryptophan/serotonin was first realised. In the last few years much
> of that has been discounted. Probably the same will occur with
> SAM-e.
I'm not trying to be overly critical here, but that WAS point of the
thread. I'm having a little technical trouble (learning new software,
server issues, etc.), or I'd gladly paste in some abstracts here. Both
SAMe supplementation and treatment with standard antidepressants serve
to raise blood levels of SAMe. Depressives are likely to have
significantly reduced levels of SAMe. Those in remission have
normalized levels. SAMe's mode of action may include endocrine
modulation as well as neurotransmitter modulation. Whatever. I don't
need to know why it works, if it does work. And for me, it does.
That said, and due to my study of the enzymatic pathways which recycle
SAMe via homocysteine, I now use betaine supplementation to promote an
alternate recycling process which leads to enhanced natural SAMe
levels. I'm not much sold on the idea of consuming a substance which is
itself the product of an enzymatic reaction. Kinetic factors and
feedback inhibition might very well shut down my normal enzyme
activity. The alternative I have chosen seems to be more in tune with
my body's processes.
> Which is not to suggest that it doesn't work, just that its mode of
> action may be other than a simple deficiency.
You've lost me with that point.
> It is interesting that you've raised the vitamin B-12. In the quick
> medline scan I did, there were a few papers that suggested that
> SAM-e may overcome a deficiency in this and other B group vitamins,
> and that this may account for some, not all, but some of its
> antidepressive effect.
I think you've got it backwards. SAMe synthesis requires folate and B-
12. Again, whatever. Why take an SSRI if what you need is nutrition?
> >> 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.
> >
> True. But I wouldn't want to be in the position where I had only
> depression or Parkinson like symptoms to choose from.
I think there are other possible outcomes. I'm sure there are other
stations on the continuum between those two extremes.
Larry
Sent via Deja.com http://www.deja.com/
Before you buy.