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About JustNuts

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  1. If your insurer truly won't cover them at all under any circumstances, even with a prior auth, then I suggest looking into manufacturer programs for patient assistance ASAP. These usually have caps on income for eligibility (for example, household income must be no more than 4 times the Federal Poverty Level for Takeda's program), and your pdoc will have to complete some forms, but they will provide the medication to you for free if you meet the criteria. In the meantime, your pdoc may be able to give you enough samples to cover the gap while the application for the patient assistance programs are processed.
  2. I've been on Vraylar for about a month or so now (as a mood stabilizer, antidepressant, and treatment for obsessive thoughts - it's primarily prescribed because I was having really severe and persistent suicidal thoughts, but my psych thought it might help in some other areas as well due to the rather unique MOA). I wasn't able to tolerate 3 mg at all, but 1.5 mg has been more or less tolerable (there have been some annoying side effects), and it's definitely been helpful so far. After some experimentation I discovered that taking it at night instead of in the morning reduced the severity of the side effects enough for them to be much less of an issue. This definitely has worse side effects when you initially start it. It has a long half-life (and a active metabolite with a very long half life), so it takes a while for it to stabilize. The akathisia was more present initially and has reduced to very tolerable levels with time and the switch to night dosing. The insomnia was a significant problem until I switched to night dosing, although it lessened with time prior to that. With regards to the insomnia, I noticed that it generally caused more problems with disrupted sleep quality and too-short sleep duration than with directly falling asleep, although initially it was doing all three of those. There has been some minor weight gain but considering that I am actively trying to gain weight (a very difficult prospect when you're on this dose of Adderall/Fetzima and have other preexisting problems with eating), I don't think this data point has much value. Nausea was a minor issue initially but quickly faded away. Little to no difference. I am on HRT though so I am not the best person to evaluate this.
  3. In the case of citalopram vs escitalopram, the differences in binding profiles / receptor affinities are actually significant enough to matter (especially so for 5-HT2C, H1, and α1). In the case of dexmethylphenidate vs methylphenidate, the differences in binding profiles / receptor affinities are nowhere near significant enough to matter.
  4. Np. Yes, there are no erythro- diastereomers in any modern formulation of methylphenidate. Only threo- diastereomers are used. "Regular Ritalin" (i.e. racemic methylphenidate) contains 50% dextro-threo-methylphenidate and 50% levo-threo-methylphenidate. "Focalin" (i.e. dexmethylphenidate) contains 100% dextro-threo-methylphenidate. Good to hear that it's working.
  5. This is glaringly incorrect. threo- and erythro- are diastereomers of methylphenidate, not metabolites of methylphenidate. The primary metabolite of methylphenidate is ritalinic acid, which is pharmacologically inactive. Racemic methylphenidate is a 50/50 mix of d-threo-methylphenidate and l-threo-methylphenidate (so it's dl-threo-methylphenidate, or d,l-threo-methylphenidate). The erythro- diastereomers are never used in modern formulations of methylphenidate due to being pressor amines that do not have useful clinical effects. Clinical research has proven that dl-threo-methylphenidate is indistinguishable from equivalent doses of d-threo-methylphenidate in its efficacy and tolerability. d-threo-methylphenidate is a classical example of an evergreened drug, in fact one might say that it's literally one of the best possible examples out there of clear-cut evergreening.
  6. There is literally no functional difference whatsoever between methylphenidate and dexmethylphenidate other than the fact that dexmethylphenidate is exactly twice as potent by weight as methylphenidate (i.e. that 5 mg of dexmethylphenidate = 10 mg of methylphenidate). There is no reason to take dexmethylphenidate instead of methylphenidate.
  7. Diazepam for me. Lorazepam and I don't get along very well (very short duration of effect, exceedingly weak effects, some problematic side effects), I've never tried clonazepam (the half-life is too long anyways), and I'm unwilling to touch alprazolam.
  8. Hi, Sorry about the delay in responding, I've had a bad week. Thank you for reinstating my private messaging system access, I understand the conditions and will comply with them.
  9. The science says otherwise: https://www.ncbi.nlm.nih.gov/pubmed/27143896 There may be some minor anxiolytic properties, but it's agreed that vortioxetine has not been demonstrated as a viable primary treatment for anxiety. ECT scares me too—anyone in their rightful mind should be scared about a procedure that involves electrically induced seizures—but it's extremely effective for depression, the risks and side effects are quite a bit lower than most people realize, and for treatment-resistant cases, it can be a godsend. It's a SNRI with a highly unusual 1:2 SERT:NET ratio (the three other major SNRIs used for depression have ratios of 30:1 and 10:1), so it's quite stimulating, although often too much so (many people can't tolerate it due to initially-nasty side effects and the increased anxiety, especially people with significant uncontrolled existing anxiety). Esketamine is the S(+) enantiomer of ketamine. It's formulated as an intranasal spray and indication is being sought for adjunctive use in treatment resistant depression, although it has been designated as a breakthrough drug from the FDA for treatment resistant depression and MDD with associated suicidal ideation, so those indications may be developed as well. Ketamine itself is known for being a very useful and widely used human/animal anesthetic, a significant drug of abuse (with some nasty side effects in chronic abuse, major risks in abusing it, and several notable deaths of famous people having been associated with its abuse), and being one of the very few rapid-acting antidepressants (exhibiting a completely novel mode of action in the process - a big deal in this field). The dietary restrictions for MAOIs are actually not as bad as you'd expect, and you can eat most processed cheeses while taking MAOIs, it's the aged cheeses that have enough tyramine in them to cause trouble. But if you're already having trouble eating enough, it's certainly reasonable to avoid MAOIs (although low-dose Emsam is exempt from dietary restrictions and is still an option you could potentially consider). Then let me list off the antidepressants often classified as atypicals: bupropion (Wellbutrin) mirtazapine (Remeron) vilazodone (Viibryd) vortioxetine (fluvoxamine trazodone nefazodone (rarely prescribed) There are some niche drugs occasionally prescribed off-label as antidepressants that could possibly be thrown in the atypical pool, but I've omitted them. There are also a lot of TCAs out there (and MAOIs, but we'll ignore those). And a ton of SSRIs. And a bunch of SNRIs. I'll list off the SSRIs and SNRIs. SSRIs: citalopram (Celexa) escitalopram (Lexapro) fluoxetine (Prozac) - can be useful for OCD in high doses. sertraline (Zoloft) paroxetine (Paxil) fluvoxamine (Luvox) - this SSRI is indicated for OCD only in the US but is an effective antidepressant as well. SNRIs: venlafaxine (Effexor) desvenlafaxine (Pristiq) duloxetine (Cymbalta) levomilnacipran (Fetzima) Have you tried any other atypical antipsychotics? Other atypical antipsychotics used for augmentation other than olanzapine include: quetiapine (Seroquel) ziprasidone (Geodon) lurasidone (Latuda) aripiprazole (Abilify) brexpiprazole (Rexulti) cariprazine (Vraylar) Lamotrigine is definitely a good option for augmentation, although an atypical antipsychotic may be a better choice. Understandable. In some ways it is, but in others it's not. Things were far worse even just a few decades ago. But it's true that they'll only keep getting better as we move forwards, and that treatment options for some things aren't currently all that ideal. Gave you most of what I know earlier in this reply. With luck you'll be seeing it released in 2018. If you're interested, there's at least one long-term open-label clinical trial of the drug that's currently recruiting: https://clinicaltrials.gov/ct2/show/NCT02497287 Oh, sorry, I meant method/mechanism/mode of action (essentially the way it works), not monoamine oxidase. Acronyms like that can get quite confusing if you're unaware of them or don't catch the context, I should have just written it out since it was a bit overly ambiguous in that context. Depression, very likely to see benefit over the short/medium term, but may not be sustained over the long term (however more treatments can be done in that case). Anxiety or OCD - evidence for ECT in those disorders is limited, I'd say the evidence for OCD is a bit stronger than that for anxiety (yet still weak and limited), but I only briefly surveyed the literature. No problem! I'm always glad to help. We're actually in somewhat similar situations, and one of the numerous things I do to try to distract myself from my problems is research topics like these ones and answer questions on crazyboards. Yes and no. Serotonin is important in depression and anxiety, but GABA is much more specific for anxiety (hence the efficacy of benzodiazepines), and depression-related neurotransmitters such as norepinephrine and dopamine usually increase anxiety (although there are some exceptions - SNRIs for example). Other neurotransmitters involved in anxiety and depression generally have less overlap. This is a major oversimplification and focuses only on the most commonly targeted neurotransmitters.
  10. Hello board staff, My access to the private messaging system was revoked due to an incident a while ago involving the sharing of a link to copyrighted materials with another member. I would like to discuss regaining access to the private messaging system, as I wish to contact a certain member to discuss some sensitive topics and ideas in private (none of which are related to piracy or the illicit distribution of copyrighted material). I am willing to agree to permanently avoid the use of the private messaging system on this forum for sharing copyrighted content despite my personal stance on the matter. This should completely resolve any lingering concerns that I could expose the forum to any legal liability, which is the reason that was cited for revoking my access to the private messaging system in the first place. Is this acceptable? (For any curious members reading this, I am posting this as a topic because I currently have absolutely no access to the private messaging system (cannot send, receive, or read/access private messages, including old ones) and thus cannot even contact the forum staff directly regarding this issue, so I was forced to resort to this method of communication.)
  11. Interestingly enough, ECT's effect size for depression is similar to that of stimulants for ADHD, which is infamously high (massively higher than any other psychiatric medication - it still blows my mind every time I think about it). The only issues with ECT are that the response isn't always sustained long-term (although additional rounds of ECT will often still work), and that there are some potentially major/unacceptable risks involved (variable-duration memory loss following treatment is the most concerning). These are all excellent recommendations for meds and med combos.
  12. My pdoc is in the early access prescribing program (or something similar); as far as I can tell the drug hasn't officially launched yet outside of that program. It'll be publicly launched by the end of the year, or early in 2018 at the absolute latest, and copay coupons will definitely be released at that point. If you're really interested in trying it, I suggest signing up on https://www.mydayis.com/ to get notified when there's more information available about the public launch. Just remember that if you're still on a PPI, it will likely mess with the pharmacokinetics.
  13. It actually won't really give you anything significant that's new unless you already suspect CYP2D6 duplication(s) are present (assuming that the test even assesses that - not all of them do). I'm assuming you're already able to competently interpret your results and have ran your raw data through Promethease - if the latter isn't true, run your raw data through there and interpret it properly! Generally speaking medical PGx testing only gives you verrrry simplified conclusions, which can usually just be be reached on your own with if you understand what you're doing, use the right tools, do enough research, and devote enough time to the issue (and I'm pretty sure that you are quite capable of doing this).
  14. Vortioxetine (Trintillex) is not an effective anxiolytic medication, it is only approved for the treatment of MDD, and the scientific literature does not support its use for GAD or any other form of anxiety. Esketamine is supposed to potentially hit the market in 2018, so that's a major new antidepressant with a novel MOA and strong efficacy that'll be available soon. You've tried TMS, have you tried ECT? ECT is generally extremely effective for depression. It may be a bit difficult finding someone willing and able to administer ECT though. Have you tried all of the SNRIs/SSRIs (including levomilnacipran (Fetzima))? Which atypicals (broadly classified as such) other than mirtazapine have you tried? Have you tried MAOIs yet? How about atypical antipsychotics - have you gone through all of the major candidates, or just a few of them? Have you tried mood stabilizers such as lithium, lamotrigine, divalproex sodium (Depakote), etc?
  15. You can get the same effects from XR and an IR booster. Mydayis is just a single-pill version of that with no chance of forgetting to take the IR booster at the right time. Yes, proton pump inhibitor is what I meant by "PPI". Esomeprazole is a PPI and if taking it chronically yes it will definitely screw with the extended release mechanism because chronic PPI use significantly raises gastric pH, which screws up basically all pH-based forms of extended-release/delayed-release/time-release/slow-release/sustained-release/etc mechanisms. However, exactly how much it screws with the extended release mechanism is variable. For Adderall XR, the primary measured change in the only trial done that directly assessed the impact of a course of PPIs is a decrease in the median Tmax from 5 hours to 2.75 hours [total amphetamine], 4 hours to 2.8 hours [d-amp only], and 5 hours to 2.75 hours [l-amp only] (as well as some other significant stuff - the most significant probably being the rather considerable pharmacokinetic variability in subjects taking XR+PPI - see the full text of https://www.ncbi.nlm.nih.gov/pubmed/19820270 for all of the details).