Posted by Marty on July 3, 2008, at 14:26:53
NOT that I think people SHOULD be interested in what (little me) think about what and how depression is and how antidepressant works BUT.. I wrote the whole thing in a reply to Linkage about Neurogenesis and Tianeptine and though this part of the post could start a thread on his own.
It's lengthy but I think it's worth the read.
My theory is influenced by the neurogenesis research paper, psychology, evolutionism, some years of interest/reading in psychopharmacology while trying on myself 30+ drugs in the last 10 years.. and also by my engineering background (most in the computer science field) .... oh and
So here's the copy/paste :
... MUCH MORE (70% + ?) results IN THE LAST COUPLES YEARS point to the theory that most AD drugs induce/stimule SOME KIND OF BRAIN PLASTICITY MECHANISM/PHENOMENON and that it would be that effect which brings *MOST* -ALLIVIATED- DEPRESSED PATIENT out of their misery. While this is not quite what I would call a scientific concensus (!!) it's seems this theory is already as good as the other ! .. and at this pace, will surpass the infamous monoamine theory and others in the next decade. In fact, it's already a more respected/elegant theory that any other.
Btw, Here's how I see the whole thing: (oversimplified version)
Depression is a biological mechanism which kicks in when the brain evaluate (RIGHTFULLY OR WRONGLY !) solely based on HIS PERCEPTION OF RESULTS (which has MANY point-of-failure and evoluated in a world QUITE DIFFERENT that the one we are living in in 2008 ! and so is often maladapted) that the organism, which he's part of, behaviours/strategies are badly performing to the point where it become a viable/acceptable risk, from a evolutionism point of view, TO FORCE THE ORGANISM TO ADOPT A "SICKNESS BEHAVIOURS" STRATEGY (WITHDRAWAL AND AVOIDANCE, ECONOMY OF RESOURCES ETC ETC) TO PROTECT ITSELF WHILE HE PROGRESSIVELY *UNBUILD/UNLINK* IN A *BRUTEFORCE* KIND OF WAY SOME NEUROLOGICAL COMPONENTS (neurons, intraneuronal Unknows, dentrites, glials etc etc) IN SOME BRAIN ORGANS (ie. hypotalamus. hypocampus, amygdala etc) WHICH ARE SUITABBLE/VIABLE TARGETS FOR POSSIBLY INHIBITING, IN THIS *BRUTEFORCED* MATTER (some randomness/luck, some more somehow calculated moves), THE PROBLEMATIC UNVIABLE BEHAVIOURS/STRATEGIES.
Now 1 of 2 things could happen and both are viewed from OKAY to BEST from this strategy point of view:
1- BEST = the brain evaluated (again, RIGHTFULLY or WRONGFULLY by the up mentioned, PARTLY OBSOLETED by mordern day, "Organism objectives/results evaluation mechanism") that ENOUGH UNVIABLE behaviours/strategy are OUT and/or ENOUGH NEW (Coping? Adapting?) VIABLE behaviours/strategy came IN .. and so the brain GRADUALLY STOP (fadeout) this mecanism to start another one (fadein) which kick in to REBUILD to some extent the implicated (and so impaired) neurological organs base on NEW experiences...
2- OKAY= the operation has failed and the organism die OR doesn't reproduce (at all, or as much) because of the unviable/failing behaviours/strategy + the sickness behaviour induced by the 'depression' mechanism. And the whole thing is OKAY from an evolutionary point-of-view because it STATISTICALLY serves well the familly/clan by allowing the resources to go to the 'stronger' member AND serves well the species by helping getting pulling some unviable/inferior genes out of the species pool. Species > Clan > Organism (member) .. what's important is the GENES survival at the biggest scale, a single organism entity/instance (and his genes) has not much value in the big scheme.. in doubt one can spread some bad genes (combinaison etc) -> sacrifice is OKAY.
So.. at least 3 strategy/mechanisms is involved in this obviously oversimplified theory:1- Sickness behaviour : kicks in, in part, for a safer depression.
2- Depression : WANTED Partial-Bruteforce (semi-dumb, random) neurodegeneressance in some brain organs well suited (evoluated/ready for this operation)
3- Growth : increased but prudent neurological growth (structural, operational, etc etc.. neurogenesis is of the bunch) to the organs implicated in the depression. That mechanism COULD BE activated at the same time as the 'depression' in order to help find some coping/adaptating strategy ? .. kicks in from the start VERY WEAKLY and then goes from prudent to confident as the depression fadeout ?
Now where does the AD fits in this theory ? What about:
1- SOME would initially increase mechanism #1(sick.Behav) + #2(depres) and somehow after ~2 weeks forces the brain to promote #3 (Growth)in order to compensate or something ? (Increased Turnover Link ?) Prozac and Cie (SSRIs/SNRIs etc)2- SOME would just promote #3(Growth) and leave the other alone... but after awhile indirectly (by way of recovery) inhibits #2 and so #1 ? SSRE like Tianeptine ?
3- SOME would JUST kill the pain of the process and so in 'adjusted relieving' would allow the organism to NOT be paralized too much by the sickness behaviour and so find more easily what's working for him .. completing the process with success .. AND so in 'TOO MUCH relieving' would deprive the organism of some helpful (to some extent) CUES IN FORM OF PSYCHOLOGICAL PAIN and so would leave the organism with LESS CHANCES of completing succesfully the process than a more 'adjusted relieving' .. or not relieving at all in case of not-paralyzing-already-okay psychological pain... (Benzo style? .. which are, of course, not ADs in the strict sense)
Anyway this whole theory (which Neurogenesis is part of and support) makes ALOT of senses from an engineering/evolutionist point of view.. don't you think ?Any toughts ? ..
/\/\arty
poster:Marty
thread:837855
URL: http://www.dr-bob.org/babble/20080626/msgs/837855.html