Posted by SLS on December 2, 2022, at 7:26:07
In reply to Re: Saw doctor today, posted by rjlockhart37 on November 30, 2022, at 3:30:53
> wellbutrin from my limited knowledge is less worked on dopamine, and more norepinephrine. It always gave me jitters and anxiety, edgy. I tolerated it for a while, but then edgy side effect happened. Hope ritilin works good
Your characterization of Wellbutrin falls in line with those of some experts. However, I think most the research community will tell you that they still have no idea how Wellbutrin works - this after 56 years of study.
With Wellbutrin, I didn't experience anything close to the strange stimulation / anxiety that the tricyclics produced in me as a startup side effect. These drugs act to great degree as norepinephrine (NE) reuptake inhibitors. These phenomena doesnt occur with me and TCAs anymore. Something is different, now that I have been exposed to TCA multiple times. The drugs that you trial and fail to respond to therapeutically nevertheless produce lasting alterations in brain function. Ask yourself if there are any drugs that affect you differently now compared to the first time you tried it. Baron Shopsin gave me the advice to remain as "clean" as possible during the time between trying new compounds or newly discovered combinations of old drugs.
Frederic Quitkin and Wilma Harrison of Columbia Presbyterian / New York State Psychiatric Institute told me that it was never a good idea to "pulse" antidepressants - on/off/on/off... It often leads to treatment-resistance and side effects that are either new or of greater magnitude. This is perhaps most true of Paxil (paroxetine) among the SSRIs. After the first exposure to a psychotropic drug, the brain is left altered in some way, probably indefinitely or persistently. Treatment choices should take this into consideration.
Paxil is the SSRI most likely to work, the SSRI most likely to stop working, and the most likely to become ineffective once stopped and restarted. Paxil is also the SSRI likely to produce the most robust side effects. Weight gain, sedation, anticholinergic effects, and perhaps anorgasmia. They tend not to mitigate over time. However, Paxil is the go-to SSRI for anxiety disorders.
When I first took a MAOI for the first time, I experienced a complete cessation of dreaming or at least had no memories of dreaming. This was most likely due to a ubiquitous side effect related to the inhibition of REM sleep. So much was it inhibited in me, that upon a rather abrupt discontinuation, I was dreaming while my eyes were wide open. I could see my bedroom, but could not get myself to move, despite my efforts to get out of bed and stand up. This is called sleep paralysis. It is a manifestation of the REM-rebound effect caused by the discontinuation of a potent REM sleep inhibitor like the MAOIs.
Interestingly, many people with depression feel less depressed the day after one nights total sleep deprivation. I found that the improvement I experienced didnt last much beyond late morning. After that, I deteriorated again. Scientists have remarked on this phenomenon as early as the 1970s. Some people incorporate a sleep deprivation schedule to augment drug therapy.
For a healthy person, REM sleep begins no sooner than 90 minutes after falling asleep (REM latency). For depressives, it is 45-60 minutes. The more severe the depression, the shorter is the period of REM latency. The sleep rhythm is somehow altered by the exposure to an antidepressant particularly TCAs and MAOIs. I now dream on both Parnate and Nardil regardless of dosage. I also no longer experience drug-discontinuation REM rebound. Its been like this for over 20 years.
I think we might be better off not f*ck*ng around with drugs so cavalierly
- Scott
Some see things as they are and ask why.
I dream of things that never were and ask why not.The only thing necessary for the triumph of evil is that good men do nothing.
poster:SLS
thread:1121154
URL: http://www.dr-bob.org/babble/20220917/msgs/1121180.html