In article <2kk5ussv4mi7qf19u78chpa8cmsik54is5 at 4ax.com>,
et_al at my-deja.com wrote:
For some reason, my earlier reply was truncated, leaving out the
following (reconstructed from memory, and expanded):
> 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.
Perhaps you ought to peruse the medline database, as I did, wherein it
was clearly shown that depressed individuals are significantly more
likely to show low circulating levels of SAMe. This was the reason that
nutritive supplementation of this substance was first tested. For some
individuals, it has proven to be a very effective remedy. SAMe is
involved in a large number of different biochemical pathways. Chronic
stress, for example, might easily deplete SAMe levels, due to
activation of the HPA axis. The end result could be depression, despite
normal brain receptor activity, due to reduced neurotranmsitter
formation over time. And this in otherwise "normal" people.
Please note that I have not invoked the genetic inheritance issue in my
discussion, until I do so here. Depression is one of the most heritable
of all disorders, let alone mental disorders. I'm sure you wouldn't
argue that the biochemistry of the brain and its supporting structures
is exceedingly complex. It would not take very much imagination at all
to consider that a variety of different pathways might be disrupted by
flaws in enzymatic processes, absorption or transport, all mediated by
peptides under genetic control. One doesn't question the need for
nutritive supplementation for those individuals lacking in intrinsic
factor (necessary for B-12 absorption). Why would you categorically
exclude nutritive factors from the list of etiological affecting
Let me invoke a simile, at this point. It's not a great one, but off
the top of my head, I am using it to express the difficulties arising
in treating a heterogenous disorder using an exclusionary hypothesis.
Consider depression as analogous to a car not starting. The potential
reasons for the car not starting are varied. If one looks at a group of
such cars, some might be out of gas. Others might have dead batteries.
And others still might have damp ignition wires. Putting gas in the car
will help some cars start (analogous to nutritive supplementation).
Charging the short circuit that drained the battery will help others
(loosely similar to stress/load reduction). And correcting the damp
ignition wires will help others (receptor-active medication). However,
putting gas in the car will do nothing to help the other cars start,
will it? Nevertheless, that in no way negates the effectiveness or need
to resolve the fuel problem for that limited group.
> 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 let us not forget that chronic depression is a fatal
disorder. That side effect is a little bit more difficult to address.
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