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::::We already link to [[ΔFosB]] in that section and no one is saying we shouldn't. This is a misuse of the main template as it is not a page specifically about the pathophysiology of alcoholism. You appear to be attempting to overlink to a page that you have written. We do not typically link to the same article multiple times. [[User:Doc James|<span style="color:#0000f1">'''Doc James'''</span>]] ([[User talk:Doc James|talk]] · [[Special:Contributions/Doc James|contribs]] · [[Special:EmailUser/Doc James|email]]) 13:18, 16 May 2015 (UTC)
::::We already link to [[ΔFosB]] in that section and no one is saying we shouldn't. This is a misuse of the main template as it is not a page specifically about the pathophysiology of alcoholism. You appear to be attempting to overlink to a page that you have written. We do not typically link to the same article multiple times. [[User:Doc James|<span style="color:#0000f1">'''Doc James'''</span>]] ([[User talk:Doc James|talk]] · [[Special:Contributions/Doc James|contribs]] · [[Special:EmailUser/Doc James|email]]) 13:18, 16 May 2015 (UTC)
:::::The only reason that hatnote should remain is that it points out that FOSB contains more detail on its pathophysiology. If overlooking is your concern, I don't mind removing the link in the text. [[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']]&nbsp;([[User Talk:Seppi333|Insert&nbsp;'''2¢''']]) 13:29, 16 May 2015 (UTC)
:::::The only reason that hatnote should remain is that it points out that FOSB contains more detail on its pathophysiology. If overlooking is your concern, I don't mind removing the link in the text. [[User:Seppi333|'''<font color="#32CD32">Seppi</font>''<font color="Black">333</font>''''']]&nbsp;([[User Talk:Seppi333|Insert&nbsp;'''2¢''']]) 13:29, 16 May 2015 (UTC)
:::::: ''We do not typically link to the same article multiple times''...I concur with DocJames --[[User:Ozzie10aaaa|Ozzie10aaaa]] ([[User talk:Ozzie10aaaa|talk]]) 13:33, 16 May 2015 (UTC)

Revision as of 13:33, 16 May 2015

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Good articleAlcoholism has been listed as one of the Natural sciences good articles under the good article criteria. If you can improve it further, please do so. If it no longer meets these criteria, you can reassess it.
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October 25, 2006Peer reviewReviewed
April 28, 2010Good article nomineeListed
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Untitled

Could the picture on long term effects of ethanol use be put next to the indes and enlarged as there is already a large whtite space present there. — Preceding unsigned comment added by 124.183.182.151 (talk) 13:48, 1 October 2013 (UTC)[reply]

No Alcohol fMRI studies?

I noticed there is no coverage of fMRI studies on Alcholism yet there is ample information.

Searched google with "alcoholic fmri" and many articles came up.

  • How Alcohol Affects the Brain: a fMRI Math Study - Department of ...
  • Brain-mapping increases understanding of alcohol's effects on first ...
  • fMRI Differences Between Subjects with Low and High Responses ...
  • Brain Regions Impaired by Alcoholism Identified
  • Specific areas of the brain impaired by ...
  • Functional MRI can locate and assess levels of brain activation associated with motor, sensory, or cognitive processes that may be impaired by alcohol over time ...
  • Why we like to drink: a functional magnetic resonance imaging study ...
  • fMRI measurement of brain dysfunction in alcohol-dependent young ...
  • Alcoholism and Social Exclusion - Blog Network - Scientific American
  • “Disrupted Regulation of Social Exclusion in Alcohol-Dependence: An fMRI Study” Neuropsychopharmacology, Dysfunction of reward processing correlates with alcohol craving in ...
  • Alcohol addiction is based on well-learned behavior of ...
  • Finger tapping shows that alcoholics may recruit other brain regions ...

Would be a great project for grad student, professor or research pro to digest the fMRI (and other imaging) research and add a good size section to what has been established. Rick (talk) 00:47, 25 March 2013 (UTC)[reply]

Uncertain as to how to fix

There is a section of the article: "Benzodiazepines, whilst useful in the management of acute alcohol withdrawal, if used long-term cause a worse outcome in alcoholism. Alcoholics on chronic benzodiazepines have a lower rate of achieving abstinence from alcohol than those not taking benzodiazepines."

Alcoholism has long been defined differently from alcohol dependence in that it involves all cross-tolerant substances. No addiction expert would prescribe an alcoholic benzodiazepines for anything other than acute detox. And all would recognize that abstinence from alcohol is useless if the patient is using benzodiazepines. That would break the sobriety date and leave the patient in an actively using state. You may as well prescribe two cans of Budweiser per day.

This portion of the article seems to ignore this and approach benzodiazepines from the other direction. There are plenty of references as to the information noted in my ¶ above. Should we reword this section? Drgitlow (talk) —Preceding undated comment added 16:35, 20 March 2011 (UTC).[reply]

Gin Lane

It's a great little image, but it's not actually about the damaging effects of alcohol. It's only half the picture - the other half is Beer Street, where everybody's healthy, happy and prosperous. There was a panic about gin specifically in eighteenth-century London; drinking huge amounts of beer was considered perfectly fine.82.36.138.46 (talk) 07:47, 23 March 2011 (UTC)[reply]

Social barriers

Your social barriers section should be changed to more gendered language such as "Gender and alcoholism." This is because social barriers exist in a wide variety of contexts. Gender is one of many ways to categorize social contexts. What about culture? Class? Etc?

Second, your cited research under that section is outdated. The Blum, et al. article (although very important) is thirteen years old. You are making a great argument for 1998, but I'm sure there is more research on this issue today. I read the Karoll article. It is more current than Blum et al., but is still nine years old, and it merely pulls together even older research (as old as Blum et al.), but it does make a good argument that women were more likely to seek help from mental health professionals instead of physicians in the late 90's. Do you know of any recent (2001-present) empirical critical feminist research that explores this issue of gender and alcohol abuse? The Karoll article is more of a meta-analysis and only cites research from the late '90's on this. This research needs to be refreshed.

Thanks! —Preceding unsigned comment added by 24.9.122.211 (talk) 00:54, 28 March 2011 (UTC)[reply]

Disability-adjusted life year

What is this crap? I've read enough documents and news articles to know that US rates of alcohol use do not match UK rates per capita or in any other relevant fashion so why the higher US disability adjustment?

Seems as dumb as trying to make out alcohol is responsible for silly little crimes rather than the broad spectrum such as murder it really is and trying to pretend it's a harmless little substance rather than categorizing it with crack where it belongs instead of safer than cannabis. Ignoring this true but emotionally taxing to the deluded paragraph the former paragraph needs attention. 87.112.178.244 (talk) 23:02, 28 May 2011 (UTC)[reply]

Alcoholism as a "disease" =

This is horse manure, anyhow.

Alcoholism is one hundred percent a decision that selfish or weak-minded people make to escape their situation, rather than facing it. That is a fact and no amount of holistic, "sympathetic" BS can alter that fact.

My mother was/is an alcoholic and is neither weak-minded or especially selfish. I make no excuse for her. However, your use of the word "fact" (stated twice)is extremely loose and without substance. — Preceding unsigned comment added by 98.119.151.233 (talk) 07:21, 15 September 2013 (UTC)[reply]

People make bad decisions, and there's no excuses to be made; this article is a sham. — Preceding unsigned comment added by 193.1.218.210 (talk) 11:20, 19 September 2011 (UTC)[reply]

Like it or not, it is the prevailing viewpoint of the medical community as there many similarities with traditional "biomedical" diseases, though it is not entirely free from controversy, as mentioned under "Dissenting opinion". See Disease theory of alcoholism#Criticism. This talk page is primarily for constructive discussion to improve the article, not a forum for opinions on the article content. If you think the article is lacking in some way, and have reliable and preferably peer-reviewed sources, improve it. Dallas (talk) 09:31, 22 September 2011 (UTC)[reply]

Trying to improve the lead

I've taken a bit of a stab at this, but honestly I'm attempting to make use of my vague familiarity but fundamental ignorance of medical topics to try and rewrite the leads of articles so that they aren't horrifyingly technical. Unforunately, the lead of this article is not only technical, it's also got some other issues, so I'm doing a bit more than just replacing and explaining jargon. Feel free to revert. SDY (talk) 18:15, 2 October 2011 (UTC)[reply]

I'm not sure what to do with what I've left as the last paragraph. The Thombs thing looks out of place, it should really be in the article proper with some sort of summary in the lead rather than in the lead as a whole bit. Not sure where to put it though. Social effects? SDY (talk) 19:59, 2 October 2011 (UTC)[reply]

This article is missing updated research on the physical causes of alcoholism, and there is plenty of it. This is the reason why different races/ethnicities tend to be more or less prone to alcoholism. Native Americans process alcohol twice as fast as caucasians. Caucasians process it is faster than Hispanics, and Hispanics process it fast than Asians. The faster you process alcohol, the less likely you are to have messages sent to your brain telling you to quit. In fact, the brains of alcholics are different on MRIs than non-alcholics. In an alcoholic, the brain's cells are shaped perfectly for alchol, and the body actually needs alcohol. I'm Hispanic, and when I have one beer, my body already tells me to stop because of the effects. I am no saint because I don't drink. And someone who drinks is not a demon. We need to be more objective in order to help people with this problem. Blame does nothing for it. — Preceding unsigned comment added by 162.82.215.197 (talk) 20:25, 9 March 2012 (UTC)[reply]

do prohibition of alcohol good or bad

i dont think it will help . i want the comment and reason for your justification. — Preceding unsigned comment added by 115.240.120.223 (talk) 15:13, 27 November 2011 (UTC)[reply]

GA review

This article seems to need some work. Lots of primary research presented as fact. A bunch of formatting issues. Will try to address some of it but may need to delist it.--Doc James (talk · contribs · email) 20:46, 6 December 2011 (UTC)[reply]

Are you sure there are a lot of primary sources used? I thought they were addressed and removed during the GA, but I could be wrong or maybe some have been added since then. Perhaps my memory is failing me. Hmmm.--Literaturegeek | T@1k? 01:32, 19 March 2012 (UTC)[reply]
Ref 54 is a study of 28 people, ref 55 a study of 16, ref 56 is looking at rat neurons in culture, ref 57 is from 1989 and also looked at rats. Ref 61 is a news page, 109 is a cohort study. A this is just on a cursory examination.--Doc James (talk · contribs · email) 03:57, 19 March 2012 (UTC)[reply]
I have made a start addressing the references. I have got rid of the worst offenders, references 54, 55, 56, 57 and rewrote the withdrawal section with high quality sources.--Literaturegeek | T@1k? 08:30, 17 April 2012 (UTC)[reply]

Evolutionary perspective

I think some addition of evolutionary perspective might improve this article a bit, I just saw this study today. Mark Arsten (talk) 19:22, 5 January 2012 (UTC)[reply]

File:The children - victims of adult vices (bahus).jpg Nominated for Deletion

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opening sentence for 'alcohol dependence'

since thetalk page foracoholdependence redirectsheri willask/suggest thishere. currenty theopening sentence at that article reads: Alcohol dependence is a psychiatric diagnosis (a substance related disorder DSM-IV) describing an entity in which an individual uses alcohol despite significant areas of dysfunction, evidence of physical dependence, and/or related hardship, and also may cause stress and bipolar disorder.

i don't think entity is the correct word in this situation. i think it should be 'describing a situation'...an entity for me is a tangible, sentient, thing; something that has a real existence; i.e., not a concept. if i haven't seen a respnse in a few days i will change this. cheers.Ruraltexas (talk) 10:48, 25 February 2012 (UTC)[reply]

Introductory paragraphs & definitions

The need for concise entries may sometimes jeopardise a comprehensive overview of any subject. My concerns about the first two paragraphs are:

The definition seems to ignore the vernacular history and specific contextual uses of the term "alcoholism" - views on this may differ on different sides of the Atlantic!

Allusion to the nature/nurture debate is omitted, as is an explanation of the WHO's reason for rejection of the term "alcoholism" in favour of the word "dependence"

Reference to "alcohol abuse disorder" as a subcategory of "alcohol dependence disorder" (DSM IV) is erroneous

Assertion that "tolerance and physical dependence occur with minimal use of alcohol over a short term period" is erroneous.

Below I am inserting a suggested re-write of these first two paragraphs. Feel free to tear me to shreds! : >

The term alcoholism has been used, in common parlance, to describe a state of extreme physical addiction to alcohol, since the 1850s. Its readily recognised characteristics of craving, loss of control leading to large and frequent consumption, prioritising of alcohol use in the face of more normal demands on time and money supply, and consequent loss of family, friends, employment and housing, made it easy to identify and label. At a time when little was known about other harms which excess drinking might cause, it was generally assumed that if a person was not "alcoholic" then their drinking was unproblematic.

The increasing interest in intervention which emerged with the Alcoholics Anonymous (AA) movement in the early part of the 20th century served to reinforce this classification; indeed, "sufferers" were (and still are) encouraged to accept and own the label of “alcoholic” as a first step on the road to recovery. The AA movement conceptualised “alcoholism” as a disease over which its victims had little control. They advocated complete and total abstinence as the only means of “recovery”. During the 1960s, psychologists espousing social learning theories started to oppose what they saw as rigid biological determinism, arguing that alcohol addiction derived from imperfectly learned or inappropriate drinking norms, and maintaining that, with appropriate support, addicted individuals might learn or re-learn how to drink in moderation. They eschewed the use of the terms “alcoholic” and “alcoholism” as derogatory and unhelpful to the process of therapeutic intervention. In 1979 an expert World Health Organization committee discouraged the use of "alcoholism" in medicine, preferring the category of "alcohol dependence syndrome". (See ICD10). The American Psychiatric Association (APA) uses the term “alcohol dependence disorder”. (See DSM IV). Other categories of problematic drinking were recognised, with the APA defining also “alcohol abuse disorder” where excess drinking causes social, criminal justice or health problems to the individual, in the absence of an inner compulsion to drink. “Hazardous”, “harmful” “lower risk” and “increasing risk” are other commonly used descriptors of various degrees of excess drinking behaviours, current in public health circles in the UK.

Recent advances in neuro-imaging and psycho-pharmacology have led to the development of theories of neuro-adaptation as the underlying mechanism producing alcohol dependence in the individual. Twin studies suggest that elements of genetic predisposition may play a role in increasing vulnerability, and social mores and environment, stress, gender, age and ethnic origin may also be risk factors. Generally speaking, the lead-in time to addiction to alcohol is much longer than with other psychoactive drugs, so that a heavy drinking male may continue to drink for a decade or so before succumbing to physical addiction. For women this period of time is much shorter, so that dependence may be achieved in as little as 2 or 3 years. Young people, and especially young women are at particular risk, with some studies indicating a 40% lifetime risk of dependence with the onset of regular drinking at 14 years. Whereas it was initially assumed that only “alcoholism” harmed the individual, it is now recognised that medical and psychological damage can precede and exist independently of addiction. Liver disease, cancers, heart disease, strokes, diabetes, digestive disorders, accidents, unwanted pregnancy and memory loss are but a few of the perils of excess drinking, and all harms occur more quickly and at lower levels of consumption in females.

Damosel (talk) 17:33, 29 August 2012 (UTC)[reply]

Defining Alcoholism

Just as Epilepsy is a common and diverse set of chronic neurological disorders characterized by seizures, so Alcoholism is a chronic neurological disorder characterized by obsessive compulsive drinking (of alcoholic drinks). Technically speaking, alcoholism is a neurobiochemical disorder that alters the reward cascade that controls subconscious decision making. Hence the 'addiction' characteristic. In fact many addictions have similar pathways but based on a different substance. What appears most confusing, are the causes of such disorders, since science has not yet been able to provide a comprehensive set of causes and pathways that can be easily understood. What is understood at present, is that genetics has a major role in a majority of addiction disorders.— Preceding unsigned comment added by 125.239.191.252 (talk) 19:18, 10 September 2012 (UTC)[reply]

Unbiased suggestion

Wikipedia mainly focuses on side effect and negative aspects of alcoholism. It asserts alcohol causes detriment of the drinker's health, personal relationships, and social standing. Throughout wikipedia, it warns alcohol addiction, a long-term misuse of alcohol, and its effects to physical and psychiatric. I totally agree with the prevalent research results in those negative aspects of alcoholism, but wikipedia significantly shows a lack of unbiased position in informing knowledge. Wikipedia is considerably required to inform people not only dark side of alcoholism, but also benefits by the moderate use of alcohol. I have experienced an effective method by alcohol to enhance my blood circulation and heart ability when I was sick in age of 10. As one of evidences, WebMD Health news tells that moderate alcohol intake can significantly reduce heart disease risk by up to 25% and it has positive effects on HDL. — Preceding unsigned comment added by Hosung83 (talkcontribs) 02:34, 1 October 2012 (UTC)[reply]

Thanks for your feedback, Hosung. Alcoholism is an addictive and neurodegenerative brain disease caused by chronic excessive intake of alcohol; it has nothing to do with moderate intake (e.g. 1 or 2 light glasses of wine per day). The benefits of moderate intake of alcohol are addressed in the appropriate article, long-term effects of alcohol, which you may wish to take a look at.--MrADHD | T@1k? 13:06, 28 October 2012 (UTC)[reply]

"Alcohol damages almost every organ in the body, including the brain."

The source cited in "Drink, Drugs and Dependence: From Science to Clinical Practice By J. De Belleroche" employs the word "can" in the statement this draws from. The significant damage alcohol does to the body is well documented, so let's not turn subjunctive statements into blanket facts, yo. 86.17.188.129 (talk) 01:57, 27 January 2013 (UTC)Ygnil[reply]

Thank you for spotting this. I have tried to improve the wording. Hopefully this issue is now resolved. :-)--MrADHD | T@1k? 12:20, 27 January 2013 (UTC)[reply]

Cultural

Unless this article is only about alcoholism in the US, there is still a lack of other countries approach. I wanted to add this link under section, "cultural" but I notice the page is in some kind-of lock. Please consider this addition since it covers multi-country cultural phenom., (Ireland, Russia to name 2) http://en.wikipedia.org/wiki/Seven_Drunken_Nights[[3]]24.0.133.234 (talk) 19:45, 12 February 2013 (UTC)[reply]
Found this under requests for review/open tasks[[4]]:"Alcoholism luckily only affects people in N. America. Rich Farmbrough 15:59 7 March 2006 (UTC). I spoke to Rich Farmbrough and he said the bias was "mostly" edited away but that "It should still touch on the alcohol problems in post-communist Russia, and the treatment, self-help and diagnosis have a Western bent, but nothing like what it was 5 years ago." Cloveapple (talk) 06:59, 17 May 2011 (UTC)"

Baclofen

There is no discussion here of the use of baclofen as a medicine for alcoholism, that it has been approved in France for off-licence use, that it is now being studied in the US by the NIH for use in anxiety related alcoholism [1]. There are references to this development under the baclofen and Olivier Ameisen entries on Wiki but nothing here. This medication should be added to the list of medications being used to treat alcoholismBaclofenuk (talk) 14:16, 22 February 2013 (UTC)[reply]

perhaps you should refer to Wikipedia's conflict of interest guidelines. Additionally we use reliable sources here, and a call for participants doesn't really qualify. Right now I think this section should be deleted as a promotional attempt.Coffeepusher (talk) 14:37, 22 February 2013 (UTC)[reply]

Baclofen

Some studies suggest that baclofen may reduce alcohol craving and use by reducing anxiety in alcoholics, which in turn can help to reduce cravings.

In May 2011 a Scottish team from Glasgow presented: "Baclofen at a Tailored Dose Reduces Alcohol Use, Craving and Consequences of Drinking in Alcoholics with Medical Disease due to Alcohol Dependence" at the "Royal College of Psychiatrists Faculty of Addictions Psychiatry Annual Meeting". They used doses between 15 and 360 mg of baclofen per day and winning the conference prize for the best poster raised the profile and increased interest in baclofen as anti-craving drug. 1

In 2012, baclofen was approved for use in the treatment of alcoholism on a case by case basis by the AFSSAPS.2

In the United States, the National Institutes of Health began recruiting participants in December 2012 for a study of baclofen for anxiety related alcoholism. The study is sponsored by the National Institute on Alcohol Abuse and Alcoholism (NIAAA).3

The use of Baclofen for the treatment of alcoholism came to widespread public attention as a result of the publication of The End of My Addiction by Dr. Olivier Amesen in 2008. [4] After hearing anecdotal reports that the muscle relaxant baclofen was, like naltrexone, acamprosate and topiramate, modestly effective at reducing the cravings of addictions, he experimented on himself, and proposed a new treatment model for addiction that is evidence-based. He first postulated that unlike other diseases where which suppression of symptoms is not associated with improvement of prognosis (such as: bacterial pneumonia, relief of unstable angina with medical means without surgery etc...), in addiction, suppression of symptoms (craving, preoccupation, thoughts etc...) should suppress the disease altogether since addiction is, as he observed, a "symptom-driven disease". Of all "anticraving medications used in animals, only one - baclofen - has the unique property of suppressing the motivation to consume cocaïne, heroin, alcohol, nicotine and d-amphetamine. The effect is dose-dependent.5 All other medications reduce but do not suppress the urge of the animal to consume alcohol or related substances. Ameisen hypothesized that these unique dose-dependent motivation-suppressing properties of baclofen in animals could be transposed to humans and suppress dependence altogether. He designed a protocol of baclofen dose -escalation (the same protocol that experienced neurologists use for comfort-care, going up to 300 mg/d for the treatment of spasticity. At the dose of 270 mg/d, Ameisen observed that he had become completely indifferent to alcohol. This, unlike abstinence which requires constant efforts, has occurred effortlessly. There were no side effects other than "welcome" mild somnolence in patient with anxiety. Ameisen stayed at this dose for only 10 days, progressively reducing to 120 mg/d at which there were no symptoms of alcohol-dependence altogether, and no side effects at all. Since 2003 Ameisen has been diagnosed as cured. Since complete suppression of dependence using a medication had never been described in the medical literature, Ameisen wrote up his own case report and the peer reviewed Journal Alcohol and Alcoholism published it on December 13, 2004, after praising the paper. In his paper, like in those that followed in JAMA, Lancet, CNS Drugs etc., Ameisen urged for randomized trials to test suppression of alcohol dependence using high-dose baclofen.6



1 ^ "'Anti-alcoholism' drug cleared for use in France".http://medicalxpress.com.+April 25, 2012.

2. http://www.rcpsych.ac.uk/pdf/baclofen%20poster2011%20masson_a0.pdf

3. http://clinicaltrials.gov/ct2/show/NCT01751386

4. ^ Hugh Schofield (6 Dec 2008), France abuzz over alcoholic 'cure', BBC 5.^ Ameisen, JAMA, 2005: Naltrexone for alcohol dependency

6. ^ Complete and prolonged suppression of symptoms and consequences of alcohol-dependence using high-dose baclofen: a self-case report of a physician. Ameisen O. Alcohol Alcohol. 2005 Mar-Apr;40(2):147-50. Epub 2004 Dec 13. http://alcalc.oxfordjournals.org/cgi/content/abstract/40/2/147Burdenedwithtruth (talk) 17:09, 23 February 2013 (UTC)[reply]

Burdenedwithtruth. Are you the same user as User:Baclofenuk? I ask because wikipedia has guidelines for using multiple accounts that you should be aware of and if you are the same user there is a simple way to make sure you don't get in trouble. I also ask because I have been speaking to Baclofenuk about different policies and I am wondering if I need to repeat myself or if we have already been talking about how to add Baclofen into this article.
Now your suggested addition (I am assuming that is what this post is about) on first glance looks good, but it really needs to be reduced quite a bit to follow wikipeida's guidelines on how much text should be used in an article in relation to other ideas. Right now, if you look at the medicine section of Alcoholism, each medication is only allocated approx. 1-3 sentences. This means that an entry for Baclofen should not exceed this amount of text, especially in relation to drugs like Antibuse which has a much longer history in the treatment of alcoholism, and has generated a significant amount of literature describing its use for alcohol treatment. You may want to also look at Baclofen, and see if those editors would be willing to allow a larger history of baclofen's treatment of alcoholism.Coffeepusher (talk) 17:49, 23 February 2013 (UTC)[reply]

Here is the most recent edit. I am the same user. I could not figure out how to change the name other than to open an account using the same details and type in a different username. I would prefer just to delete the baclofenuk account if that is ok. Here is the new edit. I expect you will say it is still too long. I hear what you are saying about weight but this drug is the only one which is going through trials at the moment in France and the US so it is hard to say that in a short space unless one summarizes it by simply referring to that fact and putting the trials as footnotes. Let me know. I am having difficulty formatting text for some reason and I have not figured out how to add links to Ameisen and baclofen pages.

Baclofen is an agonist for the GABAB receptors.[1][ 2] The use of baclofen for the treatment of alcoholism came to widespread public attention as a result of the publication of The End of My Addiction by Dr. Olivier Amesen in 2008. [3] Baclofen works by suppressing the motivation to consume cocaine, heroin, alcohol, nicotine and d-amphetamine. The effect is dose-dependent.[4] Research has shown baclofen to be effective in the treatment of alcohol dependence and withdrawal, by inhibiting both withdrawal symptoms and cravings.[5]In May 2011 a Scottish team headed by Dr. Mathis was awarded a prize for the best poster by the Royal College of Psychiatrists after using doses of 15 mg/d to 360 mg/d to treat alcoholics with medical disease due to alcoholism and raised the profile of and increased interest in baclofen as anti-craving drug. [6] Following studies, [7] a clinical trial of Baclofen began in France on 20 May 2012. The French Agency for the Safety of Health Products (AfSSAPS) has now authorized the prescription of Baclofen on a case by case basis by health professionals experienced in treating and managing dependency on alcohol.[8] Also in 2012 French doctors published a Guide for the prescribing of baclofen to treat alcoholism. [9] In December 2012 the United States’ National Institutes of Health began recruiting participants in December 2012 for a study of baclofen for anxiety related alcoholism. The study is sponsored by the National Institute on Alcohol Abuse and Alcoholism (NIAAA).[10] A support community has formed on the Mywayout forum for users of baclofen, many of whom purchase the drug on-line and self prescribe and many of whom report similar results to Dr. Ameisen. 1^ Mezler M., Müller T., Raming K. (February 2001). "Cloning and functional expression of GABA(B) receptors from Drosophila". Eur. J. Neurosci. 13 (3): 477–486.doi:10.1046/j.1460-9568.2001.01410.x. PMID 11168554. 2^ Dzitoyeva S., Dimitrijevic N., Manev H. (April 2003). "Gamma-aminobutyric acid B receptor 1 mediates behavior-impairing actions of alcohol in Drosophila: adult RNA interference and pharmacological evidence". Proc. Natl. Acad. Sci. U.S.A. 100 (9): 5485–5490. Bibcode 2003PNAS..100.5485D. doi:10.1073/pnas.0830111100.PMC 154371. PMID 12692303.


3. ^ Hugh Schofield (6 Dec 2008), France abuzz over alcoholic 'cure', BBC 4.^ Ameisen, JAMA, 2005: Naltrexone for alcohol dependency 5. ^ Addolorato, G.; Leggio, L.; Ferrulli, A.; Cardone, S.; Vonghia, L.; Mirijello, A.; Abenavoli, L.; D'Angelo, C. et al. (Dec 2007). "Effectiveness and safety of baclofen for maintenance of alcohol abstinence in alcohol-dependent patients with liver cirrhosis: randomised, double-blind controlled study". Lancet 370 (9603): 1915–1922. doi:10.1016/S0140-6736(07)61814-5. PMID 18068515. 6. http://www.rcpsych.ac.uk/pdf/baclofen%20poster2011%20masson_a0.pdf 7. “Abstinence and ‘Low-Risk’ Consumption 1 Year after the Initiation of High-Dose Baclofen: A Retrospective Study among ‘High-Risk’ Drinkers.” Laurent Rigal, Constance Alexandre-Dubroeucq, Renaud de Beaurepaire, Claire Le Jeunne and Philippe Jaury, Alcohol and Alcoholism, 19 March 2012. 8 ^ "'Anti-alcoholism' drug cleared for use in France".http://medicalxpress.com.+April 25, 2012. 9 https://dl.dropbox.com/u/59463672/Prescribing-Guide-for-Baclofen-in-the-Treatment-of-Alcoholism-Don.pdf 10. http://clinicaltrials.gov/ct2/show/NCT01751386Burdenedwithtruth (talk) 20:07, 23 February 2013 (UTC)[reply]

Ok, that actually looks really good. You are citing what you are saying and using reliable sources (a good rule of thumb is to try and put two citations for every sentence, that way no one will say that you are adding bad information). Additionally you followed the format used in the medicine section which is a stylistic trick that most new users don't pick up on. Kudoes! Now you are correct that it is a bit longer than will stand. So now we need to figure out what to reduce. I am happy to peruse it down for you, but this is your edit and I want to give you the chance to finish it off and add it to the article yourself. So take a look at it and figure out what an encyclopedia article entry would look like. The block of information about awards and countries it has been used in could probably be put into one sentence with multiple citations, technical details are probably not useful, but your intro is really great and I would recommend merging sentences one, three, and five into one complete sentence. Why don't you give it a shot and see if we can make this into a three/four sentence entry which will stand scrutiny by the other editors. again, if you would like I am happy to show you what I would do (this is a collaborative project and your edits will rarely stand the way you wrote them) but I do want you to have a good shot on your first mainspace edit.
as for your user name, I will see if the admins will approve a deletion of the original account. Coffeepusher (talk) 20:32, 23 February 2013 (UTC)[reply]
ok, i've looked over the policy and it seems unlikely that we will be able to argue to get your original account deleted. Don't worry too much about that right now. I would tag both accounts with the information I have given above regarding identifying that you have multiple accounts and you won't have any problems. (wikipedia is really big on keeping track of user edits so that we can keep track of problem behavior, you haven't displayed any issues so identifying both accounts won't hurt you.).Coffeepusher (talk) 20:37, 23 February 2013 (UTC)[reply]
also, before I forget, don't worry about the external links etc right now. Go ahead and do the citations the way you are doing them and when we get a product we want to add to the mainspace I will show you how to format them. Right now let's focus on getting the text right.Coffeepusher (talk) 20:48, 23 February 2013 (UTC)[reply]

Here is my newest draft. I hope I am almost there.


Baclofen is an agonist for the GABAB receptors.[1][ 2] Baclofen is dose dependant. [3][4] Two randomised controlled trials of fixed-dose baclofen have found significant improvements in alcohol intake, craving and duration of abstinence when compared to placebo controls by inhibiting both withdrawal symptoms and cravings.[5][6] Dr. Olivier Ameisen drew attention to the use of baclofen for the treatment of alcoholism by publishing a case study of his own use of high doses of baclofen[7] and a book about his treatment called The End of My Addiction 2008, later re-released as Heal Thyself [8]. A number of studies have been completed or are under way in Scotland, France and the United States with a view to having baclofen licenced as a treatment for alcoholism.[9][10][11]. The French Agency for the Safety of Health Products (AFSSAPS) has authorized the prescription of Baclofen pending the result of further trials [12]. A guide has been published to assist doctors in prescribing baclofen.[13] 1^ Mezler M., Müller T., Raming K. (February 2001). "Cloning and functional expression of GABA(B) receptors from Drosophila". Eur. J. Neurosci. 13 (3): 477–486.doi:10.1046/j.1460-9568.2001.01410.x. PMID 11168554. 2^ Dzitoyeva S., Dimitrijevic N., Manev H. (April 2003). "Gamma-aminobutyric acid B receptor 1 mediates behavior-impairing actions of alcohol in Drosophila: adult RNA interference and pharmacological evidence". Proc. Natl. Acad. Sci. U.S.A. 100 (9): 5485–5490. Bibcode 2003PNAS..100.5485D. doi:10.1073/pnas.0830111100.PMC 154371. PMID 12692303. 3.^ Ameisen, JAMA, 2005: Naltrexone for alcohol dependency 4. ^ Addolorato, G.; Leggio, L.; Ferrulli, A.; Cardone, S.; Vonghia, L.; Mirijello, A.; Abenavoli, L.; D'Angelo, C. et al. (Dec 2007). "Effectiveness and safety of baclofen for maintenance of alcohol abstinence in alcohol-dependent patients with liver cirrhosis: randomised, double-blind controlled study". Lancet 370 (9603): 1915–1922. doi:10.1016/S0140-6736(07)61814-5. PMID 18068515 5. Addolorato G et al. Baclofen efficacy in reducing alcohol craving and intake: a preliminary double-blind randomized controlled study. Alcohol 2002: 37; 504-508. 6. Addolorato G et al. Effectiveness and safety of baclofen for maintenance of alcohol abstinence in alcohol dependent patients with liver cirrhosis: randomised, doubleblind controlled study. Lancet 2007: 370; 1915-22.


7. ^ Hugh Schofield (6 Dec 2008), France abuzz over alcoholic 'cure', BBC . 8. ^ Complete and prolonged suppression of symptoms and consequences of alcohol-dependence using high-dose baclofen: a self-case report of a physician. Ameisen O. Alcohol Alcohol. 2005 Mar-Apr;40(2):147-50. Epub 2004 Dec 13. http://alcalc.oxfordjournals.org/cgi/content/abstract/40/2/147 9. http://www.rcpsych.ac.uk/pdf/baclofen%20poster2011%20masson_a0.pdf 10. “Abstinence and ‘Low-Risk’ Consumption 1 Year after the Initiation of High-Dose Baclofen: A Retrospective Study among ‘High-Risk’ Drinkers.” Laurent Rigal, Constance Alexandre-Dubroeucq, Renaud de Beaurepaire, Claire Le Jeunne and Philippe Jaury, Alcohol and Alcoholism, 19 March 2012. 11. http://clinicaltrials.gov/ct2/show/NCT01751386 12 ^ "'Anti-alcoholism' drug cleared for use in France".http://medicalxpress.com.+April 25, 2012. 13 https://dl.dropbox.com/u/59463672/Prescribing-Guide-for-Baclofen-in-the-Treatment-of-Alcoholism-Don.pdfBurdenedwithtruth (talk) 11:34, 24 February 2013 (UTC)[reply]

What I am picking up on in your edits is that you are used to technical writing. We are going to need to change that style when contributing to an encyclopedia. We are not talking to professionals, but to the general public so the tone should be conversational rather than "point A (full stop) point B (full stop) point C..." Give enough information to show it is different from other medications, but not too much. Get to the heart of what you are trying to say without bogging it down with details. I'll give you my suggestion based on what you have written.
"Baclofen is an agonist for the GABAB receptors which suppresses the motivation to consume cocaine, heroin, alcohol, nicotine and d-amphetamine by inhibiting both withdraw symptoms and cravings. The use of baclofen for the treatment of alcoholism came to widespread public attention as a result of the publication of The End of My Addiction by Dr. Olivier Amesen in 2008, later re-released as Heal Thyself. Currently, licencing agencies in several countries in Europe and the United States are engaging in clinical trials to research the use of baclofen for the treatment of alcoholism."
What do you think?Coffeepusher (talk) 14:53, 24 February 2013 (UTC)[reply]

That is fine. I would like to say that there is a guideline published because this is what led the French association to change their views on its use off licence. Is that going too far?? Whose decision is it ultimately?Burdenedwithtruth (talk) 14:48, 26 February 2013 (UTC)[reply]

To answer your question of "whose decision is it ultimately?" the answer is "all of us" but I believe it is ultimately up to you since you wanted this material added. Placing the information about the treatment guide is going to be difficult. The main reason is that to all appearances the guide is distributed exclusively by the Baclofen company, and adding it to this page would be seen as promotional. If you can find a reliable source which makes the claim that "Baclofen guide=change in attitude of France" then we could put a short blurb and link to that article, but the initial search doesn't turn up anything that would qualify. If you are satisfied I will add the references and give you instructions on how to add this to the mainspace.Coffeepusher (talk) 15:15, 26 February 2013 (UTC)[reply]

The Prescibing Guide isn't published anywhere in English. It is a guide produced by the doctors who conducted the study. I don't think there is any reference to it anywhere as it is not, in English, a publicly released paper but the doctors who wrote it are the ones conducting the studies in France. The decisions by the French authorities to advise doctors to use baclofen on an off-licence basis is reported and is cited. Can that go in? I think it is important and would be happy with that, but to leave out the prescribing guide. There is no baclofen company. It is a molecule. There are a number of pharmaceutical companies which make the drug containing it under various brand names. I have nothing to do with any of them.Burdenedwithtruth (talk) 16:25, 26 February 2013 (UTC)[reply]

why don't we work with the text without the guide for now. Bring those sources and we will have a look at them and see what, according to wikipedia guidelines, we can place into the article. Today I am a bit buisy but will have the text and instructions to you before the end of business today. Coffeepusher (talk) 16:59, 26 February 2013 (UTC)[reply]

That's fine. — Preceding unsigned comment added by Burdenedwithtruth (talkcontribs) 18:16, 26 February 2013 (UTC)[reply]

I think we should change the last sentence as follows:

"Baclofen is an agonist for the GABAB receptors which suppresses the motivation to consume cocaine, heroin, alcohol, nicotine and d-amphetamine by inhibiting both withdrawal symptoms and cravings. The use of baclofen for the treatment of alcoholism came to widespread public attention as a result of the publication of The End of My Addiction by Dr. Olivier Amesen in 2008, later re-released as Heal Thyself. Currently, clinical trials of baclofen are underway in several countries in Europe and the United States with a view to having baclofen licenced for the treatment of alcoholism"

I say this because,strictly speaking, it is not the licencing authorities who are conducting the trials. If that is ok please feel free to move on to the next stageBurdenedwithtruth (talk) 11:01, 27 February 2013 (UTC)[reply]

not a problem, I am still busy but I will get to it shortly.Coffeepusher (talk) 12:56, 27 February 2013 (UTC)[reply]

I can finish this if you tell me what to do.Burdenedwithtruth (talk) 19:10, 1 March 2013 (UTC)[reply]

no no. Don't worry, it is Friday and I SWEAR my real life is about to let up enough to finish those citations. Sorry about the delay.Coffeepusher (talk) 23:56, 1 March 2013 (UTC)[reply]

alright, here we go. The template for doing citations is <ref name="name"> {{cite journal |author= |title= |journal= |volume= |issue= |pages= |year= |pmid= |doi= }}</ref> just fill in the spots. Once you do the whole thing once in an article you can subsequently reference it by simply saying <ref name="name" />. So let's get the paragraph set up.

Looking at the medical section it should probably look like this in wiki code, Hit the "edit" icon to display the actual code and copy that:

  • Baclofen is an agonist for the GABAB receptors[2][3] which suppresses the motivation to consume cocaine, heroin, alcohol, nicotine and d-amphetamine[4] by inhibiting both withdraw symptoms and cravings.[5] The use of baclofen for the treatment of alcoholism came to widespread public attention as a result of the publication of The End of My Addiction by Dr. Olivier Amesen in 2008[6], later re-released as Heal Thyself. Currently, clinical trials of baclofen are underway in several countries in Europe and the United States with a view to having baclofen licenced for the treatment of alcoholism.[7][8]

Ok, now go ahead and copy this (in the code) and then go to the mainspace. once there, simply move to the medical section, hit "edit" and then paste this text where it seems most appropriate (if it is alphabetical, great! if it looks like they are using some other ordering system on medications then figure out what that is. Please do not put it "first" as that will really look suspicious especially since Antibuse is ahead of it alphabetically).

Good luck!Coffeepusher (talk) 04:46, 3 March 2013 (UTC)[reply]

  1. ^ http://clinicaltrials.gov/ct2/show/NCT01751386
  2. ^ "Cloning and functional expression of GABA(B) receptors from Drosophila". European Journal of Neuroscience. 13 (3): 477–486. 2001. doi:10.1046/j.1460-9568.2001.01410.x.. PMID 11168554. {{cite journal}}: Check |doi= value (help); Unknown parameter |author 1= ignored (help); Unknown parameter |author 2= ignored (help); Unknown parameter |author 3= ignored (help)
  3. ^ Dxitoyeva S.; Dimitrijevic N.; Manev H. (2001). "Gamma-aminobutyric acid B receptor 1 mediates behavior-impairing actions of alcohol in Drosophila: adult RNA interference and pharmacological evidence". Proceedings of the National Academy of Sciences, USA. 100 (9): 5485–5490. doi:10.1073/pnas.0830111100.PMC 154371.. PMID 12692303. {{cite journal}}: Check |doi= value (help)
  4. ^ Ameisen (2005). "Naltrexone for alcohol dependancy". Journal of the American Medical Association.
  5. ^ Addolorato, G.; Leggio, L.; Ferrulli, A.; Cardone, S.; Vonghia, L.; Mirijello, A.; Abenavoli, L.; D'Angelo, C.; et al. (2007). "Effectiveness and safety of baclofen for maintenance of alcohol abstinence in alcohol-dependent patients with liver cirrhosis: randomised, double-blind controlled study". Lancet. 370 (9603): 1915–1922. doi:10.1016/S0140-6736(07)61814-5.. PMID 18068515. {{cite journal}}: Check |doi= value (help); Explicit use of et al. in: |author8= (help)
  6. ^ Schofield, Hugh (December 6, 2008). "France abuzz over alcoholic 'cure'". BBC News. Retrieved March 2, 2013.
  7. ^ “Abstinence and ‘Low-Risk’ Consumption 1 Year after the Initiation of High-Dose Baclofen: A Retrospective Study among ‘High-Risk’ Drinkers.” Laurent Rigal, Constance Alexandre-Dubroeucq, Renaud de Beaurepaire, Claire Le Jeunne and Philippe Jaury, Alcohol and Alcoholism, 19 March 2012. 11. [1]
  8. ^ 'Anti-alcoholism' drug cleared for use in France".[2]

Vaccine for alcoholics

Croatian writer Giancarlo Kravar: New vaccine developed by scientists from Chile could help alcoholics, because if you drink even the slightest amount of alcohol will experience a bad hangover, the Croatian daily Glas Slavonia. Vaccine biochemical sends a message that does not produce liver genes that metabolize alcohol. The action takes between six months and one year.78.2.88.251 (talk) 16:47, 24 February 2013 (UTC)[reply]

Edit request on 12 June 2013

The citation #19 is formatted incorrectly. Here is a link to the paper which I assume is being cited. http://www.ncbi.nlm.nih.gov/pubmed/14628177 Thanks! 75.157.1.34 (talk) 05:34, 12 June 2013 (UTC)[reply]

Done! Thanks for pointing this out. 78.26 (I'm no IP, talk to me!) 15:30, 12 June 2013 (UTC)[reply]

Alcohol habituation and Opiate addiction

Alcohol inhibits oxidation (by ALDH) of Acetaldehyde to Acetic Acid, causing it to build up in acute or chronic alcoholism. High levels of Acetaldehyde in alcoholism lead to other reactions such as alcohol released Adrenalin and Acetaldehyde forming Opiate-like Isoquinolines. Narcotic antagonists, like Natrexone, induce immediate DTs (Delirium Tremens; withdrawal) when injected into alcoholics (yes, I need to find the references). Neither Alcoholism or Narcotics addiction have a simple "cure" (Kurt Cobain committed suicide while sober). However treatment with agonist-antagonists like Methadone may present an intermediate solution. Shjacks45 (talk) 05:16, 14 June 2013 (UTC)[reply]

Medications

This section is kind of a mess, given that we have mixed in drugs that have been approved by the FDA, for example, with other drugs that are undergoing current research but must be used "off-label" for alcoholism. I propose that we separate the drugs into two subcategories: "Approved" and "Experimental". Approved would have disulfiram, acomprosate, and naltrexone. The others would go into Experimental and their descriptions would be primarily that they are under study. The downside of this is that it would be very US-centric. To cure that, we could at least find out which drugs are approved in Europe without too much trouble. Any thoughts?Desoto10 (talk) 22:35, 11 July 2013 (UTC)[reply]

I like the idea of separating them, I agree that it is a little tricky. Would a third category "approved for alcoholism in some countries" work? We could explain in the sections which countries have approved use and which are experimental. This would make the third "experimental" category for drugs that are used for other treatments, but haven't been approved for alcoholism in any country .Coffeepusher (talk) 23:04, 11 July 2013 (UTC)[reply]
Good idea. One trouble that I find is that the FDA website does not have a search function (that I know of) for indications so that you can look up easily what drugs are approved for what diseases. Fortunately (or, actually, unfortunately) there are not a lot of drugs approved for alcoholism anywhere. We will need to add topirimate as well. A review just came out from the VA that shows, from prescription records, that topirimate is prescribed for alcohol abuse more than disulfiram and acomprosate combined, even though it is off-lable. What I want to avoid is a laundry list of drugs that somebody somewhere tried on patients, got a positive result and is now promoting its use without quality clinical trials and secondary sources.Desoto10 (talk) 02:56, 12 July 2013 (UTC)[reply]
I would say that we have the culling criteria in what you just stated. Lets say that a WP:RS must indicate that the drug has been either approved or is being tested for alcoholism specifically by one or more countries, not just a reliable source that says it is being used by one or more doctors. What do you think? Coffeepusher (talk) 03:05, 12 July 2013 (UTC)[reply]
I might go a little further to separate the drugs that are actually approved by each country from those "under investigation". I would also limit our "under investigation" to those drugs that have some clinical (ie., not animal or in vitro) studies to back them up. The major failure point in drug development is the transition from preclinical (animal studies) to human trials. Lots of compounds show promise in preclinical but just don't work in humans.Desoto10 (talk) 22:39, 13 July 2013 (UTC)[reply]
I like that criteria, so you are saying ONLY those drugs that are actually approved for human testing, with a separation of "Approved for alcoholism" (with a reliable source naming at least one country where it is specifically approved for alcoholism, with proper notations on any other countries where it is in the trial stage), "under investigation" (with a reliable source stating that it is currently in human trials for Alcoholism). Now do you still want an "experimental" section for drugs not approved for alcoholism, but approved for other treatments?Coffeepusher (talk) 22:46, 13 July 2013 (UTC)[reply]
I think that would be appropriate, particularly for this disease, because, as I mentioned earlier, some off-label drugs are used more than the on-label drugs. Still, I think we ought to put the bar up fairly high for the experimental drugs. Of course, this may all be academic as I cannot find a high quality list of drugs for alcoholism that have been approved in, for example, the European Union, to say nothing of South America, Asia, etc. Desoto10 (talk) 20:44, 15 July 2013 (UTC)[reply]

You need to start by looking at Wikipedia in other languages. Baclofen has now been approved for use in France just this summer even though trials are still underway because the results over the last 6 or 7 years are such that it is obviously working and there have been numerous successful trials. Here is a Google translate from Wiki.fr: Other molecules are being tested , such as baclofen . It is a muscle relaxant indicated for the treatment of muscle spasticity, a Benin disorder but highly uncomfortable observed for example in the aftermath of a stroke, in paraplegics , or cerebral palsy patients with multiple sclerosis but also in the simple spasmodique28 torticollis . It is marketed under the name of Lioresal , but from generics since the 1980s . It is prescribed as a treatment since 1966 comfort. The AMM allows up to 80 milligrams per day. Beyond 80 milligrams per day , it is question of high doses. Baclofen , however, was tested as a treatment for mild comfort in doses of 300 milligrams per jour29 disorders for several consecutive years in adults and 180 milligrams per day (eg torticollis in children) 28 without effects second limiting. They emphasize that he never met with significant side effects. The most common are drowsiness or muscle weakness that both always regress in 24 or 48 hours without sequelae .

Also, here is the entry for "baclofene" in the French Wiki page: Le 3 juin 2013, le président de l'Agence nationale de sécurité du Médicament (ANSM) Dominique Maranchini annonce une prochaine Recommandation Temporaire d'Utilisation (RTU) pour le baclofène en France24, qui courra sur 3 ans, en attendant la fin de 2 essais contre placebo. Ainsi, le baclofène à haute dose sera autorisé dans l'indication d'alcoolo-dépendance.

Tranalated with Google gives you this: June 3, 2013, the President of the National Security Agency of Medicines (MSNA) Dominique Maranchini announces next Recommendation Temporary Use (RTU) for baclofen in France24, which will run for 3 years, until the end of 2 trials against placebo. Thus, the high-dose baclofen be allowed in the indication of alcohol dependence.

Which means that baclofen is now approved and used in France by all doctors for treatment for treatment of alcoholism. It is now also being considered by the NICE in England and is under study by the US equivalent.Burdenedwithtruth (talk) 06:00, 23 November 2013 (UTC)[reply]

Someone has again edited the medicines section of this page without discussion, removing the agreed content about baclofen and substituting a reference to one study only. The study referred to is in relation to alcohol withdrawal so it is not appropriate to this topic. There was no discussion of this and this is the second time this edit has been made by a person unknown with no discussion here which violates the rules of Wiki. I have reinstated the content as agreed with Coffeepusher but the cites have also been interfered with so these need to be reinstated properly.Burdenedwithtruth (talk) 06:20, 29 December 2013 (UTC)[reply]

The prescribing guide for baclofen has now been published in English: British Journal of Medicine and Medical Research, ISSN: 2231-0614,Vol.: 4, Issue.: 5 (01-15 March) - See more at: http://www.sciencedomain.org/abstract.php?iid=315&id=12&aid=2459#.Ur--v_QW3RIBurdenedwithtruth (talk) 06:20, 29 December 2013 (UTC)[reply]

With respect to baclofen the best available evidence does not support its use.[5] Doc James (talk · contribs · email) (if I write on your page reply on mine) 08:39, 29 December 2013 (UTC)[reply]

The most senior alcohol specialists in the world are using it in treatment. You are not a specialist in that field. Check the Baclofen section where you will find their names. They are supported by the UK Royal College of Psychiatry and the editor of the Oxford Journal of Alcohol and Alcoholism. You breached Wiki rules by failing to discuss this. I suggest something be put back in even if it is not what I drafted.Burdenedwithtruth (talk) 21:42, 30 December 2013 (UTC)[reply]

This edit of yours was a complete mess and you removed two review articles on the topic.[6]. I have moved this content to the research section of the article. It is unclear what text you wish to add and what refs you wish to use to support it. Doc James (talk · contribs · email) (if I write on your page reply on mine) 02:45, 31 December 2013 (UTC)[reply]
Also please read WP:MEDRS. Doc James (talk · contribs · email) (if I write on your page reply on mine) 02:46, 31 December 2013 (UTC)[reply]

Okay found a 2013 French review that says baclofen for alcohol dependence is worth studying further [7]. Doc James (talk · contribs · email) (if I write on your page reply on mine) 09:02, 31 December 2013 (UTC)[reply]

Ok, can you put it in? I suggest this part be put in: "Three uncontrolled retrospective series reported the results obtained in 300 alcohol-dependent patients, most of whom were in treatment failure. They were treated with high, escalating doses of baclofen (on average about 150 mg per day, up to 400 mg per day) with the intention of reducing their craving for alcohol. After 3 to 24 months of follow-up, about half of the patients reported moderate or zero alcohol consumption."Burdenedwithtruth (talk) 09:23, 2 January 2014 (UTC)[reply]

Uncontrolled retrospectives series are not really notable and do not / should not determine treatment. This is summed up in "tentative evidence". Doc James (talk · contribs · email) (if I write on your page reply on mine) 11:39, 2 January 2014 (UTC)[reply]

http://www.google.com/patents/WO2012020170A1?cl=en — Preceding unsigned comment added by 93.106.112.138 (talk) 20:54, 16 January 2015 (UTC)[reply]

Reference #6

Reference #6, the AMA document, no longer appears to exist, or perhaps no longer represents AMA policy. Thoughts as to how to proceed? Drgitlow (talk) — Preceding undated comment added 21:08, 15 March 2014 (UTC)[reply]

found another source for this. Jytdog (talk) 00:48, 16 March 2014 (UTC)[reply]

18% of alcoholics commit suicide?

According to the article some 12% of American adults are (or will be) alcohol dependent at some point in their lifetime - if the terms "alcohol dependent" and "alcoholic" are taken to be interchangeable (as in the article), then 12% of American adults are alcoholics. If 18% of alcoholics commit suicide, then at least 2.16% of American deaths should be suicides (not counting suicides by non-alcoholics) This is simply not plausible as suicide accounts for 1.6% of all US deaths (2010) according to the cdc's report at http://www.cdc.gov/nchs/data/nvsr/nvsr61/nvsr61_04.pdf Also in the article a WHO estimate of the world's population of chronic alcoholics is given as 140 million (or 2% of total world population at 7 billion). There is a general inconsistency in the numbers. I also just have serious misgivings about a statement like "18% of all alcoholics commit suicide" - if it was "18% of all suicides are committed by alcoholics", then it'd be plausible. I notice that the reference is to a text "Drug Abuse Prevention: A School and Community Partnership" - texts geared towards drug abuse prevention among children tend to be more hyper-alarmist and fear-mongering rather than fact-based and informative - I also don't know where in that reference (which is a book of 346 pages) one is to find that dire and fatalistic factoid. Anyone else have thoughts on this? Qdiderot (talk) 20:58, 9 July 2014 (UTC)[reply]

Agree and have replaced with a better ref.Doc James (talk · contribs · email) (if I write on your page reply on mine) 17:13, 10 July 2014 (UTC)[reply]

This has nothing to do with alcoholism

"In a study done on Korean immigrants in Canada, they reported alcohol was even an integral part of their meal, and is the only time solo drinking should occur. They also believe alcohol is necessary at any social event as it helps conversations start.[156]"

Under "Society and Culture". It deals with alcohol consumption, but nothing about alcoholism. I think I'm going to delete it. — Preceding unsigned comment added by 71.207.108.86 (talk) 06:41, 27 July 2014 (UTC)[reply]

New image found

probably dont need this, but its newly discovered, 1870s california

285-WHEN SHALL WE THREE MEET AGAIN

Mercurywoodrose (talk) 03:08, 12 September 2014 (UTC)[reply]

Annotated signal transduction diagram for alcohol addiction

I'm waffling over whether or not it's worth creating an annotated signal transduction diagram for alcohol addiction (analogous to Template:Psychostimulant addiction, which is the image in the collapsed tab below and the references/color legend that transclude with it). I figured I'd seek input from others before doing this: is it worth creating a diagram like this (the image would illustrate the bottom diagram in this link) to show the neuronal mechanisms that alcohol acts through to produce a state of addiction? I'm asking on this talkpage since I just redirected alcohol addiction to this article (it was redirecting to alcohol dependence before, which is a distinct concept).

This article's pathophysiology section only covers alcohol dependence, which isn't the same concept and arises through a different mechanism; I'm not sure the causes/mechanism of alcohol addiction are covered in any wikipedia article (besides ΔFosB) at the moment. Seppi333 (Insert  | Maintained) 23:54, 1 November 2014 (UTC)[reply]

@Boghog: I'm wondering what you think about creating this diagram for the article - is it too technical? I'd seek your feedback like last time if I go ahead with this. Seppi333 (Insert  | Maintained) 00:06, 2 November 2014 (UTC)[reply]
Hi Seppi333. I think the bottom diagram (chronic alcohol) in the link would be way too technical for a general article about alcoholism. Can the diagram be simplified (e.g., remove the intermediate steps of the MAPK signaling pathway) while maintaining technical accuracy? Boghog (talk) 08:13, 9 November 2014 (UTC)[reply]
It wouldn't be out of the ordinary to do that; I've seen the cAMP/CaMK/MAPK pathways merely indicated with a line and no intermediate steps in some reviews. I'm getting a bit ahead of myself though; I should probably expand the section on mechanisms to include coverage of how ethanol interacts with the mesolimbic pathway before starting on the image, assuming I decide to make one. Based upon my reference texts, ethanol has some pretty complex dynamics in that pathway, so I actually need to do a literature search for current sources on the topic. Seppi333 (Insert  | Maintained) 00:05, 10 November 2014 (UTC)[reply]
Annotated image diagram for psychostimulants
Signaling cascade in the nucleus accumbens that results in psychostimulant addiction
The image above contains clickable links
This diagram depicts the signaling events in the brain's reward center that are induced by chronic high-dose exposure to psychostimulants that increase the concentration of synaptic dopamine, like amphetamine, methamphetamine, and phenethylamine. Following presynaptic dopamine and glutamate co-release by such psychostimulants,[1][2] postsynaptic receptors for these neurotransmitters trigger internal signaling events through a cAMP-dependent pathway and a calcium-dependent pathway that ultimately result in increased CREB phosphorylation.[1][3][4] Phosphorylated CREB increases levels of ΔFosB, which in turn represses the c-Fos gene with the help of corepressors;[1][5][6] c-Fos repression acts as a molecular switch that enables the accumulation of ΔFosB in the neuron.[7] A highly stable (phosphorylated) form of ΔFosB, one that persists in neurons for 1–2 months, slowly accumulates following repeated high-dose exposure to stimulants through this process.[5][6] ΔFosB functions as "one of the master control proteins" that produces addiction-related structural changes in the brain, and upon sufficient accumulation, with the help of its downstream targets (e.g., nuclear factor kappa B), it induces an addictive state.[5][6]


References

  1. ^ a b c Renthal W, Nestler EJ (September 2009). "Chromatin regulation in drug addiction and depression". Dialogues in Clinical Neuroscience. 11 (3): 257–268. doi:10.31887/DCNS.2009.11.3/wrenthal. PMC 2834246. PMID 19877494. [Psychostimulants] increase cAMP levels in striatum, which activates protein kinase A (PKA) and leads to phosphorylation of its targets. This includes the cAMP response element binding protein (CREB), the phosphorylation of which induces its association with the histone acetyltransferase, CREB binding protein (CBP) to acetylate histones and facilitate gene activation. This is known to occur on many genes including fosB and c-fos in response to psychostimulant exposure. ΔFosB is also upregulated by chronic psychostimulant treatments, and is known to activate certain genes (eg, cdk5) and repress others (eg, c-fos) where it recruits HDAC1 as a corepressor. ... Chronic exposure to psychostimulants increases glutamatergic [signaling] from the prefrontal cortex to the NAc. Glutamatergic signaling elevates Ca2+ levels in NAc postsynaptic elements where it activates CaMK (calcium/calmodulin protein kinases) signaling, which, in addition to phosphorylating CREB, also phosphorylates HDAC5.
    Figure 2: Psychostimulant-induced signaling events
  2. ^ Broussard JI (January 2012). "Co-transmission of dopamine and glutamate". The Journal of General Physiology. 139 (1): 93–96. doi:10.1085/jgp.201110659. PMC 3250102. PMID 22200950. Coincident and convergent input often induces plasticity on a postsynaptic neuron. The NAc integrates processed information about the environment from basolateral amygdala, hippocampus, and prefrontal cortex (PFC), as well as projections from midbrain dopamine neurons. Previous studies have demonstrated how dopamine modulates this integrative process. For example, high frequency stimulation potentiates hippocampal inputs to the NAc while simultaneously depressing PFC synapses (Goto and Grace, 2005). The converse was also shown to be true; stimulation at PFC potentiates PFC–NAc synapses but depresses hippocampal–NAc synapses. In light of the new functional evidence of midbrain dopamine/glutamate co-transmission (references above), new experiments of NAc function will have to test whether midbrain glutamatergic inputs bias or filter either limbic or cortical inputs to guide goal-directed behavior.
  3. ^ Kanehisa Laboratories (10 October 2014). "Amphetamine – Homo sapiens (human)". KEGG Pathway. Retrieved 31 October 2014. Most addictive drugs increase extracellular concentrations of dopamine (DA) in nucleus accumbens (NAc) and medial prefrontal cortex (mPFC), projection areas of mesocorticolimbic DA neurons and key components of the "brain reward circuit". Amphetamine achieves this elevation in extracellular levels of DA by promoting efflux from synaptic terminals. ... Chronic exposure to amphetamine induces a unique transcription factor delta FosB, which plays an essential role in long-term adaptive changes in the brain.
  4. ^ Cadet JL, Brannock C, Jayanthi S, Krasnova IN (2015). "Transcriptional and epigenetic substrates of methamphetamine addiction and withdrawal: evidence from a long-access self-administration model in the rat". Molecular Neurobiology. 51 (2): 696–717 (Figure 1). doi:10.1007/s12035-014-8776-8. PMC 4359351. PMID 24939695.
  5. ^ a b c Robison AJ, Nestler EJ (November 2011). "Transcriptional and epigenetic mechanisms of addiction". Nature Reviews Neuroscience. 12 (11): 623–637. doi:10.1038/nrn3111. PMC 3272277. PMID 21989194. ΔFosB serves as one of the master control proteins governing this structural plasticity. ... ΔFosB also represses G9a expression, leading to reduced repressive histone methylation at the cdk5 gene. The net result is gene activation and increased CDK5 expression. ... In contrast, ΔFosB binds to the c-fos gene and recruits several co-repressors, including HDAC1 (histone deacetylase 1) and SIRT 1 (sirtuin 1). ... The net result is c-fos gene repression.
    Figure 4: Epigenetic basis of drug regulation of gene expression
  6. ^ a b c Nestler EJ (December 2012). "Transcriptional mechanisms of drug addiction". Clinical Psychopharmacology and Neuroscience. 10 (3): 136–143. doi:10.9758/cpn.2012.10.3.136. PMC 3569166. PMID 23430970. The 35-37 kD ΔFosB isoforms accumulate with chronic drug exposure due to their extraordinarily long half-lives. ... As a result of its stability, the ΔFosB protein persists in neurons for at least several weeks after cessation of drug exposure. ... ΔFosB overexpression in nucleus accumbens induces NFκB ... In contrast, the ability of ΔFosB to repress the c-Fos gene occurs in concert with the recruitment of a histone deacetylase and presumably several other repressive proteins such as a repressive histone methyltransferase
  7. ^ Nestler EJ (October 2008). "Transcriptional mechanisms of addiction: Role of ΔFosB". Philosophical Transactions of the Royal Society B: Biological Sciences. 363 (1507): 3245–3255. doi:10.1098/rstb.2008.0067. PMC 2607320. PMID 18640924. Recent evidence has shown that ΔFosB also represses the c-fos gene that helps create the molecular switch—from the induction of several short-lived Fos family proteins after acute drug exposure to the predominant accumulation of ΔFosB after chronic drug exposure
  1. ^
      (Text color) Transcription factors

Removal of a primary reference

I understand some of the reasons why Jytdog removed this primary source from 30 years ago, but I suggest that reference was useful (and the shock expressed in the edit summary was unwarranted). I coupled it with a high-quality secondary source that verifies the concepts (i.e. they are aligned conceptually). The primary source described the supported concept in a publicly available abstract, whereas the secondary source is behind a paywall. In such situations, older references are not bad, just inferior to recent sources (I would welcome one that served as well, but you simply removed it). I also think it's worth highlighting that in such a situation, WP:PRIMARYNOTBAD. WP:MEDRS states, "Research papers that describe original experiments are primary sources. However, they normally contain introductory, background, or review sections that place their research in the context of previous work; these sections may be cited in Wikipedia with care." - and I did place this one with care, next to a higher-quality but less-accessible source that agrees. I have no intention of reverting this edit myself - it's not a big deal and I have immense respect for the editor who did this removal - but I think we should focus on improving the article, and in fact I think this removal made the concepts less available to most readers. Replacement with a better, more recent ref that serves the same purpose would be a substantial improvement, so I hope we find one. Sometimes, it's worth airing one's thought process - hence this note. -- Scray (talk) 21:33, 22 November 2014 (UTC)[reply]

it is very very hard to imagine a situation where a 30 year old primary source would be acceptable in health-related article in Wikipedia, especially for such a well-researched and discussed topic as alcoholism. this is not some obscure disease. i found a recent review and replaced all the sources with it. it is free access too. took like three minutes to find that.... Jytdog (talk) 22:03, 22 November 2014 (UTC)[reply]
Agree that's a big improvement. Replacement is much better than removal. -- Scray (talk) 23:37, 22 November 2014 (UTC)[reply]

Nov 23 deletion by User:Doc James questioned: (→‎Long-term misuse: not a symptom or sign really)

User:Doc James, could you please clarify your reason "not a symptom or sign really" for deleting two small paragraphs, one citing the new large study from CDCP for the National Survey on Drug Use and Health? The reported results appear to me to be highly relevant to the article, although this citation might be better located elsewhere in the article. thanks. Layzeeboi (talk) 21:59, 23 November 2014 (UTC)[reply]

Ah, now I see that in your next edit, you re-introduced the deleted material in the section Urine_and_blood_tests under Diagnosis. How can a study of the correlation between alcohol dependence and either consumption or binge drinking belong there? Layzeeboi (talk) 22:12, 23 November 2014 (UTC)[reply]
Sure lets move it here will we discuss. The text in question is:
"The National Institute on Alcohol Abuse and Alcoholism (NIAAA) defines binge drinking as the amount of alcohol leading to a blood alcohol content (BAC) of 0.08, which, for most adults, would be reached by consuming five drinks for men or four for women over a 2-hour period. According to the NIAAA, men may be at risk for alcohol-related problems if their alcohol consumption exceeds 14 standard drinks per week or 4 drinks per day, and women may be at risk if they have more than 7 standard drinks per week or 3 drinks per day. It defines a standard drink as one 12-ounce bottle of beer, one 5-ounce glass of wine, or 1.5 ounces of distilled spirits.[1] Despite this risk, a 2014 report in the National Survey on Drug Use and Health found that only 10% of either "heavy drinkers" or "binge drinkers" defined according to the above critera also met the criteria for alcohol dependence, while only 1.3% of non-binge drinkers met this criteria.[2]"
This is a definition for diagnosis. Thus IMO should go somewhere in the diagnosis section. Also we should be really using secondary sources rather than primary sources. Doc James (talk · contribs · email) 00:28, 24 November 2014 (UTC)[reply]

References

  1. ^ http://pubs.niaaa.nih.gov/publications/aa68/aa68.htm
  2. ^ Esser, Marissa B.; Hedden, Sarra L.; Kanny, Dafna; Brewer, Robert D.; Gfroerer, Joseph C.; Naimi, Timothy S. (20 November 2014). "Prevalence of Alcohol Dependence Among US Adult Drinkers, 2009–2011". Preventing Chronic Disease. 11. doi:10.5888/pcd11.140329.
I agree! I finally realized that our misunderstanding was due to my omission of the main motivation of the Esser study. It really belongs in the article binge drinking, but I also inserted it as second paragraph of Definition here, as it follows nicely the last sentence of the first paragraph. Layzeeboi (talk) 22:08, 6 January 2015 (UTC)[reply]

Proposal for an addition of MicroRNA information under "Causes"

I have made an addition to the microRNA page about the role of microRNAs in alcohol addiction, and would like to add a section on this alcoholism page connecting the research. Although this material is very heavy in molecular neurobiology, I only took the simplest of information from my miRNA edit to allow biologically-oriented readers to follow up if interested.

The edit would be as follows:

"One paper has found that alcohol use at an early age may influence the expression of genes which increase the risk of alcohol dependence." Chronic alcohol abuse results in persistent changes in brain function mediated in part by alterations in gene expression. [1] MicroRNAs, or small non-coding RNA molecules, have been shown to significantly regulate gene expression in mammals. [2] miRNA global regulation of many downstream genes deems significant regarding the reorganization or synaptic connections or long term neuroadaptions involving the behavioral change from alcohol consumption to withdrawal and/or dependence.[3] Up to 35 different miRNAs have been found to be altered in the alcoholic post-mortem brain, all of which target genes that include the regulation of important cellular processes. [1] Altered miRNA levels were also found in specific areas of the brains of alcohol-dependent mice, suggesting the role of miRNA in orchestrating cellular changes where complex cognitive behavior and decision making likely originate. [4] Jbryfonski (talk) 00:51, 10 December 2014 (UTC)[reply]

Your refs are broken. Please read WP:MEDHOW Doc James (talk · contribs · email) 01:06, 10 December 2014 (UTC)[reply]
I might add something on that at a later date when the critical microRNAs in alcoholism are identified, but at this point it's basically just a summary of everything that's currently stated at the not-so-well-covered-here ΔFosB article. All addictions involve common epigenetic mechanisms (CREB in most types, ΔFosB in all known types), but with distinct downstream targets from those common elements. That downstream component is still an active area of research for drug & behavioral addictions. Seppi333 (Insert  | Maintained) 01:28, 10 December 2014 (UTC)[reply]

References

  1. ^ a b Cite error: The named reference Lewohl was invoked but never defined (see the help page).
  2. ^ Ambros, V (Sep 16, 2004). "The functions of animal microRNAs". Nature. 431 (7006): 350–5. doi:10.1038/nature02871. PMID 15372042.
  3. ^ Template:Citepmid
  4. ^ Template:Citepmid
Not done for now: Your requested edit seems to be lacking proper references and there seems to be a lack of consensus to make the changes as requested. Please discuss and reactivate the edit request when consensus has been reached on text to add. Thank you. — {{U|Technical 13}} (etc) 20:24, 10 December 2014 (UTC)[reply]

Semi-protected edit request on 13 May 2015

Simple grammar fix.

This: In the United States it results in economic costs of $224 billion USD in 2006.

Should be this: In the United States it resulted in economic costs of $224 billion USD in 2006. Robertew54 (talk) 23:45, 13 May 2015 (UTC)[reply]

Adjusted Doc James (talk · contribs · email) 01:01, 14 May 2015 (UTC)[reply]

Main links are for subarticles that contain just a summary here. Thus the main link for the pathophysiology section would be pathophysiology of alcoholism. This is not the main link and thus removed {{main|ΔFosB}} Term is already linked in the article. Doc James (talk · contribs · email) 11:53, 16 May 2015 (UTC)[reply]

It does not exclusively deal with the pathophysiology of alcoholism. It deals with the pathophysiology of a number of addictions. Doc James (talk · contribs · email) 11:55, 16 May 2015 (UTC)[reply]
I wrote FOSB in a way that covers the role of ΔFosB in any addiction, independent of the stimulus, be it an addictive drug or an addictive behavior. Literally the only things in the addiction section on that page which is stimulus specific is a note on cross-sensitization between amphetamine reward/addiction and sexual reward/addiction and the amphetamine addiction diagram, but the transcriptional elements in the nuclear membrane are common to other stimuli (e.g., c-fos repression via ΔFosB/HDAC1/SIRT1). There's almost no coverage of epigenetic mechanisms (that's even more complicated), which is where massive differences exist between the mechanisms that help ΔFosB establish and maintain an addictive state toward a specific stimulus; without that, ΔFosB overexpression by viral vectors simply promote compulsivity toward anything rewarding until stimulus-specific epigenetic remodeling occurs. Compulsive reward seeking toward arbitrary rewarding stimuli fits the definition of an addiction though, which is why it doesn't matter at all about what pathophysiology section links to ΔFosB. It is literally the single common and critical element across all addictive stimuli which alone (when overexpressed) can induce an addictive state. That's why ΔFosB and its addiction subsection, as written, equally cover the pathophysiology of amphetamine addiction, alcoholism, cocaine addiction, opioid addiction, sexual addiction, and addiction to any other addictive stimulus.
Just some of the epigenetic mechanisms, most of which differ across stimuli, include HDAC1, HDAC2, HDAC3, HDAC4, HDAC5, HDAC10, sirtuin 1, histone acetyltransferases like CBP, histone methyltransferase like G9a (that's the most significant/notable mechanism among these and it's common to all drugs) and G9a-like protein (sad that we don't have an article for that enzyme), and others. The epigenetic remodeling and microRNAs that I mentioned is where addiction pathophysiology varies across all stimuli, and I assume this neuroepigenetic component is what makes an addiction specific to a particular stimulus. It is very complicated (that reviews addictive drug epigenetics) compared to what I've written on the biomolecular mechanisms so far, but as that review indicates, in spite of amphetamine and cocaine producing similar effects, their epigenetic mechanisms are markedly different. This review on amphetamine[1] and epigenetics of cocaine addiction show that their epigenetic mechanisms differ a lot, although there a few elements in common (e.g., sirtuin 1, HDAC1 and G9a are involved in both) in how they go about chromatin remodeling in the nucleus accumbens.
Now, with that said, until there's a detailed article on epigenetics of alcoholism like the one for cocaine, the pathophysiology section really should link to ΔFosB, as it covers content which is entirely relevant alcoholism pathophysiology and isn't already covered here (e.g., what ΔFosB actually does in the nucleus accumbens, how changes in its expression affects behavior, the transcriptional targets table, and the graph showing how it's expressed over time during acute exposure and builds up during chronic exposure to drugs). It doesn't indicate alcoholism in particular in its coverage of addiction because ΔFosB's effects are relevant to all addictive drugs/behaviors, as stated on that page... several times. Seppi333 (Insert ) 13:03, 16 May 2015 (UTC)[reply]

References

  1. ^ McCowan TJ, Dhasarathy A, Carvelli L (February 2015). "The Epigenetic Mechanisms of Amphetamine" (PDF). J. Addict. Prev. (S1). Avens Publishing Group: 1–7. ISSN 2330-2178. Retrieved 30 April 2015. Epigenetic modifications caused by addictive drugs play an important role in neuronal plasticity and in drug-induced behavioral responses. Although few studies have investigated the effects of AMPH on gene regulation (Table 1), current data suggest that AMPH acts at multiple levels to alter histone/DNA interaction and to recruit transcription factors which ultimately cause repression of some genes and activation of other genes. Importantly, some studies have also correlated the epigenetic regulation induced by AMPH with the behavioral outcomes caused by this drug, suggesting therefore that epigenetics remodeling underlies the behavioral changes induced by AMPH. If this proves to be true, the use of specific drugs that inhibit histone acetylation, methylation or DNA methylation might be an important therapeutic alternative to prevent and/or reverse AMPH addiction and mitigate the side effects generate by AMPH when used to treat ADHD.
We already link to ΔFosB in that section and no one is saying we shouldn't. This is a misuse of the main template as it is not a page specifically about the pathophysiology of alcoholism. You appear to be attempting to overlink to a page that you have written. We do not typically link to the same article multiple times. Doc James (talk · contribs · email) 13:18, 16 May 2015 (UTC)[reply]
The only reason that hatnote should remain is that it points out that FOSB contains more detail on its pathophysiology. If overlooking is your concern, I don't mind removing the link in the text. Seppi333 (Insert ) 13:29, 16 May 2015 (UTC)[reply]
We do not typically link to the same article multiple times...I concur with DocJames --Ozzie10aaaa (talk) 13:33, 16 May 2015 (UTC)[reply]