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About browri

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  • Birthday 05/14/1991

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    Bethlehem, PA

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  1. Such a shame. Good and available pdocs are so hard to find these days. If I'm having an issue, I can just call in and let them know I'm having an issue and to have my pdoc call me back when he has time and we'll talk it through over the phone. If your pdoc is anything like mine, he'll want to increase whatever the mood stabilizer is. My pdoc usually just bumps me up on Rexulti if I call in and I sound agitated.
  2. Well going back to Lamictal was nice for the Spring/Summer but it clearly is not helping me with Fall/Winter at all. Transitioning back to Trintellix: (doses are Lamictal/Trintellix) Week 1: 50mg/5mg Week 2: 25mg/5mg Week 3: 25mg/10mg Week 4: 12.5mg/10mg Week 5: Discontinue lamotrigine Last time I took Trintellix from 8/2017-6/2018 I had to go to a lower Vyvanse dose because they work synergistically and I could tell because I started to get the stimulant facial tics when we added in Trintellix and I think the tics started kicking in around 15-20mg. I'll probably back the Vyvanse down to 30mg. Towards the end of this past June as well, I noticed I was getting a bit mixed and we should have just decreased the Trintellix to 5mg for the Spring/Summer and upped the Rexulti. So now that I've learned my lesson (lol), here's where we're likely headed: AM Trintellix 10-20mg (not sure, we'll see how the dice roll) Vyvanse 30mg PM Depakote ER 1250mg Rexulti 2mg And don't forget the fish oil! For those that don't know about it, Vascepa is an EPA-only fish oil which is much better for triglycerides and LDL than the DHA/EPA mixed fish oil (Lovaza). It also has known anti-inflammatory properties even in the brain which can help immensely with depression. I take 2 grams twice a day. Be careful though, there have been several cases of omega-3 supplements triggering hypomania similarly to antidepressants. I was so worried the insurance wouldn't cover it. I've been on many generics before, so step therapy usually isn't a problem for me, but with BCBS of NC and Prime Therapeutics, apparently not only do you have to try several other medications, but they will only approve step therapy for a "restricted agent" if it's being used for its FDA-approved indication. Trintellix is for MDD. I'm BP2. I was so worried they wouldn't approve it, but we submitted the paperwork on Tuesday, and it was just approved today! No need for appeal. So needless to say I'm a TAD euphoric at the moment. As for what these do for me: Trintellix (depression, also does truly help significantly with cognitive symptoms, focus/attention, etc.) Vyvanse (ADHD, works synergistically with the Trintellix to get the same effect in a lower dose, also helps quite a bit with depression) Rexulti (depression, really positive effect on my sleep and anxiety. On its own doesn't have much mood stabilizing action. However, in a pinch we can raise the dose and it does quiet intrusive and racing thoughts) Depakote ER (this is the most important and forms the backbone of the whole cocktail. Rexulti augments its mood stabilizing action but offsets Depakote's mood depressing effects. Trintellix assists there as well of course. also assists the Rexulti with anxiety issues. Depakote is also the only reason I can tolerate the same dose of Vyvanse without taking "low-dose holidays" to unwind from the stimulation)
  3. I wouldn't advise doing anything without your doctor's permission. Sure you are on low doses. But if you really feel like your mood is "up" then better to call the pdoc. He may prefer to increase the Depakote and keep you on Zoloft+Cymbalta until things calm down. However if you haven't already, make sure you explain that this is the effect that you get from most antidepressants and you think based on your experience that removing one might help. If you're only on 25mg of Zoloft then I would say to get rid of the Cymbalta. 25mg of Zoloft should help you maintain while you continue increasing the Depakote. I would say you would want to shoot for 1000mg on the Depakote and THEN see how you feel.
  4. Yeah my partner and our pdoc have both emphasized that it HAS to be taken early enough. Sometime between 7pm and 8pm would be best. Smart idea. Should help to give some pep to offset the morning fogginess from clonazepam.
  5. @Bobo77 If you're taking sertraline and duloxetine together then you're actually pretty much taking a potent SNDRI (serotonin-norepinephrine-dopamine reuptake inhibitor). Zoloft is already a fairly potent at serotonin, but it also modestly inhibits the dopamine transporter. The real effects of that are seen more at higher doses. HOWEVER, because duloxetine is potent at norepinephrine and norepinephrine and dopamine are both catecholamines, increasing norepinephrine could have a downstream action on dopamine. So in that regard, sertraline+duloxetine in low doses could be synergistic. However, they are both extremely activating relative to other options. @argh made a good point that perhaps you should be looking at TCAs. In a perfect world, your pdoc increases the Depakote to a healthy level (let us know, btw when you do the lab work and what your valproic acid level comes back as), then you remove Zoloft and Cymbalta to try to stabilize a bit. Then, perhaps, your doctor may be willing to let you try amitriptyline. It can be very effective in small doses like 10-20mg at bed time. It has anti-histamine actions which should assist with sleep, and it will help to combat any new depression that might be caused by the Depakote. This leads into another important discussion. If you start to feel new depression since starting Depakote, talk to your pdoc about it, and don't just stop taking it. There are changes he could make to try and improve your mood. Adding amitriptyline at night like I suggested is one option, but another option which can have very positive effects on mood is ziprasidone (Geodon) like 20-40mg at bedtime. When it's used to control mania, it's dosed closer to 160mg but low doses can have a very positive effect on affect/mood.
  6. Careful though not to confuse Adderall's Afternoon Poop-Out with mood cycling. Adderall contains both levoamphetamine and dextroamphetamine. Levo has a stronger effect on norepinephrine, where dextro has a stronger effect on dopamine. However, levo has a longer half-life than dextro, which means that in the afternoon, dextro may have largely cleared your system, with the levo component still quite active. This is likely what is causing the zombie effect, but it isn't necessarily post-hypomania depression. ADHD and Bipolar disorder cross over more than you would think. They have high comorbidity statistics, but I'm not entirely sure of the number off the top of my head. I take Vyvanse with Depakote+Rexulti. One thing is for sure though, Depakote is the reason that I can tolerate Vyvanse long-term. Previously I would have to back down to a lower dose for a few weeks before increasing back to the usual dose because I would get tightly wound and stressed. Not since starting Depakote.
  7. According to Stephen Stahl's prescriber's guide, titration from Geodon to Vraylar should be overlapped by one week. However, you're on such a low dose of Geodon that it's hard to actually titrate. So perhaps you try to remove it after you've been on 3mg for a few days. Are you taking Vraylar morning or night? Your fogginess could also be the increased clonazepam dose. My partner always feels that way after his pdoc raises his clonazepam.
  8. Vraylar is definitely activating for sure. You're on 3mg at this point, right? Maybe you need to step down to 1.5mg.
  9. I took a moment to look back on the meds you took and how you described the "tension". That COULD be antidepressant-induced hypomania, but you may also be one of those people who is genetically predisposed to not respond well to antidepressants. Most modern antidepressants inhibit the serotonin transporter which is encoded by a gene called SERT (or SLC6A4 if you're feeling fancy). This gene has several different SNPs (single nucleotide polymorphisms) which alone may not have much effect, but together can be formidable. On the SERT, you can have a long or short allele, which I won't get into in great depth, but it's most important to know in this context specifically that short means less transporter, and long means a normal amount of the transporter or more than most. The ratio of shorts to longs varies from person to person. I have 3-4 short "repeats" which predispose me to lower levels of the serotonin transporter. Therefore, inhibition of the transporter with an SSRI should theoretically be bad, right? Not necessarily. The only correlation that they've been able to find is that people with a few repeats of the short allele are USUALLY more likely to have tolerability issues with antidepressants, but even that is inconsistent, and some people with several short repeats may have tolerability issues in the beginning but may respond really well with long-term treatment. I for example always eventually fall into depression without antidepressants, but without mood stabilizers, antidepressants make me worse. So it's about finding balance. However, if you are one of those people who does adhere to the statistic, then you may do better on something like mirtazapine. Because you've tried a fair amount of medications already, doing genetic testing may be useful, but not ones that just look at drug metabolism. There are better ones like GenoMind that look into some of the genes that encode brain functions as well. They really aren't perfect. There have been so many stories of people who take the test and then try a medication that the report says they will do well with, and ultimately they find that it wasn't a match. Pharmacogenomics is still kind of an art more than a science. We just don't know enough yet to really be entirely sure what will stick.
  10. I think I can actually answer this. I've done a lot of research on valproate and lamotrigine since I'm taking both of them right now. They do work differently, and I'll try to explain it. A primer though. Glutamate and GABA are effectively "opposites" and they form a see-saw in the brain. Glutamate converts to GABA and GABA converts back to glutamate. Activating GABA receptors reduces glutamate release and increased glutamate signaling would reduce GABA signaling. Glutamate is activating. GABA is inhibiting. Valproate works at both ends of the GABA/glutamate see-saw. It increases the conversion of glutamate into GABA and then inhibits GABA's breakdown back into glutamate. The increased levels of GABA in the brain result in lower glutamate signaling, which is hypothesizes to be one of the core reasons why valproate is so effective for mania. Other reasons would be that it induces MAO-A which would encourage the metabolism of excess serotonin and inhibits the synthesis of catecholamines like norepinephrine and dopamine, which could contribute to mania or depression. Lamotrigine works a bit differently. It reduces the RELEASE of glutamate from neurons. By reducing glutamate signaling, it too could potentially increase GABA signaling by suppressing the glutamate pathways. It's a different mechanism of action altogether. Therefore, valproate and lamotrigine can be combined to create a pretty formidable cocktail (I mean that in the best possible way). A study was done where the patients in the study were given both valproate and lamotrigine for the first half. Then for the second half, lamotrigine was replaced with placebo for half the patients. The patients who had lamotrigine replaced with placebo said that they preferred the valproate+lamotrigine combo over valproate alone. This was a double-blind trial meaning the doctors and the patients didn't know whether they were on the valproate+placebo or valproate+lamotrigine for the second half of the trial. Another interesting point is that the metabolism of neurotransmitters like GABA and glutamate occurs intracellularly (inside neurons). This metabolism is responsible for the conversion of glutamate to GABA and GABA back to glutamate. By taking lamotrigine, you reduce glutamate release, leaving more in the cells for valproate to do its job which is to convert that excess glutamate into GABA and "lock it in" that way to keep it from converting back to glutamate. To answer your other question, the one medication that is most similar to lamotrigine in regards to actual mechanism of action would be topiramate (Topamax). However, there is far less evidence in favor of its use in bipolar disorder than there is for lamotrigine.
  11. My mother-in-law has developed sleep issues in older age. Her pdoc told her to take Klonopin about an hour before she goes to bed. Like 0.5mg, then if she wakes up around 4am when she usually does, take a Xanax and go back to sleep. Because Xanax is shorter acting, it's less likely to leave you groggy when you wake up if you take it in the early morning unlike taking another Klonopin which would make you feel like a zombie when you wake up.
  12. Klonopin actually has a half-life of 19-60 hours and a duration of effect of 6-12 hours. For that reason they never made an extended release version. It has one of the longest half lives of benzos.
  13. 600mg of Depakote isn't necessarily a low dose. My pdoc says "1000mg is the average dose". He also doesn't put as much stock in blood levels and doses based on symptoms and references the blood level if there is an issue. A "therapeutic" level of valproic acid is 50-100mcg/mL with the level for acute mania being more like 80-100mcg/mL. A 600mg dose of Depakote will likely not yield these concentrations, but it does depend on weight. I take 1250mg of Depakote, but I'm also 6 feet tall and weigh 210 pounds. I have a level of around 69 right now. More than likely 600mg isn't the target dose unless your doctor is more progressive in their thinking and will dose based on response. The "therapeutic" blood level isn't necessary for everyone and for those that require it, it may not be necessary for the entire duration of treatment. Some adjustments may be temporary. So it would be good to go along with your pdoc and see how this goes. When I was first diagnosed with bipolar 2 disorder, my pdoc cut my Cymbalta from 60mg to 30mg and immediately started Lamictal. Then we used Prozac to titrate off the Cymbalta entirely, then discontinued the Prozac. Unfortunately, after trying the usual treatments for bipolar disorder, we did find that my depressive episodes return almost invariably every Fall/Winter if I'm not taking an antidepressant. So going off antidepressants now doesn't necessarily mean you can't take them later if the situation warrants it.
  14. You aren't depressed and you aren't "up". You're in between, right where you should be. Being interested to the point of excitement and pouring large amounts of energy into your interests COULD be a sign of bipolar disorder but on its own isn't necessarily. It's when your latest obsessions start to eclipse all else that it starts to border on bipolar. People with bipolar 1 often have issues holding down jobs because their mood swings are too extreme. People with bipolar 2 on the other hand could be very high functioning individuals, sometimes quite intelligent. However, their condition doesn't regularly impede normal functioning in the world like getting out of bed and going to work or meeting your other non-work obligations that way that it can in bipolar 1 disorder. Interestingly enough, people with bipolar 2 disorder in particular seem to have prominent impulsivity issues which translates into a high rate of suicide attempts. Additionally, bipolar 2 disorder can go undiagnosed for a while. I knew in 2004 I had mood issues but wasn't appropriately diagnosed as bipolar 2 until 2013. Everything changed when I started taking the appropriate medications. I take a combination of Depakote and Rexulti as a mood-stabilizing backbone but the core of it is really the Depakote. I have a tendency to rapidly cycle and become mixed, and it does suit me better per the evidence in its favor for these kinds of conditions. Rexulti has positive effects on my depression and anxiety and also calms intrusive or racing thoughts when I get a little "wobbly". I'm also currently taking Lamictal as a preventative measure against depression and added mood stabilization. However, I'm likely going to be going back to Trintellix at my next appt, which is what I was on previously, and it worked quite well. Lamictal hasn't been cutting it for my depression going into Fall/Winter.
  15. I can't find much data on the metabolites. It looks like pharmacology data for them is on file, but you have to have a subscription to some of these sites to get access to the articles because they're so new and haven't been released freely for public consumption. However, what I have been able to find is that desmethylcariprazine and didesmethylcariprazine both have pretty similar pharmacology to cariprazine.