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About mikl_pls

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    Alabama, US (not native Alabamian!)

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  1. Only when the clomipramine doses get high enough for the levels of its active metabolite, N-desmethylclomipramine, to get high enough to work on norepinephrine sufficiently. (N-desmethylclomipramine is a secondary amine TCA, meaning it acts mainly on norepinephrine.) At low doses of clomipramine, it primarily occupies the SERT (quite potently), and NET occupancy isn't very high at low doses due to the low levels of N-desmethylclomipramine. For me, personally though, it worsened my depression and anxiety a lot... But everyone is subject to their own experience with any medicine. Nope, as @Skeletor said, Fetzima actually works more on norepinephrine than serotonin, which is unique amongst the SNRI class of medications. Milnacipran, marketed as Savella in the US specifically for Fibromyalgia (and not for depression, but is marketed for depression in other countries in the world), is the racemic version of Fetzima (levomilnacipran, which is the levorotatory enantiomer of milnacipran, or the left-hand side of the molecule). I forget where you reside, @Blahblah, but check it out, milnacipran may be available where you live. Some common brand names are Ixel, Dalcipran, and Toledomin (other than Savella). There may be other trade names that I don't know about... Yes, it is. Side effects are more pronounced in the tertiary amine TCAs definitely, but in the secondary amine TCAs, not so much. I know I already listed them, but I'll list them again. Tertiary amine TCAs in the US include: (more side effects, more serotonin except in higher doses which act include more norepinephrine) amitriptyline (Elavil) doxepin (Sinequan) (basically a glorified antihistamine, not that effective for depression) imipramine (Tofranil, Tofranil-PM) clomipramine (Anafranil) trimipramine (Surmontil) (this one does not cause any reuptake inhibition of any neurotransmitters; rather, it has atypical antipsychotic properties similar to clozapine) Secondary amine TCAs in the US include: (less side effects, more norepinephrine and indirectly dopamine, higher doses include serotonin too) nortriptyline (Pamelor) desipramine (Norpramin) protriptyline (Vivactil) Don't forget about the tetracyclic antidepressants! (TeCAs) amoxapine (Asendin) This is the active matabolite of the first-generation (sometimes debated as an atypical) antipsychotic loxapine (Loxitane). It is a potent norepinephrine reuptake inhibitor and a weak serotonin reuptake inhibitor. It has "built-in" atypical antipsychotic properties, with D2 antagonism and potent 5-HT2A, 5-HT2C, and 5-HT6 antagonism. It, too, has some active metabolites that have D2 antagonism. One active metabolite has more potent serotonin reuptake inhibition, balancing out its monoamine reuptake inhibition profile. maprotiline (Ludiomil) A potent norepinephrine reuptake inhibitor, 5-HT7 antagonist, and H1 antagonist (antihistamine). This medication has a narrow therapeutic index due to its propensity to causing seizures. It's not very commonly used anymore, and is very hard to find nowadays. mirtazapine (Remeron) Considered a tetracyclic antipsychotic, though its mechanism of action differs vastly from the other two, which more closely resemble those of the tricyclics (sometimes they're even referred to as secondary amine TCAs). Causes no reuptake inhibition. Potent 5-HT2A and 5-HT2C inhibition, leading to disinhibition of dopamine and norepinephrine release. Potent 5-HT3 antagonism, resulting in antiemetic effects, as well as release of acetylcholine and other neurotransmitters. Potent presynaptic α2A and α2C antagonism, leading to disinhibition and enhancement of norepinephrine an serotonin release (leading to indirect increased 5-HT1A stimulation, presynaptically causing downregulation of the autoreceptors in time which disinhibits serotonin release and postsynaptically causing downstream dopamine release) Potent H1 antagonism, leading to increased appetite and weight gain (especially when combined with the potent 5-HT2C antagonism that this medicine has) This medicine is commonly paired with SNRIs to get a more potent response for treatment-resistant depression (prototypically Effexor XR), called "California Rocket Fuel" by Dr. Stephen Stahl, a psychopharmacologist. It is typically more sedating in lower doses (7.5-15 mg), and less sedating and maybe even stimulating to some in higher doses (30-45 mg). (This, however, was not the case for me at all...) Some people need supratherapeutic doses of 60-90 mg. I'm sorry, but I have never heard of this. Looking at the molecule, it does not have the prototypical tricyclic structure. Can you please provide a source for this?
  2. PANICKING but somewhat relieved. Kay Ivey, governor of Alabama, is being pressured into issuing shelter in place. If she does, IT'S ABOUT FUCKING TIME!!!!! But that means I won't get to bro-cuddle with @THE_REAL_Bryan and watch YouTube videos with him!! 😢
  3. Kay Ivey is being pressured into issuing shelter in place for Alabama. She should've fucking done it a long time ago!! But yet I'm panicking big time because I won't get to see my best friend, @THE_REAL_Bryan! 😢 I guess Facebook Chat or some other video chat will have to do... :( 

    1. saintalto


      Video chat has been helping me. I chat with all my friends as regularly as they’ll let me and it keeps my spirits up considerably. 

  4. When I was a very young kid (2-4 years old), the house we lived in had the washer and dryer in the basement (which flooded often). Oftentimes my mom would put a load of laundry in the washer at bedtime. Well, sometimes the washer would get off balance and start thrashing around. That used to terrify the ever living shit out of me. I would scream and cry hysterically and would be inconsolable for half an hour. That lasted until the next house we lived in where the washer and dryer were in the actual laundry room which was closer to my bedroom. It would happen, and I would start screaming bloody murder. I think I outgrew that "phobia" by the time I was 6 or 7 years old. Another phobia I had (and still to this day as a 32 year old grown assed man) is bathroom fans. I don't know why, but they freak me the fuck out. They're loud, I don't like them, I don't know where the air is going they're sucking out of the bathroom... OR:EGJEO:IRGJ:EOIGRJIO:WEJOGP:IJWEGOI:JWE:OIGJW:OIEGJO:EOIJG"PO NO! JUST NO! Even worse are the bathroom heaters! They're so fucking loud! They're going to kill me I just know it! There are more but I can't think of them, and it's probably best that I not do so...
  5. That's what makes me wonder if an amphetamine would be better for you over a methylphenidate-based because with methylphenidate and bupropion I believe you have to already have dopamine and norepinephrine there to inhibit the reuptake of. If there's a deficiency of them, then you won't be able to get any benefit from them. Amphetamines forces the release of those catecholamines. You could get some benefit out of taking amino acids like DL-phenylalanine or L-tyrosine, but there haven't been any proven benefit from taking them (they metabolize into dopamine and norepinephrine supposedly). As for the SNRIs, you've tried Effexor and Cymbalta to no avail... What about Pristiq or Fetzima? Honestly I think that would be a fantastic idea. The tertiary TCAs are pretty potent SRIs in lower doses, but as the dose increases, the become very potent SNRIs because the active metabolites (secondary amines which work on norepinephrine) increase in your system. Tertiary amine TCAs in the US include amitriptyline (which produces nortriptyline), imipramine (which produces desipramine), clomipramine (which produces desmethylclomipramine), doxepin (which produces nordoxepin), and trimipramine (which produces desmethyltrimipramine). Trimipramine is considered a second generation or "atypical" TCA because it does not produce any significant reuptake inhibition of any neurotransmitters. Instead, it possesses antipsychotic properties similar to clozapine (without the bad side effects). It has 5-HT2A antagonism and D2 antagonism, but preferentially antagonizes the presynaptic D2 autoreceptors in lower doses which leads to disinhibition of dopamine release. It's also a potent antihistamine and an anticholinergic. Clomipramine is regarded as the "golden standard" SNRI. Personally, I had a horrible experience with it, but be my guest and try it. It's supposed to work wonders for people. It just wan't my cup of tea. What I like are the secondary amine TCAs. Nortriptyline, desipramine, and protriptyline. They work primarily on norepinephrine, have less side effects, rather than being sedating are actually stimulating, especially protriptyline (which is taken during the day instead of night). (Desipramine can be taken during the day too.) These really help me with alertness, vigilance, and energy along with the SSRI that I take (Zoloft). I find that taking a secondary amine TCA with a SSRI (to create a customizable SNRI) is best for me. If I need more or less of one, all my pdoc has to do is tweak one or the other. It's super simple. As for MAOIs, I personally loved Parnate (tranylcypromine), but it caused me so much weight gain which is very paradoxical. It's supposed to cause weight loss. But it along with the combo of Adderall had me out of my existential depression and I was so happy to be alive I could've burst into confetti. Literally. Emsam wasn't all that great, but it was better than the other one that I tried, Marplan. Marplan was kinda crappy and didn't work well, and it cost way too much for me. I never touched Nardil because of the menacing weight gain threat it has. That and it is supposedly sedating or stimulating—it can go either way. Also it can cause liver failure and vitamin B6 depletion which if left untreated can cause neuropathy. Emsam and Nardil are the safest, Marplan is the least researched and understood, and Parnate is most likely to cause both orthostatic hypotension and hypertensive crisis, paradoxically. (The orthostatic hypotension is how you know it's working.) Don't be afraid of MAOIs though. The dietary restrictions aren't that bad or super restrictive. Just watch fermented and pickled foods and you should be okay. That and aged cheese and certain alcoholic beverages. (Really you shouldn't be drinking alcoholic beverages on psych meds anyway, but.........) If your pdoc doesn't seem to be progressing with you or helping you, I would advocate as strongly as you can for a TCA or MAOI. MAOIs, believe it or not, have less side effects than SSRIs (if you take them right, watch food and drug interactions, etc.) and definitely less than TCAs.
  6. I know what you mean by tics. I have Tourette's disorder and have suffered from it from age 3 or 4 years old (now 32 years old). I also know what you mean by this surge of electrical impulse feeling. It could be a number of things. Zoloft is not known for causing this (Effexor however is), but some serotonergic meds with particularly short half-lives (like Effexor), if you miss a dose by just a few minutes than when you normally take it, it creates electric shocking/zapping sensations in your brain ("brain zaps"). Paxil does this too quite badly, even though its half-life isn't as short as Effexor's. It could be that you're particularly sensitive to Zoloft and that you need to make sure that you take it exactly on time. I don't think the divalproex is the culprit, but in doing some research, I did find an interesting tidbit... Sodium valproate (basically same thing) use is associated with reduced parietal lobe thickness and brain volume. Here's the link: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3908352/ Ambien could possibly be causing it, but that's just a guess from me. Next time you see your pdoc, be sure to write a note on a piece of paper or write a note on your smart phone or something to remind you to bring it up to them. You may need a referral to a neurologist.
  7. That's what I figured based on previous questions about chat rooms, and that's why I really wanted a moderator to weigh in on this. Personally, I'm not opposed to PMs or anything from anyone, but I don't want my inbox to blow up or anything, and also just know that I'm currently dealing with my own things, so if I don't get back to you immediately, it's nothing personal against you.
  8. I'm actually more involved in politics now than I ever have been, and angrier than I ever have been at the government. Now I'm shutting down because I don't have the coping mechanisms to deal with all the anger from all the news I'm reading about how poorly the US is handling this.
  9. Hello! Do you have a seizure disorder? That's the first thing that comes to my mind.
  10. Hey there everybody! I just got a prescription for Caplyta (lumapeterone) today from my GP (couldn't get to my pdoc today) as Latuda wasn't doing anything to help me at all. I took the prescription to the pharmacy and it's going to need a prior auth. I'm wondering if it's because I'm not schizophrenic, and so far, that's the only indication for it. Is anyone else on this drug? (Schizophrenic or not?) I'm bipolar type 2 but have psychotic features when very depressed. If anyone is on this drug, could you please describe your experience on it?
  11. I've heard glucomannan is a pretty good supplement for if you're trying to lose weight. It not only promotes fullness, but absorbs water and has a bunch of other health benefits as I glossed over some articles about it. I remember reading about it when I was doing the keto diet and decided against it for some reason (probably because it would kick me out of keto) but read up on it before you go purchase any. Also, I can't speak highly enough of the ketogenic diet. It's hard to get on, but once you get on it, it's wonderful. Your energy levels increase and your mood stabilizes. Or at least mine did anyway, and that's the general consensus about it... But while I know it's not sustainable for long periods of time (over 2 years is not recommended medically), you can see a nutritionalist to help you gradually reintroduce carbs and lower fat down into your diet so you don't gain all the weight back. Also, inb4 "keto is a fad diet!" No, it's a medical diet for treatment-resistant epileptics. It just so happens that it has become a fad diet.
  12. This could very well blow up in our faces, mods please feel free to input here, but I just had an idea pop up in my mind. Maybe we could start a Discord server. We don't have to do the voice chat thingy, but we could do the text chat thingy if we wanted. Mods could mod it if they like. Just an idea to throw on the table. 🤷🏻‍♂️
  13. I wasn't able to find much, but I too believe I suffer from this. I believe my antipsychotic also contributes to this as well. As for the antidepressant (specifically SSRI) induced indifference, I found one single link from pubmed that seemed to be somewhat reputable. I recommend checking it out. I'll summarize a little of it below. Personally I have gotten rid of it by adding a moderately high dose of desipramine (100 mg) to my SSRI. That's a secondary amine TCA which works primarily on norepinephrine (actually is the most selective NRI on the market in the US). Atomoxetine (Strattera) would work too theoretically (I've tried it and it didn't work too terribly great for me). Fluoxetine and atomoxetine was a good combination until Strattera went generic (then all hell broke loose). MAOIs are really great for depression that are treatment resistant (if you're able to find a psychiatrist who's willing to prescribe them). They're even more effective when prescribed with a stimulant, which is classically contraindicated, but can be done under the close supervision of an expert psychiatrist.
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