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Hi everyone :)

I have serious Bipolar II depression, and my pdoc recently put forth the idea of trying a new drug, Trintellix (Vortioxetine). It hasn't been on the market for very long, and as the old adage goes, "Wait for a new drug to be out for 7 years before you take it." Well, this one has been on the market for 3, so I'm trying to learn more about it and I'm having a hard time finding anyone who's actually taken the drug.

My main concern is the number of receptors it hits. First-generation anti-depressants typically only hit 1 receptor. Newer anti-depressants, like Effexor, hit 2. But Trintellix hits 7, and that worries me. It worries me because I'm prone to having withdrawals from just about every drug I've ever been on, and I am also medication-resistant, which means I go on a new drug, it may work for a few months, then it "poops out" and I have to come off it, thus experiencing the withdrawals. Effexor was awful to come off of, and it only hits 2 receptors. This new drug hits 7! :(

It almost reminds me of an atypical anti-psychotic in terms of how many receptors it hits. It's as if Big Pharma decided to package what is essentially an anti-psychotic as an anti-depressant to get away from the stigma that anti-psychotics have developed over the years given their side effects. When I came off of Zyprexa, I had the worst experience of my life and ended up in the emergency room. It took 2-3 months for the W/D to stop.

Is Trintellix anything like Zyprexa, or any other anti-psychotic for that matter?

From what I can tell, Trintellix hits 7 receptors, and Zyprexa hits 31 ... does that sound about right?

   

I got this from Wikipedia:

Trintellix:

Target Affinity Functional activity Pharmacodynamic action
Ki (nM) IC50 / EC50 (nM) IA (%)
SERT* 1.6 5.4 Inhibition
NET* 113 Inhibition
5-HT1A* 15 200 96 Agonist
5-HT1B* 33 120 55 Partial agonist
5-HT1D* 54 370 Antagonist
5-HT3* 3.7 12 Antagonist
5-HT7* 19 450 Antagonist
β1-adrenoceptor 46[6]

Zyprexa:

Receptor Ki (nM)[63] Biologic action and notes[64]
5-HT1A 2282 Antagonist.
5-HT1B 585  ?
5-HT1D 1061  ?
5-HT1E 2209  ?
5-HT2A 2.4 Inverse agonist. May underlie the "atypicality" of the newer antipsychotics like olanzapine. May contribute to sedating effects.
5-HT2B 11.9 Inverse agonist/antagonist.
5-HT2C 10.2 Inverse agonist. May underlie the appetite-stimulating effects of olanzapine.
5-HT3 202 Antagonist. Possibly responsible, at least in part, for its antiemetic action.
5-HT5A 1212  ?
5-HT6 8.07 Antagonist.
5-HT7 105.2 Antagonist.
α1A 112 Antagonist. Likely responsible for the orthostatic hypotension seen with its use.[64]
α1B 263 Antagonist.
α2A 315 Antagonist.
α2B 81.8 Antagonist
α2C 28.9 Antagonist.
M1 26 Antagonist. Likely the chief receptor responsible for the anticholinergic effects seen with olanzapine's use.[64]
M2 63.5 Antagonist.
M3 52.67 Antagonist. Possible role in type 2 diabetes side-effects.[65]
M4 17.33 Antagonist.
M5 7.5 Antagonist.
D1 70.33 Antagonist.
D2 3.00 Antagonist. Likely responsible for the therapeutic effects of olanzapine against the positive symptoms of schizophrenia.[64]
D2Long 31 Antagonist.
D2Short 28.77 Antagonist.
D3 47 Antagonist.
D4 14.33 Antagonist.
D5 82 Antagonist.
H1 2.19 Inverse agonist. Likely responsible for the sedative effects of olanzapine.[64]
H2 44 Antagonist.
H4 >10000 Antagonist.
   
     
     
     

So it appears that Zyprexa hits a whole swath of the brain that Trintellix doesn't touch, so it's not like Zyprexa or other anti-psychotics then? It's still overlapping over the same 7 receptors as Trintellix, which makes me think that tardive dyskinesia could potentially be an issue. Trintellix has only been out for 3 years, so the number of patients from whom such statistics would point to tardive dyskinesia are unavailable simply because not enough people have taken the drug. Zyprexa, by comparison, has been on the market for much longer and likewise we have better stats as to the likelihood of developing tardive dyskinesia.

Another thing, since it's so new, it hasn't been properly studied as to how it treats anxiety and OCD, both of which I have severely. Do any of you know if it helps with OCD/anxiety?

Have any of you taken Trintellix? Can you share your experiences with me, and if you had any withdrawals coming off of it?

Can anyone speak to the above information I provided regarding the receptors? If a single-receptor AD causes me W/D (such as Prozac), and a double-receptor drug like Effexor was even worse (way worse), what will a 7-receptor drug do? <_<

As always, thanks guys :)

troop

   
     
     
     
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i really dont' know too much about the way the medication works. but i am wondering why the insomnia iv been experiencing after a week at 10 mg of trintellix hasn't gone away yet. hoping that's not a bad sign. aside from that iv noticed very mild improvements in depression/anxiety symptoms and maybe some cognitive benefits too (difficult  to tell for sure right now)

have you seen this thread?

this link might help also: https://www.crazymeds.us/pmwiki/pmwiki.php/Meds/Brintellix

Edited by y1gFwo
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Keep in mind what really matters is how much affinity it has for each receptor. That is the Ki number, lower numbers mean more affinity. You might as well disregard receptors with a Ki in the thousands, their effect is infinitesimal. 

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I wouldn't get too hung up on the mechanism of action. Everybody reacts differently, so if you're not totally opposed to it, give it a shot. MoA is not a good way to judge a drug. 

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I'm not familiar with how drugs interact with different receptors, or "mechanisms of action." I know many of you are, which is why I'm hoping you can enlighten me on some of the issues I raised in the original post.

Honestly though, looking at the Brintellix- Is anyone else actually taking this? ... thread, it doesn't seem like anyone knows much at all about Trintellix due to its newness, which is what's frightening to me.

As always, thanks in advance! :)

Edited by troop111
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On 10/6/2016 at 1:12 AM, troop111 said:

[...] My main concern is the number of receptors it hits. First-generation anti-depressants typically only hit 1 receptor. Newer anti-depressants, like Effexor, hit 2. But Trintellix hits 7, and that worries me. [...]

[...] It almost reminds me of an atypical anti-psychotic in terms of how many receptors it hits. It's as if Big Pharma decided to package what is essentially an anti-psychotic as an anti-depressant to get away from the stigma that anti-psychotics have developed over the years given their side effects. When I came off of Zyprexa, I had the worst experience of my life and ended up in the emergency room. It took 2-3 months for the W/D to stop.

Is Trintellix anything like Zyprexa, or any other anti-psychotic for that matter? [...] 

[...] So it appears that Zyprexa hits a whole swath of the brain that Trintellix doesn't touch, so it's not like Zyprexa or other anti-psychotics then? It's still overlapping over the same 7 receptors as Trintellix, which makes me think that tardive dyskinesia could potentially be an issue. Trintellix has only been out for 3 years, so the number of patients from whom such statistics would point to tardive dyskinesia are unavailable simply because not enough people have taken the drug. Zyprexa, by comparison, has been on the market for much longer and likewise we have better stats as to the likelihood of developing tardive dyskinesia. [...]

[...] Another thing, since it's so new, it hasn't been properly studied as to how it treats anxiety and OCD, both of which I have severely. Do any of you know if it helps with OCD/anxiety? [...]

Can anyone speak to the above information I provided regarding the receptors? If a single-receptor AD causes me W/D (such as Prozac), and a double-receptor drug like Effexor was even worse (way worse), what will a 7-receptor drug do? <_<

7

 

Yes, Trintellix hits many receptors. It is an inhibitor of the serotonin transporter (SERT) (which is how it inhibits serotonin reuptake to increase serotonin levels in the synaptic cleft); a near full agonist at 5-HT1A (a serotonin receptor, which when an agonist for this receptor combined with SSRI action, more serotonin production is capable than with 5-HT1A agonism or SSRI action alone, is believed to accelerate the antidepressant response, is believed to have anxiolytic actions when agonized or "partially" agonized, and is believed to enhance dopamine release via downstream effects of agonism of postsynaptic 5-HT1A receptors) with an intrinsic activity of 96% (how "much" the receptor is activated by the drug in comparison to an endogenous ligand like 5-HT or serotonin, which would be 100%); a partial agonist at 5-HT1B (which are autoreceptors) with intrinsic activity of 55% (roughly half of serotonin), which I speculate would act competitively with serotonin and act kind of more like an antagonist, which would disinhibit, or "cut the brake line" for serotonin release from these neurons; a 5-HT1D antagonist (which are also autoreceptors), which has the same results as 5-HT1B antagonism/partial agonism with low to moderate intrinsic activity, which is disinhibiting/enhancing serotonin release; a 5-HT3 receptor antagonist, which induces release of norepinephrine and acetylcholine, and possibly histamine, dopamine, and serotonin too; a 5-HT7 receptor antagonist, which is thought to have effects on learning, circadian rhythm, and enhance serotonin release; and a β1-adrenergic receptor ligand (doesn't specify if it's an agonist or antagonist, so I can't say what it would do).

Trintellix is far from being like an atypical antipsychotic. An atypical antipsychotic typically has dopamine D2 receptor antagonism or partial agonism and serotonin 5-HT2A receptor antagonism whose affinity is near or greater than that of D2 antagonism (but not always). Trintellix has neither 5-HT2A nor dopamine receptor antagonism or dopamine receptor partial agonism.

Your chances of getting tardive dyskinesia from a serotonergic medicine are much less than getting it from an antidopaminergic drug (like an antipsychotic, typical or atypical). Trintellix does not antagonize dopamine receptors, which is believed to be the common cause of TD, so the worries of TD with Trintellix do not compare with that of the antipsychotics because they don't share the same mechanism of action believed to cause it. Now if you were taking the antidepressant amoxapine (Asendin), then things would be different—you'd have to worry about TD and EPS like akathisia and all that because it has "built-in" dopamine receptor antagonism with it and its metabolites.

As for its efficaciousness for treating anxiety or OCD, we know that serotonergic drugs like SSRIs and SNRIs and some of the TCAs are particularly effective in treating anxiety disorders, including but not limited to OCD, so we can likely safely extrapolate that since this drug is also serotonergic (with a few enhancements), it, too, may be able to treat anxiety disorders including OCD. Is it the best drug for these indications? We don't know yet. But it doesn't hurt to try it and see.

I can't say anything about its withdrawal effects. It says in the PI sheet, I believe, that if you're on 10 mg or lower, you can just stop taking it, but if you're on any higher dose than that, you must titrate down to 10 mg for a certain amount of time before ceasing it.

 

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Wow Mikrw33 you're a pro man! :goofy:

How do you know all of this? Are you a psychopharmacologist or psychopharmacology student?

I posted something a while back here on CrazyBoards about how there are some cases of Prozac causing tardive dyskinesia. Have you ever heard of that?

And thanks for such a greatly informed response! I don't understand a lot of it though because it's in science-speak.

Are you able to summarize, based on your pharmacological knowledge (and perhaps first/second-hand experience) of Trintellix, what this drug does in real terms? I admit my ignorance in this area, and I very much appreciate the time and effort you put forth in your response :)

troop

 

Edited by troop111
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Thanks :)

No, I'm just someone with a lot of free time and an interest in psychopharmacology.

It seems I've read of SSRIs, in general, being able to cause tardive dyskinesia, but I think the chances of that happening are far less likely than those of atypical antipsychotics.

I'll try to summarize its actions. Trintellix is a "multi-modal" antidepressant according to Stephen Stahl, and on Wikipedia, it calls it an SMS (serotonin stimulator and modulator). This is because it not only causes reuptake of serotonin (and subsequently raise serotonin levels) but also enhances serotonin release by actions at multiple receptors, as well as induce dopamine release (should help with affective brightening and the overall antidepressant response as well as possibly countering sexual side effects), norepinephrine release (should help the overall antidepressant response, help with attention and wakefulness, etc.), and acetylcholine release (should help with the brain fog and cognitive deficits associated with depression).

I've personally not had a good response from it, but my dad takes it and he seems to be getting a wonderful experience from it. He's bipolar type II (like me and I believe you too, but he doesn't grapple with depression as much as we do I don't think). It seems to have not only lifted his depression but also has a markedly positive impact on his cognitive functioning (which is currently declining as he may have dementia), and he seems less agitated and aggressive with it. He was on 20 mg but his (our) pdoc bumped him down to 10 mg because his kidney function wasn't doing so well (he has a bunch of health issues), and there was a noticeable difference in his behavior and even personality when she lowered him to 10 mg—next visit we're going to ask that she raise him back up to 20 mg since he was doing so well with it at that dose. It was a slow response, though, granted, he started at 5 mg and went up slowly. But after a month or so on 10 mg, there was a definitely a difference, and the real difference was noticeable at 20 mg. He tolerates it well with no side effects that he complains of.

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On 10/8/2016 at 2:02 PM, mikrw33 said:

I'll try to summarize its actions. Trintellix is a "multi-modal" antidepressant according to Stephen Stahl, and on Wikipedia, it calls it an SMS (serotonin stimulator and modulator). This is because it not only causes reuptake of serotonin (and subsequently raise serotonin levels) but also enhances serotonin release by actions at multiple receptors, as well as induce dopamine release (should help with affective brightening and the overall antidepressant response as well as possibly countering sexual side effects), norepinephrine release (should help the overall antidepressant response, help with attention and wakefulness, etc.), and acetylcholine release (should help with the brain fog and cognitive deficits associated with depression).
 

Thank you for this summary :) How do the things you've outlined here separate Trintellix from other anti-depressants in real terms? Does it just mean "It's supposed to work better," or do you have a better (different?) way to put it? Is this new drug a "game-changer," showing tremendous potential as compared to other ADs that do less?

I know the first generation of anti-depressants hit 1 receptor (Prozac, Zoloft, etc.), the second, and to my knowledge latest, generation of ADs (before the introduction of Trintellix, such as Effexor, Cymbalta, etc.) hit 2. Trintellix hits 7. I guess this means that the "newer" ADs (the newest-until-now generation, Effexor, Cymbalta, etc.) are now relegated to the old-school category given the introduction of Trintellix?

Regarding tardive dyskinesia  and ADs, I would think it would be exceedingly rare for someone to develop TD from ADs. Otherwise it'd be a known issue, just as it is so widely-known for anti-psychotics. But most people never associate TD with ADs, which tells me it's super, super rare. Do you agree?

I'm sorry to hear Trintellix didn't help you. Did you have negative side effects, or did it just not do the trick? I'm glad though to hear it's helping your dad. Regarding the kidney issue, is Trintellix potentially damaging to the kidneys (or any other organ for that matter), or was it more of an issue of your dad's separate health problems, unrelated to the Trintellix?

Thanks again! :)

troop

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This drug is intended to act in many different ways to treat depression via actions at multiple sites and receptors vs. just one or two, so in a way I guess if you wanted to say, yes, "it's supposed to work better," with the caveat that it may not work "better" for everyone. Some people may not respond to it at all, just as with all antidepressants. I don't know if I'd call it a "game changer," but it's definitely a trend in the positive direction in innovation as far as antidepressants go and how they work. In other words, it's not like Pristiq or Fetzima (yay, two more SNRIs...). Viibryd is very similar to Trintellix, but doesn't have the same actions at the same receptors. It's basically a SSRI + 5-HT1A partial agonist is about all, with "some action" at 5-HT2A and 5-HT2C, but I haven't been able to figure out what type of "action" (antagonist/agonist?).

The "first generation of antidepressants" would be referring to the MAOIs and tricyclics, the SSRIs and SNRIs are second-generation antidepressants. Just a little nuance in how to refer to antidepressants I guess. So the "older second-generation antidepressants" hit one or two receptors, sometimes more (Prozac is a 5-HT2C antagonist and a norepinephrine reuptake inhibitor in higher doses [3]; Paxil is an anticholinergic [6]; Zoloft is also a dopamine reuptake inhibitor and probably even a norepinephrine reuptake inhibitor in higher doses, a σ1 receptor agonist, and an α1 receptor antagonist [4-5]; Luvox was also a σ1 receptor agonist [2], Effexor in high doses is a dopamine reuptake inhibitor, too, making it a triple reuptake inhibitor [3]; Cymbalta is believed to have the same effect as Effexor [3]). The only one that truly hits just one site is probably Lexapro (the SERT), and maybe Celexa (SERT) (except it seems to have some antihistaminergic qualities that are somewhat prominent, which would make 2 binding sites). Whether these "older-newer" antidepressants have been rendered "old school" just because Trintellix has such a novel mechanism of action would be a question for a doctor. I personally don't think so, but that's just me.

Yes, I would be willing to posit that TD from ADs is an exceptionally rare occurrence. I agree with that statement.

I had negative side effects from Trintellix, but I think I'm going to give it another try and see if I can manage it. I never made it to 20 mg which is apparently where the magic happens for many people, at least that I've noticed. No it's not potentially damaging to the kidneys, she just wanted to take some load off of his kidneys where she thought she could (my/his pdoc). I'm not even sure if Trintellix is excreted by the kidneys at all. I haven't done any research into it.

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  • 2 weeks later...

Hi Mik,

Thanks for your great response and I apologize for my late one.

I'd love to get your opinion on something. I have withdrawals from everything, even Prozac (which is supposed to be WD-free, at least that's what many doctors believe). I had a very hard time coming of Effexor (which is known for bad WDs), but all my other drugs, save Zoloft, I've had very bad WD effects. It's my understanding that the more receptors a drug hits, the tougher the WD would be, hypothetically at least.

So, with Trintellix hitting 7 receptors (as compared to the 1 or 2 that other ADs hit), I'm very concerned that the WD would be unbearable for my system, as I tend to be prone to having WD from drugs. Do you have any thoughts about that?

Also, could coming off of Lamictal cause a rash? I know going up on the drug can, but I'm decreasing and suddenly I have all these skin conditions. I'm going to make a separate post about it in the Bipolar section of the forum, but I'd like to see if you know anything about that.

Thanks Mik, and you should really consider getting paid for your keen mind and knowledge regarding these matters :)

troop

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I've not heard of this theory regarding the more receptors a medicine hits the harder it is to discontinue. If that were the case, antipsychotics would be hell to discontinue! As far as Trintellix goes, the PI sheet says as long as you're at 10 mg, you can just stop taking it. If you're on anything higher than 10 mg, you need to titrate down to 10 mg for a week (I believe) and then D/C.

I don't know enough to say whether coming off Lamictal could cause a rash. Usually when a drug causes a rash, they discontinue it as rapidly as possible, so my personal uneducated guess would be no, but don't quote me on that.

Thanks troop. Lol I actually am considering becoming a psychiatrist. :)

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  • 3 weeks later...

You should Mik :)

As far as receptors and withdrawals, I weaned off Zyprexa and had such bad WDs I ended up in ER. Prior to ending up there, I went 11 days without eating, constant diarrhea, dry heaving, little to no sleep, and an AWFUL feeling that I can't describe. That lasted for months, and as you know Zyprexa hits many receptors. It would make sense logically that the more of your brain that's affected by a drug, the more WDs one would have.

Also, I've heard from others who take anti-psychotics, notably Seroquel, that if they miss a day or two it's like "coming off heroin."

I never trust what the drug companies put as the "official" way to "discontinue" a drug. They won't admit to withdrawals, just "discontinuation symptoms." They don't want to be sued.

What do you think of all this? I mean, the receptor thing seems logical, and based on the anecdotal evidence I've shared, the theory seems logical.

troop

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Another thing to remember when looking at the pharmacological profiles of these medications. Many people would look at the receptor lineup and say, "antagonist...well doesn't that mean it blocks serotonin". Sure, but when receptors are antagonized, the brain increases its serotonin output to compensate. In the end, serotonin release increases, activity at the antagonized receptors decreases, and activity at any other receptors that aren't touched by the medication would increase due to the brain's natural upregulation of serotonin caused by the medication at other receptors.

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  • 1 year later...

My wife is now on Trintellix.  We are not sure if this is related to Trintellix or possibly one of the other drugs that she was on but she has developed Tardiv Dyskenesia.  She was taking abilify but the doctor took her off of it assuming that this was possibly the cause.  It has been over 6 months now but still has the TD symptoms.  I am concerned is this a side effect of the Trintellix or is this something that was caused by the other medication and is irreversible.  

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  • 3 weeks later...
  • 2 weeks later...

I've been on this for about a week and a half now.  Taking 10mg at the moment.  So far this is working really well for SAD.  Until it kicked in I was starting to feel really depressed, the loss of energy, and wanting to sleep all the time.  Now the early evening is really not bothering me and I am staying up all day.  I have been able to function fairly normally and even lift weights pretty much every day.  Thanks to @browri for recommending this AD for SAD in another thread.  It's the first AD I have ever taken and had positive results.  It's pretty amazing how fast this has worked.  I am praying that this isn't just a temporary feeling. 

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4 hours ago, gb84 said:

I've been on this for about a week and a half now.  Taking 10mg at the moment.  So far this is working really well for SAD.  Until it kicked in I was starting to feel really depressed, the loss of energy, and wanting to sleep all the time.  Now the early evening is really not bothering me and I am staying up all day.  I have been able to function fairly normally and even lift weights pretty much every day.  Thanks to @browri for recommending this AD for SAD in another thread.  It's the first AD I have ever taken and had positive results.  It's pretty amazing how fast this has worked.  I am praying that this isn't just a temporary feeling. 

Amazing that this is working so well for you! I’m currently struggling with not being able to stay up all day and loss of energy and want to sleep all the time. I don’t know if depression is creeping in or not. But I have been keeping an eye on trintellix. I think I might call my pdoc about trying this med! I would do anything to be able to function through the day. 

Good luck to you and I hope it keeps on working well for you!

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15 minutes ago, Wonderful.Cheese said:

Amazing that this is working so well for you! I’m currently struggling with not being able to stay up all day and loss of energy and want to sleep all the time. I don’t know if depression is creeping in or not. But I have been keeping an eye on trintellix. I think I might call my pdoc about trying this med! I would do anything to be able to function through the day. 

Good luck to you and I hope it keeps on working well for you!

Thank you.  Try and give it a shot if you can.  I was skeptical at first but it's definitely working out for me so far. 

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46 minutes ago, gb84 said:

Thank you.  Try and give it a shot if you can.  I was skeptical at first but it's definitely working out for me so far. 

I called and left a message asking her if I could try it. I want to stay on top of things this year. We qualify for patient assistance even. No co-pays if I'm looking at the paperwork right. 

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I just started taking Trintellix a few days ago. I'm lucky that so far (although I'm not up to where she wants me yet), I'm not having any side effects. Fingers crossed that sticks. I'm really, really hoping it'll work for the OCD/anxiety.... I still have trouble calling it OCD, but I'm going to have to get past the denial one day.

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Is anyone on the patient assistance program? I don’t mean the copay card (which would still make this med unaffordable to me), but the patient assistance program? If you’re not on it you should look into it.

We qualify (if I’m reading everything correctly) and usually we make like a penny too much to qualify for any extra help but then can’t afford many meds either. It’s a sticky situation. Don’t qualify for help, but can’t afford a lot of meds either even with their copay cards. So I’m shocked that trintellix offers such a generous assistance program. But thankful they do!

Now here’s hoping my pdoc sees my plea and agrees that trying an AD is needed to help and also prevent things from getting even worse.

 

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  • 3 weeks later...

I started taking Trintellix on October 26th at 10mgs and decreased Prozac to 10mgs and nothing.  I still feel the same and I even stopped the prozac and increased the Trintellix to 20mgs and all I do is sit on the couch and stuff my face and cry.  I told the NP that it wasn't helping me and it enhanced my BED so much that my therapist wanted me to go inpatient to control my eating.  The NP put me on Vyvance and I started it yesterday.  It takes away my urge to binge but then I go all day without eating.  It also makes my thoughts all jumbled in my head so it's hard to get out what I want to say and then I get angry and I can feel my heart pound in my chest.  I feel like the older i get the more difficult it is to find a medication that will help me.  To be continued...

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13 minutes ago, Beth45 said:

I started taking Trintellix on October 26th at 10mgs and decreased Prozac to 10mgs and nothing.  I still feel the same and I even stopped the prozac and increased the Trintellix to 20mgs and all I do is sit on the couch and stuff my face and cry.  I told the NP that it wasn't helping me and it enhanced my BED so much that my therapist wanted me to go inpatient to control my eating.  The NP put me on Vyvance and I started it yesterday.  It takes away my urge to binge but then I go all day without eating.  It also makes my thoughts all jumbled in my head so it's hard to get out what I want to say and then I get angry and I can feel my heart pound in my chest.  I feel like the older i get the more difficult it is to find a medication that will help me.  To be continued...

sounds like the stimulant dose may be to high if your having racing thoguhts, anger, and rapid heart rate......just a thought, good luck

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  • 2 weeks later...

I love me some Trintellix. I started taking it in April, titrated from 5mg, to 10mg, then 20mg, and that's where I've been since June. Only side effect is some occasional nausea. It's allowed me to decrease my Rexulti from 2mg to 0.5mg and remain stable, although I did experience a mood shift with each step-down of the Rexulti dosage. I still think there is some sort of synergistic effect between the two drugs, because I went from 5mg Trintellix/2mg Rexulti to 20mg Trintellix/0.5mg Rexulti and have remained equally balanced, with fewer side effects, thanks to the decrease in Rexulti. I may try to step down to 0.25mg of Rexulti, but right now my life is too unstable to risk it.

Trintellix seems to be one of those drugs that you don't really notice is working until you've gone a few months and realize that your feelings are no longer irrational.

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Honestly I've tried Zoloft, Celexa, Lexapro, Wellbutrin, Viibryd, Pristiq, Effexor, Cymbalta. All of them had some issue that I couldn't overcome. Zoloft made me agitated and gave me a stony cold affect. Celexa and Lexapro left me feeling like an apathetic slug that was content eating ice cream and watching Lifetime all day. Wellbutrin ramped up my anxiety and made me snappy and mean. Viibryd made me cycle faster and definitely made me more hypomanic. It also gave me chronic diarrhea. Effexor pooped out. Cymbalta also made me hypo.

Trintellix is the only antidepressant that makes me feel like a functioning human again without spinning me out of control and it's just as good for SAD as Wellbutrin in my experience. However, it is definitely a STRONG antidepressant. 20mg is only okay for me in the DEEP of Winter.

@Beth45 you may find that the combo of Vyvanse+Trintellix is extra stimulating the way I do. I definitely think those two meds work synergistically. As I increase my Trintellix, I have to decrease my Vyvanse. I'm taking 40mg now and will likely be decreasing to 30mg at my next appt in January. We had to do the same thing when I took it last winter for seasonal depression.

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On 10/22/2016 at 4:30 PM, mikl_pls said:

I've not heard of this theory regarding the more receptors a medicine hits the harder it is to discontinue. If that were the case, antipsychotics would be hell to discontinue! As far as Trintellix goes, the PI sheet says as long as you're at 10 mg, you can just stop taking it. If you're on anything higher than 10 mg, you need to titrate down to 10 mg for a week (I believe) and then D/C.

I don't know enough to say whether coming off Lamictal could cause a rash. Usually when a drug causes a rash, they discontinue it as rapidly as possible, so my personal uneducated guess would be no, but don't quote me on that.

Thanks troop. Lol I actually am considering becoming a psychiatrist. :)

 

I think psychopharmacolgist would be a good fit for you. Or a clinical pharmacist in a psych facility. Your knowledge could help a larger population of people given that role. I wanted to do that myself. 

Edited by Persona_Is_Life
Dear God spelling. I should really proofread my posts.
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On 11/19/2018 at 6:18 PM, Wonderful.Cheese said:

Is anyone on the patient assistance program? I don’t mean the copay card (which would still make this med unaffordable to me), but the patient assistance program? If you’re not on it you should look into it.

 

I read this when I started trintellix, and I just got my assistance-approved meds in the mail this week.  The program is available for people making up to 5 times the poverty level.  Otherwise the med would have cost me over $1000.  Thank you so much for mentioning the program in this thread!  The only thing I'm not sure about is if you can use the program again after you run out of the first batch of approved meds.  But at least I know I'm good for the next 6 months!

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