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browri

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About browri

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  1. Rexulti has been wonderful for my depression. However, I'm still feeling out whether or not it's strictly relegated to the lower doses or not. I had to start low and go slow similarly to Abilify (which I could NOT tolerate). Started at 0.5mg for 2 weeks and that was TOO much. We went down to 0.25mg for 6 weeks then increased again to 0.5mg and it was totally different the second time around. I'm now on 1.5mg but dropping down to 1mg tonight because I've been feeling some Winter depression. Rather than take a risk by increasing the Trintellix, we're going to try peeling back things to clear my head a bit and regroup. All-in-all though, I LOVE Rexulti. This is after Latuda, Saphris, Fanapt, Abilify, Loxitane, Zyprexa. If I had to pick a second choice after the Rexulti, Zyprexa would be it. Both cause weight gain, but with Rexulti it's been WAY less of an issue than with Zyprexa. My blood sugar and lipids are more under control too.
  2. Of the ones I've tried, Rexulti and Zyprexa tie for the top. I usually respond fairly well to -pines, but Rexulti was the first time that I was able to get outside of that box. In a crisis scenario, I would probably go back to Zyprexa, but Rexulti has worked so well for me, I see no reason to at this point. EDIT: Saphris wasn't half bad either. Only thing is it gave me HORRIBLE hiccups. I don't know how or why, but it did.
  3. I personally didn't have too much nausea from Trintellix. It felt more like an overly-acidic stomach to me. But not like I was going to vomit. Alcohol and cannabis haven't been an issue for me.
  4. browri

    Adderall to vyvanse to adderall

    Yeah I never found Adderall to really be mood-boosting the way that Vyvanse is. Vyvanse makes me feel more social whereas Adderall makes me more grouchy.
  5. browri

    Adderall to vyvanse to adderall

    It can take some time for levels to build. With Vyvanse, you were already taking dextroamphetamine. So you likely already have steady levels of that. Switching from Vyvanse to Adderall, you now have to build up levels of levoamphetamine which has a longer half-life than dextro and therefore can take a bit longer. But still only about a week. So expect the first week to be more energy and motivation. Perhaps a little amped. Then it calms down after a week.
  6. It's not THC you should be focusing on. It's CBD. The other cannabinoid that's been getting a lot of attention. It's actually a dopamine partial agonist like Abilify, Rexulti, and Vraylar. It modulates dopamine activity like an antipsychotic. I only bring in THC to the mix because when atypical antipsychotics block 5HT2A it also increases dopamine release as when THC activates CB1. So theoretically, cannabis strains with low THC and high CBD could theoretically provide control of mood disorders. Well risperidone will certainly help if some emotional blunting is what you need. But it can also improve emotional blunting for some people in low doses. It's possible that risperidone could increase your nicotine buzz because risperidone can block adrenaline receptors thus enhancing adrenaline release and possibly a deeper buzz. Not sure. Grasping at straws.
  7. Haha yes I understand. Good analogies are so hard to find these days!
  8. You're right. It is really confusing. Consider what you pointed out about risperidone's higher affinity for 5HT2A than D2. Antagonism of 5HT2A leads to downstream dopamine release. And with a higher affinity for that receptor than for D2, there theoretically would be more dopamine release than blockade at lower doses. And of course keep in mind that as you said, the pre-synaptic D2 receptors are auto-receptors so antagonism will lead to MORE dopamine release. In a way, dopamine blockers and modulators can enhance the effects of THC. Cannabis already does this now between THC and CBD. THC binds predominantly to the CB1 receptors which are concentrated mostly in the brain. This leads to dopamine release. CBD on the other hand binds predominantly to CB2 receptors which are found pretty much everywhere else in the body but are strongly focused on the surface of white blood cells. Activation of CB2 receptors reduces inflammation caused by our immune system, which is why CBD can be used in certain inflammatory or auto-immune conditions with great effect. Now bring in the cannabis entourage effect and you have a party. Not only does CBD bind to CB2 receptors, but it also binds to D2 receptors as a partial agonist like Abilify, Rexulti, and Vraylar. With THC increasing dopamine release through activation of CB1 receptors and CBD modulating that dopamine activity by binding to D2 receptors, you kind of have yourself an atypical antipsychotic don't you? Pure THC administered via IV caused patients to experience psychotomimetic effects akin to something like drug-induced schizophrenia. However an even 50/50 administration of THC/CBD caused no such effects. Cannabidiol does in fact prevent the psychosis-inducing effects of THC. But there is something else that it does in the process that every stoner would be familiar with: couch lock. Cannabis strains with high THC content and negligible CBD can actually be quite activating, but as you introduce more and more CBD, the strain becomes more sedating. CBD on its own can't cause couch lock, but THC and CBD together can be formidable. So really when you feel stoned and sluggish because of your AAP, just think of it as couch lock, the feeling you get when your synapses are flooded with dopamine and the door on the far side of the synapse is locked! Risperidone on its own certainly would reduce serotonin activity. However, when you mix it with an SSRI, it kind of does the opposite. Remember that many of those serotonin receptors pre-synaptically are auto-receptors. This means that blockade leads to serotonin release. If you mix this with an SSRI, inhibiting the transporter would perpetuate risperidone's activity and vice versa. Risperidone sees to it that more serotonin is released into the synapse and the SSRI makes sure that it stays there. An SSRI on its own does slowly over time increase serotonin in the synapse, but this leads to a lot of activation of receptors that possibly shouldn't be activated like 5HT2A. Activation of some of these receptors slows down serotonin release, like an automatic shut-off valve when flow is too high. Risperidone makes sure a dysfunctional shut-off valve doesn't shut off serotonin outflow prematurely and ensures stability between the serotonin and dopamine systems. Increasing serotonin and not blocking any of the serotonin receptors would lead to inhibition of dopamine release. This is where the SSRI startup effects like insomnia come from. An out-of-balance system where serotonin is high and dopamine is low. Dopamine is supposed to be the calming chemical that provides reward and positive reinforcement to the things that we do. With SSRIs, anhedonia (or loss of ability to feel pleasure) is a hard symptom to crack because it's the one thing that doesn't seem to get better (exception being Wellbutrin/bupropion) unless you add an AAP, which will rebalance the serotonin and dopamine systems after an SSRI has been introduced. Highlighting on 5HT2A and psychosis, one of our most potent hallucinogens is LSD being a super high affinity 5HT2A agonist with a long-acting binding constant. Some receptors are tricky ones though. While 5HT2C does lead to norepinephrine and dopamine release when blocked and thus antidepressant effect, blocking it also makes you feel hungry. That particular receptor is connected to satiety. 5HT7 is one of the new favorite receptors to antagonize because it can improve SSRI-induced sexual dysfunction. It can also eliminate insomnia by correcting the circadian rhythm. By correcting the sleep cycle, it lends to antidepressant effect. @HydroCat to understand an inverse agonist, just think of it on a number scale of 0-100. An antagonist has no intrinsic activity at a receptor and thus its number would be 0. A partial agonist at D2 like Rexulti would be a 45. Abilify would be a 60. An inverse agonist is essentially "below 0". Said another way an agonist pushes a mechanism forward, whereas an inverse agonist is like a hypothetical "vacuum". Antagonizing a receptor has a certain effect. An inverse agonist would just have an even more strong of a downstream effect than an antagonist. In the case of 5HT2C for risperidone, it does truly just mean even more norepinephrine and dopamine release downstream than would be rendered by simply blocking the receptor. It's like the receptor essentially works "in reverse".
  9. I've always found this to be the case since starting to take AAPs. Pot is definitely more intense. Makes for a lot of calming dopamine release between an AAP and cannabis This does sound more like akathisia for sure. Curious. Does it seem to "calm down" when you smoke? Are you able to sit still more? This may reinforce the akathisia theory. One of the components in cannabis, cannabidiol, is a negative allosteric modulator of acetylcholine receptors which may assist with restlessness.
  10. Glad the recommendation worked out for you! Funny you mention SAD, I'm amazed myself at how well Trintellix squashes winter depressions. Wellbutrin did work but I just couldn't handle the anxiety as a side effect. Talk to your pdoc about trying the 20mg. Maybe it could work for you. Best of luck! Interesting you mention the patent. Takeda and Lundbeck's initial 5-year marketing exclusivity was supposed to end in September (even though the patent goes for much longer). They managed to get it extended because of the results from the clinical trials that showed Trintellix improved cognitive function in people with depression. Now the marketing exclusivity is up in May of 2021. So no Trintellix generic for a while unfortunately However, if you can get through a prior auth with your insurance, with the savings card on a 30-day prescription, you pay the first $10, they pay $100, then you pay the remainder. So it may help with the cost, but I know that if Trintellix isn't even on your formulary, a prior auth'd copay can still be horrendous.
  11. Quite the contrary. I think it would make sense to do the combo of valproate+Cipralex+Rexulti if Rexulti is available to you. The worry with eliminating Cipralex is that valproate and Rexulti on their own might not be enough for depression. But more than likely you'll find that Rexulti tones down a lot of the tension you're perceiving from Cipralex.
  12. It is that time of year, and I found I needed the 20mg in the winter time. However it was pretty stimulating for me so I couldn't stay on it as we got towards Spring. It made me a bit mixed to be on that high a dose. We have optimized my Rexulti and Depakote doses since then though so it could be totally different now for me. Of course your mileage may vary. Last time taking Trintellix, I didn't really start to feel better until 15mg. But 20mg really did make a difference. I just personally don't need 20mg at this point
  13. Yeah that would have been like 20mg at that dose, which packs quite a punch on its own but with Wellbutrin, woah.
  14. Getting to the basics. When a compound binds to a receptor; whether the compound be a neurotransmitter like serotonin, norepinephrine, or dopamine or a drug like Rexulti, it has some sort of activity at that receptor. Receptors in the brain for the most part are named for whatever naturally occurring substance binds to it with 100% intrinsic activity. Serotonin receptors are named as such because serotonin binds to them and has 100% intrinsic activity. This would make it a full agonist of the serotonin receptors. Rexulti has near 100% intrinsic activity at 5HT1A making it also a full agonist there. However, for 5HT2C it is a partial agonist because it does not have 100% intrinsic activity at that receptor the way that serotonin does. Partial agonists have some blocking effects and some activating effects. So the best analogy is to think of receptors like light switches. An agonist turns the light switch on. An antagonist turns the light switch off. A partial agonist is like replacing that regular On/Off switch with a dimmer switch instead and running the lights on a lower setting. You still get light, but not TOO much light Cipralex (escitalopram) does not bind to receptors. It only binds to the transporter. So if you think of two neurons as islands in the brain, and receptors are ports or piers where the boats can dock, the transporter would be the boat. The boats take serotonin across the lake from the pier on Island A to the pier on Island B, then the boat is released back into the ocean to return to Island A. Only Cipralex slows down this process making more serotonin persist in the water between the two islands. Over a long period of time, this results in more activity at the piers on Island A and Island B, and the net result is less depression. However Cipralex does not do its work "at the piers" like you are suggesting. In fact, Cipralex is regarded as the "most pure SSRI" in that regard. Rexulti blocks adrenergic receptors in the brain. The net result is fewer adrenergic symptoms. Like the tense feeling in your chest when you're on edge. Sudden rise in heart rate in stressful situations. When I started Rexulti I was going through kind of a traumatic time back in September 2017 and developed some mild PTSD from it. I'm getting better, but Rexulti has helped to make me feel calmer from an adrenaline perspective. It's very good for anxiety and panic in my personal experience. BPIII isn't really a thing. What you've described does sound like SSRI-induced hypomania, but if you continue to control with valproate that should improve over time. Your symptoms collectively seem more like BPII since you seem to be high functioning and you've gone undiagnosed for so long. People with BPI typically are diagnosed earlier and correctly on the first try, whereas over 50% of BPII cases start out as some other diagnosis.
  15. Rexulti is stronger at both serotonin and adrenergic receptors. What this means for therapeutic effect isn't as clear at this point because these two meds are so new. However, it seems like Rexulti is garnering a reputation as an antidepressant because of it's potent effects at serotonin receptors. Its effects at adrenergic receptors may explain its positive effect on PTSD. Prazosin is used as an adrenergic blocker for PTSD and Rexulti has similar actions. This being said, I do believe that Vraylar is "closer" to getting approval for bipolar depression. Rexulti is still in trials for bipolar mania, where Vraylar got that indication at launch with its schizophrenia indication. Just know that Rexulti was the one that got the indication for adjunct to an antidepressant for MDD and seems to have better data in favor of its positive effects on mood. I took Trileptal before switching to Depakote and I found that it didn't control the "tensions" that you describe. It was very calming. Pretty effective. But not as effective as valproate for mania. Valproate generally doesn't have any antidepressant effect, and if you are feeling less depressed, it is almost definitely from the Cipralex even if it is causing you tension. Trileptal (oxcarbazepine) can have some antidepressant effect for some people. It was "soothing" to me. No other way to really describe it. However, I feel like I have fewer cognitive issues on valproate. Trileptal made me confused sometimes. More so than Lamictal which only gave me issues with word recall. With Trileptal, I sometimes had to have people explain something to me 2 or 3 times before I got it. It got a lot better as I adjusted to it, but it was a bit weird in the beginning. Although from what I understand, it doesn't come close to Dopamax (topiramate). At low doses like you're taking probably not. Really the most important part of valproate blood testing other than the therapeutic blood level itself is liver monitoring to make sure your body is handling it well because valproate can cause liver toxicity for some people. I haven't had any issues and I have a blood level of 69mcg/mL
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