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
serotoninergics(zimelidine,indalpine,fluvoxamine):
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.
