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browri

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  1. Typically with mirtazapine or trazodone, you would have to take them regularly. I wouldn't be surprised if single dose helped from time to time, but really it's about consistency and changes in receptor sensitivity. An orgasm requires neurotransmitter signaling to be able to burst See when you have mood swings, an AAP can be very important. The cognitive dulling is sometimes there, but I push it to the side because I don't usually like how I feel without an AAP. I do actually, and we're getting married next month! Actually believe it or not I have trouble with erectile dysfunction on a fairly regular basis and general sexual desire. It's something was a problem in our relationship, but it really isn't anymore. With communication, he has become a lot more understanding, and honestly our relationship really has grown from it. Sex is important, but acknowledging that it's not the most important is the higher road sort of.
  2. Are your anxiety/panic attacks hallmarked by somatic adrenergic symptoms like a tight chest or racing heart? I sometimes wonder if an alpha-1 antagonist might be a good option here. Little background: There are two major types of adrenergic receptors, alpha receptors and beta receptors, which can be further broken down into sub-types. The alpha receptors are broken down into type 1 and type 2. Alpha-2 receptors act as the feedback loop. Activating them reduces adrenergic release, and blocking them increases it. On the other hand, activation of alpha-1 receptors is what causes the exhibition of adrenergic symptoms of anxiety/panic. Therefore, if you activate alpha-2 receptors, then theoretically you can slow down the adrenergic system. Examples include clonidine and guanfacine. Have you tried either of these? Well if lorazepam didn't do much for you relative to clonazepam, then you can safely expect that alprazolam will be even less helpful, I would think. Glad we were able to clarify the sexual dysfunction. It's safe to say that the anorgasmia is likely serotonergic in its roots, but the erectile dysfunction very well could be adrenergic in nature. May be TMI for some but I'll explain it anyway. The problem is that messing with the adrenergic system impacts the dilation and contraction of smooth muscle as well as blood flow. Ramping up the adrenergic system reduces blood flow to the penis via contraction of blood vessels and because of the desensitizing effect this has on the adrenergic system, also impacts the ability of smooth muscle to contract, namely, the sphincter that ensures blood remains in the penis (an erection). So in fact, while Cymbalta may be stimulating and a silver bullet for your anxiety when combined with clonazepam+pregabalin, the impact on the adrenergic system could reduce "performance" in this manner. It's also why even stimulants and their illicit cousins like ecstasy (MDMA) and methamphetamine can cause erectile dysfunction. Even cocaine can cause erectile dysfunction to a certain extent for the same reason. The way sildenafil works is by causing blood vessels to dilate thus facilitating blood flow into the penis. Anything pro-adrenergic works against this process. Keep in mind that dextroamphetamine (D-AMP) is significantly more dopaminergic than it is noradrenergic. This is in contrast to its sibling levoamphetamine (L-AMP) which is more noradrenergic than dopaminergic, and this may underlie Adderall's higher propensity for sexual dysfunction. In short, D-AMP is a bit more pure than Adderall which combines both D-AMP and L-AMP. Not sure why you had such an experience with Vyvanse though, which at the end of the day is just dextroamphetamine which is bonded with lysine to keep it from being abused via methods such as inhalation through the nose. It has to be digested to be bioavailable. Otherwise it's pretty useless powder in a gelatin capsule. But at the end of the day, Vyvanse is just dextroamphetamine with a solid extended release mechanism. It doesn't serve a good purpose in your case though because you use D-AMP specifically for sexual dysfunction, so you don't need it to last all day. Just long enough for the encounter itself. So immediate release D-AMP (Dexedrine) makes more sense in this case. I would imagine that pregabalin+clonazepam together could have a potent suppressant effect on the brain which would inhibit proper arousal, but you are right that it's a different mechanism than serotonin. While it's a name that sounds similar to buspirone, I imagine we should all give it the benefit of the doubt. Think that trazodone and vilazodone sound very similar but are VERY different medications in practice. The former is quite sedating and the latter is quite stimulating. There are critical things that will make gepirone different. Firstly, while buspirone and gepirone are both partial agonists of 5HT1A, gepirone is comparatively higher in intrinsic activity, meaning that gepirone will act as more of an agonist or activator of those receptors than buspirone does, thus lending to higher dopamine output. Additionally, gepirone's affinity for the dopamine receptors is 30- to 50-fold lower than buspirone, which should theoretically allow it to be used as an antidepressant because it doesn't throttle dopamine output that is occuring downstream of the 5HT1A activation. One thing they have in common though is that they both metabolize to 1-(2-pyrimidinyl)piperazine which is a potent alpha-2 blocker, thus increasing norepinephrine output. This would complement the duloxetine by enhancing noradrenergic signaling further than duloxetine could do on its own. As each day goes by I'm becoming more and more convinced by ziprasidone. The 60mg dose is mild really compared to what you were likely taking.
  3. No problem! I find this stuff to be fascinating so talking through cocktails and what's been tried and what hasn't is interesting to me. Jesus. Bless your soul for putting up with it, and good that you have found a combo that mostly works well for you. I've found that valproate, vortioxetine, and dextroamphetamine (in Vyvanse) are core for me but I'm not totally settled on an antipsychotic just yet myself. Yep all makes sense, particularly trying to tune the clonazepam dose against the pregabalin and also reducing the duloxetine because doses greater than 60mg work for some people but statistically speaking not a great deal of additional response is seen from most people in doses higher than 60mg, just more side effects without any additional efficacy. You are correct, the mechanisms are different. Sertraline is stimulating via inhibition of the dopamine transporter (a dopamine reuptake inhibitor), whereas fluoxetine is stimulating via the antagonism of 5HT2C receptors (which increases norepinephrine and dopamine release from neurons) and also via inhibition of the norepinephrine transporter by its metabolite norfluoxetine. So you are correct that they are both stimulating, but they do so in different ways. I read through the whole post before replying and the fact that you found both sertraline and bupropion to be uncomfortably stimulating is likely due to their effects on the dopamine transporter. In the case of sertraline, dopamine reuptake inhibition would indirectly increase norepinephrine signaling because when dopamine is up, norepinephrine generally is up as well. In the case of bupropion, the norepinephrine transporter is DIRECTLY inhibited like the dopamine transporter which would make it effectively worse than sertraline was. Indeed you were. Being on a combo of pregabalin and gabapentin is irresponsibly redundant. Being on a combo of risperidone and ziprasidone....as @mikl_pls would say, "Holy sedation, Batman!" Don't personally feel strongly one way or the other about memantine but it was likely necessary simply because of all the other medications you were on. Like I said, haven't taken mirtazapine personally so I don't really know for sure. I think what is important about mirtazapine is the serotonin antagonist effects at 5HT2 type receptors specifically. This can have calming effects, particularly when its also an anti-histamine. The concern with alprazolam is that the half-life is too short and that it's potency is roughly half that of clonazepam. At your current dose of 4mg/day, you would have to take 8mg/day of alprazolam to achieve the same sedative effect. Alprazolam XR is only dosed to 6mg/day, and they only make it in up to 3mg tablets. Some patients do take more than that, but psychiatrists generally move patients to clonazepam if they need to take that much alprazolam because clonazepam has a lower tendency to cause tolerance to anxiolytic effects. The other concern is that your insurance company may put a quantity limit on alprazolam XR 3mg tablets of 2 per day which would prohibit you from achieving the dose necessary to achieve the same effect as your clonazepam dose unless you did a prior authorization for a quantity limit exception. Have you ever tried lorazepam? It's known to have an intermediate duration of action where alprazolam is considered short and clonazepam is considered long. Perhaps lorazepam would be a happy medium with TID dosing and less effect on acetylcholine or serotonin. When was the last time that you took 60mg of duloxetine? Perhaps you may be getting some excess serotonergic stimulation which could also be causing activation. Like I said above, statistically speaking most people should function well on 60mg but I do also see that you are treatment refractory. So you could adjust duloxetine down, move clonazepam to TID dosing, or switch clonazepam to lorazepam. This may explain why you responded so well to fluvoxamine and paroxetine. This may be a stretch but there is another option as well, and I'll put it out there even though you mentioned you didn't really want to take more than 3 medications. However, it has been tried in practice and appears to be effective in more difficult cases of OCD, panic and anxiety. Not sure if you've heard of clomipramine or taken it, but clomipramine and fluvoxamine can be combined in low to moderate doses very carefully to create a potent combo. Clomipramine (CMI) is metabolized into desmethylclomipramine (DMC). The parent compound (CMI) is more serotonergic, whereas the metabolite (DMC) is more noradrenergic making clomipramine very similar to other tricyclic antidepressants. Additionally, the metabolite circulates at much higher levels than the parent compound making it mostly noradrenergic. However, when it is combined with fluvoxamine, its metabolism is inhibited and CMI circulates at much greater levels than DMC. This makes it more serotonergic. The premise is that you start them both at the lowest doses possible and then VERY slowly increase them to the most effective dose combination. And this should only be done by an experienced pdoc. Sexual dysfunction on any sort of serotonin reuptake inhibitor is pretty much par for the course, but there are options to reduce sexual dysfunction. I know you've already said that bupropion is a panic attack in a pill, and personally I agree. I did take it for quite some time but ultimately the anxiety it caused me from day to day was totally not worth any positive it brought. However, mirtazapine is generally regarded as the other best augmenting option for reducing sexual dysfunction caused by SSRIs. This is because it acts as a low potency antagonist at 5HT1 receptors and a high potency antagonist of 5HT2 and 5HT7 receptors. There is an FDA-approved medication called Addyi (flibanserin) which is for women with Hypoactive Sexual Desire Disorder (HSDD) but theoretically could be used by men as well. It is termed a norepinephrine-dopamine disinhibitor in that it acts as a full agonist of 5HT1 receptors in some brain regions and a partial agonist (part agonist, part antagonist) in others. It is also a potent 5HT2A antagonist. By blocking certain types of serotonin signaling, it enhances norepinephrine and dopamine signaling which can promote sexual arousal. Another option would be the newer antidepressant that is coming out, Travivo (gepirone). It is chemically related to buspirone but makes some great improvements on the mechanism of action that address some of the core problems with buspirone. Particularly, where buspirone acts as a partial agonist of dopamine receptors at higher doses thus tempering any antidepressant response, gepirone does not. Therefore, its partial (near-full) agonist actions at 5HT1A are not blunted by the throttling of dopamine signaling. 5HT1A activation causes dopamine release in the pre-frontal cortex, but at higher doses, the dopamine partial agonist actions actually cause dopamine output to decrease. Therefore, lower doses of buspirone can have antidepressant effect when combined with an antidepressant, but higher doses may reduce this. Gepirone does not do this and can produce antidepressant effect at all doses tested. It also I believe has different affinities for pre-synaptic versus post-synaptic receptors which theoretically allow it to pull out all the stops on serotonin acting as a partial agonist at pre-synaptic causing serotonin release and full agonist at post-synaptic thus further enhancing the response. Gepirone is new so of course it will be difficult to get insurance to cover it and it's technically meant to be taken as monotherapy but anecdotally could be used as an augment like its cousin, buspirone. Yeah dopamine agonists really aren't a good answer to the sexual dysfunction problem. Really bupropion, mirtazapine, and trazodone are your three best options. Additionally, even dextroamphetamine can cause some sexual dysfunction. Like it may increase sexual desire but still cause erectile dysfunction because of its effect on the cardiac system. Serotonin activation in the beginning can be quite stimulating because it causes downstream release of dopamine. However, after a few weeks the brain does adjust. In fact it's quite normal in the beginning for doctors to prescribe short-term benzodiazepines like Klonopin, Xanax, or Ativan to be taken with the antidepressant for the first 2 weeks until the brain starts to adjust to the increased stimulation. In this case, you were already taking a benzodiazepine. So a dose increase may be temporarily necessary until you adjust.
  4. So of the benzos, clonazepam is most often used for panic because of its long half-life and also because tolerance to the anxiolytic effects takes much longer than for other benzodiazepines. Meaning specifically, when you start clonazepam, for the first few days to weeks you feel the sedation/hypnotic effects, but those go away after a time and you're left with just the anxiolytic effects. Kind of like how stimulants in the beginning give you a lot of motivation and energy but after 1-2 weeks, the extra energy goes away and you're left with pure focus. As a general rule, alprazolam causes the patient to develop tolerance to the anxiolytic effects faster than other mainstream benzodiazepines. There are other benzos with much longer half-lives like flurazepam, which has such a long half-life that it actually accumulates in the system to the point that it becomes more and more sedating as the days go by. It's only supposed to be used for the short term treatment of insomnia. In short, its half-life is too long to be useful. Earlier on in the post you had talked about switching from BID dosing to TID dosing. That is actually how my doctor prescribes it for anxiety and panic. He starts you out at 0.25mg in the morning, 0.25mg at noon, and 0.5mg at bedtime and he works up from there. So perhaps you do 1mg when you wake up, 1mg at noon, and 2mg at bedtime. It may be worth discussing with your pdoc. Remember that an important reason why SNRIs are more effective for anxiety than most SSRIs is because of their noradrenergic effect. In essence, things get worse before they get better via desensitization. Because SNRIs like Cymbalta increase norepinephrine signaling, over time adrenergic receptors become desensitized to the increased adrenergic activity and therefore adrenergic "bursting" that comes with anxiety/panic attacks nets a smaller effect on the cardiac system. Basically, if your adrenaline is up all the time, then your body doesn't take notice to the short bursts of norepinephrine that can occur during a panic attack that cause those somatic, adrenergic symptoms like tightness in the chest or your heart is pounding. Even Paxil (paroxetine) is a known norepinephrine reuptake inhibitor but at the time it wasn't considered to be clinically relevant because of the low affinity. So it was relegated to the SSRI class even though it's a wannabe SNRI. May be part of the reason why Paxil is so commonly prescribed for anxiety. The premise here is that those with anxiety and panic may have lower base norepinephrine signaling, which means when there are norepinephrine bursts, adrenergic receptors are overly sensitive to this extreme increase in signaling. So if you increase the baseline norepinephrine signaling level, then it can lead to less bursting and therefore potentially fewer panic attacks and generally less anxiety. Although some still report feeling tense or nervous when their core anxiety and panic symptoms have subsided. I personally have not taken Remeron (mirtazapine). However, it has demonstrable effects on anxiety and in combo with an SNRI can work synergistically similarly to the way pregabalin or gabapentin mix well with benzos. It would certainly be worth a try. You may find it stimulating, and that may not be such a bad thing. The stimulation may help to desensitize you to your anxiety symptoms. It's hard to say though. This is another option you'd have to discuss with your pdoc. He would have more experience with the combo. In fact, if you're in California, then he should be intimately familiar with California Rocket Fuel (mentioned earlier in the thread) which classically combines Effexor (venlafaxine) with Remeron, but theoretically the same effect can be achieved by combining any SNRI with Remeron including Cymbalta, Pristiq, and possibly even Fetzima in higher doses (because Fetzima behaves as an NRI at lower doses with effects on serotonin in escalating doses). The SNRI increases serotonin and norepinephrine levels in the synapse. Normally, activation of central 5HT1 serotonin receptors and alpha-2 adrenergic receptors by the increases in serotonin and norepinephrine would reduce serotonin and norepinephrine output. This is the "braking system" in the brain. Remeron acts as an antagonist or blocker at alpha-2 adrenergic receptors, thus "cutting the brake line". This can increase norepinephrine and serotonin output. It also acts as an antagonist of 5HT2 receptors similarly to AAPs, which can increase output of serotonin, norepinephrine, and dopamine. Taken with the inhibition of serotonin and norepinephrine transporters by the SNRI, it's a potent combo. The concern with long-term high-dose clonazepam treatment is the fact that it is an acetylcholine reducing agent, which can cause cognitive issues in the short term and the long term. What other SSRIs and/or SNRIs have you tried beside duloxetine? I ask because fluoxetine is known to increase circulating levels of allopregnanolone, which is a GABA-A positive allosteric modulator, and fluoxetine itself is a known positive allosteric modulator. Allosteric modulators "tune" the receptors up (positive) or down (negative) in their sensitivity to ligands that bind at the orthosteric site. So in this case, GABA is the ligand that binds to the orthosteric site of the GABA-A receptor, and allopregnanolone and fluoxetine would both INCREASE the effect that GABA has at the receptor effectively making less GABA go further. GABA being the main inhibitory neurotransmitter in the brain is how anxiolytic medications like benzodiazepines typically mediate their effects. This allosteric modulation is suspected to be how fluoxetine is effective in anxiety disorders or panic. If you think that you might be feeling too stimulated from an adrenaline perspective, switching to venlafaxine or desvenlafaxine will have somewhat less of an adrenergic effect and still retain efficacy in anxiety or panic. If you aren't interested in replacing the clonazepam because you feel it is a core medication for you, perhaps you could look at replacing pregabalin with something else like the older gabapentin or the newer tiagabine or vigabatrin if those are available in your country. If you wanted to get by with fewer medications, I imagine that a combo of clonazepam+buspirone would be effective and might allow you to go without duloxetine and/or pregabalin. There's also the option of Trintellix (vortioxetine) which isn't an SNRI but is also not a pure SSRI, acting as a full agonist at 5HT1A, a partial agonist at 5HT1B, and an antagonist of 5HT1D, 5HT3, and 5HT7. A few studies have been done to determine the effect that vortioxetine has on anxiety. They ultimately determined that for those that don't have much or any anxiety or those that do have anxiety but have a low baseline, vortioxetine can increase anxiety levels, but in those that have a very high anxiety baseline in that they are mostly anxious most of the time, vortioxetine had a total positive effect on anxiety. I believe someone else spoke to the glutamate side of things (opposite of GABA). Vortioxetine can stabilize glutamate and GABA signaling. There are lots of options as you can see, and they all work in different ways, but you're probably better off going to TID dosing with clonazepam and keep everything else the same if you don't feel foggy or medicated from the combo of pregabalin+clonazepam.
  5. this would be correct. I believe the safest anticonvulsant medications during pregnancy are Lamictal (lamotrigine) and Keppra (levetiracetam). That being said all anti-convulsants carry some sort of warning about birth defects because there is some data, there just is less data for some medications, like in this example. They have some indication of problem in animals but lack much if any supporting data in humans. Doesn't mean they haven't tested the theory, just means there's less data. Not for lack of trying I imagine. Lamictal is an old medication. I do believe Keppra is newer, so perhaps the latter's excuse is that there hasn't been enough time to collect the data. But the former has been around for a long time, and I imagine that birth defects would have been reported by now if there were any.
  6. Fingers crossed! I hope Flonase helps you. Fluticasone will work differently from oxymetazoline in that the former is a glucorticosteroid, and the latter activates alpha adrenergic receptors. Theoretically oxymetazoline should work for this particular side effect because Seroquel is an alpha adrenergic blocker and oxymetazoline should work in the opposite direction in the nasal area to open the airways but in my experience oxymetazoline isn't nearly as potent at opening my airways as fluticasone. And like I said, if you end up getting regular Flonase and find it to just taste disgusting and leave a chemically floral smell in your nose, make sure you try Flonase Sensimist because it's the same fluticasone but a different "experience" so to speak.
  7. Theoretically the XR may have less weight gain than the IR formulation but I can't speak to the other side effects. However, that IR dose in the evening may be part of your problem and it may be worth going to 250-300mg of the XR in the morning because at that dose Seroquel should start to become more stimulating via norepinephrine activation (usually begins after 200mg). My thinking is that you have this 150mg that's distributed throughout the day and then a booster of 100mg at night which could be exacerbating the nasal congestion. It may be better to do more of the XR in the morning and less of the IR in the evening. More than likely any of the anti-histamines will just dry you out as Seroquel itself is an anti-histamine, so I personally wouldn't recommend Zyrtec (cetirizine), Xyzal (levocetirizine), Claritin (loratadine), Clarinex (desloratadine), Allegra (fexofenadine). However, I would recommend Flonase, particularly the Sensimist which is fluticasone furoate instead of fluticasone propionate. Less spray volume so less post-nasal drip and it doesn't have a terrible taste or floral smell the way the regular Flonase does. Fluticasone is a steroid and should reduce inflammation. Whether it will reduce inflammation caused by vasodilation via alpha 1 adrenergic antagonism idk, but I'm inclined to think it'll work better than anti-histamines would.
  8. Make sure to take that stat in context. That stat doesn't cover those where it SEEMS like the antidepressant poops out but a dose increase resolves the problem. If your antidepressant "stops working" but you do respond to a dose increase, that isn't antidepressant tachyphylaxis. That just means you weren't on the optimal dose to begin with. However, if you hit poop-out on a moderate to maximal AD dose, then you switch to another antidepressant. Here's a purely hypothetical scenario: Pdoc starts you out on 10mg of Prozac and after a few weeks increases you to 20mg. You're on 20mg for a few months and find that it isn't working the way it used to in the beginning. So your pdoc bumps you up to 40mg and you do well for several more years. After many years of treatment with 40mg of Prozac, you start to feel like it isn't working again, so the pdoc increases it to 60mg. This causes more side effects but not a whole lot of improvement. So the pdoc tries bumping it to 80mg, but you are unable to tolerate the dose and you don't notice much of any improvement over the 60mg dose. So the pdoc decides to switch you to either 50mg of Zoloft or 30mg of Paxil. The statistic indicates in this SPECIFIC example that with the switch from Prozac to either Paxil or Zoloft the chances of you responding to Paxil or Zoloft after being on Prozac for several years and maxing out the dose are <50% and with each subsequent switch, the chances of treatment success (i.e. prognosis) actually get WORSE not better. This scenario above and the corresponding statistic also does not apply to antidepressant-induced hypomania. For example, you've been diagnosed with major depressive disorder but the pdoc is not yet aware of your manic tendencies and prescribes Prozac first at 10mg then to 20mg as in the previous scenario. Except this time, after just a few weeks you feel depressed again and need to increase to 40mg, which resolves the depression but again after a few weeks you're depressed again. This is cycling. Separating undiagnosed bipolar disorder from antidepressant tachyphylaxis is really tricky business. For someone with MDD, each subsequent AD trial reduces the chance of treatment success, and for someone with bipolar disorder each AD failure increases likelihood of bipolarity. It's very weird separating the two.
  9. No they don't poop out for everyone by default but the statistic is really high the longer you take a medication. The missing part there though is that once you reach poop-out, switching to another medication doesn't always fix the problem. For many who have reached poop-out, switching the antidepressant for another antidepressant helps less than 50% of the time. Usually augmentation is required to reverse tachyphylaxis.
  10. Omg the total opposite Yes it definitely would. You totally wouldn't even need Linzess anymore I would think lol Edit: I'm actually pretty sure there were studies done on Viibryd treatment in those with depression or anxiety who also had IBS-C.
  11. I would more likely think lamotrigine. But I can't be sure. And I also don't know that it's considered a serious side effect either unless of course they start showing up everywhere rapidly. But really with lamotrigine, the only thing that you really have to be worried enough about to call the doctor is the rash.
  12. At least a step in the right direction. Therapy and medication are each a leg and most people have a hard time walking with one leg No really good alternatives to Wellbutrin other than Ritalin. It's a stimulant but more so an NDRI than anything. I would take your docs suggestion of going higher on the Pristiq because you can fill a 100mg and 50mg tablet prescription without insurance complaining about it and Pristiq does have somewhat more effect on norepinephrine than Effexor does.
  13. Oh well Linzess should be able to handle any diarrhea because if I understand linaclotide reduces gut motility. So Viibryd could be a great option for you.
  14. And your neuros are probably right lol. That's actually a brilliant idea to use iron, because other than the fact that Viibryd caused a major increase in GI motility (and consequential diarrhea), it was a great antidepressant. I wasn't on a mood stabilizer when I was taking it though, so I'm not totally sure how it would work for me now. @looking for answers she is right that Viibryd is pretty activating and it may be a suitable substitute for the Wellbutrin while also improving anxiety rather than worsening it.
  15. It's good to strike a balance between stimulating and sedating. In your case though, it's mostly sedating. That's a solid dose of quetiapine (assuming you are still taking 150mg) as well as trazodone at 100mg and clonazepam at 1mg. On the other end of the spectrum 300mg of bupropion and 40mg of Vyvanse is nothing to shake your head at. Because anxiety lends to dysphoria, it would make sense to remove something that could potentially cause you anxiety or make you feel agitated and you've clearly called out bupropion. From there you would probably want to roll back the clonazepam because long-term benzo use is definitely not ideal. Continuing on amantadine and melatonin as well as the Vyvanse makes sense to me. I'm not sure I see the point in taking both trazodone and quetiapine together though in moderate doses like that. It's kind of redundant. The only things the quetiapine does that trazodone doesn't is norepinephrine reuptake inhibition (which bupropion is also doing) and dopamine antagonism. The lithium can also be sedating. That is something to consider, but it should be less impactful during the day if it's all taken at night. A solid combo of lithium+quetiapine and add on the Vyvanse should be really good for depression and mood stability all on its own. You could also increase it further to get some stimulation out of it that's lost by stopping the bupropion. It just comes down to whether or not the lithium+quetiapine combo is ENOUGH for your depression. And some people can't get by without an antidepressant. I would honestly say go back to Trintellix just because it's going to have fewer side effects than some of your other previous SSRI trials like paroxetine.
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