The Fenfluramine-Prozac-Serotonin Connection

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Friends,

You should find the following to be of particular interest. It was written

by a medical doctor I associate with.

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Dawn, the neuroscience research literature from as far back as 1975 knew

that fenfluramine was brain damaging to lab animals and yet Big Pharma went

ahead and marketed it to humans because of its powerful anorexic effect. The

big emphasis was on the heart valve toxicity at the time it was banned and

they couldn't get around that. They did manage to obscure any evidence of

the less easily provable brain toxicity that was also likely happening

(subtly), but which the corporate powers managed to keep out of the

consciousness of the patient-victims (quite successfully).

Ask somebody who has access to the brain research journals of the last 25

years (PubMed is a good place to start) do that for you and they will find

the references (type in " fenfluramine " and " neurotoxicity " for starters and

follow the leads).

Fenfluramine and fluoxetine (Prozac) both have similar qualities and

molecular structures (both have three fluoride atoms of the benzene ring for

starters) and both also have potent effects on appetite suppression

initially, despite the common fairly high incidence of later weight gain

(probably when the " down regulation " /disappearance of the serotonin

receptors kicks in).

There were quite a few MDs who immediately substituted Prozac for the Fen

part of the Fen-Phen combination and that worked nicely for weight loss. Of

course that was an off-label usage and Lilly couldn't advertise it as much

as they probably wanted to (actually they had to be simultaneously concerned

about the high probability of neurotoxicity, especially in combination with

a substituted amphetamine drug like fenfluramine).

Although Lilly wants to deny it, Prozac, besides its serotonin reuptake

inhibition properties, also has serotonin agonist properties (which made

fenfluramine such a great appetite suppressant, since it caused serotonin to

be vigorously secreted from intravascular platelets as well as from

serotonergic neurons in the brain - thus the heart valve fibrosis).

Apparently Prozac is a somewhat weaker serotonin agonist than fenfluramine

was.

I'll bet that there is subtle brain damage happening to some or all of the

Prozac users, although they won't realize it until they get some form of

dementia later, and then it will be too late. (Some of the early mice

experiments with fluoxetine actuallly had 100% mortality with the highest

doses.)

And, of course, the psychiatrists and BigPharma will be able to use their

infamous " plausible deniability " plea in court ( " try to prove it, " they will

say) to escape culpability.

You know, it isn't the brain serotonin within the intraneuronal vesicles of

the nerve terminals that is the problem, it is the serotonin in the

extracellular space in the synapse that is potentially toxic in high

concentrations. HIgh levels of intrasynaptic serotonin causes some of the

receptor sites to disappear because of too much stimulation.

So when the drug company and its reps and the prescribing docs and the ads

claim that the SSRIs raise serotonin levels in the brain, they are telling a

big white lie, because there is no net gain of serotonin in the brain, only

a transient increase in the synaptic cleft. In fact there is actually a net

loss of serotonin because the act of reuptake inhibition by the synthetic,

non-nutritive, foreign, toxic chemical SSRI does not allow the nerve

terminal to actively suck it back up and recycle the molecules of serotonin

back into the inside of the nerve where it is taken back up into the storage

vesicles and subsequently reused (I read somewhere that normally there is an

85% efficiency in that recycling process at best, and obviously much worse

with interfering xenobiotics circulating around everywhere and messing up

the cellular metabolism.

Instead some of the extracellular serotonin gets metabolized/detoxified (and

some of the metabolic byproducts are apparently toxic to the brain) or

wasted and some of it stimulates the autoreceptors which causes the nerves

to shut down the process of metabolizing serotonin from tryptophan.

So there is a lot going on that the drug companies don't want us to know

about, especially concerning the non-prescription and nutritional options of

depression treatment.

Well I could go on and on, but it's getting late so I must stop.

Keep up the great sleuthing. I use a lot of what you send me, and the stuff

from <www.prozactruth.org> and other websites, to help in my understanding

of this serious, complex and politically-charged issue. I also use a lot of

it in my practice, political activism and teaching. Thanks a lot, .

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