Has anyone read any studies linking KAPPA-OPIOID activity to SLEEP DEPRIVATION ??
I subscribe to the belief that one of the main processes leading to dysphoria/dysthymia/depression is the reduction of dopaminergic transmission in the reward system as a result of increased kappa-opioid activity, if not in all cases, than at least in the subset of people with active or past addiction. In any case, based on all the studies I've read, I've come to the conclusion that the inversely related kappa-opioid and mu-opioid receptor modulation of the reward system is the foremost agent demonstrating the ability to determine human mood, emotions, feelings, and affect. Cognitively, after reviewing the literature, I believe that dysphoria/dysthymia/depression all boils down to the dominance of kappa-opioid activity over mu-opioid activity, leading to excessive depression of the reward system and over-activation of the fear/aversion circuitry.
That being said, I would advocate that the closest thing to a cure for depression would lie in either 1) a kappa-opioid antagonist that does not induce upregulation of the kappa system (i.e. it continues working), or 2) a treatment regime based on regularly administering a potent kappa-opioid agonist that floods the receptor (such as salvia), thereby causing down-regulation of the kappa receptor. Ideally, I should be able to back this theory up by personal experience and experimentation.
Accordingly, I've worked up the courage to do salvia just a handful of times in the past, and experienced subsequent relief of depression and severe anhedonia. The issue is merely that the experience for me can be terrifying, so each time I have a huge aversion to doing it the next time, and therefore it can become a difficult treatment regime to maintain, although I plan to try it again soon. The big advantage here of course is that the intensely dysphoric period is so short (about 15 minutes), providing relief that lasts much longer (1-3 days). In other words, it's a good value for your time, but there is no way around experiencing that short but terrifying trip on a semi-regular basis.
The only other treatment that has ever worked for me, including the slew of prescribed and non-prescribed drugs that I've taken, has been sleep deprivation. It has a near miraculous effect on me, like flipping a light switch allowing me to experience joy and pleasure again versus anhedonia and anxiety. It lasts until I sleep again. Accordingly, after a night or two of sleep deprivation, I feel normal and happy, but there's no way sustain it without eventually crashing. This brings me to my question above -- Has anyone read any studies linking sleep deprivation to kappa and/or mu opioid activity? There must be a link here, even if the effect of sleep deprivation is indirect and relies on some other chain of systems such as the pituitary axes.
Accordingly, anyone who might be able to elucidate this link would be profoundly appreciated. Thank You !!
By the way, I'm new to Bluelight, so how does one go about making this a separate thread, because I don't know that it belongs here.
I subscribe to the belief that one of the main processes leading to dysphoria/dysthymia/depression is the reduction of dopaminergic transmission in the reward system as a result of increased kappa-opioid activity, if not in all cases, than at least in the subset of people with active or past addiction. In any case, based on all the studies I've read, I've come to the conclusion that the inversely related kappa-opioid and mu-opioid receptor modulation of the reward system is the foremost agent demonstrating the ability to determine human mood, emotions, feelings, and affect. Cognitively, after reviewing the literature, I believe that dysphoria/dysthymia/depression all boils down to the dominance of kappa-opioid activity over mu-opioid activity, leading to excessive depression of the reward system and over-activation of the fear/aversion circuitry.
That being said, I would advocate that the closest thing to a cure for depression would lie in either 1) a kappa-opioid antagonist that does not induce upregulation of the kappa system (i.e. it continues working), or 2) a treatment regime based on regularly administering a potent kappa-opioid agonist that floods the receptor (such as salvia), thereby causing down-regulation of the kappa receptor. Ideally, I should be able to back this theory up by personal experience and experimentation.
Accordingly, I've worked up the courage to do salvia just a handful of times in the past, and experienced subsequent relief of depression and severe anhedonia. The issue is merely that the experience for me can be terrifying, so each time I have a huge aversion to doing it the next time, and therefore it can become a difficult treatment regime to maintain, although I plan to try it again soon. The big advantage here of course is that the intensely dysphoric period is so short (about 15 minutes), providing relief that lasts much longer (1-3 days). In other words, it's a good value for your time, but there is no way around experiencing that short but terrifying trip on a semi-regular basis.
The only other treatment that has ever worked for me, including the slew of prescribed and non-prescribed drugs that I've taken, has been sleep deprivation. It has a near miraculous effect on me, like flipping a light switch allowing me to experience joy and pleasure again versus anhedonia and anxiety. It lasts until I sleep again. Accordingly, after a night or two of sleep deprivation, I feel normal and happy, but there's no way sustain it without eventually crashing. This brings me to my question above -- Has anyone read any studies linking sleep deprivation to kappa and/or mu opioid activity? There must be a link here, even if the effect of sleep deprivation is indirect and relies on some other chain of systems such as the pituitary axes.
Accordingly, anyone who might be able to elucidate this link would be profoundly appreciated. Thank You !!
By the way, I'm new to Bluelight, so how does one go about making this a separate thread, because I don't know that it belongs here.
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