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Sun Apr 10 21:20:03 EST 2005

serotoninergic "anti-depressants(thymoanaleptics)are not,in fact,anti-depressants per 
se but should,logically,be classified as thymoanesthesisers(thymoanesthésiants).
Thymoanesthesisers are molecules which anaesthesise emotions.Emotional 
blunting,induced by these molecules and by some alleged anti-depressants(such as 
maprotiline or captopril,for instance),is misinterpreted,by those scientists who have 
never tested the effects of these molecules on themselves and normal volunteers,as an 
"anti-depressant" effect because simply patients DO NOT COMPLAIN anymore!!!
Thymoanesthesisers have spectacular effects on lovers(amoureux):they will efficiently 
block their love feelings,which will be replaced by indifference.Thus,such molecules 
induce an EMOTIONAL DEFICIT.Can then we really call such molecules which induce a 
deficit,reminiscent of the negative symptoms of schizophrenia,true anti-depresssants?
The answer is a categorical "No".
In fact,my researches have demonstrated that the conceptually only authentic 
serotoninergic thymoanaleptic is TIANEPTINE which DECREASES serotonin 
neurotransmission.It is also a well-known fact that such molecules as M.D.M.A (3,4 
Methylenedioxymethamphetamine),which also decrease serotoninergic 
neurotransmission,enhance pleasurable emotions,an observation which is consistent with 
the fact that SSRIs are thymoanesthesisers and NOT thymoanaleptics(MDMA is also a 
serotonin releaser but this gives rise to su
bjective effects similar to those one can observe under fluvoxamine).
So,experimentation clearly demonstrates that enhancement of serotonin action normally 
leads to emotional blunting while reduction of serotonin action leads to mood 
stimulation.The concept of thymoanaesthesia rationnally clarifies why molecules with 
opposite effects on serotonin,such as tianeptine and fluvoxamine,for instance,are 
grossly both "anti-depressants" as seen by OUTSIDE OBSERVERS.
The second thing which I discovered is that the typical 

a.Decrease the quantity of thoughts reaching consciousness per unit of time(they act 
on a CNS structure called the "Attenuator" of which the function is to control the 
quantity of information flowing from memory to consciousness).
b.Decrease or suppress dream recalls.
c.Induce sleep.
d.Relieve,to some extent,different kinds of pains(headaches,etc).

Fluvoxamine is considered by this author as the reference typical SSRI.

Fluoxetine,on the other hand,was found to be atypical:

a:It does not substantially decrease the quantity of thoughts reaching consciousness.
In fact it promotes the opposite under the form of subhallucinations.
b.It induces insomnia
c.It causes pain such as headaches.
d.It increases dream recalls.

All this suggests 5-HT2A preferential stimulation!
Fluoxetine effects are all antagonised by fluvoxamine.For instance if you cannot sleep 
because of fluoxetine then you can take an equipotent dose of fluvoxamine and you will 
feel sleepy.
An hypothesis which I devised to try to understand these opposite effects is the 
concept of the "serotonin/serotonin balance".
This concept says that any NET global behavioural serotoninergic effect is the ratio 
of those serotoninergic processes which decrease dopamine neurotransmission and those 
serotoninergic processes which increase dopamine neurotransmission,such as 5-HT2A 
receptors stimulation.
According to this hypothesis,typical SSRIs would INCREASE this ratio and 
thus,preferentially,stimulate those 5-HT receptors which decrease dopamine 
neurotransmission while atypical SSRIs would,preferentially,stimulate 5-HT2A receptors 
and so stimulate dopamine neurotransmission.
Fluoxetine seems to be the only SSRI which can induce subhallucinations.This effect is 
evidently mediated through 5-HT2A serotoninergic receptors.
The concept of the serotonin/serotonin balance is an extension of a previous 
hypothesis which I devised and which I called the "dopamine/serotonin balance".This 
hypothesis states that,very often,dopamine and serotonin act in opposite 
directions.For instance dopamine increases behavioural activation while serotonin 
decreases all behaviours to a quiescent state.
The consequence of this is that both neurotransmitters should always be studied 
SIMULTANEOUSLY in order to appraise properly the effects of "serotonin" or "dopamine" 
on behaviour.
In conclusion,fluvoxamine and fluoxetine represent different types of SSRIs.
Typical SSRIs seem better in practice than the atypical fluoxetine which has more 
unwanted side-effects.

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