Wait, so ibogaine and salvia are kappa agonists right? But are you sure it was the kappa antagonism of Suboxone that helped, and not the mu-agonism?
From a simplistic perspective, I thought kappa antagonism helped regulate the reward-system and that improved hedonic tone could increase obsessions/compulsions, but who knows .. it's too hard to read right now with akathisia anyway, but I found this which suggests low activity in the nucleus accumbens, particularly in contamination phobias: http://www.ncbi.nlm....pubmed/21272861 .. which is interesting, because I thought high dopamine in the Nacc was implicated in OCD .. but maybe it's just disordered dopamine, and a kappa-antagonist could normalize it?
Then again, dexamphetamine is recommended as monotherapy for OCD and increases dopamine in the Nacc while doing other stuff like modulating glutamate.
My biggest problem, other than the obsessions, is the intense sense of fear that accompanies them.. the overwhelming freefloating anxiety makes even walking up the road to the store a tremendous battle; I am plagued by a constant sensation that something awful is going to happen 24/7 and it *feels* real. I know what reduced fear feels like because on e.g. stimulants the obsessions are still there, but suddenly they don't stress me/phase me so much and I can face them. But no medication has really touched the core hypervigilance and fear, even SSRIs. I'm hoping that even if JDTic doesn't help the obsessions very much, it could remove the phobia and physical restrictions on my life.
I also have a lot of shitty personality-related compulsions/addiction .. like compulsively doing stuff to get attention all the time, even in subtle ways, to fill my inner 'emptiness'. I'm not sure whether they come from .. some interplay between ADD, narcissism and that dysthmic/schizoid-emptiness that has never let me feel close to people. I hope the JDTic can influence that too.
Oh -- and when I say JDTic, I'm just using that as easy shorthand for kappa-antagonism. Since I'm in a pretty desperate situation, I'm going to be buying Suboxone and combining it with LDN a la celebes to see if kappa-antagonism is a worthwhile road for me to go down.
Yeah i think low dopamine and high glutamate in the nacc are found in ocd....dexedrine, like other ampetamines and stimulants do work well for ocd but can exacerbate it... i.e skin picking, repetitive ritualistic behavior, irrational phobias etc are all symptoms of stimulant psychosis and to a lesser extent even after a single dose etc....
Glutamate levels are increased in response to increased dopamine because as drive increases so does the need for celular excitation...glutamate acts like a throttle on neurotransmission, it's an oversimplification but if dopamine levels are high, glutamate acts supportively to that state but it works both ways. When the levels are low, it amplifies that too.
With dexedrine for example, as the drug wears off and dopamine levels drop, the glutamate levels stay high a while which explains the ocd like comedown symptoms. the emptiness of the dopamine receptors is being amplified by the glutamate so the body tries to remedy this with rituals and repitition in attempt to recreate a response which have worked before....
For example popping pimples or picking scabs, checking that your environment is safe The body, like a computer, runs through sequences over and over desperately to illicit an increase in dopamine to no avail because dopamine stores have been used up. So you check if the door's locked but the feeling of safety you usually get isn't there because the dopamine isn't there so you try again...then it tries another one etc
I don't know why they call it ocd, obsessions and compulsions are really the same thing. obsessing about something is just feeling compelled to give it your attention...but anyway it's really just that comfort seeking gets put much higher on the priority list because discomfort(empty dop receptors) is being amplified by glutamate.
In a natural situation(not drug induced) depression dampens dopamine response to pleasurable activities and fear increases glutamate levels creating this dysregulation between dopamine and glutamate. the severity etc varies respectively. It's a self perpetuating. self supportive function which is why it's so hard to reverse.
Like i say though this is a massive oversimplification i would imagine that almost every chemical and functional component in the body is invloved to some extent in all maladies but i digress...
Jdtic, as opposed to amphetamine, increases dopamine by inhibiting dynorphan which in turn fails to inhibit dopamine. So rather than just generally promoting the release of dopamine(which is unsustainable), it just allows it to act naturally as if there were no aversive signal recieved.
This is interesting:
These data suggest that although KOR antagonists may be able to reverse reductions in DA caused by increased KOR tone, they have a limited ability to enhance DA function to the degree that would make the drugs rewarding. In addition, these results suggest that KOR antagonists would not be likely to produce mania-like states, a problem seen with stimulants and, sometimes, with standard antidepressants.
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