Talk:Addiction/Archive 3
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Archive 1 | Archive 2 | Archive 3 | Archive 4 |
Neutral point of view
This article seems heavily biased toward genetic explanations for addiction, based inappropriately on one or two papers that seem to have had little real influence in the professional literature, in violation of Wikipedia:Neutral point of view#Due and undue weight. A Google Scholar search for Nestler 2013 and Ruffle 2014, on which a great deal of material in this article is based, shows 44 citations and 1(!) citation, respectively, compared to 704 for Dube et al. 2003, which advances a psychosocial interpretation. Meanwhile, the National Institute on Drug Abuse (USA) says that genetic factors account for only about half of a person's vulnerability to addiction.
— Coconutporkpie (talk) 23:06, 29 January 2016 (UTC)
- You're confusing risk factors with pathophysiology. The transcriptional and epigenetic proteins that the article refers to are mechanisms that mediate the development of an addiction (pathophysiology), not the proclivity for developing one (risk factor). AFAIK, the transcriptional and epigenetic mechanisms to which the article refers aren't associated with polymorphisms that affect individual susceptibility to developing an addiction. Even if a few are associated, their contribution to overall risk is likely insignificant since they're just individual genes. The article doesn't actually say anywhere that transcription factors and epigenetic mechanisms are risk factors, excluding the transgenerational epigenetic inheritance section, although that's a risk factor associated with a gene-environment interaction, not genes alone. Seppi333 (Insert 2¢) 00:42, 30 January 2016 (UTC)
- Probably worth pointing out that the Nestler review that you've linked above covers genetic/environmental risk factors and is consistent with the NIDA statement you mentioned.
Genetic factors account for roughly 50% of this individual variability in addiction vulnerability, and this degree of heritability holds true for all major classes of addictive drugs, including stimulants, opiates, alcohol, nicotine, and cannabinoids.2 It has not yet been possible to identify most of the genes that comprise this genetic risk, likely due to the involvement of perhaps hundreds of genetic variations summating in a single individual to confer addiction vulnerability (or, in other individuals, resistance). The other 50% of the risk for addiction is due to a host of environmental factors, occurring throughout a lifetime, that interact with an individual's genetic composition to render him or her vulnerable to addiction to a greater or lesser extent. Several types of environmental factors have been implicated in addiction, including psychosocial stresses, but by far the most powerful factor is exposure to a drug of abuse itself. Certain “gateway” drugs, in particular, nicotine, have been shown to increase one's vulnerability to an addiction to another drug.3 Moreover, there is increasing evidence that, despite a range of genetic risks for addiction across the population, exposure to sufficiently high doses of a drug for long periods of time can transform someone who has relatively lower genetic loading into an addict.4 |
I've added the material from the above excerpt to the Addiction#Risk factors section to make this clear to other readers. Seppi333 (Insert 2¢) 02:36, 9 February 2016 (UTC)
Recent edit
This edit introduced content based upon a minority perspective on addiction to the lead. The statements that were introduced were too vague to be useful to readers, so the material needs to be revised so as to make a more concrete statement about what addiction is from this viewpoint; simply saying something along the lines of "some object to the notion that addiction is a brain disease" is not useful. After an appropriate statement for the lead is decided upon, this content will also need to be covered in the body of the article. Seppi333 (Insert 2¢) 14:57, 31 July 2016 (UTC)
- Changing this sentence:
Despite the involvement of a number of psychosocial factors, a biological process – one which is induced by repeated exposure to an addictive stimulus – is the core pathology that drives the development and maintenance of an addiction.
- to
Despite the involvement of a number of psychosocial factors, a biological process – one which is induced by repeated exposure to an addictive stimulus – pathology is widely seen as the key the development and maintenance of an addiction.
- is not supported by the citations given or the citations added. Seppi333 (Insert 2¢) 13:00, 1 August 2016 (UTC)
Environmental factors - traumatic experiences
@JzG and Jg16540: Please discuss this content here. Seppi333 (Insert 2¢) 20:16, 17 August 2016 (UTC)
- Not necessary, since this is a routine action removing evident self-citation. I have adivsed the user that if he wants his work cited here, as pretty much every single one of his edits indicates to be the case, then he should propose it on Talk. I have no opinion on its merits, only that it should not be added by a co-author. Guy (Help!) 20:35, 17 August 2016 (UTC)
- The self-publication policies are as follows:
- "Using material you have written or published is allowed within reason, but only if it is relevant, conforms to the content policies, including WP:SELFPUB, and is not excessive. Citations should be in the third person and should not place undue emphasis on your work. When in doubt, defer to the community's opinion."
- "Self-published and questionable sources may be used as sources of information about themselves, usually in articles about themselves or their activities, without the self-published source requirement that they be published experts in the field, so long as: the material is neither unduly self-serving nor an exceptional claim; it does not involve claims about third parties; it does not involve claims about events not directly related to the source; there is no reasonable doubt as to its authenticity; the article is not based primarily on such sources."
- Therefore, a co-author can most definitely cite a paper as long as it is relevant, accurate and not excessive. Writing two sentences and citing multiple papers is most definitely not self-promotion. All that matters here are the merits of the citation: child abuse is an important risk factor for addiction. Therefore, the peer-reviewed research supporting this should be included. Please add the following back:
- "Traumatic experiences have been linked to the development of addictive and substance-related problems.[33][34] Interpersonal traumas, such as child abuse and violent assaults, are particularly predictive of substance-related problems.[35][36][37]"
- 33) Stewart, S.H. Alcohol abuse in individuals exposed to trauma: A critical review. Psychol. Bull. 1996, 120, 83–112
- 34) Bailey, K.M.; Stewart, S. Relations among trauma, PTSD, and substance misuse: The scope of the problem. In Trauma and Substance Abuse: Causes, Consequences, and Treatment of Comorbid Disorders, 2nd ed.; Ouimette, P., Read, J.P., Eds.; American Psychological Association: Washington, DC, USA, 2014; pp. 11–34
- 35) Guina, Jeffrey; Nahhas, Ramzi; Goldberg, Adam; Farnsworth, Seth (10 August 2016). "PTSD Symptom Severities, Interpersonal Traumas, and Benzodiazepines Are Associated with Substance-Related Problems in Trauma Patients". Journal of Clinical Medicine. 5 (8): 70. doi:10.3390/jcm5080070. PMID 27517964.
- 36)Ford, J.D.; Elhai, J.D.; Connor, D.F.; Frueh, B.C. Poly-victimization and risk of posttraumatic, depressive, and substance use disorders and involvement in delinquency in a national sample of adolescents. J. Adolesc. Health 2010, 46, 545–552.
- 37)Sullivan, T.P.; Cavanaugh, C.E.; Buckner, J.D.; Edmondson, D. Intimate partner violence (IPV) and drug and alcohol use problems among community women: The roles of physical, sexual, and psychological IPV and PTSD. J. Trauma Stress 2009, 22, 575–584. — Preceding unsigned comment added by Jg16540 (talk • contribs) 20:47, 17 August 2016 (UTC)
I have 43 years experience. Research and I believed a long with consular, scientists. And seven treatment sent errors. That all said I'm extremely to short on this ,I've done everything. Tar bits hard so do s coca Kimberly milanoski (talk) 06:14, 1 September 2016 (UTC)
Missing concepts
Specific to drugs:
- Addiction liability of a drug as a risk factor
Operant/classical conditioning (reviews[1][2][3] and pp. 365-367 of molecular neuropharmacology text[4])
- Description of Self-administration
- Explanation of the relationship between conditioned reinforcers and primary reinforcers Added (still needs work)
- Drug/environmental cues: cue reactivity (conditioned reinforcers) and conditioned place preference (classical conditioning) Added (still needs work), but haven't covered CPP yet
- Relapse/Reinstatement of drug-seeking behavior
- Describe incentive salience as it relates to a reward[5] Partly done
Seppi333 (Insert 2¢) 12:01, 3 February 2016 (UTC)
References
- ^ Edwards S (2016). "Reinforcement principles for addiction medicine; from recreational drug use to psychiatric disorder". Prog. Brain Res. 223: 63–76. doi:10.1016/bs.pbr.2015.07.005. PMID 26806771.
- ^ Milton AL, Everitt BJ (2012). "The persistence of maladaptive memory: addiction, drug memories and anti-relapse treatments". Neurosci Biobehav Rev. 36 (4): 1119–1139. doi:10.1016/j.neubiorev.2012.01.002. PMID 22285426.
- ^ Torregrossa MM, Taylor JR (2013). "Learning to forget: manipulating extinction and reconsolidation processes to treat addiction". Psychopharmacology (Berl.). 226 (4): 659–72. doi:10.1007/s00213-012-2750-9. PMC 3466391. PMID 22638814.
- ^ Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 15: Reinforcement and Addictive Disorders". In Sydor A, Brown RY (ed.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 365–367. ISBN 9780071481274.
{{cite book}}
: CS1 maint: multiple names: authors list (link) - ^ Pool E, Sennwald V, Delplanque S, Brosch T, Sander D (2016). "Measuring wanting and liking from animals to humans: A systematic review". Neurosci Biobehav Rev. 63: 124–142. doi:10.1016/j.neubiorev.2016.01.006. PMID 26851575.
animal wanting, which relies on affective relevance, consisting of the perception of a cue associated with a relevant reward for the organism's current physiological state.
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Study or review?
See edit here.
An addiction to loud music is seen more often in non-professional musicians than in non-musician control subjects.[1]
References
- ^ Schmuziger, Nicolas; Jochen, Patscheke; Stieglitz, Rolf; Probst, Rudolf (2012). "Is there addiction to loud music? Findings in a group of non-professional pop/rock musicians". Audiology Research. 2 (1). doi:10.4081/audiores.2012.e11. ISSN 2039-4349. PMC 4630946. PMID 26557326.
PubMed indicates it is a review. They may have examined their own previous research. QuackGuru (talk) 20:04, 16 October 2017 (UTC)
- I've come across two Pubmed-indexed and Pubmed-classified "Reviews" on addiction that are absolute/utter crap; the studies which were reviewed in them were a biased selection of research which supported their assertions, whereas they ignored a large body of contradictory evidence. Consequently, IMO, if a pubmed-classified "review" on addiction seems to have dubious (WP:FRINGE) quality, then it should not be cited in this article. For some reason, the topic of addiction seems to generate more sketchy secondary medical research than any other topic I've researched and written about on WP.
- In relation to the article you're discussing, "loud music" is not actually a stimulus; rather, it describes a magnitude of a stimulus. A type of music would be a more specific, but still general class of stimuli, whereas a particular song would be a specific auditory stimulus. Some genres of music are classes of rewarding stimuli since music can induce pleasure/motivational states in approximately 95% of the population; consequently, it is plausible that some people are drawn to listening to music more than others, but compulsively listening to arbitrary songs which are loud seems like a very far-fetched phenomenon; consequently, the implications of that review about an "addiction to loud music" being an actual phenomenon seem very sketchy to me (i.e., the review seems WP:FRINGE). If more independent secondary medical research is published on this topic in the future, I'd be okay with covering it in the article; however, right now, there doesn't seem to be adequate medical consensus supporting this concept. Seppi333 (Insert 2¢) 19:42, 11 December 2017 (UTC)
- Just to be perfectly clear, not all music is rewarding. Some people find some types of music highly aversive and others highly rewarding; e.g., trance (music) songs are rewarding to me because I like to listen to them, but death metal songs are aversive to me because I would turn them off or move away from a source which is playing them. Consequently, music in general is not, and can not be, a potential class of addictive stimuli. Seppi333 (Insert 2¢) 19:56, 11 December 2017 (UTC)
Arts & humanities approaches to addiction
The article as it currently stands only contains quite a narrow scientific description of addiction. This is a topic on which there has been considerable research in other disciplines.
History Concepts of addiction emerging in the sixteenth century; link to religious treatises in seventeenth century; associated with temperance movements in eighteenth and nineteenth centuries; rise of the 'disease model' in twentieth century; current trend towards recognition of behavioural addictions. See Jessica Warner, Rebecca Lemon, Melvyn London, HG Levine, Roy Porter, etc.
Philosophy Ongoing and controversial debates around the morality of addiction, the responsibility of the addict, the balance between free will and compulsion. Tied into questions surrounding whether addiction is a disease or a choice.
Politics The war on drugs, harm reduction policies (abstinence vs maintenance, methadone clinics etc), gambling restrictions. — Preceding unsigned comment added by Ada cree (talk • contribs) 12:38, 20 June 2018 (UTC)
- @Ada cree: Wikipedia just cites and summarizes professionally-published mainstream academic (and in some cases journalistic) sources. While the ideas you are suggesting would be good, they would need to be supported by sources (preferably secondary or tertiary, not primary). Ian.thomson (talk) 15:02, 20 June 2018 (UTC)
- Here's a few to start (mostly historical):
- Cree, JM, 'Protestant evangelicals and addiction in early modern English', Renaissance Studies 32 (June 2018), pp. 446-462
- Ferentzy, P., 'From Sin to Disease: differences and similarities between past and current conceptions of substance abuse', Contemporary drug problems 28 (2001)
- Lemon, R., Addiction and Devotion in Early Modern England (Philadelphia, 2018)
- Lemon, R., ‘Scholarly Addiction: Doctor Faustus and the Drama of Devotion’, Renaissance Quarterly, 69 (2016)
- Levine, H. G., 'The discovery of addiction. Changing conceptions of habitual drunkenness in America', Journal of Studies on Alcohol 15 (1978)
- London, M., 'History of Addiction: A UK Perspective', American Journal on Addictions 14 (2005)
- Perry, L. M., 'The Word for an Addict in Geneva (Calvin on Addiction)', Christian Bioethics 20 (2014), pp. 80-96
- Porter, R., 'The Drinking Man's Disease: The ‘Pre-History’ of Alcoholism in Georgian Britain', British Journal of Addiction 80 (1985), pp. 385-96
- Robert, W., and West, R., Theory of addiction, (Oxford, 2006)
- Room, R., 'The Cultural Framing of Addiction', Janus Head 6 (2003), pp. 221-34
- Warner, J., '"Resolv'd to drink no more": addiction as a preindustrial construct', Journal of Studies on Alcohol 55 (1994), pp. 685-191
- Willis, D., ‘Doctor Faustus and the Early Modern Language of Addiction’, in Placing the Plays of Christopher Marlowe (Aldershot, 2008) — Preceding unsigned comment added by Ada cree (talk • contribs) 08:45, 22 June 2018 (UTC)
- Here's a few to start (mostly historical):
Reviews, medical references, and content to add
High Priority: Need to add coverage of these sources since they're recent and very comprehensive.
- Nestler's 2018 review on the neuroepigenetics of addiction.[1] (note to self: Nestler covers the same 5 structures in Fig 48.1 that we cover in Addiction#Mesocorticolimbic pathway: the amygdala, hippocampus, PFC, NAcc, and VTA; also specifies that NAcc innervation by the hippocampus, PFC, and amygdala is glutamatergic) Seppi333 (Insert 2¢) 10:50, 13 August 2018 (UTC)
Excerpts from Nestler's review
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Stopped on page 5/15 at the beginning of the section on histone modifications. Need to finish reading through this later to decide on what to quote for this ref and what to cover in the article. Seppi333 (Insert 2¢) 10:50, 13 August 2018 (UTC)
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- United States Surgeon General's report on addiction (published November 2016).[2]
- Review of the neurobiology of addiction[3]
- Other content to add
Epigenetic effects of drugs
- Drug-specific epigenetics reference
- Amph/meth-specific epigenetics reference
- [4][5]
- (First?) clinical trial with an HDACi for addiction - PMID 27656618; need a review of this paper in order to update Addiction#Research (3rd paragraph)
Neuropsychology
- [6]
- [7] Review that covers motivational salience, stimulus control, and Pavlovian-instrumental transfer in addiction
Seppi333 (Insert 2¢) 21:35, 28 January 2017 (UTC); updated 01:57, 21 July 2018 (UTC)
References
- ^ a b Walker DM, Nestler EJ (2018). "Neuroepigenetics and addiction". Handbook of Clinical Neurology. 148: 747–765. doi:10.1016/B978-0-444-64076-5.00048-X. PMID 29478612.
- ^ "Facing Addiction in America: The Surgeon General's Report on Alcohol, Drugs, and Health" (PDF). Office of the Surgeon General. US Department of Health and Human Services. November 2016. Retrieved 28 January 2017.
- ^ Koob GF, Volkow ND (August 2016). "Neurobiology of addiction: a neurocircuitry analysis". Lancet Psychiatry. 3 (8): 760–773. doi:10.1016/S2215-0366(16)00104-8. PMID 27475769.
Drug addiction represents a dramatic dysregulation of motivational circuits that is caused by a combination of exaggerated incentive salience and habit formation, reward deficits and stress surfeits, and compromised executive function in three stages. The rewarding effects of drugs of abuse, development of incentive salience, and development of drug-seeking habits in the binge/intoxication stage involve changes in dopamine and opioid peptides in the basal ganglia. The increases in negative emotional states and dysphoric and stress-like responses in the withdrawal/negative affect stage involve decreases in the function of the dopamine component of the reward system and recruitment of brain stress neurotransmitters, such as corticotropin-releasing factor and dynorphin, in the neurocircuitry of the extended amygdala. The craving and deficits in executive function in the so-called preoccupation/anticipation stage involve the dysregulation of key afferent projections from the prefrontal cortex and insula, including glutamate, to the basal ganglia and extended amygdala. Molecular genetic studies have identified transduction and transcription factors that act in neurocircuitry associated with the development and maintenance of addiction that might mediate initial vulnerability, maintenance, and relapse associated with addiction. ... Substance-induced changes in transcription factors can also produce competing effects on reward function.141 For example, repeated substance use activates accumulating levels of ΔFosB, and animals with elevated ΔFosB exhibit exaggerated sensitivity to the rewarding effects of drugs of abuse, leading to the hypothesis that ΔFosB might be a sustained molecular trigger or switch that helps initiate and maintain a state of addiction.141,142
- ^ Eserian JK (July 2013). "Vitamin D as an effective treatment approach for drug abuse and addiction". Journal of Medical Hypotheses and Ideas. 7 (2): 35–39. doi:10.1016/j.jmhi.2013.02.001.
Vitamin D is a potent inducer of endogenous GDNF. The most prominent feature of GDNF is its ability to support the survival of dopaminergic neurons. ... The protective effects of vitamin D might be due to a mechanism of up-regulation of GDNF [14], as it was shown that when GDNF is administered directly into the striatum before methamphetamine treatment, complete protection against the dopaminergic toxicity of methamphetamine, such as reductions in striatal DA release and content, could be observed [22]. Vitamin D also increases glutathione levels and inhibits inducible nitric oxide synthase (iNOS) production, which could reduce methamphetamine toxicity to the DA system by reducing methamphetamine free radicals' production [14].
- ^ Chandel N, Malhotra A, Singhal PC (August 2015). "Vitamin D receptor and epigenetics in HIV infection and drug abuse". Front Microbiol. 6: 788. doi:10.3389/fmicb.2015.00788. PMC 4541325. PMID 26347716.
Interestingly, vitamin D may not be able to augment VDR expression optimally in several instances where epigenetic contributes to down regulation of VDR; however, reversal of epigenetic corruption either by demethylating agents (DACs) or histone deacetylase (HDAC) inhibitors would be able to maximize expression of VDR in these instances. ... Vit D works through its receptor- VDR ... VDR is a member of the nuclear receptor (NR) family of transcription factors ... VDR heterodimerizes with Retinoid X Receptor (RXR) and forms VDR-RXR complex, which recruits either repressor or activator complexes depending on its unliganded or liganded status ... Vit D provided protection against the serotonin-depleting effect of [methamphetamine] in the brain of animals in the setting of repeated dosage administration. Vit D deficient rats traveled farther in locomotion test after acute dosage administration (Cass et al., 2006; Kesby et al., 2012). Vit D treated animals also showed reduction in [methamphetamine]-induced dopamine [depletion] ... HIV and drugs provide an environment which is conducive to short term and long term epigenetic modifications leading to alterations in gene expression. Epigenetic alterations are also dependent on use of single or multiple drugs. ... Therefore, epigenetics is a complex issue in drugs of abuse in general and specifically in the presence of HIV infection. However, epigenetic alterations are reversible and thus strategies can be developed to reverse them.
{{cite journal}}
: CS1 maint: unflagged free DOI (link) - ^ Tibboel H, De Houwer J, Van Bockstaele B (October 2015). "Implicit measures of "wanting" and "liking" in humans". Neurosci. Biobehav. Rev. 57: 350–364. doi:10.1016/j.neubiorev.2015.09.015. PMID 26432503.
- ^ Corbit LH, Balleine BW (2016). "Learning and Motivational Processes Contributing to Pavlovian-Instrumental Transfer and Their Neural Bases: Dopamine and Beyond". Current Topics in Behavioral Neurosciences. 27: 259–289. doi:10.1007/7854_2015_388. PMID 26695169.
Other US-related content
Reflist
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References
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Reward system
I am researching articles in order to add to the "reward system" section, but I would appreciate any suggestions--Blb6175535 (talk) 21:55, 29 September 2016 (UTC)
- @Blb6175535: Hi there. Sorry for responding so late – I didn't notice this until now. I'm not sure if you're still interested in adding material on the reward system; however, if you still intend to do so, I'd strongly recommend that you only look at medical reviews of literature on this topic. The use of medical reviews to cite medical statements is required by WP:MEDRS and it's generally a good practice to cite such literature even when citing non-medical statements, such as statements which are more related to molecular neurobiology, in medicine-related articles like this one. This link provides a list of all medical reviews from the past 5 years that mention both "addiction" and "reward system" in the title or abstract – it'd be best if you use only the articles listed in these search results to add new content in the Addiction#Reward system section.
- On a related note, I intend to add content from one of the reviews in that list at some point (PMID 27475769 - this is the 2nd citation in the #Incentive salience / neurobiology reviews to add section above this one). If you want to summarize the material on the reward system from that review, please feel free to do so! It'd reduce my workload. You can view the full text of that review article by following this link. Seppi333 (Insert 2¢) 22:41, 13 December 2016 (UTC)
Other refs
I haven't read through these papers yet, so I'm just putting these links here for now.
- Reviews on the endocannabinoid system and DA interactions/addiction: PMID 26733830 PMID 26373473
- Interesting primary source on 12 step programs: PMID 26306329
Seppi333 (Insert 2¢) 07:13, 9 October 2016 (UTC)
Environmental enrichment-based behavioral therapy
- The paragraph on physical exercise in the quote of this review currently cites/supports statements in this article, but the material on environmental enrichment-based therapies (i.e., the use of "environmental" positive reinforcers to promote healthier alternative behaviors that substitute for drug use) hasn't been added yet.[1] A summary of this material should be added under Addiction#Behavioral therapy at some point. Full quote of the review's environmental enrichment subsection on clinical research in humans:[1]
Seppi333 (Insert 2¢) 22:20, 13 December 2016 (UTC)In humans, non-drug rewards delivered in a contingency management (CM) format successfully reduced drug dependence [for a review see Ref. (188)]. In general, CM programs promote drug abstinence through a combination of positive reinforcement for drug-free urine samples. For instance, voucher-based reinforcement therapy in which medication compliance, therapy session attendance, and negative drug screenings reinforced with vouchers to local business (e.g., movie theater, restaurants, etc.) directly reinforces drug abstinence, provides competing reinforcers, enriches the environment, and it is a robust treatment across a broad range of abused drugs (189). Another example of using social rewards to reduce drug addiction was given in the Naimi et al. (156) study, comparing younger and older adults, who reported that enhancing non-alcohol-related campus social programing had decreased alcohol use.
In summary, both animal and human studies indicate that environmental enrichment is an important intervention that moderates the development and progression of drug addiction. There is little information regarding sex differences in social reward at present; however, once drug use patterns have developed, non-drug rewards, such as social interaction, have the advantage of being self-sustaining and are effective in both sexes.
References
- ^ a b Carroll ME, Smethells JR (February 2016). "Sex Differences in Behavioral Dyscontrol: Role in Drug Addiction and Novel Treatments". Front. Psychiatry. 6: 175. doi:10.3389/fpsyt.2015.00175. PMC 4745113. PMID 26903885.
Environmental Enrichment ...
In humans, non-drug rewards delivered in a contingency management (CM) format successfully reduced drug dependence ... In general, CM programs promote drug abstinence through a combination of positive reinforcement for drug-free urine samples. For instance, voucher-based reinforcement therapy in which medication compliance, therapy session attendance, and negative drug screenings reinforced with vouchers to local business (e.g., movie theater, restaurants, etc.) directly reinforces drug abstinence, provides competing reinforcers, enriches the environment, and it is a robust treatment across a broad range of abused drugs (189). ...
Physical Exercise
There is accelerating evidence that physical exercise is a useful treatment for preventing and reducing drug addiction ... In some individuals, exercise has its own rewarding effects, and a behavioral economic interaction may occur, such that physical and social rewards of exercise can substitute for the rewarding effects of drug abuse. ... The value of this form of treatment for drug addiction in laboratory animals and humans is that exercise, if it can substitute for the rewarding effects of drugs, could be self-maintained over an extended period of time. Work to date in [laboratory animals and humans] regarding exercise as a treatment for drug addiction supports this hypothesis. ... However, a RTC study was recently reported by Rawson et al. (226), whereby they used 8 weeks of exercise as a post-residential treatment for METH addiction, showed a significant reduction in use (confirmed by urine screens) in participants who had been using meth 18 days or less a month. ... Animal and human research on physical exercise as a treatment for stimulant addiction indicates that this is one of the most promising treatments on the horizon. [emphasis added]{{cite journal}}
: CS1 maint: unflagged free DOI (link)
Facing Addiction: A National Summit - November 21, 2016
This section was added by botonduty. I'm moving it here for further consideration. In my opinion this section does not fit on the article page. It seems mainly to be a promotional piece for the non-profit that held the summit and, as a one-off event, may not have the notability or impact needed to have it appear on this topic page.
(Redacted)
“Addressing the addiction crisis in America will require seeing addiction as a chronic illness – not as a moral failing,” said Murthy. “Addiction has been a challenge for a long time, but we finally have the opportunity and the tools to address it. By bringing together researchers, treatment providers, policy makers and key influencers, this summit will help our country see that a united front is necessary to address a public health challenge of this magnitude."[1]. The event was streamed live & archieved.
(Redacted)
References
- ^ [https://www.facingaddiction.org/news/2016/11/03/facing-addiction-america-national-summit Surgeon General of the United States’s report on Alcohol, Drugs, and Health
If the consensus is for keeping it, there are a number of issues with the text that will still need to be addressed (dab links, use of "motive", spelling, promotional language, mis-matched quotes, etc – most of them easily fixed, but I'll wait on that until others have had a chance to comment. —jmcgnh(talk) (contribs) 06:01, 29 November 2016 (UTC)
Could it not be both? Some people grow up in households and are exposed to drugs from a young age before their brains are fully developed and are lacking a moral compass, therefore in those situations it could be seen as a chronic illness within our society. However, I could also see it being a moral failing of adults that choose to try drugs. Drugs are usually a coping mechanism people use as a response to an untreated mental illness and that could also argue the point that drug use is a symptom of untreated chronic illness. Mgomil1 (talk) 18:18, 7 September 2018 (UTC)
- The prose is copied from https://www.facingaddiction.org/news/2016/11/03/facing-addiction-america-national-summit and is thus a copyright violation. Sorry but we can't include it in the article unless it's thoroughly re-written. I have removed it from the talk page as well. — Diannaa 🍁 (talk) 16:47, 30 November 2016 (UTC)
Criticism Section ?
Social sciences can have a tendency to employ circular definitions, and utilize "correlation implies causation" arguments.
Lately, they have tacked hard science onto the end of dubious assertions, to make them look more authoritative.
For example, this article starts with "Addiction is a brain disorder characterized by compulsive engagement in rewarding stimuli despite adverse consequences." This sentence is followed by many paragraphs of undoubtedly solid biomedical and neuroscience research about reward systems. However, the first sentence has so many dubious aspects:
- Brain disorder is not defined.
- Compulsive is not defined.
- Adverse consequences is not defined.
- Normal brain functioning and normal human behavior are not defined. According to Evolutionary Psychology, neither of those has existed for 12,000 years, since homo sapiens mammals are evolved to live in tribes among groups of 200 individuals known for a lifetime. Life among thousands of strangers is at odds with homo sapiens' genetic programming. Any human culture will automatically define typical current behavior as "normal", but for scientists to fall into that error can entirely throw off any research done with that unexamined assumption.
If an organism is given a choice of accepting a well known positive reward or declining it, why is it "pathological" or a "disorder" to accept it?
So, the definitions of "compulsive" and "adverse consequences" are of huge importance here. Millions of people have been jailed in cases where a government reserves the right to define "adverse consequences" for individuals (as opposed to circumstances where someone checks themselves into "rehab"). 162.205.217.211 (talk) 20:41, 21 October 2018 (UTC)
- Adverse consequences are simply the ones that cause harm or oppose our interests. If the harm happens to be illegal, most governments will specify the precise violation before sending someone to jail. It varies, case-by-case, but is usually public, unless you're thinking of somewhere I'm not. Compulsive engagement is just engagement we're compelled to engage in by a compulsion (that irresistible persistent impulse to perform an act). Your guess is as good as mine as to what a brain disorder might be. InedibleHulk (talk) 19:47, 22 October 2018 (UTC)
- A brain disorder is any pathology that involves impaired cognition and/or distressing behaviors and arises from abnormal structural and/or functional changes within the brain. "Adverse consequences" is subjective and pertains to a case-by-case basis, although its definition should be fairly straightforward given that it's not jargon. A compulsion is simply an irresistable urge to do something; to be more precise, it is a behavior which one elicits despite an attempt to exert inhibitory control (NB: this is a cognitive process) over their behavior. Seppi333 (Insert 2¢) 23:03, 9 November 2018 (UTC)
Dead links
External links section contains dead links. — Preceding unsigned comment added by 85.221.158.44 (talk) 13:43, 22 June 2019 (UTC)
False/misleading statements - needs to be changed
Gnarmpf (talk) 18:46, 20 July 2019 (UTC) There are serveral statements in this article that are misleading. First: "Despite the involvement of a number of psychosocial factors, a biological process – one which is induced by repeated exposure to an addictive stimulus – is the core pathology that drives the development and maintenance of an addiction. The two properties that characterize all addictive stimuli are that they are reinforcing (i.e., they increase the likelihood that a person will seek repeated exposure to them) and intrinsically rewarding (i.e., they are perceived as being inherently positive, desirable, and pleasurable)."
The first sentence is taken from Nestler (2013): "Despite the importance of numerous psychosocial factors, at its core, drug addiction involves a biological process: the ability of repeated exposure to a drug of abuse to induce changes in a vulnerable brain that drive the compulsive seeking and taking of drugs, and loss of control over drug use, that define a state of addiction" (S. 431). This conclusion is drawn from animal models: „We focus here on stimulant and opiate drugs of abuse, which produce more dramatic effects in animal models compared with other drugs“ (Nestler, 2013, S. 432). Animal models cannot possibly replicate human psychosocial factors, thus the statement is misleading and almost certainly false. To this day (and to my knowledge) there is no sound explanation - let alone empirical evidence - for what constitutes the supposed "vulnerability" of the brain mention by Nestler. This means that from a purely biological standpoint no one can explain why millions of people around the world are taking drugs regularly yet only a relatively small percentage (typically less than 10%) acutally become addicted, even when it comes to the 'worst' drug: Heroin (Robins, 1993). Nor can they explain why people get addicted to things that are not in fact addictive in themselves, which is a common observation in clinical trials of non-addicitve pharmaceuticals (e.g. Bandelow et al., 2015). Theories about this vulnerability are contradictory and often times do not account for the fact that this "vulnerability" is very likely to be a misdiagnosed primary mental health disorder, in most cases depression - which is why drugs of abuse are used as a form of selfmedication to compensate for debilitating effects of depression or anxiety (among the most common comorbidities are depression, anxiety/social phobia, trauma, ADHD; Wittchen et al., 2011).
The second false statement is that addicitve stimuli are instrinsically rewarding. In reality, since addiction is demonstrably a coping mechnism in the majority of clinical cases, what really drives compulsive drug seeking is negative reinforcement, i.e. supressing the aversive states/thoughts/feelings caused by primary mental health disorders and many other -psychosocial- burdens. Especially when taken in excess drugs are in fact not enjoyable but it is still a very strong stimulus powerful enough to "overwrite" and supress most human misery, if only temporarily. In that sense, it is comparable even to self-injurious behaviors (see Nock, 2010). The implication of statements about the reinfocing nature and hedonistic properties of drugs of abuse is that addicts are undisciplined and purely driven by pleasure which is false and disparagingly disregards all personal accounts of those affected (for example in autobiographical books or Movies like "Factory Girl" or "Wir Kinder vom Bahnhof Zoo") That disregard and the resulting schism of understanding between the physician and the user, which allows distrust and confusion, prejudice and fear, to arise around the condition (Foxcroft, 2007, S. 3), leads to false assumptions in scientific and clinical practice, as Thomas Insel, former director of the National Institute of Mental Health (NIMH) pointed out long ago: "The literature on the hedonic properties of drugs of abuse has been our major source of information about the neurobiology of reward. Drugs such as cocaine are an easily manipulated stimulus and thus have permitted rigorous dissection of the pathways and the candidate genes involved in reward. It seems likely that these pathways and genes evolved not for drug abuse but for mediating the motivational aspects of social interaction, including pair bonding, maternal attachment to infants, and presumably infant attachment to mother" (Insel, 2003, S. 356) This also points to the fact that attachment theories of addiction have long since deepened our understanding of addiction and it has been shown that shallow descriptions of simply persuing rearding behaviours for fun are false and not even close to capturing the true nature of addiction (for example Philip J. Flores (2004). Addiction as an Attachment Disorder).
The third false statement is this: "Addiction is a disorder of the brain's reward system which arises through transcriptional and epigenetic mechanisms and develops over time from chronically high levels of exposure to an addictive stimulus (e.g., eating food, the use of cocaine, engagement in sexual activity, participation in high-thrill cultural activities such as gambling, etc.)" This cannot be said for ANY mental disorder: „However, there are no known biomarkers of Internet addiction at this point in time. Indeed, there are no known biomarkers of any mental disorder. Ever since Kraepelin, and thus for a century, psychiatrists have been searching to understand mental disorders as underlying physiological diseases […].“ (Kuss, 2013, S. 132). The evidence that was what has happened and is happening to people in their lives plays a major role in creating various forms of emotional distress and behavioral problems – including psychosis – is very strong […] this evidence is stronger than any we have for genetic or biological causes" (Boyle, 2011, S. 27) Genes are not "autistic" but are in fact highly adaptive and gene activity can adjust to changing enviromental circumstances and interpersonal relationships, only around 1-2% of all known diseases are caused by gene mutations (Bauer, 2005). Thus all others can be attributed to lifestyles, human relationships, societal problems/inequalities, human misery - or in other words: psychosocial factors. Findings about supposed genetic causes for addiction are very likely to simply be the effects of tolerance on a genetic level and thus are not cause of addiction but consequence (see for example Wang, Kapoor & Goate, 2012). Or they could be expressions of other (misdiagnosed) mental health disorders. Data derived from cross-sectional studies does not allow claims about the direction of the relationship between addiction and neurobiological/neurochemical and genetic abnormalitites. Presenting as matter of fact that addiction "arises through transcriptional and epigenetic mechanisms" is false and misleading.
This article needs to be changed to reflect the fact that in reality addiction in many if not most cases is caused by misery and used as a (dsysfunctional) coping mechanism by people who are desperate and suffering. In other words addiction is often symptomatic of underlying mental health disorders including child-hood trauma (e.g. Beutel, 1999; Felitti, 2002; Beckham et al., 2005; Karadag et al., 2005; Schnieders, Rassaerts, Schäfer & Soyka, 2006; Chen et al., 2010; Wittchen et al., 2011; Cashmore & Shackle, 2013; Bandelow et al., 2015; Brisch, 2015).
This must be the guiding principle in diagnosis in order to avoid overlooking underlying problems and initiating misguided treatments that can do more harm than good in worst case scenarios, i.e. addiction treatment can be a genuin risk factor, perpetuating addiction instead of alleviating it (see Robins, 1993).
(I dont know how all of this editing works Im sorry!)
Brisch, K.H. (2015). Bindung und Sucht. (Attachment and addiction.) Stuttgart: Klett-Cotta.
Karadag, F., Sar, V., Tamar-Gurol, D., Evren, C., Karagoz, M. & Erkiran, M. (2005). Dissociative disorders among inpatients with drug or alcohol dependency. Journal of Clinical Psychiatry, 66, 1247–1253.
Beutel, M. (1999). Sucht und sexueller Mißbrauch. (Addiction and sexual abuse.) Psychotherapeut, 44, 313-319.
Chen, L. P., Murad, M. H., Paras, M. L., Colbenson, K. M., Sattler, A. L., Goranson, E. N., Elamin, M.B., Seime, R.J., Shinozaki, G., Prokop, L.J. & Zirakzadeh, A. (2010). Sexual abuse and lifetime diagnosis of psychiatric disorders: systematic review and meta-analysis. Mayo Clinic proceedings, 85(7), 618–629.
Felitti, V.J. (2002). The relationship of adverse childhood experiences to adult health: Turning gold into lead. Zeitschrift für Psychosomatische Medizin und Psychotherapie, 48, 359–369.
Beckham, J.C., Feldmann, M.E., Vrana, S.R., Mozley, S.L., Erkanli, A., Clancy, C.P. & Rose, J.E. (2005). Immediate antecedents of cigarette smoking in smokers with and without posttraumatic stress disorder: a preliminary study. Experimental and clinical psychopharmacology, 13 (3), 219-228.
Bauer, J. (2005). Das Gedächtnis des Körpers. (The body's memory.) München: Piper.
Boyle, M. (2011). Making the World Go Away, and How Psychology and Psychiatry Benefit. In M. Rapley, J. Moncrieff & J. Dillon (Hrsg.), De-Medicalizing Misery. Psychiatry, Psychology and the Human Condition (S. 27–43). London: Palgrave Macmillan.
Nock, M.K. (2010). Self-Injury. Annual Review of Clinical Psychology, 6, 339–363.
Foxcroft, L. (2007). The Making of Addiction. The 'Use and Abuse' of Opium in Nineteenth-Century Britain. London: Routledge.
Kuss, D.J. (2013). Internet gaming addiction: Current perspectives. Psychology Research and Behavior Management, 6, 125–137.
Nestler, E.J. (2013). Cellular basis of memory for addiction. Dialogues in clinical neuroscience, 15 (4), 431–433.
Wang, J.C., Kapoor, M. & Goate, A.M. (2012). The genetics of substance dependence. Annual review of genomics and human genetics, 13, 241–61.
Insel, T.R. (2003). Is social attachment an addictive disorder?. Physiology & Behavior, 79 (3), 351–357.
Robins, L.N. (1993). Vietnam veterans’ rapid recovery from heroin addiction: a fluke or normal expectation? Addiction, 88, 1041–1054.
Bandelow, B., Wiltink, J., Alpers, G.W., Benecke, C., Deckert, J., Eckhardt-Henn, A., Ehrig, C., Engel, E., Falkai, P., Geiser, F., Gerlach, A.L., Harfst, T., Hau, S., Joraschky, P., Kellner, M., Köllner, V., Kopp, I., Langs, G., Lichte, T., Liebeck, H., Matzat, J., Reitt, M., Rüddel, H.P., Rudolf, S., Schick, G., Schweiger, U., Simon, R., Springer, A., Staats, H., Ströhle, A., Ströhm, W., Waldherr, B., Watzke, B., Wedekind, D., Zottl, C., Zwanzger, P. & Beutel M.E. (2015). S3-Leitlinie Angststörungen. (S3 guideline for anxiety disorders.) Berlin, Heidelberg: Springer.
Wittchen, H.U., Jacobi, F., Rehm, J., Gustavsson, A., Svensson, M., Jönsson, B., Ole-sen, J., Allgulander, C., Alonso, J., Faravelli, C., Fratiglioni, L., Jennum, P., Lieb, R., Maercker, A., van Os, J., Preisig, M., Salvador-Carulla, L., Simon, R. & Steinhausen, H.-C. (2011). The size and burden of mental disorders and other disorders of the brain in Europe 2010. European Neuropsychopharmacology, 21 (9), 655–679.
Schnieders, M., Rassaerts, I., Schäfer, M. & Soyka, M. (2006). Der Einfluss kindlicher Traumatisierung auf eine spätere Drogenabhängigkeit. (The influence of child trauma on later drug addiction.) Fortschritte der Neurologie (Advances in neurology), Psychiatrie, 74(9), 511-521.
- THIS! MY GOD, THIS! Robshort (talk) 00:36, 9 November 2019 (UTC)
- 1. Facepalm
- 2. You're thinking of of dependence, not addiction.
- 3. "Internet addiction disorder" is not an addiction.
- This article isn't going to change without citing WP:MEDRS-quality sources. Please read that before inundating this page with garbage citations. Seppi333 (Insert 2¢) 15:27, 6 May 2020 (UTC)
- @Seppi333: (1) I beseech you to discuss this topic in a civil manner, e.g., no "face palms". (2) It is not accurate to describe Gnarmpf's post as discussing "dependence, not addiction", in part because the terms have been used interchangeably or as being closely related for decades. Since the publication of DSM-5 in 2013, a more clearly defined demarcation between the two terms is developing, but one would still be hard-pressed to find clear, consistent distinctions between the two words in peer-reviewed, academic publications. (3) Whether or not "addiction" to various forms of Internet use is a legitimate psychiatric diagnosis is a matter of much debate. Although I'm not yet convinced that proposed diagnostic descriptions or criteria possess adequate convergent and discriminant validity, it's not accurate to categorically dismiss the concept. (4) I cannot speak to the German publications, but the remainder of the citations Gnarmpf listed are WP:MEDRS-quality sources. With regard to the German citations, we should not dismiss out of hand references written in another language without some investigation into the matter, e.g., consulting with bilingual editors active on the German Wikipedia. Thank you - Mark D Worthen PsyD (talk) (I'm a man—traditional male pronouns are fine.) 14:31, 7 May 2020 (UTC)
- I'm perfectly fine with discussing alternative viewpoints in any article. I'm not open to reading a half-assed "peer-review" of literature when (1) the OP isn't even peer-reviewing an article correctly from an academic perspective (e.g., who the fuck argues that an author's assertions are false in a formal peer-review?) and (2) we don't do that on Wikipedia to begin with.
- Addiction isn't a formal diagnosis in the DSM-5. If you want to write about a substance use disorder, navigate to that article instead.
- I don't even need to bother looking up most of the sources above because they're well outside WP:MEDDATE. Arguing that they're mostly WP:MEDRS-quality when you can visually verify that fact seems a bit asinine. Seppi333 (Insert 2¢) 17:01, 7 May 2020 (UTC)
- (a) I agree that the OP's post could have been written better, but, as he noted, he's not an experienced editor like you, so while I respect all humans, and human-like beings, we don't want to scare off potentially good editors. (b) I understand that "addiction" is not a formal diagnosis, and yet we have an article on the topic, so it must be important. (c) You wrote, "Arguing that they're mostly WP:MEDRS-quality when you can visually verify that fact seems a bit asinine." Did you mean "... when you cannot visually verify ..."? If not, I don't understand your sentence. If so, I think you recognize that one could say the same about your statement: "This article isn't going to change without citing WP:MEDRS-quality sources. Please read that before inundating this page with garbage citations." - Mark D Worthen PsyD (talk) (I'm a man—traditional male pronouns are fine.) 00:28, 8 May 2020 (UTC)
- @Seppi333: (1) I beseech you to discuss this topic in a civil manner, e.g., no "face palms". (2) It is not accurate to describe Gnarmpf's post as discussing "dependence, not addiction", in part because the terms have been used interchangeably or as being closely related for decades. Since the publication of DSM-5 in 2013, a more clearly defined demarcation between the two terms is developing, but one would still be hard-pressed to find clear, consistent distinctions between the two words in peer-reviewed, academic publications. (3) Whether or not "addiction" to various forms of Internet use is a legitimate psychiatric diagnosis is a matter of much debate. Although I'm not yet convinced that proposed diagnostic descriptions or criteria possess adequate convergent and discriminant validity, it's not accurate to categorically dismiss the concept. (4) I cannot speak to the German publications, but the remainder of the citations Gnarmpf listed are WP:MEDRS-quality sources. With regard to the German citations, we should not dismiss out of hand references written in another language without some investigation into the matter, e.g., consulting with bilingual editors active on the German Wikipedia. Thank you - Mark D Worthen PsyD (talk) (I'm a man—traditional male pronouns are fine.) 14:31, 7 May 2020 (UTC)
- To be sure,
he takes drugs because otherwise cannot cope with life
(meaning recreational drugs, not medicines) is a claim I heard often. So, I am not completely unsympathetic to such approach. But WP:RULES have to be obeyed and certainly WP:MEDRS has been adopted in order to prevent a deluge of fake medical claims. So, MEDRS has to be obeyed, regardless of we like it or not. While I have my own opinions on e.g. health effects of salt, I know that Wikipedia isn't for my own opinions, but it is a place to render the medical orthodoxy. Tgeorgescu (talk) 02:44, 14 May 2020 (UTC)
- To be sure,
Huffington Post source
I read that article. The gist is: do we know that antidepressants work? Yes. Do we know why they work? No. About the modest effects: the newer antidepressants were not meant for the treatment of mild depression. They are targeted at severe cases of depression. It's unlikely that a drug + placebo test (double blinded) would be tested on people having severe depression. Tgeorgescu (talk) 04:13, 15 May 2020 (UTC)
Due and undue weight
I made edits on 2 May 2020 (diff) with these explanations: "The brain disease model of addiction is the prevailing explanation for addictive behaviors, but it is not the only one with scientific evidence in its corner. We need to err on the side of general descriptions OR discuss the competing theories from an international, interdisciplinary perspective in a balanced manner", and "Trying to begin the long process of writing a more balanced (less reductionistic) description and explanation of addiction based on *all* the scientific evidence, not just the brain disease model." Seppi333 reverted my edits (diff) with the explanation, "It was fine before".
I believe this article currently places undue weight on the brain disease model of addiction to the exclusion of other models that have also received substantial empirical support from diverse reliable sources, including reliable biomedical sources. One aspect of this disproportionate coverage is regional, i.e., the brain disease model is more widely accepted (some might say promoted) in the United States compared to the United Kingdom (and Europe generally), Australia, New Zealand, and other countries. Thus, one reason for describing and explaining addiction in a more balanced manner is to avoid a USA bias. The second and even more important reason is to strive for an article written in an impartial tone that documents and explains major points of view, giving due weight with respect to their prominence.
I believe that concerned editors express sincere beliefs, in good faith, based on their reading of the relevant scholarly literature. I look forward to discussing this issue in a civil manner, with the goal of reaching consensus. - Mark D Worthen PsyD (talk) (I'm a man—traditional male pronouns are fine.) 14:00, 7 May 2020 (UTC)
- See above. Feel free to cite some quality sources to justify what you're asserting is missing and I'll be more amenable to revision. Seppi333 (Insert 2¢) 17:02, 7 May 2020 (UTC)
- Fair enough, I will do that. Thanks - Mark D Worthen PsyD (talk) (I'm a man—traditional male pronouns are fine.) 00:10, 8 May 2020 (UTC)
- Just a comment: Dutch professors have to publish in English in select US journals in order to fulfill their publications quota. So, yeah, science is generally speaking US-centric, meaning reputable US scientific journals. Tgeorgescu (talk) 02:24, 14 May 2020 (UTC)
- Fair enough, I will do that. Thanks - Mark D Worthen PsyD (talk) (I'm a man—traditional male pronouns are fine.) 00:10, 8 May 2020 (UTC)
Addiction is a multidisciplinary field of study
Of course, neuroscience and biomedical research generally is important in the addiction field. But we would be naïve and woefully uninformed if we were to assume that only biomedical disciplines contribute to our understanding of addiction, including its phenomenology, etiology, clinical assessment, how to help people suffering from addiction (counseling, mutual support, psychoeducation, harm reduction, prevention), comorbidity with other psych disorders, etc.
Here is a quote on the topic:
The modern study of substance use and substance use disorders (SUDs) is highly multidisciplinary, involving basic and applied research in numerous behavioral, social and biomedical disciplines. This is because the use and consequences of psychoactive substances are influenced by a range of factors from the molecular to the cultural, traversing almost every conceivable level of causal explanation with no single discipline holding a monopoly on the key to understanding who uses psychoactive substances, why they use them, how it affects them, and what to do about it. Perhaps the greatest challenge to those interested in understanding substance use and SUDs is how to integrate these different factors into comprehensive explanatory models that can form the basis of a more rational approach to assessment, treatment, prevention, and social policy. Indeed, it is difficult to imagine any area of study that brings together more disciplines with a common interest than the study of substance use and SUDs.[1]
References
- ^ Kenneth J. Sher, and Alvaro Verges, "Introduction and Overview", chap. 1 in The Oxford Handbook of Substance Use and Substance Use Disorders: Volume 1, edited by Kenneth J. Sher (New York: Oxford University Press, 2016): 2.
Frontiers in Psychiatry citations
I cited two articles in Frontiers in Psychiatry, currently references # 13 and # 14. I understand that Frontiers journals have a mixed reputation, for mostly good reasons. This journal has decent metrics (that's just a quick subpage I created for this purpose); falls under this guidance:
The CiteWatch cannot determine the full context in which a source is used, therefore use common sense and judgement before removing a citation from an article (see Q8 in the FAQ);
and, most importantly, these two articles are written by prominent scholars in their respective fields (philosophy, psychiatry, and psychology). If you doubt the reliability of these two articles, please read them, familiarize yourself with the authors' scholarship generally, and offer a cogent explanation why they are not reliable sources. Thank you - Mark D Worthen PsyD (talk) (I'm a man—traditional male pronouns are fine.) 02:35, 30 May 2020 (UTC)
Citation [3]
The third citation in the lead refers specifically to "drug addiction", but drugs are not mentioned in the first sentence. Or in the cited sentence. This seems like a problem. 216.8.188.31 (talk) 14:08, 7 December 2020 (UTC)
- Good point. I made some edits (diff) that hopefully rectified the problem. Mark D Worthen PsyD (talk) [he/his/him] 15:08, 7 December 2020 (UTC)
Multiple issues
I added a multiple issues tag to the article.
This article or section may contain misleading parts. - The article conveys a sense that the brain disease model (BMD) is the only widely-accepted theory of addiction, which is not the case. I edited the lead paragraph and the first sentence of the second paragraph (diff), but the body of the article contains misleading information of the same type.
This article may contain an excessive amount of intricate detail that may interest only a particular audience. - Particularly the mechanisms section, although there are some other overly technical sentences elsewhere in the body and lead. The mechanisms section is certainly interesting, but it should significantly condensed and the detailed version could be a separate article or part of a neuroscience article.
This article may be unbalanced towards certain viewpoints. - The brain disease model (BMD) dominates this article. While the BMD is prominent in the United States, the same is not true in Europe, Australia, New Zealand, and other parts of the world. In addition to being USA-centric, this lack of due weight does not accurately represent the scholarly literature on addiction. I have added references in the lead section to support this point, and I will gradually do so in the body of the article. I encourage other editors to do the same.
For those of you who (perhaps) believe that the BMD is the only scientifically valid theory of addiction, I ask that you please read scientific articles that posit competing or complementary theories of addiction and please explain here why those articles are not scientifically valid. Thank you. Mark D Worthen PsyD (talk) [he/his/him] 15:24, 7 December 2020 (UTC)
- For example, many of the articles and books that Gnarmpf posted on 20 July 2019 are relevant to this discussion, despite the fact that another editor derided Gnarmpf for his good-faith contribution, and disparaged these references. I suggest taking into consideration the tone of an editor's response—regardless of how exalted their Wikipedia standing—particularly when that editor does not follow one of Wikipedia's simple expectations (one of the Five pillars): Wikipedia's editors should treat each other with respect and civility. - "Respect your fellow Wikipedians, even when you disagree. Apply Wikipedia etiquette, and do not engage in personal attacks. … Act in good faith, and assume good faith on the part of others. Be open and welcoming to newcomers." - Mark D Worthen PsyD (talk) [he/his/him] 15:56, 7 December 2020 (UTC)
Lead and how to define addiction
- @Markworthen: Sure, happy to discuss. Let's keep this NPOV, shall we? The article body doesn't reflect what you wrote in the lead. Secondly, you don't justify your assertion that what you call the "brain disease model of addiction" is not the scientific consensus. You just source-dumped some authors that disagree with virtually every other major source cited in this article. The lead as written is highly biased toward a minority viewpoint, and downplays the mainstream view of what addiction is. You can revert me again, but I'll just take this to WT:MED and the NPOV noticeboard if you decide to restore it without toning down the bias. Seppi333 (Insert 2¢) 01:55, 27 May 2021 (UTC)
- @Seppi333: I will not revert your revert of my revert of your revert of my edit, for which I created a new section on the Talk page for discussion.
- We both have a point of view and we both believe that our POV is neutral. Therefore, I will work very hard to better understand your point of view.
- You wrote, "The article body doesn't reflect what you wrote in the lead." That is a fair critique. I will work on fleshing out the points I made in the lede.
- You wrote, "Secondly, you don't justify your assertion that what you call the 'brain disease model of addiction' is not the scientific consensus." I was using the term used by Volkow and others,[1] but I'm open to suggestions. What would you call the model? Mark D Worthen PsyD (talk) [he/his/him] 16:55, 27 May 2021 (UTC)
- We will need to come to an agreement, based on Wikipedia policies of course, on what constitutes "scientific consensus", "minority view", and "mainstream view".
- In general—and you might very well agree—we should consider professional guidelines, association position statements, government policies, books, and journal articles from the United States and other nations. In other words, we should guard against being USA-centric. Mark D Worthen PsyD (talk) [he/his/him] 17:13, 27 May 2021 (UTC)
- Insofar as I can tell, the scientific consensus on the pathophysiology of addiction is that it is a "brain disease" (e.g., see the US Surgeon General's view and NIDA's). Interestingly, when I searched for the EMCDDA's position on this, I came across this publication on addiction models (see chapter 2 table 2.1 on page 22). Their critique of the "brain disease" model is that it neglects the socio-environmental aspects of the disorder. That is an entirely valid critique if you ignore the entire field of neuroepigenetics. Animal models support that social pressures and novel changes in the environment can act through epigenetic mechanisms (e.g., (de-)acetylation/(de-)methylation/etc. of specific amino acid residues on one or more histones) in the brain and impinge upon addictive behavior. It's certainly true that these critiques exist in the literature; they just don't account for the current perspective on the neurobiological underpinnings of addiction, which almost makes the argument against the brain disease model a straw man.
- I am perfectly fine with covering other theories in this article so long as they don't misrepresent the current perspective on the neuropathophysiology of addiction. Seppi333 (Insert 2¢) 02:38, 28 May 2021 (UTC)
- FWIW, whether or not it's correct to lump disorders like depression, ADHD, addiction, and the like in with neurodegenerative disorders and TBI is debatable. It seems pretty clear at this point is that addiction occurs as a −result of largely reversible abnormalities in the brain that arise from aberrant gene transcription and are influenced by social and environmental pressures through histone modifications. I have read many papers on epigenetic marks in addiction. Still, I have neglected to cover the significance of addiction neuroepigenetics because it is incredibly complex, even compared to the current material in this article. Until there's a much better understanding of that set of molecular mechanisms and their influence on animal behavior, I don't think it's worth covering in detail. Hence why I never expanded that section of this article.
- In any event, I am far too busy to work on Wikipedia right now. I will probably be back in 12-18 months after I raise our Series A, and my work-life balance isn't 100% work, 0% life. Seppi333 (Insert 2¢) 02:58, 28 May 2021 (UTC)
References for this Talk page section
References
- ^ Volkow, Nora D., and George Koob, “Brain Disease Model of Addiction: Why Is It so Controversial?” Lancet Psychiatry 2, no. 8 (August 2015): 677–79. https://doi.org/10.1016/S2215-0366(15)00236-9
Drug addicts
By removing the words drug addicts
the text is no longer clear. Please refrain from such changes. It also created a non-functional wikilink. tgeorgescu (talk) 21:22, 19 August 2021 (UTC)
new essay source in treatment section
User 121.200.5.219 recently added content to the treatment section, some of which I removed for having a non-medical source. The other piece of content cites an essay published in a journal (currently ref number 111). Are essays like this one considered reliable medical sources?--Megaman en m (talk) 17:17, 27 August 2021 (UTC)
Overquote in references
Is it really necessary to quote paragraphs of text from so many sources that have a free online version? — Chris Capoccia 💬 20:36, 27 August 2021 (UTC)
- Academic disciplines have varying opinions regarding the value of extended quotations. As a I reader, I find extended quotations to be helpful. At the same time, your critique has merit and I shall henceforth trim quoted text or not include it at all out of respect for your viewpoint, which I imagine others share. Mark D Worthen PsyD (talk) [he/him] 03:19, 29 January 2022 (UTC)
Wiki Education Foundation-supported course assignment
This article is currently the subject of a Wiki Education Foundation-supported course assignment, between 19 January 2022 and 17 May 2022. Further details are available on the course page. Student editor(s): Friedchickenprincess.
- Welcome, Friedchickenprincess. I hope you find ways to improve this article. You probably want to read the l-o-n-g section above, in which we talk about changing the first few sentences of the article. WhatamIdoing (talk) 18:47, 21 February 2022 (UTC)
RfC re: is addiction a "biopsychosocial disorder" or a "brain disorder"?
Consensus reached; RfC closed. For more info, click "show" →
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We reached consensus on compromise language that satisfied the concerns of the editors involved in the discussion and that was consistent with the majority of comments offered by editors who responded to the request for comment but elected to not engage in the ongoing discussion. (RfCs rely on such "one-time comments" to garner thoughtful responses from a variety of editors. Offering one's opinion and not commenting further is the modal response to a request for comments.) See Suggested rewrite for the concluding discussions. See also Workspace for referencing for the final consensus version for the article's introduction. We waited one month since the last comments before closing this RfC. Mark D Worthen PsyD (talk) [he/him] 05:25, 25 March 2022 (UTC)
Should addiction be called a "biopsychosocial disorder" or a "brain disorder"? Mark D Worthen PsyD (talk) [he/him] 22:29, 30 January 2022 (UTC)
General discussionNote: I moved my response to StarHOG's reply to this RfC because I think they (StarHOG) has a good point about the purpose of an RfC (see below, "I came to this page as a result of an RfC ..."). My intention is to keep their (StarHOG's) RfC reply "pure" so to speak and move the debate, which they did not seek, down here. Mark D Worthen PsyD (talk) [he/him] 02:34, 1 February 2022 (UTC)
Our differing viewpoints perhaps reflect the ongoing debate among specialistsIt is not surprising that tension exists here on Wikipedia about this question as it has been hotly debated for many years in academia, among researchers, in the law, and by policy-makers among others. A forthcoming book,[1] for example, contains 44 chapters covering pro, con, not sure, and new viewpoints. (See the publisher's site for the table of contents.)
Sources:
References
Compromise languageHere is a proposed beginning for the lead:
(a) Lumping together drug addiction and non-drug behavioral addiction is problematic because in most instances the evidence for equivalency, as the behavioral addiction section acknowledges, rests largely on preclinical research findings. (Note that buttressing a section with preclinical evidence is a practice WP:MEDRS discourages. See WP:MEDANIMAL). For readers interested in the topic, we can refer them to relevant articles, e.g., Problem gambling. A related reason for concentrating on drugs is that if we are going to refer to addiction as a brain disorder (along with calling it a biopsychosocial disorder), are we comfortable stating that problem gambling, for example, is a brain disorder? I know that some medical institutions or groups do so, but the scientific support for such a conclusion remains controversial. (b) You will notice that my proposed first sentence differs from the current version (although not from previous versions) in the following manner:
I changed "brain" to "biopsychosocial" to incorporate the emerging consensus that both terms should be used. I argue that the more comprehensive term—biopsychosocial—should come first, immediately followed by introducing "brain disorder" and the rationale for its descriptive value. I changed "compulsive engagement in rewarding stimuli" to "persistent use of a drug" for a couple of reasons. First, the adjective "compulsive" lacks clarity. If we plan to retain the word, we should define it and explain exactly what it means in this context. For example, does it mean, from Webster's, "having power to compel"?[1] If so, we ought to define "compel" too. Turning to Webster's again, "compel" means to force, drive, or impel.[2] If you accept these definitions, then addiction forces a person to use drugs. If that is the case, how have so many people overcome drug addiction? If their malady forces them to use, how did they ever stop? So, we should jettison "compulsive" because it serves only to confound. (There are many other reasons to omit "compulsive", which Heather (2017)[3] examines in detail.) Similarly, the muzzy phrase "engagement in rewarding stimuli" should go. If someone can explain exactly what that phrase means, please do. I will listen with an open mind. Finally, we should include "harm" along with "adverse consequences" because, for example, a person mugging another for drug money might not regard the cash thereby obtained as an adverse consequence, whereas the robbery victim likely suffers harm. Mark D Worthen PsyD (talk) [he/him] 06:48, 7 February 2022 (UTC)
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Rethinking the premise of the RfCI'm beginning to think that the premise of the RfC, that there should be a choice between "brain" and "biopsychosocial", is going to prove unable to reach a satisfactory consensus. It's entirely appropriate to discuss these concepts as part of the page, but it may not work to do it in the lead paragraph, because that forces too much simplification. In a sense, neither of these words has to be the first word we use to describe addiction. I was looking for possible source material, and came upon this 2021 review article: [2]. It starts off by saying: "
Suggested rewriteBased on the subsection just above, I'd like to suggest something along the lines of the following:
WorkspaceBased on the talk section just below, I'd like for interested editors to collaborate on the rewrite here, before actually implementing it on the page. Here is a somewhat clumsy copy-and-paste of the text just above, into the current version of the first paragraph of the lead. I need other editors to revise it further, especially in terms of the correct placement of inline citations. --Tryptofish (talk) 18:33, 20 February 2022 (UTC)
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Workspace for referencingLet's get the inline citations into the revised version. --Tryptofish (talk) 22:45, 23 February 2022 (UTC)
References Close this RfC?It has been 21 days since I posted this Request for Comment (RfC). It seems we have reached a consensus. I therefore suggest: (1) If no one objects within the next five days (120 hours from the timestamp of this comment), Tryptofish will edit the lead in a manner consistent with the consensus reached here. (Presuming Tryptofish is willing to take on this task.) (2) If someone objects, we will make a formal request for closure, which for those relatively new to Wikipedia means that an uninvolved editor will assess, summarize, and formally close this discussion. Mark D Worthen PsyD (talk) [he/him] 18:16, 20 February 2022 (UTC)
The discussion above is closed. Please do not modify it. Subsequent comments should be made on the appropriate discussion page. No further edits should be made to this discussion.
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