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browri

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Everything posted by browri

  1. Guess what the other name is for niacin? Nicotinic acid. Nicotinamide if it's the water-soluble form. If you're taking high levels of that, it is possible that perhaps you are building up some low levels of cotinine that make you appear as a passive smoker. What I find disturbing is that your life insurance finds a urinalysis to be acceptable proof. A blood test should be done to properly quantify the amount of cotinine in the blood and sometimes the blood tests are more accurate than the urine tests. I had to get a cotinine test as well for my employer for health insurance to get a discounted premium and that was definitely a blood test. Although you could decline the blood work and go for a cotinine mouth swab.
  2. Yeah when I first get back on Klonopin, I sometimes feel grogginess for the first 3-5 days. After that, I usually do okay. But it can linger for up to two weeks.
  3. This sounds like a good plan of attack to me. I'm not surprised your pdoc would prefer you on Caplyta + long-term benzo if needed over Zyprexa because the metabolic safety issues with Zyprexa are a serious concern, whereas Caplyta so far seems to show very little metabolic impact, at least when compared to Risperdal. Theoretically you should be less likely to develop tolerance to Klonopin with consistent dosing as well unlike Valium which does have tolerance issues.
  4. Agreed. If certain symptoms are manageable for the time-being, address the more severe ones first. There's always the option of changing the citalopram later too, but you start by adding the risperidone because, generally speaking, OCD symptoms can be distressing and further exacerbate existing depression. Unfortunately, our pdocs only see us for so long each visit though, and they can try to make a clinical judgement call based on what they see right in front of them, but they do still rely on us to tell them what distresses us most. In my mind, it makes more sense to augment first just because it has a higher chance of success at resolving all reported issues instead of an AD switch strategy which may only resolve one issue. This of course is an option as well. If you're on 40mg citalopram, it wouldn't hurt to talk to your doctor about at least trying escitalopram 10mg to see if there's any difference. There may not be, but citalopram is a racemic mixture where the R- enantiomer isn't completely silent. It actually antagonizes some of the effects of the S- enantiomer. So where escitalopram could be more effective, ar-citalopram, makes it less effective. Some people report improvements converting from citalopram to escitalopram. And there's room for dose increases too. Some say that citalopram is half as potent, but with the added antagonist effect of the R-enantiomer, 40mg citalopram doesn't necessarily equal 20mg escitalopram. Citalopram is probably more like a third as potent where 20mg, 40mg, and 60mg citalopram translate more to 5mg, 10mg, 20mg escitalopram, respectively. Except they don't prescribe citalopram up to 60mg anymore due to prolonged QT interval which is apparently less pronounced with escitalopram?
  5. So if your goal is to switch to a benzo regimen that is a little less "moreish" (in that you want more and can barely wait for your next dose), you truly would want to consider clonazepam (Klonopin) around the clock. It has one of the longest half-life of the benzos leaving pretty much only diazepam and flurazepam being longer. However, diazepam is broken down into several metabolites and definitely falls into the "moreish" category. My pdoc loves clonazepam for its long half-life and lower propensity to develop a tolerance than something like diazepam. When I'm more panicky than usual, my pdoc has me do 0.25mg with my morning meds, 0.25mg somewhere between noon and 2PM, and then another 0.5mg at bedtime for a total of 1mg in the day. I do sometimes find myself anxiously awaiting the noon dose sometimes, but I don't feel panicky in the mornings and by the afternoon I'm usually not jonesing for the evening dose.
  6. Risperidone should reach steady state in the blood stream around 4.5 days after daily administration. But there are changes in receptor sensitivity and expression that can occur for the 2-4 weeks beyond that steady state being reached. @Iceberg @CeremonyNewOrder My pdoc thinks of this like a game of chess. What's the next move? In the case of the OP @OCDme, the pdoc has noticed that citalopram 40mg isn't working the way it used to, so you either switch or augment. However, the patient also reports issues with rumination and obsessive thoughts. Those issues likely wouldn't be addressed with a switch to a different AD (like going from citalopram 40mg to escitalopram 20mg or fluoxetine 40mg). However, you could address both rumination and antidepressant poop-out with an augmenting agent like an atypical antipsychotic. Of course when thinking about augmenting an AD it's natural to gravitate towards aripiprazole. However, the patient reports having issues settling their thoughts, and aripiprazole is liable to push them in the opposite direction. Risperidone and quetiapine (Risperdal and Seroquel, respectively) are the only two atypical antipsychotics that are "silent" dopamine antagonists and can settle the thoughts enough to address obsessive rumination. They both seem to have the most evidence in treating OCD when high dose serotonin reuptake inhibitors aren't an option (like clomipramine 120mg or fluoxetine 80mg) +1 It is normal for the brain to adjust over time, even to the medications that we feed it. Think about it this way. When you work out to build muscle mass, you oftentimes need to rotate between different kinds of exercises of a specific muscle group in order to get continuous results or your muscle growth will plateau. This is because the muscles adjust over time to being worked out in a certain way. The brain isn't so different.
  7. What you're describing sounds more like a combination of Zyprexa withdrawal and Caplyta startup effects at the same time actually. Most commonly for the "-pines" like olanzapine and clozapine is the issue of cholinergic and adrenergic rebound upon discontinuation. Olanzapine is a potent anticholinergic, which has calming properties. It can also reduce gut motility. Coming off an anticholinergic not to mention an antiserotonergic (serotonin is also responsible for gut motility) could explain the diarrhea. Olanzapine potently blocks alpha adrenergic receptors (both auto-receptors and hetero-receptors). So you might be experiencing some adrenergic sensitivity that may come across like an overly sensitive fight-or-flight response. Nausea is listed is one of the most common side effects of Caplyta next to somnolence. I've never taken Caplyta but have heard from one other person that the nausea starting up on Caplyta was no joke but they adjusted to it. Intuniv (guanfacine) is an alpha-2 receptor agonist. The alpha-2 recepors act as auto-receptors for norepinephrine and epinephrine/adrenaline. When activated, they slow adrenergic output, when blocked or inactivated, they increase output. It's a feedback loop. Olanzapine has been blocking those receptors thus increasing the amount of signaling norepinephrine. Olanzapine also blocks alpha-1 receptors, so you don't feel that increase in adrenergic flow. Now all the stops are pulled out and your adrenergic system is responding in a sensitive way. Guanfacine will work by activating alpha-2 receptors to reduce norepinephrine output which should help to calm the over activated alpha-1 receptors. To answer your second question, yes clonidine is generally regarded as somewhat more potent than guanfacine and works in the same way. Klonopin is more potent by dose than Valium, but Valium is probably broader spectrum. Can't say for certain though. 10mg of diazepam is roughly equivalent to 0.5mg of clonazepam. When I'm having anxiety/activation like what you're describing, I usually need 1mg clonazepam. Caplyta supposedly takes 5 days to reach steady state. And you can reasonably expect adjustment for 2 weeks beyond that point, and further adjustment with each decrease of Zyprexa. Remember that Zyprexa and Caplyta work very differently though, and it's possible you may be incompatible. Just be sure you give it enough time and be patient. Keep your pdoc in the loop. If he gave you the okay to manage these breakthrough symptoms with Valium and Intuniv then definitely do it. If there's a chance that Caplyta will work for you, it can apparently REALLY work.
  8. I was on it for 6-8 months. And yes, oh so calming. I tried Latuda, Saphris, Fanapt, Abilify, Rexulti, loxapine, Zyprexa, probably missing some. My favorites were Zyprexa or loxapine, but loxapine I had to push into akathisia dose space for full symptom control. Zyprexa made my weight balloon and my lipids and blood glucose go out of control after just 6 months on 5mg. If it didn't make me so metabolically dysfunctional, I might have actually been able to live on it. However, after Zyprexa and loxapine, I found Rexulti and it has provided a similar calm paired with a cool stimulation that I just can't beat and it doesn't cause as much weigh gain as Zyprexa either. That being said, Rexulti is brand only right now and if I were to lose my insurance I PROMISE YOU I will be back on Zyprexa stat because it's the only thing that manages my anxiety, mania, and depression all in one pill.
  9. General sentiment is that for bipolar disorder, lamotrigine blood levels aren't as relevant to treatment response as those blood levels would be when treating epilepsy. Meaning if you have seizures you want to make sure you have steady levels throughout the day to ensure proper seizure control. However, for bipolar disorder, steady levels throughout the day don't seem to be necessary for mood control for most people unlike valproate or lithium. Speaking of valproate though, there are scenarios where you could be prescribed valproate and lamotrigine, at which point a doctor would likely always test the lamotrigine level. I was on the combo briefly, and because those two meds can do unpredictable things to each other's metabolism, it's best to keep an eye on the level. Valproate can increase lamotrigine's level, but lamotrigine can either increase or decrease valproate. Depends on the person. When you have interactions like that, then you test lamotrigine levels. Otherwise, you only test them if you have epilepsy and you're on higher dose lamotrigine (>200mg).
  10. Lamotrigine is predominantly a glutamate-reducing agent. But it has been shown to increase glutamate signaling in some ways such as very weak 5HT3 antagonism. There is a fringe group of patients whose depression is glutamatergic in nature versus serotonergic. Those patients typically respond to lamotrigine over typical antidepressants that focus on increasing serotonin signaling. You wouldn't want to take lamotrigine with ketamine infusions because lamotrigine would interfere with that subsequent glutamate outflow caused by ketamine's NMDA receptor antagonism. Just a guess really. But you wouldn't want to block NMDA glutamate receptors (ketamine) AND reduce glutamate output (lamotrigine) even if either on their own could result in improvements in glutamate signaling.
  11. I can describe a few different pieces to a puzzle with trillions of pieces. What I know is that clonazepam is depressogenic. It doesn't matter that it may reduce anxiety and thus make someone more at ease and potentially LESS depressed. If I'm having anxiety, I take it regularly. After about 2-3 weeks, I start to feel depressed. The point is that the way clonazepam works is by depressing the brain via GABA-A receptors, GABA being the chief inhibitory neurotransmitter in the brain. Glutamate, on the other hand, is the chief excitatory neurotransmitter in the brain. The brain tends to release more of it when other receptor systems are activated, and activation of the glutamatergic system subsequently inhibits the release of neurotransmitters, creating a feedback loop. Glutamate is GABA's opposite. Like day and night. When you take amphetamine, it activates TAAR1 receptors which cause neurotransmitter efflux. Activation of central dopamine receptors leads to increased release of glutamate, which in turn slows down the release of dopamine. So if you block the glutamate receptors (NMDA receptors, specifically), what happens? You've just cut the brake line, leading to a complete disinhibition of the brain and subsequently release of neurotransmitters, particularly dopamine. Ketamine, furthermore, is not just an NMDA receptor blocker, but interacts with many other receptor systems like the sigma receptors and opioid receptors. It does even have some affinity for dopamine receptors as well. Glutamate, while excitatory and an important part of the nervous system, is toxic in high levels and not modulated properly. Inhibiting NMDA receptors with a substance like ketamine would not only disinhibit the brain and encourage nerve growth, but because the brain detects no glutamate binding to NMDA receptors, it will increase glutamate output. While glutamate can be neurotoxic in high levels, when modulated correctly, it can actually have positive effects on depression. This is part of the reason why some people respond to no antidepressants, but they try lamotrigine or ketamine and it's a game-changer. Those are both glutamatergic agents meant to increase glutamate output, dampen glutamate signaling (simultaneously), and subsequently activate numerous other neurotransmitter systems both directly and indirectly. Additionally, this may be why vortioxetine may be more effective for some people than other antidepressants. It potently antagonizes 5HT3 receptors which increase glutamate output as well. The problem with clonazepam is that as an activator of the GABA inhibitory system. It could potentially dampen the positive response from ketamine. While ketamine blocking NMDA receptors may help the brain to reset, any neurotransmitter outflow downstream of ketamine would be dampened by clonazepam. So when the nurse says it's "not that big a deal", what they mean to say is for ketamine, you ideally want to do it with as clear a head as possible. The goal with ketamine infusions is to hopefully reduce polypharmacy. You may even find that ketamine infusions make it easier to go without clonazepam, but make sure you always discuss these things with your pdoc.
  12. I can definitely +1 the anxiety feeling of both starting AND stopping Lamictal. Going up is always a challenge on the first few dose hops. I felt like 25mg and 50mg were difficult jumps. 100mg wasn't so bad, and beyond that the dose changes were more tolerable. However, yes the Lamictal titration is rocky. If it's going to work for you though, it will likely do so with little to no side effects. The only side effect I had from it after the titration period that didn't really go away with time was issues with word recall. Definitely should continue up if you can handle it. However, if you haven't tried it yet and you don't plan on having any children, Depakote is actually a wonderful option. More tolerable than lithium in my experience. Lithium made me feel downright ill. Depakote makes me feel like I can sit still for a moment and be calm. It's really nice.
  13. To answer your question directly, I believe the two that you're most likely to be prescribed by a doctor would be either nortriptyline (metabolite of amitriptyline) or desipramine (metabolite of imipramine). Both or far more noradrenergic than their parent compounds, and they theoretically should be stimulating where the parent compounds would probably be sedating. The other one which you probably wouldn't be able to get prescribed is protriptyline, which is more of an NDRI like bupropion. Your signature indicates schizoaffective, bipolar type. You're on 1500mg lithium and 1250mg valproate, which will cause a fair bit of sedation. Coming off of dextroamphetamine won't help either. However, your saving grace is that you are reducing clozapine and increasing aripiprazole, which should be more stimulating. Not to mention clozapine on its own can be quite sedating for some people. If you can tolerate aripiprazole no problem, then I would say to wait until you've completely titrated across to aripiprazole and you've been on your target dose of aripiprazole for at least 3 weeks and off dextroamphetamine for 2 weeks before making a decision of whether an antidepressant is needed.
  14. It is worth noting initially that the diagnosis is written using DSM-IV methodology. The DSM acts as a guidebook for mental health clinicians to diagnose various disorders. The DSM-IV used a multi-axial system to describe various portions of a patient's mental condition. Axis I: mental health and substance use disorders Axis II: personality disorders and mental retardation Axis III: general medical conditions Axis IV: psychosocial and environmental problems (e.g. problems at home or at work) Axis V: Known as the GAF Score/scale, was an assessment of overall functioning Axis 1 would describe mental health disorders like major depressive disorder, bipolar disorder, schizophrenia, etc. This indicates that you have a recurrent depressive disorder. In ICD-10 coding, this would be F33, but your pdoc seems to imply here that he would rather diagnose you as a bipolar disorder, unspecified (F31.9) or cyclothymia (F34.0). F41 is the ICD10 major code for some anxiety disorders including panic disorder, generalized anxiety disorder, etc. It does not include social phobia (otherwise known as social anxiety disorder). F41.2 is a relatively new code to imply a mixed anxiety and depressive disorder as he has described. Many times people feel that their anxiety or their depression is stronger, one leading to the other. This statement by your psychiatrist implies that anxiety is tightly intertwined with depression in a way that cannot be described with other anxiety disorders. This is not unusual for a comorbid anxiety diagnosis with a mood disorder like bipolar disorder or cyclothymia (a possibly less mild form of bipolar disorder). This all could also explain why you didn't respond well to imipramine, which is a fairly strong tricyclic AD. Axis 2 would imply personality traits independent of any mental disorders. In a nutshell, your pdoc has assessed you as having an avoidant personality with obsessive qualities and that these qualities combined with a lack of coping mechanisms can lead to a problem. Don't take this as an attack on who you are as a person but rather as an assessment of what you're capable of under stress. For example, one of my favorite coping skills for anxiety is 4-7-8 breathing: https://www.healthline.com/health/4-7-8-breathing This is a physical coping mechanism for my anxiety. When I feel anxious or stressed, I'm out of my CBD:THC tincture, and I don't want to take a clonazepam or don't have time for it to kick in (which can take a few hours), 4-7-8 breathing is my godsend. Your doctor is looking to see if you have these kinds of coping mechanisms to handle your day-to-day. In summary: Under the DSM-V, you have been re-diagnosed as having bipolar disorder comorbid with a mixed anxiety/depressive disorder, most likely a secondary diagnosis to the bipolar disorder. A comorbid diagnosis (having 2 or more conditions simultaneously) is a fairly common diagnosis for those with bipolar disorder. However without the actual ICD-10 codes that the pdoc's office is using, it's hard to say for sure what their final diagnosis is, and they usually keep that pretty close to the chest (i.e. you usually can't just call your pdoc and ask them what they're using as their diagnosis for your billing claims). Considering that you're already taking Seroquel and Lamictal for some time now, a re-diagnosis as bipolar isn't that far-fetched at all, as both of those medications are for bipolar disorder (although Seroquel has an indication for treatment-resistant MDD and Lamictal is used off-label for that as well).
  15. Yeah but it still unfortunately doesn't have an indication for bipolar depression or manic/mixed episodes in bipolar disorder. They are working on the bipolar depression indication now I believe, but the trials for mania were a flop. In my experience it is a stellar med for bipolar depression.
  16. Coming off Lamictal, I actually became more anxious and agitated during the titration process (titrating up as well). Lamictal is interesting that the experience titrating up and down seems to be pretty much the same for me at least. Anxiety and agitation no matter what direction the dose is going. As for a relapse into depression afterwards? No, because I was on other medications maintaining that, which leads me to my question: Have you ever tried valproate? Even in low doses, it can be very helpful for mixed states. Not sure if it would be necessary to take with lithium, but my combo of Depakote+Rexulti does wonders for me when it comes to irritability, agitation, and sleep.
  17. It may be worth trying. Although issues with energy/motivation and grogginess and tiredness definitely won't be addressed by oxcarbazepine, it will definitely augment your current regiment of fluoxetine/bupropion assuming your signature is correct. Will say though that oxcarbazepine and carbamazepine (it's cousin) are not typically used in unipolar depression the way that lamotrigine and lithium are sometimes used.
  18. That's good to hear! Oh then you have plenty of room to grow then if you needed to. Although it sounds like maybe a lithium increase isn't so necessary? Worth still talking to your pdoc about it because hypomanic episodes can be followed by depressive episodes or further cycling without an adjustment.
  19. and for many also really hard to treat too. Absorption can be a real problem. I have to take 5,000IU daily with 10,000IU on Saturday and Sunday and my last check in end of June was 49ng/mL. Used to be in the high teens to low 20s. Correcting it has really helped my mood in tandem with fish oil and meds.
  20. That would make sense. I remember at the top end of the fluoxetine dose range that it was pretty stimulating. Even at 40mg. Improvement in agoraphobia and personal hygiene on a combination of fluoxetine/brexpiprazole wouldn't be surprising. That's the kind of combination that will put a jazz in your step However, starting to have this sense that all of your problems are suddenly effortlessly surmountable could border on "grandiosity" or "invincibility" both of which are dangerous parts of the array of bipolar symptoms. Have you found yourself smoking more or less since getting to this dose of brexpiprazole? Good you were able to start a diet and get to the gym again. Okay so this is usually one of MY red flags. I truly think that everyone's bipolar disorder is unique or that there are certainly many subgroups beyond bipolar 1 and 2. With that, there would be certain symptoms that are more prominent than others and also from person to person, the "red flag" symptoms (i.e. the ones that show up first). I, like you, generally lie in bed for a bit before getting up. Or I might fall back asleep and wake up later if it's not time to wake up yet. When I'm headed towards hypomania or I'm in hypomania, I may still get tired in a day, MAYBE. But the most noticeable thing is that I wake up in the morning feeling WIDE AWAKE, rip-roaring ready to go. Now since we've gotten my valproate level in the normal range, that doesn't really happen anymore. So it may be worth bringing up that brexpiprazole has been associated with a modest deterioration in impulse control as well as compulsive behaviors like gambling, online shopping, risky sex like you've mentioned above. I believe aripiprazole was far worse for this, but I haven't seen long-term numbers from brexpiprazole yet to say for sure one way or another. it SHOULD, but brexpiprazole and lurasidone are the two AAPs that really failed to treat (hypo)mania effectively but they're very effective for treating bipolar depression. They seem to be good for the depressive side of things, whereas when it comes to mania, they really need to be used in tandem with something else for complete symptom control, like lithium or valproate (have you ever tried valproate?) I think that you should present all of this to your pdoc exactly the way that you presented it to us. And I know that's easier said than done sometimes, being this open with your pdoc. But if I were your pdoc and you described this to me, I would be grateful because your self-awareness and attention to those details seems to be pretty impeccable. So you give him the list of symptoms you've been experiencing that you think are problematic like the increased spending, risky sex, feeling like you can conquer all of your problems, etc. Then tell him the reasons why you think you aren't hypo like you described above: delusions and paranoia are well-treated, getting good sleep and feeling tired if you don't sleep, only slight pressure of speech, etc. If I were a clinician, that gives me as complete a picture as any. Increasing lithium may not be a half bad idea, but that would depend greatly on your lithium level and if there's even room to increase (most people taking 900-1200mg/day). You may know this already, but a safe therapeutic blood level of lithium is 0.6-1.2mEq/L. Toxicity can happen at 1.5mEq/L and higher. Severe toxicity at 2.0mEq/L and medical emergency at 3.0mEq/L. I'm assuming you're on 1000mg based on your signature. I'm also assuming you have access to lithium CR (controlled release) in 300mg and 450mg tablets. It would be possible to go to 1200mg, I think. Like I said above, being wide awake pretty much from the moment I wake up gives me pause and I start to pay closer attention to my mood. Irritability is another major problem for me. I can be in a much cheerier mood than usual, but I will still inexplicably snap at people. Like my actions towards others may completely contradict my mood. I usually don't gauge myself off of how I feel though. Like if I feel like I can achieve my goals, who am I to say that I can't? However, when my reactions to my environment around me (e.g. people) don't make sense or my responses are out-sized relative to the "stimuli", and when physically the gears start to feel like they're running hotter, I pay closer attention.
  21. This is more how I've been feeling. Like I need to start taking clonazepam again because my irritability and anxiety have both been on the uptick Yeah so I can't figure out for myself if starting valproate played any role. You hear about lithium causing hypothyroidism all the time but not so much from valproate. It can happen but.......I'm also considering that my father has hypothyroidism and has never even taken psych meds so I don't read into this too much.
  22. Do you experience thyroid issues because of the lithium (i.e. did the thyroid issues start after you started lithium) or was the thyroid issue pre-existing?
  23. A few years ago, I found out from my father (who I don't see often) that he was diagnosed late in life with hypothyroidism. Making due diligence, my family doctor started testing my TSH and Free T4. Tested it once in 2017 where TSH was normal and T4 was just barely low. Tested again in 2018 about 6 months later and TSH was still normal and T4 still lowish. Wasn't until early last year that I started testing high TSH numbers. The initial high was only 4.77uIU/mL, which isn't that high relatively speaking. However, a subsequent test of my TSH and T4 showed the same high TSH but now I had lower T4 than in 2017 or 2018. It was apparent that either something was going on in my body or I just had hypothyroidism that was progressing. So in November of last year, my general doctor starts me on Synthroid at my request. My father takes 100mcg a day, but there's also a family history of heart issues on both sides of my family where the one side specifically is cardiac arrhythmia. So my gdoc wanted to start at the bottom and work our way up. Started on 25mcg and tested again this past January. TSH is still high at 4.61 but T4 is now 0.97ng/dL. Whoopee! I'm actually in the normal free T4 range! So we increased to 50mcg because no jitters or cardiac side effects to speak of. Test again in April and TSH is now 7.18 and T4 back down to 0.76ng/dL. So at this stage my gdoc recommends I see an endocrinologist. Got one. She has me take an additional 50mcg on Sundays (100mcg total) which seems to start making a real difference. Latest TSH is 5.90 and T4 is 1.01ng/dL. Looks like we're headed somewhere. Now, all that to tell you this: My current psych meds are: Trintellix 5mg AM Rexulti 1mg AM Vyvanse 40mg AM Depakote ER 1250mg This combo has worked well for me since 2017 when my pdoc and I pieced it together. My bipolar disorder follows a seasonal pattern. So we typically adjust meds as the seasons progress. Usually just the antidepressant, but sometimes the Rexulti as well. Standard dose on Trintellix for me is usually 10mg but in the Summer I need to back down to 5mg for a few months because it can cause me to go a little hypomanic. On the flip-side in the Fall and Winter, I typically require Trintellix at 15mg and 20mg respectively. The problem though is that since introducing Synthroid, my normal seasonal rhythm feels like it's been thrown off. I find myself feeling over-stimulated on a semi-regular basis. Sometimes a little anxious. The weirdest thing for me though is that caffeine usually goes right through me (I'm a CYP1A2 rapid metabolizer, hence I remove caffeine from the body faster than most), yet recently I'm finding that after 1 MAYBE 2 coffees, I'm finding I'm a little too stimulated when I usually need like a whole pot of coffee to get by. I started on Vyvanse because I was having issues with focus and concentration but also motivation/fatigue. My pdoc and I weren't 100% sure what I was experiencing was ADHD and not some unrelated problem rooted in anhedonia or anxious inattention. However from where I'm standing now, it would seem that all I really needed was some Synthroid and that the Vyvanse was just a bandaid covering up the real problem. I tried going off Vyvanse for a month before I had started Synthroid or knew there was a thyroid problem. Mixed success. My mood was less stable, but I found myself in good moods more often. Couldn't focus on anything for the life of me, and I was DOG tired. As a side note, the endocrinologist did some further blood tests and we did determine that I do have Hashimoto's disease, which is why my thyroid is under-performing. My immune system is attacking it. So I did some research on Hashimoto's disease and psychiatric impact and come to find that there are plenty of people with similar stories. Psychiatric diagnoses (bipolar and major depressive especially) were super common in these people, who would then go on to start thyroid hormones that resolve a significant portion of their psychiatric issues. I'm not saying that Synthroid is my answer and that I or anyone should throw out their psych meds when they get a Hashimoto's diagnosis. What I want to know is who here has been treated for some sort of affective/mood disorder, then been diagnosed with some sort of thyroid problem, start taking thyroid hormones, only to find that it really did change the psych med merry-go-round for you?
  24. Yeah you certainly have to weigh benefits against side effects. For me, I don't really have any side effects from valproate at this dose, but my threshold for akathisia on AAPs is pretty low not to mention other metabolic side effects. Throughout my treatment the one most important thing I've learned is that my overall condition is much better if an AED pulls most of the mood stabilizing weight. Then use an AAP at a lower dose if necessary. I've always speculated that this is because epilepsy runs in my family even though I have never personally had a seizure. I know in the past I've tried 1500mg of valproate, but it started making me depressed. 1250mg though is a sweet spot that gets me a blood level between 50 and 100 mcg/mL but doesn't make me feel sedated, depressed, cause my weight to balloon, etc. Risperidone has its own side effects, but if you tolerate it well at your current dose then maybe an increase makes sense if you're noticing a negative trend in your mood and increasing valproate isn't as good of an option. Everyone is different.
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