All antidepressants work the same way through the same mechanism, by
increasing Brain Derived Neurotrophic Factor (BDNF) in the
hippocampus. It used to be believed that there is a serotonin juicing
effect that takes place, or a MAO inhibitor effect takes place.
Actually, there is no evidence for any of those mechanisms, since
there is a "waiting period" for mood to improve.
What *is* known is that neurogenesis in the hippocampus is achieved
via antidepressant therapy. What actually happens? Studies have shown
that antidepressants increase *zinc* concentrations in the hippocampul
region, which in turn stimulates neurogenesis. That is *all* that we
know that ADs actually do.
Studies have shown that this only occurs after long-term therapy with
zinc, or with antidepressants.
What causes poop-out? We can trace it back to the AD's themselves and
a lack of zinc. Serotonergic agents delete dopamine in the striatum,
causing sexual dysfunction, loss of libido, and emotional flatness.
People then compensate to raise their dopamine by drinking caffeine,
Coke,and the like--even smoking. Then we have a zinc depletion again
thanks to the fact the these substances suck the zinc out of our
system, as does stress, the pill for women, and junk food. In other
words, the antidepressant rapidly increased zinc concentrations in the
brain, but did not have an available supply to keep neurogenesis
*going* and enough for the striatum to work properly.
Without zinc neurogenesis is impossible. Zinc activates the D-2 system
involved in pleasure. So we have a tradeoff--better mood but a
flattened one. We have allowed most of our small pool of zinc to
stimulate neurogenesis, at the expense of dopamine depletion in the
striatum, the latter requiring zinc.
Yes, we need B-6, Folic Acid, Iron, Magnesium, and B-12. However,
only zinc has been shown to alter in concentration in the hippocampus
of the brain after AD therapy.
We don't know why zinc is the only known mechanism of action in the
role of ADs.
Zinc is the most overlooked mineral clearly involved in neurogenesis.
No neurogenesis, no mood stability, no serotonin, no dopamine, no
melatonin. Eventually hippocampul cells begin to die. We rotate our
meds and again "feel good" when an additional spurt of zinc gets into
the hippocampus and some seeped into the striatum during the washout
period.. Then the cycle repeats itself.
Lather, rinse, repeat.
Zinc turns excess estrogen in men into testosterone.
Valproate, a mood stabilizer (downer) depletes zinc. It causes mood to
go down by depleting the body of nutrients.
Everything seems to involve zinc and now the NIMH has acknowledged
that zinc somehow is the "bottom line" of mood disorders, with
secondary roles played by folic acid, B-6, B-12, and magnesium.
I take 10 mg Selegiline daily, in tablet form, and have not had to restrict
my diet. (I measured my blood pressure before and after meals for a few
weeks to confirm that I wasn't having any hypertension problems.) As you
increase the oral dose, food interactions also increase, and at some point
you do need to be careful about what you eat.
The transdermal form of Selegiline, as you've noted, bypasses the digestive
tract, and has even less risk of food-related hypertension. (I take the oral
form because it is cheaper, and hasn't caused me any problems. )
I always recommend buying an inexpensive blood-pressure gauge, and
self-monitoring blood pressure for any MAOI medication. It's good to have
guidelines for what foods can cause problems, but it's better to measure
your own response and know, rather than guess, what effects different foods
may have.
I tried Parnate once, for a short time. It made me very tired, which seems
to be an unusual reaction.
> I don't wish to change my meds in the near future, as I have a chronic
> health problem which affects moods as well. I won't see a specialist
> for this condition until early Nov(I had to wait 6 months). Then I
> might need surgery etc. Also, I don't like switching. I've done this
> before and gone off of my Effexor to try something else. The
> something else didn't work and I was in trouble for a few works. I've
> tried to change a few times. Ouch! Effexor works. It just doesn't
> work as well as Elavil did for me once upon a time as I've stated
> before. So I've always got my eye on improving.
--
Nom dePlume, Ph.D.
Why, yes, in fact, I am a rocket scientist.
Find my book, Medicines for Mental health, and free drug information, at
www.MentalMeds.org
=====
(Another rare side-effect I experienced in the realm of
antidepressants: I had to discontinue desipramine because of itching.)
Did you get much itching on your shins? I ask this because when I was
self medicating with heroin, that's where I got lots of itching. btw,
sorry if my former illicit drug use offends some, but where I'm coming
from is: illicit dope should not be illict. Besides, I no longer use/
misuse illicits.
I had itching on my legs, but I can't remember if my shins were
involved (this was at a time when desipramine was the most-prescribed
antidepressant in the US, before the advent of SSRIs).