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Dopamine, the contradiction

Quick heads up, using SWIM is not actually allowed. Also I feel for you, if you suffer from depression. Personally i have had bouts of moderate depression and have basically suffered from low motivation my entire life. However opiates seem to fix this entirely. Which is why i wonder howcome the hydrocodone you got from the dentist didn't work. What was your dosage when trying it if i may ask?


Well, too bad if SWIM isn't allowed, maybe I can use 'someone who isn't me', or 'someone I know', instead?

I was initially excited (in a depressed sense) that the Vicodin would be an answer. First time I used it I got dizzy and nauseous and had to resort to bed. A couple of other instances when taking it I didn't feel anything marked. I put it aside and then tried it again 1 or more years later, and I think it may have hinted minimally at euphoria, which possibly could've been more euphoria before I became clinically depressed. Vicodin made me excited since I had read about buprenorphine and its unique effect on some with treatment resistant depression. Btw, those who say of course hard drugs make you feel better. That's nonsense, with clinical depression what normally makes you feel good may have no effect, including drugs. That's why cocaine made me feel emotionally closer to normal, rather than high (non depressed people seem rather high to me). The effect reminded me more of days pre-depression than of an out of the ordinary high.

I guess the dose must have been 500/5 acetaminophen/hydrocodone. I took up to 1 and 1/2 tablets. A reason why it didn't work could be that my depression has been pretty severe. Maybe a stronger opiate would've had a more pronounced positive effect, or maybe made me feel even worse. My depression is of 'dead' type though, and maybe that's why stimulants work better. Even during a fire, even though I felt bodily dread, it still felt challenging to make decisions and to act, which increased the underlying sense of panic. So on one hand I may feel great fear, on the other unable to fully act on it. It's as if all proactive tasks require a manual effort to do. Thus I don't go out unless, presumably there's a need for dopamine, such as when to buy sweets, or other limited things, such as getting something done that's been on my mind (presumably releasing a bit dopamine from the reward of getting it out of the way). On that note, I may not go to a doctor's appointment, but will go to lengths just to buy some sweets even in the middle of the night. Specific sweets at it, presumably that have been associated with reward due to the positive flavor accompanying the sweet taste. If I wasn't able to get snacks though, anything sweet sugary would probably do. Sometimes salty snacks work, such as potato chips or salted peanuts. But what's interesting is these cravings kick in at specific times, usually soon after waking up, or later in the evenings. Wondering if day light or other day time distractions may supply the dopamine in between. Possibly even artificial sweeteners would work also, by triggering the same pathways.
I also suspect missing doctors appointments and other 'chores' is so easy because there's no experience of reward without external supplies, like sweets, stimulants, sometimes alcohol and other limited things, but even so the sense of reward makes them barely worthwhile, and part of it is the attached positive feeling from knowing that something may actually work, if even a just bit. Since all of them are limited in what they can do even coke feels only so worthwhile to have, mainly because the effect is ridiculously short lasting, thus the dopamine release is counteracted by the negative feeling from anticipating a return of the depressive state, along with the knowledge that using coke is expensive and risky. But clearly since I still remember the effect, it means it was good enough to be on the short list. The sugar cravings could also be part sugar addiction. Sometimes when not eating sweets for a while, I wouldn't particularly miss it, suggesting the dopamine release may be from satisfying a non-innate craving, much like nicotine doesn't do much unless you're already nicotine dependent, in which case using nicotine triggers a sense of reward/dopamine release. Or it could be since these sweet cravings keep returning, the sugar addiction is secondary to their dopamine increasing effect.

The coke experience could be likened to taking aspiring during the flu, but just enough to reduce the flu symptoms rather than eliminating them. Not sure if a bigger dose of coke would have increased the antidepressant effect, or merely exaggerated the sense of activeness, while leaving other parts untouched, especially if we assume that mental well-being is not strictly related to dopamine. Maybe being low on dopamine could be analogous to being low on insulin, in that some just suffer from it. I saw symptoms even as a kid such as often having a general sense of gloom, feeling significantly different based on if the weather was sunny vs cloudy (cloudy days would often feel gloomy, or eerie, as opposed to just less bright), social discomforts, having a regular need for sweets/snacks, and possibly became clinically depressed later as a result of it.


I had to come to bluelight to discuss these thoughts. You would think a specialist in psychiatric conditions, namely a psychiatrist would be the perfect one to discuss and clear these things out with. Unfortunately, the average psychiatrist today knows mainly two things: everything mood related boils down to low serotonin, while everything else boils down to dopamine. Take anxiety, which is robustly counteracted by benzodiazepines which work on gaba, is now also attributed to low serotonin thus ssri are first line meds for anxiety disorders :?. Not sure where they got low serotonin being the problem behind a vast amount of mental conditions, whether from Pfizer or lily's.
Wonder how many of these conclusions were derived from double blind clinical trials, vs anecdotal observations, in which case placebo hasn't been accounted for. Placebo control is always a part of serious treatment studies. If we should go by anecdotes, many more anecdotes point to cocaine, alcohol and opiates strongly reducing psychological symptoms. Since psychiatric professionals go by anecdotes, why shouldn't we.
 
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I've always wondered why Dopamine Re-uptake Inhibitors were not more widely used for the treatment of depression.

It's because depression stigma isn't limited to the general public. The powers that be also have only thing on their mind "bah, drug addicts". Depression is a major cause of suicide on one hand, on the other dopamine reuptake inhibitors are unthinkable to give them even as temporary relief. Thus in cases where only DRIs help the depressed, they may be some of ones we see sleeping on the streets. I've spoken with at least one homeless guy who lost his job due to depression, which wouldn't have been necessary if there were effective antidepressants available. And if that was the case, seeking professional help would be a logical first step to many who feel down in the throws, rather than seeking street drugs.
If you're binge eating due to an addiction to foods, then suddenly a DRI is considered useful. I.e. giving food addicts with obviously addictive personalities a drug of abuse is ok, but not the depressed regardless, save for a few rational psychiatrists. As for me being addicted to sweets, I wouldn't call it an out of control addiction, it's more almost like a preference of being addicted due to the reward from eating them. But it's also not the same as not being depressed and addicted to something. I'd call it being addicted to the pre depressed state, and anything that can bring it closer. Moreover quitting it would be no bigger deal than enduring depression itself.

In many other countries, including the European Union though, DRIs are prescribed for depression, including a couple tricyclic ones. Might be interesting to see their depression statistics, to see if it looks better or the same.
There's one exception in the US, which is wellbutrin, but it's dopamine reuptake inhibition is probably at the level of mild coffee. Was on it, did nothing, while even a small amount of coke did something, plus it hasn't been banned in the US, so it must be a very weak dri.
 
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Sorry I turned into a bit of venting, was typing the last two posts with a headache.

Feel free to add anything.

Btw, realized I hadn't eaten in a while, and then gave eating food a shot. It was one of those lucky moments when that was enough to boost my mood by i'd say 40%, the headache went away, and I got some endorphin like physical sensation along with a bit more motivation. Coke doesn't seem as attractive after the mood goes up a bit, because life's 'natural highs' then seem a step closer, around the corner.
 
I don't think your hypothesis is valid... Mirtazapine, which is effective in more patients than SSRIs, is a pretty potent antagonist of 5ht2a. If anything it seems like 5ht2a inactivation would then cause antidepressant effect.

MDMA might be weak agonist at 5ht1 and 5ht2 receptors, it's also a potent as fuck releaser. With the brain so filled up with free floating serotonin, all serotonin receptors will be getting activated plenty.

IndanylAminoPropane is more effective than Mirtazapine and is much milder than MDMA. IndanylAminoPropane creates a peaceful mindset and mild to moderate happiness. 2C-Bu and 2C-NPH(2C-G-N) works to antagonize 5HT2a receptors and seem anti-psychedelic. So it seems like both low dose psychedelics and anti-psychedelics can releive depression. Go figure.
 
There are many areas of dopamine controlling nuerons in the brain. The most notable are those that control the reward system, these are what are responsible for the quality of life experience. Others control motor functions and even involuntary muscle function regulation. They are primarily responsible for highest level aspects of motor control, motivation and decision-making. They are a very important and fragile type of nuerons, few in number at approx. 400,000 total. These nuerons while few in number STRONGLY effect their targeted areas of the brain. All senses can be effected by the nuerons. If these nuerons are altered they can produce strong euphoric effects and complete enhancements in the human experience. However constant over-exicitation of these nuerons will cause them to go beyond a tolerance reducing reaction. They will in effect downgrade themselves due to thier sensitivity to the excess of dopamine. Once this reaction occurs these nuerons do not repair, and other nuerons attempt to take up the slack.

Marked depression and lack of motivation will be noticed when this happens and slowly the mind can rehabilitate itself to an extent. While this process occurs one can notice severe changes in sight (focus issues and muted colors, lack of depth) are very noticable. Also the sense of touch is altered to exclude pleasure sensory activations. Taste is dulled and olfactory sensation lacks nuansce and sublety. This is when a depressed mood is severe, although it is unknown wether this is due to the decreased stimulation of the senses and a general "foginess" of daily experiences or a direct motivational major depression from improper regulation or depleted dopamine. In either instance we see the signifigant impact of dopamine on major systems that is more noticable than serotonin regulation problems. Serotonin producing nuerons seem to have more constitution than the dopamine effectors thus more subtle negative effects to be realized by the concious mind.
 
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