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Wiki Education Foundation-supported course assignment

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This article was the subject of a Wiki Education Foundation-supported course assignment, between 25 August 2020 and 4 December 2020. Further details are available on the course page. Student editor(s): Regal Kegle.

Above undated message substituted from Template:Dashboard.wikiedu.org assignment by PrimeBOT (talk) 14:57, 16 January 2022 (UTC)[reply]

Stimulant? Not a stimulant?

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Atomoxetine is often claimed to be not a stimulant. I find this confusing, however - despite taking weeks to do so, it eventually has the effect of raising noradrenaline (which in turn also raises dopamine), much like the traditional stimulants, and much like them it raises awareness/alertness/awakeness. It's considered useful for narcolepsy as well as ADD/ADHD. So how, exactly, is atomoxetine not a stimulant? Is it possible that the claim of being not a stimulant is marketing from the company who produces it, given how much of a bad reputation stimulants often get? Xmoogle (talk) 12:29, 6 November 2012 (UTC)[reply]

The distinction appears to come from abuse potential. I agree that no sane classification system based on pharmacodynamics alone would call nicotine and caffeine stimulants but not atomoxetine. But if we add abuse potential as a requirement, atomoxetine doesn't pass the test. At any rate, all of the medical literature I've ever come across distinguishes atomoxetine from stimulants, and we're constrained by what the literature reports even if we don't accept it ourselves. --Aurochs (Talk | Block) 20:13, 7 November 2012 (UTC)[reply]
Atomoxetine raises DA-levels directly, not only via NE. But this only in the prefrontal cortex. I disagree therefore if one can call it for a selective norepinephrine reuptake inhibitor (NRI). It is, in fact, an inhibitor of NET, but NET is not specific for NE, it reuptakes DA as well.--Vibackup (talk) 17:31, 10 June 2013 (UTC)[reply]
It is really not helpful to write in acronyms. I take it DA means dopamine, is that right? But what are NE and NET short for? 85.210.151.106 (talk) 00:59, 28 June 2013 (UTC)[reply]
Seems to be norepinephrine and norepinephrine transporter. -- Ed (Edgar181) 12:37, 28 June 2013 (UTC)[reply]
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Inhibition of CYP2D6

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The Wikipedia article states that Atomoxetine inhibits CYP2D6 and links to source number 4. The linked article[1] however says that the oral administration of Atomoxetine does not inhibit or induce the clearance of other drugs metabolized by CYP2D6 (second to last sentence). ArcticPizza (talk) 12:37, 29 November 2018 (UTC)[reply]

You are quite correct. I'll change the article to [citation needed], as they probably cited the wrong ref. Thanks.--Quisqualis (talk) 23:40, 29 November 2018 (UTC)[reply]

References

  1. ^ https://www.ncbi.nlm.nih.gov/pubmed/15910008

Lack of Research?

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I find it odd that the research section for this drug is quite bare when it could be much more dense. It would be hard to include reliable science that has yet to be strengthened but it should include more information. Regal Kegle (talk) 17:13, 6 September 2020 (UTC)[reply]

Lack of research and follow up confirming research is just the start of issues. There is also a problem with research that has incorrect dated or has misleading conclusions. The bigger issue is wiki contributors are not necessarily researchers and correcting research without doing actual studies is not feasible. So peer review of old articles relevance to current knowledge base, or quality of the research to begin with gets to be problematic to say the least.
example
"Atomoxetine prevents norepinephrine release induced by amphetamines and has been found to reduce the stimulant, euphoriant, and sympathomimetic effects of dextroamphetamine in humans" with 3 references from 2009 to 2013 (which were done poorly even then).
First reference is a meta study by the drug company itself so already there is high potential for bias and low quality results. Plus a couple researchers additionally own stock of the drug company, etc.
One referenced article lists the reference "This combination therapy has not included amphetamine because blockade of NET by atomoxetine prevents entry of amphetamine into presynaptic noradrenergic terminals". This does not support the conclusion of the statement. Only that atomoxetine can block AMPH being taken in by NET. Not why that alone is reason enough to exclude from the research. Or if researchers understood all the other factors being ignored.
Researchers know atomoxetine is an SNRI. As far as I can tell, 2 of the articles assumed its effects being combined with amphetamine is due to NET inhibition. Which is a rudimentary view of actual neurological effects and not accurate.
1. Not understanding that amphetamine has another primary route to therapeutic effect via the AMPA and NMDA/glutamate pathways. Which was known well before NE or DA was found to be effected, but everyone seems to have forgotten.
2. AMPA (enables fast synaptic transmission) / NMDA extends the effect of AMPA stimulation and additionally causes increased glutamate (primary excitatory neurotransmitter in the brain) levels in the brain. Which is strongly associated with activating the sympathetic nervous system, increasing heart rate and blood pressure.
3. Atomoxetine's secondary effect as an NMDA antagonist is being studied for other applications of atomoxetine. That alone can explain the decrease in BP, heart rate, and over stimulated feeling. Glutamate across the board, also modulates other neurotransmitters by increasing the ease which they are able to elicit a signal. NMDA antagonism reduces NMDA function and glutamate levels, which attenuates the effects amphetamine causes by raising them.
4. It is currently known that AMPH can diffuse across the cell membrane and NA and DA pathways are often combined pathways. DAT can just as easily uptake AMPH as NET. As well as many other transports and neurotransmitter interactions and effects.
5. Cortisol is a body's primary stress hormones which increased levels can elicit a physiological response. Like BP, heart rate, and respiration which increase oxygen supply to the brain and body. That alone can make a person feel stimulated. And is ignored by stating it is all due to NET inhibition of AMPH.
6. Amphetamine is lipophilic and it can diffuse across the cell membrane so NET, DAT, SET, etc. transports could all be blocked and it would still be able to get into the cell. This was already known before any of the referenced articles were done. Guess they missed that or had a bit of selective attention issues.
7. Seems they want people to believe ATX has 100% NET inhibition which if true would mean the same dose would work 100% for everyone. Don't qualify the strength of inhibition or differences in individuals. No reference I noticed of if AMPH competitively blocks ATX or if AMP reversing NET affects ATX ability to inhibit it. So many assumptions and unqualified claims.
Many other issues with old research and these references in particular. I know my own personal experience is not scientific and not considered reliable as a source of information. But I will say results would be very different if they did long term studies with people who have high tolerance to amphetamine. Poor assumptions would be revealed. I skimmed the articles, but didn't see the timing they took the meds. Taken together will elicit a much different conclusion than taken separately a few hours apart. Especially if grouped by timing and order of meds. ATX then AMPH 3 hours later, AMPH then ATX 3 hours later, taken at the same time.
If long term study and subjects had high AMPH tolerance, researchers would have concluded, WTF? Because the effects would be changing over time. And others have that same experience. And research already explains why. I'll spare everyone that.
[Strong opinion, pop psych has overemphasized DA and NE overly reductivist explanations for everything. Ignoring neurotransmitters, pathways, areas of the brain, even hormones have a complex relationship and how everything works together in the brain. Even that summary ignores most things.
ex. Some research has concluded some people have ADHD in large or in whole caused by fast glutamate metabolism. With ATX's NMDA antagonism, can see why someone may respond poorly to ATX and have the opposite effect. Where AMPH, and to a lesser degree MPH, are AMPA and NMDA/glutamate agonists which clearly would better attenuate fast glutamate metabolism. Even if NE and DA levels were the same, glutamate would make them and things they work with more effective.] HCStymie (talk) 07:58, 17 May 2025 (UTC)[reply]

Potential for withdrawal effects

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The article says that "Unlike stimulant medications, atomoxetine does not have abuse liability or the potential to cause withdrawal effects on abrupt discontinuation." Even though there are a number of anecdotes online about people experiencing withdrawal effects from tapering to a lower amount of atomoxetine (including but not limited to brain shocks that are experienced when tapering SSRI drugs). It seems inaccurrate how the article says there is no potential for withdrawal as if it's a definitive fact, shouldn't it be phrased differently?

The reference this information comes from is a study sponsored by the Lilly the manufacturer, and even they just said there was "no evidence", and with a sample size of 16 people who were all recreational drug users so it was in a specific context. — Preceding unsigned comment added by 122.60.11.75 (talk) 12:11, 10 December 2022 (UTC)[reply]

User:122.60.11.75 'anecdotes online' are not the same as definitive facts. Do you have and reliable sources that state that withdrawal may be an issue? I found another source stating that withdrawal is not an issue here https://pubmed.ncbi.nlm.nih.gov/14709944/ so it seems to be supported JeffUK (talk) 12:14, 10 December 2022 (UTC)[reply]
"I found another source stating that withdrawal is not an issue here https://pubmed.ncbi.nlm.nih.gov/14709944/"
Do you happen to work for Eli Lilly or any affiliates?
"Not an issue" is pretty vague.
The article concludes that if there is a bad reaction or adverse event, the withdrawal, that does exist, is tolerable considering the adverse event or reaction. It concludes withdrawal exists, not that it does not. Just that it does not result in a "discontinuation syndrome". Discontinuation is "well tolerated" not non existent. I only have access to the abstract, it does not say how long people were monitored after stopping.
9 to 10 week studies. It can take that long just to reach full effect for some people. I'd like to see a study that is actually long enough for people to develop tolerance and increase their doses a couple times to maintain therapeutic effect.
Atomoxetine can take up to 2 months to build up in the system. It does not stop working as soon as you stop taking it. So when the abstract says they didn't see symptom rebound upon discontinuation, not enough info to be conclusive.
Problem is quality of research, assumptions and ulterior motives etc.
Any first year psych student has probably studied the opponent process that counters exogenous changes to the brain. Which in research is more likely referred to as "acute tolerance". i.e. brain will downregulate receptors to reduce the signal resulting in decreased receptor density. Receptors that are not upregulated eventually get absorbed and taken out of play. If too many receptors are downregulated, the result is tolerance (persists). Which requires a higher dose to maintain earlier therapeutic effect. Take away the drug, try to function with reduced receptor density while nothing increasing neurotransmitter levels, that is withdrawal since now brain is operating at a much reduced level and the opposite of stimulated therapy is in effect. Sleepy, unfocused, low motivation, etc. Ignoring other routes to tolerance.
So, I would find any article that claims there to be no withdrawal as highly suspect as it does not match basic neurology. May be negligible for someone who never built tolerance. But that is a specific case only.
"'anecdotes online' are not the same as definitive facts." I agree. But often lack of research means that may be in some cases all we have. So what to do with that? Would be subjective as far as how much weight to put on any one side, even if backing articles were found. Even if stuffed into a "Controversy" or "Self reported experiences online often do not match conclusions from research" section of some sort.
I've seen people say the same about Adderall. Yet, some research states even prescribed doses can cause withdrawal that lasts for months. And ICD-11 codes say prescribed doses can cause negative long term side effects, effects by amphetamine worthy of their own ICD codes. Even the official FDA prescriber docs say there are issues. Yet, I can find articles saying there are no side effects or tolerance unless abused. Which is what my therapists were taught to say in spite of FDA doc contradictions. HCStymie (talk) 09:10, 17 May 2025 (UTC)[reply]

Grouped references

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Whywhenwhohow, you keep removing a statement from the first paragraph that is sourced later. I would simply add the <ref>, but there are 4 sources on that statement, and didn't want to have too much in the first paragraph. I do not know the syntax to group references together, but I think one exists. If there is and you know of one, or if it is better to add all 4 references, please let me know. Kimen8 (talk) 14:23, 29 December 2023 (UTC)[reply]

Each biomedical statement should have explicit WP:MEDRS-compliant sources. Medical articles should be relatively dense with inline citations. WP:MEDMOS --Whywhenwhohow (talk) 01:48, 30 December 2023 (UTC)[reply]

Probable incorrect citation re: comparison to amphetamine

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The paper cited in reference 30 does not appear to include any mention of amphetamine. The word "amphetamine" should probably be replaced with the word "methylphenidate." 2607:FEA8:991E:6800:42E:BFBC:53A8:4D8E (talk) 16:58, 4 July 2024 (UTC)[reply]

That is incorrect. It is compared with lisdexamfetamine, a derivative of amphetamine, which was shown to be more effective whilst methylphenidate and atomoxetine have equal effectiveness in not only that meta-analysis but all cited here. Димитрий Улянов Иванов (talk) 08:42, 28 September 2024 (UTC)[reply]

From Russia with lies.

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In some european countries, including Hungary, this medicine is sold (Px-only) under the brand name Bitinex. This summer it was summarily withdrawn from hungarian pharmacies based on an uncorroborated RUSSIAN federal pharmaceutical authority warning about out-of-specification active content and solvability value of the capsules. That despite Hungary not being a member of Russia/USSR/WARPAC since 1990 but is a member of the EU and NATO. Since Bitinex has no approved substitute in Hungary, tens of thousands of kids are left without medication. 94.21.229.182 (talk) 21:21, 5 September 2024 (UTC)[reply]

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