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About browri

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  • Birthday 05/14/91

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    Bethlehem, PA

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  1. The longer the half-life of a medication, the more patience you have to have, unfortunately. But some are so worth it. I realized that with Trintellix (66 hours) and Rexulti (91 hours, 86 for metabolite). When I was on them for a few weeks, I finally started to see improvements. I'm so glad that your husband has been improving. Keep faith!
  2. it's not for everyone though. For the longest time, I was very resistant with my pdoc as well for the same reason. Part of it was not accepting my bipolar 2 diagnosis and beyond that accepting that I might be a part of the large majority of people with bipolar disorder who require 2-3 medications to maintain and look where I am now lol. In all seriousness though I've been considering doing some trimming to my meds because of the same concerns that @Steve223 has
  3. oh don't get me wrong I feel mentally dull a good portion of the time How long have you been at a .4 blood level? @tommy215 how did your appt go?
  4. Fingers crossed that the appt goes well. I have read of other people's experiences that they have some confusion whether to take it morning or not because of the insomnia and it works out differently for each person. I would guess the idea behind taking it at night is it's at its lowest when you fall asleep and it's building in your system while you're sleeping so you're near peak levels when you wake up. As opposed to taking it in the morning, which with the long half-life would make for much higher levels around the time you're trying to go to sleep. But I would think it would be important to take it right before he goes to sleep and not a few hours before with dinner or something because then you have the chance of levels being higher when it's time for bed.
  5. And this is the value in GeneSight folks. They have built their business around doing a saliva test that everyone else is already doing and then furnishing doctors with reports full of information that it would have taken that doctor HOURS to glean from raw genetic data through a manual process of pulling up and reading scientific studies PER SNP in your genome (which I will remind everyone is composed of 10 million SNPs, granted the doctor in this case would only be looking at ~30 of them for a detox analysis, but still). In the end, if your insurance will pay for it in full and you have had issues responding to certain medications, you should definitely do it. If insurance only partially covers it, and you end up coughing up $50-200 in coinsurance, then you might as well do genetic testing through AncestryDNA or 23andme who are going to test more of your genome and furnish you with more information than a company like GeneSight, which only cares about specific parts of your genome. If you don't have Medicare or Medicaid and your private insurance won't cover it in full, do the Ancestry test for the fun of it and use that data for the Detox Analysis at GeneticGenie. If there are any missing that might be suspect, you can get the 23andme test done and try the report with that data instead. If you want to start out doing just one of them, I would recommend Ancestry. They actually test more SNPs than 23andme does. So your GeneticGenie reports will be more complete with Ancestry data. Their AncestryDNA tools and overall historical information are much more thorough than the ancestry info provided by 23andme, which is generally speaking more technical. Additionally, Ancestry breaks down into more specific regions than 23andme does and that's because Ancestry overall has a much larger "pool" of genetic data for reference. Will point out one critical difference though between GeneSight and Ancestry/23andme speaking specifically about the USA but may be pertinent in other countries if GeneSight is available there: GeneSight is bound by HIPAA thus they are legally obligated to protect your genetic data in a fashion that is consistent with the rest of the medical industry. And your data is subject to doctor/patient confidentiality. Ancestry and 23andme on the other hand are only bound by their Privacy Policy, which they can change as they see fit unlike a law which is quite a bit more rigid. Additionally, law enforcement can subpoena Ancestry or 23andme for your genetic data. So as you can see there are risks that I had to put out there as a disclaimer. As for me and Rexulti, we're getting along just fine. Today is 6 weeks on the dot at 0.25mg and overall the decrease really helped. It doesn't help with outright mania but it has had a positive effect on my depression and it keeps my mood relatively level more akin to Lamictal than Depakote. That being said Rexulti and Depakote together seem to be a good mood-stabilizing combo
  6. What dose did he start on, and how fast did he go up? Vraylar has a long half-life so you have to take the same dose for a while to build to a stable level. The parent drug cariprazine can take 11 to 28 days to reach steady state, and its metabolites can actually take 10-14 weeks beyond that. So it's important to start low and go slow because side effects may show up later and get worse before they get better.
  7. Yeah in my experience the nausea happens in the beginning at 5mg and 10mg but I didn't have any issues going to 15mg or 20mg. Continue to keep us posted!
  8. How long were you on 10mg before going up to 20mg? You should start to notice some change over the next 3-4 days but full effects may take up to 2 weeks in my experience.
  9. Have things gotten somewhat better since switching the Saphris back to Vraylar?
  10. You're welcome @spyker. Sorry that it can be a bit of a brain dump. I can sometimes get a bit carried away It's worth pushing past the 5mg. The stimulation at the higher doses reduces some of that fog.
  11. That's really messed up. One thing is for sure. DO NOT mess with my Vyvanse. I've concluded it's the only reason I can tolerate all of the other medications. I would be a worthless PoS without it.
  12. Yeah 300mg is a big jump. That might be where you see the energy boost. And yes it doesn't surprise me that Wellbutrin has ruined caffeine and food for you lol. It definitely has that effect. How many days now on 150?
  13. @dcfla good luck with the 5mg. Hope it works out for you. Keep with it.
  14. serotonin is the "easy" name for 5-hydroxytryptamine which you may see abbreviated as 5-HT. The space between two neurons is referred to as the synapse, and the surface of each neuron is covered with receptors. On the sending neuron, they are referred to as pre-synaptic receptors and on the receiving neuron, they are referred to as post-synaptic receptors. These receptors are designed to only accept one kind of neurotransmitter whether that be serotonin, norepinephrine, acetylcholine, dopamine, histamine, glutamate, etc. Okay. So for the sake of example, we'll just talk about serotonin. Serotonin can be broken down into several receptor subtypes. When serotonin binds to receptors, it has an effect. But the TYPE of receptor will determine what kind of effect that it has. 5HT3 is generally associated with nausea. So Zofran, being a potent 5HT3 antagonist (blocker) is prescribed for nausea, especially in cases of pregnant women with morning sickness. However, if you take a 5HT3 AGONIST (activator), you would experience the opposite effect, becoming nauseous and even vomiting. To further complicate things, these different types of serotonin receptors can have different DOWNSTREAM actions based on whether or not the receptor type in question is a heteroreceptor or an autoreceptor. Heteroreceptors accept one type of neurotransmitter and have a downstream effect on DIFFERENT neurotransmitters. Using 5HT3 as an example, blocking the receptor actually causes the downstream release of norepinephrine, dopamine, acetylcholine, and histamine. The histamine release in particular is why some people feel itchy when they start Trintellix. However, the 5HT1A receptor is an autoreceptor. When you block presynaptic 5HT1A receptors, it causes the release of MORE serotonin instead of affecting other neurotransmitters. If you activate presynaptic 5HT1A receptors it DECREASES serotonin release. The same effect would be had on norepinephrine, dopamine, acetylcholine, and histamine if you activated 5HT3, they would decrease. Back when SSRIs first came out, the psychiatric community operated off the naive theory that all you had to do was increase serotonin levels in the brain to "cure" depression. So they went from tricyclics to SSRIs which inhibit SERT (the serotonin transporter, which could be described as a chemical envelope that carries serotonin from the sending neuron to the receptors on the receiving neuron, sometimes abbreviated as 5-HTT instead of SERT). This did in fact increase serotonin in the synapse but it had the negative effect of having an agonizing or activating effect at virtually all serotonin receptors. Newer medications like Viibryd and Trintellix operate off a more learned assumption that while increasing serotonin in the brain does help with depression, activating a bunch of serotonin receptors needlessly can cause a lot of side effects and even possibly make some parts of depression worse, like anhedonia. Blocking 5HT7 can reduce SSRI-induced insomnia and sexual dysfunction. Activating post-synaptic 5HT1A and blocking pre-synaptic 5HT1A increases serotonin release and stimulation, and it also seems to decrease the time it takes for an antidepressant to start working which is why Trintellix and Viibryd can start working quickly if you do titrate up rapidly. SSRIs activating 5HT2C can reduce appetite and in some cases cause SSRI-induced anorexia. Blocking this receptor can improve appetite, but it can also cause weight gain (e.g. Remeron [mirtazapine]). The same theories are being applied to antipsychotics as well. Blocking dopamine receptors cause restlessness. So let's block a serotonin receptor that increases dopamine release in areas of the brain that are associated with restlessness. Thus the atypical antipsychotics were born. With the exception of Abilify, Rexulti, and Vraylar (EDIT: Also Latuda), all of the atypical antipsychotics have more and stronger activity at the 5HT2A receptors than dopamine and thus they generally have a much lower rate of movement disorders like restlessness than their older, typical cousins like Haldol and Thorazine. To complicate this a bit further, if activating certain serotonin receptors can effectively inhibit release or reduce the levels of neurotransmitters like dopamine, this can explain why some people experience anhedonia on some of the original SSRIs. Anhedonia might not be a symptom of your depression at all and you start taking an antidepressant, and everything gets better, but you're left with a feeling of total apathy and lack of pleasure for anything. The way Trintellix blocks certain serotonin receptors should in theory DISINHIBIT the release of certain important neurotransmitters and provide for a more thorough/well-rounded antidepressant response instead of the overactivation of serotonin leaving you feeling emotionless.
  15. Yeah I've heard that Trintellix causes GI disturbances for some people. It hasn't bothered me at all but I have heard for some people it causes diarrhea and for some people it causes constipation. About 80% of your body's serotonin is located in the gut. One of the serotonin receptors that is plentiful in the gut and is responsible for nausea is 5HT3. Trintellix even at its lowest doses blocks the 5HT3 receptor pretty potently. It binds to those receptors more potently than any other receptor it touches. The only thing it does more strongly is inhibit serotonin reuptake like any other antidepressant. Note that at higher doses, Trintellix becomes a fairly potent full agonist of 5HT1A which might move the constipation in the opposite direction and INCREASE gut motility making it easier for you to poop. Not entirely sure on this theory because Trintellix didn't have any effect on my gut that I can recall and doesn't at this point having taken 20mg now for a few months. Viibryd is another medication that is both an SSRI and 5HT1A agonist (partial only, not full, but intrinsic activity of ~60-70% which makes it pretty close to full). In my memory, Viibryd made my gut really active. I could have conversations with it because it was always gurgling throughout the day. It was pretty audible to other people too and fairly embarrassing. I also had chronic diarrhea. They're saying that Viibryd may be good for people with IBS, particularly IBS-C. Something to consider if Trintellix doesn't work out. Keep drinking lots of water and taking your Metamucil and keep trying to increase the Trintellix assuming your constipation doesn't get any worse. You may find some relief at higher doses. Some of Trintellix's activity only happens at higher doses and could reverse some of what you're experiencing.