Talk:Disulfiram

message: Article is fairly incomplete in sections.  There are many drugs that have a "disulfiram effect" that are not listed and many more drugs that can interact with disulfiram.  151.112.57.22 21:21, 18 April 2007 (UTC)
thread_title: Untitled

message: Disulfiram is an inhibitor of DA-beta-hydroxylase.  This should be mentioned  Bakerstmd (talk) 01:17, 27 April 2008 (UTC)
replies: text: should also be mentioned its been pursued as a treatment for cocaine dependence Ranamarathon (talk) 16:47, 20 February 2024 (UTC)
thread_title:  Inhibition of catacholamine synthesis 

message: i didn't see any mention in the article about implants.
http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1879293&blobtype=pdfwork  —Preceding unsigned comment added by 82.73.149.152 (talk) 13:24, 2 September 2008 (UTC)
thread_title:  implants? 

message: article references 1948 discovery of drug action.  Wright and Moore (American Journal of Medicine, 1990;88:647-653) reference a 1937 paper describing alcohol sensitivity after industrial exposure:  Williams EE:  The effect of alcohol on workers with carbon disulfide.  JAMA 1937;109:1472-1473ACMillerMD (talk) 12:22, 17 January 2009 (UTC)
thread_title:  history 

message: The section on dosage states as follows:
:"Disulfiram is supplied in 200 mg, 250 mg, and 500 mg tablets. The usual initial dose is 500 mg for 1 to 2 weeks, followed by a maintenance dose of 250 mg (range 125 mg–500 mg) per day. The total daily dosage should not exceed 500 mg."
This section has no references, and higher initial dosages are prescribed in some contries. In Finland an initial dose of 800 mg per day for two days, followed by a maintenance dose of 200 mg per day, is usually prescribed. Hence, I'm adding the unreferenced tag.  —Preceding unsigned comment added by 195.56.244.181 (talk) 19:04, 8 August 2010 (UTC)
thread_title:  dosage 

message: An editor rightly requested a WP:MEDRS for the statement (in the reaction with alcohol section) regarding the ethics of giving disulfiram without informing the patient of the potential effects.  I've add a source, , which states (regarding conduct of clinical trials, on page 650, left column): "Ethics forbid the giving of disulfiram to any patient without his or her knowledge, and the physicians could not deceive the patients by telling them they were receiving medication when this was not true."  I am confident that there are countless sources for this edict - it is common medical knowledge, but it's worthy of a reference.  -- Scray (talk) 15:26, 26 September 2010 (UTC)
thread_title:  Ethics question 

message: I am curious about this. Especially because links that have proof of such an origin exist.
-robcypher/balst32  — Preceding unsigned comment added by 108.17.66.184 (talk) 23:23, 7 October 2015 (UTC)
thread_title:  uh, why does this history say it was originally designed as an anti-parasite drug when it was really for vulcanizing rubber tires? 

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thread_title:  External links modified 

message: When identifying reliable sources in medicine, it is important to avoid cobbling together primary sources, but instead use reliable secondary sources (See WP:MEDPRI: "avoid primary sources in the biomedical field – especially papers reporting results of in vitro experiments"). Evidence quality must be assessed carefully (see WP:MEDASSESS and WP:MEDANIMAL) because in vitro studies and case reports are not considered quality evidence in medicine for determining safety and efficacy of a treatment in humans. Also, press releases from organizations that publish low quality evidence are not reliable and may be considered churnalism (See WP:NEWSORG).
Recent edits have promoted Disulfiram as a possible treatment for Lyme disease and Babesiosis. This violates WP:ADVOCACY because this is an unsubstantiated belief promoted by advocates for pseudoscientific chronic Lyme disease diagnoses and treatments. 
The edits point to an in vitro study funded by chronic Lyme advocacy group Bay Area Lyme Foundation that purported to show Disulfiram kills Borrelia Burgdorferi (the bacterium that causes Lyme disease) in a test tube. 
Activity against bacteria in a test tube does not mean that there is activity against bacteria in humans (see also "Essential Oils Can’t Treat Lyme Disease").  Lyme disease and Babesiosis treatment protocols are already well-established and use generic anti-microbials. Long term antibiotics are not considered helpful (see CDC).
 
The edits also cite a press release from the institution that published the study, a dubious series of three cases published in low-tier journal MDPI by chronic Lyme disease advocate Ken Liegner who profits from chronic Lyme treatments, a planned clinical trial by chronic Lyme advocate Brian Fallon who receives funding from chronic Lyme advocacy groups. The MDPI journal is guest edited by Eva Sapi, another advocate for chronic Lyme disease who has received funding from chronic Lyme advocacy organizations. 
The patients in Liegner's paper had unusual histories, so it is unclear whether they even had Lyme disease or Babesiosis at the times they received Disulfiram treatment. This, along with the small sample size and lack of control groups, mean Liegner's results cannot be interpreted.  Fallon's planned study is on post-Lyme symptoms, not Lyme disease. 
The edits will be reverted because none of the citations can be relied upon to say Disulfiram is considered a plausible treatment for Lyme disease or Babesia by mainstream experts. ScienceFlyer (talk) 22:39, 17 September 2019 (UTC)
thread_title:  Disulfiram improperly promoted for Lyme disease 

message: This page says 60-120 hours.  PubChem says 7.3 +/-1.5 for disulfiram and gives values for its metabolites, none of which are anywhere near 60 hours.
See section 9.7 on this page: 
AmigoNico (talk) 03:46, 29 September 2019 (UTC)
thread_title:  Elimination half-life in violent disagreement with PubChem 

message: The mechanism of action of disulfiram (i.e. acetaldehyde dehydrogenase (ADH) inhibition) is well understood. However, the chemical may also function as a dopamine beta-hydroxylase (DBH) inhibitor. This would lead to an overall increase in dopamine and decrease in norepinephrine, possibly with significant effects on mood, substance use, and related cravings. Therefore, a dopamine-based MoA for disulfiram in substance abuse may mean the drug is both doubly useful for the treatment of alcohol abuse, and may even be useful or effective in treating the abuse of drugs other than alcohol such as opiates, amphetamine stimulants, or more even without the prominent effects of ADH inhibition.
The article currently claims 'Disulfiram does not reduce alcohol cravings, so a major problem associated with this drug is extremely poor compliance.'
However, DBH inhibition has been shown to reduce cravings among those suffering from alcohol and cocaine abuse. And then disulfiram specifically has been shown to affect cocaine use, likely via that mechanism [1][2][3].
Finally, anecdotal evidence from the internet provides support for an ancillary (non-medical) psychology effect of the medication: it entirely removes the option of drinking when it's being taken. Of course, compliance is still an issue in general but the drug remains in the body for a long time and many make note of that as reducing their alcohol intake out of abject fear. As acetaldehyde toxicity is beyond discomforting and may even cause death in severe cases, I can find a few examples on the internet of those taking the medication explaining that it has helped them in that psychological way.
However, the fear of adverse effects may lead others still to skip doses. As such, this point is probably not concrete nor scientific enough to include, at least until studied more directly.
In summary, I believe that:
A) treatment of the abuse of other drugs may benefit from the DBH mechanism where acetaldehyde toxicity isn't a factor.
B) disulfiram indeed reduces cravings both via an "I physically cannot drink" thought process and via a distinct pharmacological route. 
I'll probably update the article in the coming days, but feedback is greatly appreciated.
See:
10.1016/j.pbb.2008.02.009, 10.1038/npp.2010.127, 10.1007/s43440-021-00307-2, Reddit (various posts found via search engine) Adamthedog (talk) 00:17, 17 December 2023 (UTC)
replies: text: @Adamthedog the doi.org/ refs are all WP:MEDANIMAL, they may be included in an article, in cases when a reader can't interpret them otherwise (i.e. to apply the conclusions to humans). Reddit posts do not suit to medical articles. Tosha Langue (talk) 02:53, 17 December 2023 (UTC)
replies: text: Ah, my apologies — I hadn't meant to imply the sources I linked were intended for the article without further support/explanation (if at all). Just some introductory evidence of the mechanism and anecdotes for this discussion page while I gathered sources regarding in vivo human studies (hence the vague direction to "just Google some Reddit posts"). Thanks for the heads up though! Adamthedog (talk) 08:21, 22 December 2023 (UTC)

text: I also seem to have copy-pasted one reference incorrectly from my notes anyways. Lol Adamthedog (talk) 08:23, 22 December 2023 (UTC)
thread_title:  Potential MoA for Cravings Reduction