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classification as a chlorite/caffeine

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alcohols are classified but caffeine's have yet to be put into a class I would go as far as to say the presence of oxygen make's this a chlorite and the molecule structure makes it a caffeine and that explains one of the most common side effects "the jitters"2001:558:6012:1B:3576:163:83B8:C668 (talk) 14:45, 29 July 2018 (UTC)[reply]

Anti-aripiprazole Bias (?)

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I'm concerned about what seems like an anti-medication bias throughout this article, emaphasizing flawed studies and studies with equivocal results and apparently disregarding the documentation, which is extensive, of aripiprazole's utility in clinical practice. I think this article would need an expert to correct this, however. Ucbuffalo81 (talk) 19:12, 22 October 2018 (UTC)[reply]

Hey Ucbuffalo81. I would try posting at Wikipedia talk:WikiProject Medicine. GMGtalk 19:13, 22 October 2018 (UTC)[reply]


Ok thanks GMG. I'll see if I can't attract a clinical person!

Ucbuffalo81 (talk) 19:17, 22 October 2018 (UTC)[reply]

be specific about what sources you view as poor. Jytdog (talk) 20:20, 22 October 2018 (UTC)[reply]
Indeed, I now notice lots of Cochrane citations on a few antipsychotic pages. Cochrane is a UK organization. And, those who do "reviews" of usa clinical trials, don't understand usa fda laws, including how psychiatrist are bound by doctor, american academy of psychiatry, and the law. Thus, those cochrane articles say that usa studies have bias because of dropouts or they are sponsored by the pharmacy companies. Cochrane articles really need to be limited to wikipedia.co.uk most likely. I don't think a lot of usa antipsychotics are approved for UK. They are likely many many years behind the fda in development and approval. Ap4lmtree2 (talk) 07:53, 10 September 2019 (UTC)[reply]

A detailed discussion of the mechanism

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IMO belongs in the body of the text. Also trimmed a bunch of the primary sources. Doc James (talk · contribs · email) 22:19, 5 May 2019 (UTC)[reply]

Your statement above is empty and not an invitation to a discussion. What belongs to the intro part of WP articles is strictly regulated by WP:MOSLEAD and not a matter of your opinion. If IMO does not belong, what about EMO or UMO? WP does not allow "in my opinion" anywhere in the article. The par., which I added to the lead on the mechanism of action, provided an accessible overview of the pharmacodynamics, as required by MOS:INTRO. Your statement's 2nd sentence is a private and unrelated to any discussion remark. Please, refrain from arbitrary editing vandalizing edits made in good faith by others and from making private and unrelated to any discussion remarks indicating the WP:OWNERSHIP problem. If you want to start a discussion, you need to write something constructive, justified, and written in standard English. Anything!? Good luck.--67.87.191.87 (talk) 04:18, 6 May 2019 (UTC)[reply]

This IMO is undue weight and overly detailed for the lead. And no it is not accessible.

"Known aripiprazole's mechanism of action is different from those of the other atypical antipsychotics[1][2][3][4][5][6][7][8]. It shows differential engagement at the dopamine (D2[1] It appears to show predominantly antagonist activity on postsynaptic D2 receptors and partial agonist activity on presynaptic D2 receptors.[9], D3[1][10][11], and partially D4[1][3]) and is a partial stimulant of serotonin (5-HT1A[1][12][13], 5-HT2A[1], 5-HT2B[1], 5-HT6, and 5-HT7[1][8]). It also shows lower and likely insignificant effect on histamine (H1), epinephrine/norepinephrine (α), and otherwise dopamine (D4), as well as the serotonin transporter[1][3]. Aripiprazole acts by modulating neurotransmission overactivity of dopamine, which is thought to mitigate schizophrenia symptoms[14]."

Doc James (talk · contribs · email) 04:49, 6 May 2019 (UTC)[reply]

@Doc James:,
(1) what is "IMO"? Please, use standard English, so everybody can understand. You do not write for yourself or your pals. This is not a private discussion.
(2) Your statement "[t]his IMO is undue weight and overly detailed for the lead" is a personal opinion and as such inconsistent with WP policies. You need to provide a WP policy provision to justify it and anything you object to. Otherwise your deletions indicate the WP:OWNERSHIP characteristics disallowed by WP. Please, do conform to WP policies.
(3) Your statement "[a]nd no it [IMO]is not accessible" is again your personal opinion, as unjustified by any WP policy provision. Additionally, If you do not like my IMO, do fix it as you please, if you can (please, let me know, if possible), but do not delete.
(4) Pharmacology is not a fairytale story and it is difficult. If my summary of pharmacodynamics is in addition in the lead and can be omitted when seen to difficult. It does not change or obscure the other info.
(5) It is the 4th par., so in line with the length of the lead advised by WP of 4 paragraphs. Thus, you may not claim that it is excessive unless you put something else in its place. Without such a substitute it should stay as the best available.
(6) Without the mechanism of action provided by me it is difficult to see the differences between similar medications, as they differ mainly by that mechanism. Thus, my par. is essential to distinguish aripiprazole from e.g. geodon by reading only their leads.
(7) You removed my similar par. from the ziprasidone lead that was much simpler and shorter. It means that you act in bad faith and your statement that "[t]his IMO is undue weight and overly detailed for the lead" is only a pretext to assert undue WP:OWNERSHIP.
(8) Below is the same par. simplified. I expect you put back into the lead unchanged or modified as you please:

"Known aripiprazole's mechanism of action is different from those of the other atypical antipsychotics[1][2][3][4][5][6][7][8]. It shows differential engagement at the dopamine (D2[1] It appears to show predominantly blocking activity on receiving D2 receptors and partial stimulating activity on sending D2 receptors.[9], D3[1][10][11], and partially D4[1][3]) and is a partial stimulant of serotonin (5-HT1A[1][12][13], 5-HT2A[1], 5-HT2B[1], 5-HT6, and 5-HT7[1][8]). It also shows lower and likely insignificant effect on histamine (H1), epinephrine/norepinephrine (α), and otherwise dopamine (D4), as well as the serotonin transporter[1][3]. Aripiprazole acts by modulating neurotransmission overactivity of dopamine, which is thought to mitigate schizophrenia symptoms[14]."

Please, provide justification by a WP policy provision(s) for anything you claim is appropriate for WP. Otherwise you assert undue WP:OWNERSHIP.--67.87.191.87 (talk) 19:13, 7 May 2019 (UTC)[reply]
That is overly complicated and can go perfectly well in the body of the text. We also do not need to use all the primary sources. Doc James (talk · contribs · email) 01:29, 8 May 2019 (UTC)[reply]
It does not belong to the article body, as it is already there under Pharmacodynamics. It is a compressed summary of that section. I did not add a single info or reference, but took everything already in the article body and you has not seen that. Putting summary next to the full version of the same indicates not seeing the resemblance between them that indicates not fully understanding the subject matter. Exactly the same happened in the ziprasidone article. You moved my summary par. from the lead into the body creating a repetition with that, which follows. Following is the par. further simplified:

"Known aripiprazole's mechanism of action is different from those of the other atypical antipsychotics[1][2][3][4][5][6][7][8]. Aripiprazole modulates overactivity of dopamine, which is thought to mitigate schizophrenia symptoms[14]. Specifically, it shows differential engagement at the dopamine (D2[1]: can block activity on receiving D2 receptors and partially stimulate on sending D2.[9], D3[1][10][11], and partially D4[1][3]) and is a partial stimulant of serotonin (5-HT1A[1][12][13], 5-HT2A[1], 5-HT2B[1], 5-HT6, and 5-HT7[1][8]). But, it shows min. effect on histamine (H1), epinephrine/norepinephrine (α), and otherwise dopamine (D4), as well as the serotonin transporter[1][3]."

Please, refrain from harmull editing of the essence of pharmacological articles. You edits do not account for intricacies by missing resemblances between slightly differently written texts of varying lengths, but saying basically the same. If you do not like some references, please feel free to remove them. They are not critical in the lead.--67.87.191.87 (talk) 14:19, 8 May 2019 (UTC)[reply]
Putting this mass of receptor details in the lead is not an improvement. It is simple not generally that important. You could try a RfC if you wish. Doc James (talk · contribs · email) 11:04, 10 May 2019 (UTC)[reply]
agree w/ Doc James...Putting this mass of receptor details in the lead is not an improvement--Ozzie10aaaa (talk) 11:22, 10 May 2019 (UTC)[reply]

References

  1. ^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa Cite error: The named reference pmid12784105 was invoked but never defined (see the help page).
  2. ^ a b c Starrenburg FC, Bogers JP (April 2009). "How can antipsychotics cause Diabetes Mellitus? Insights based on receptor-binding profiles, humoral factors and transporter proteins". European Psychiatry. 24 (3): 164–70. doi:10.1016/j.eurpsy.2009.01.001. PMID 19285836.
  3. ^ a b c d e f g h i Cite error: The named reference drugLabelPC was invoked but never defined (see the help page).
  4. ^ a b c Brunton, Laurence (2011). Goodman & Gilman's The Pharmacological Basis of Therapeutics 12th Edition. China: McGraw-Hill. pp. 406–410. ISBN 978-0-07-162442-8.
  5. ^ a b c Nguyen CT, Rosen JA, Bota RG (2012). "Aripiprazole partial agonism at 5-HT2C: a comparison of weight gain associated with aripiprazole adjunctive to antidepressants with high versus low serotonergic activities". The Primary Care Companion for CNS Disorders. 14 (5). doi:10.4088/PCC.12m01386. PMC 3583771. PMID 23469329.
  6. ^ a b c Newman-Tancredi A, Heusler P, Martel JC, Ormière AM, Leduc N, Cussac D (May 2008). "Agonist and antagonist properties of antipsychotics at human dopamine D4.4 receptors: G-protein activation and K+ channel modulation in transfected cells". The International Journal of Neuropsychopharmacology. 11 (3): 293–307. doi:10.1017/S1461145707008061. PMID 17897483.
  7. ^ a b c Burstein ES, Ma J, Wong S, Gao Y, Pham E, Knapp AE, Nash NR, Olsson R, Davis RE, Hacksell U, Weiner DM, Brann MR (December 2005). "Intrinsic Efficacy of Antipsychotics at Human D2, D3, and D4 Dopamine Receptors: Identification of the Clozapine Metabolite N-Desmethylclozapine as a D2/D3 Partial Agonist". The Journal of Pharmacology and Experimental Therapeutics. 315 (3): 1278–87. doi:10.1124/jpet.105.092155. PMID 16135699.
  8. ^ a b c d e f Davies MA, Sheffler DJ, Roth BL (2004). "Aripiprazole: a novel atypical antipsychotic drug with a uniquely robust pharmacology". CNS Drug Reviews. 10 (4): 317–36. doi:10.1111/j.1527-3458.2004.tb00030.x. PMID 15592581.
  9. ^ a b c Wood M, Reavill C (2007). "Aripiprazole acts as a selective dopamine D2 receptor partial agonist". Expert Opin Investig Drugs. 16 (6): 771–5. doi:10.1517/13543784.16.6.771. PMID 17501690. Cite error: The named reference "pmid17501690" was defined multiple times with different content (see the help page).
  10. ^ a b c Kegeles LS, Slifstein M, Frankle WG, Xu X, Hackett E, Bae SA, Gonzales R, Kim JH, Alvarez B, Gil R, Laruelle M, Abi-Dargham A (December 2008). "Dose-occupancy study of striatal and extrastriatal dopamine D2 receptors by aripiprazole in schizophrenia with PET and [18F]fallypride". Neuropsychopharmacology. 33 (13): 3111–25. doi:10.1038/npp.2008.33. PMID 18418366.
  11. ^ a b c Yokoi F, Gründer G, Biziere K, Stephane M, Dogan AS, Dannals RF, Ravert H, Suri A, Bramer S, Wong DF (August 2002). "Dopamine D2 and D3 receptor occupancy in normal humans treated with the antipsychotic drug aripiprazole (OPC 14597): a study using positron emission tomography and [11C]raclopride". Neuropsychopharmacology. 27 (2): 248–59. doi:10.1016/S0893-133X(02)00304-4. PMID 12093598.
  12. ^ a b c Jordan S, Koprivica V, Chen R, Tottori K, Kikuchi T, Altar CA (April 2002). "The antipsychotic aripiprazole is a potent, partial agonist at the human 5-HT1A receptor". European Journal of Pharmacology. 441 (3): 137–40. doi:10.1016/S0014-2999(02)01532-7. PMID 12063084.
  13. ^ a b c Cite error: The named reference pmid17728427 was invoked but never defined (see the help page).
  14. ^ a b c Mailman RB, Murthy V (May 2010). "Third generation antipsychotic drugs: partial agonism or receptor functional selectivity?". Current Pharmaceutical Design. 16 (5): 488–501. doi:10.2174/138161210790361461. PMC 2958217. PMID 19909227.

Cochrane and UK standards

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Cochrane reviewers and their publishing should be limited to wikipedia.co.uk rather than USA wikipedia. The UK and their MHRA are many years behind the usa and the fda. USA doctors who conduct clinical trials in the usa are bound by the american academy of psychiatry, usa law, and general researcher ethics. If you want to cite and support (non-peer reviewed) cochrane and uk reviewers, then you might as well cite them to discredit all usa fda drugs that aren't approved in the UK. However, as a general rule, for Cochrane studies, the arguments are that [1] there is "bias" from these ethically bound doctors because they are pharmacy funded studies, [2] because there is this "bias" they are "low quality," and thus, discreditable if not dismissible, [3] there ought not be a dropout rate in any antipsychotic studies because all antipsychotics are on the assumption for being highly tolerable in the first place. Indeed, from this assumption, it is shocking that there is any dropout rate and low tolerance for something that used to be referred to more as "major tranquilizers." Why would people not tolerate tranquilizers? Don't they want to sleep lots? Why would anyone not be medicine compliant for such medication. For [1] the doctors and researchers are bias rather than outright liars and frauds with doctor licenses because they are too naive and stupid to be objective. Arguably, it takes something of more self and social awareness to be an outright liar and fraud than someone to be bias; thus, these license and ethically bound doctors must be the latter. For [2], citing, what I see as anti psychiatry, in this regard merits criticism against the greater funding process for clinical trials in the first place. Indeed, perhaps if the usa were less freemarket, then perhaps usa clinical trials could have direct government supervision and funding rather than from pharmacy companies that likely get some government grants. However, the healthcare system and research is not centralized in this way. This relates more to the greater economic and healthcare structural system than picking on all individual pharmacy studies which all have this funding structure issue. Rather, it is collective and exist in all studies. Note, i would not compare and be harsh against the UK and MHRA compared to the usa fda if there isn't an apparent anti psychiatry movement going on as i see it.

What is "USA wikipedia"? Yes Cochrane reviews are peer reviewed. Cochrane is a perfectly suitable source per WP:MEDRS Doc James (talk · contribs · email) 23:02, 10 September 2019 (UTC)[reply]
Yes, I now accept as true your contention and argument that Cochrane is a reliable and reputable systemic review source. — Preceding unsigned comment added by Ap4lmtree2 (talk • contribs) 21:05, 11 September 2019 (UTC)[reply]

Please stop vandalizing the article by repeatedly removing disclosure of the FDA-mandated warning regarding Abilify causing suicide of children, adolescents and young adults.

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@Whywhenwhohow: In 9 edits, I have made 7 additions to the article. They are well-sourced. You have reverted every single time. Explain yourself. You can't keep reverting with falsehoods like implying I said children, adolescents and young adults are elderly. <sic>


And particularly relevant to your claim putting words in my mouth:

I brought this up on your talk page on the 21s of last month! RudolfoMD (talk) 03:36, 4 November 2023 (UTC)[reply]

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