Talk:Addiction

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Missing concepts[edit]

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])

Seppi333 (Insert 2¢) 12:01, 3 February 2016 (UTC)

References

  1. ^ 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.
  2. ^ 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.
  3. ^ 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.
  4. ^ 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.CS1 maint: multiple names: authors list (link)
  5. ^ 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.

Reviews, medical references, and content to add[edit]

 High Priority: Need to add coverage of these sources since they're recent and very comprehensive.

  1. 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

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)

While further investigations are necessary, a picture of genetic and epigenetic mechanisms involved in addiction is beginning to emerge and the insight gained from these studies will be key to the identification of novel targets for improved diagnosis and treatment of addiction syndromes in humans. ...

Drug addiction, or substance use disorder (SUD), is defined as the compulsive administration of drugs of abuse in spite of negative consequences to the individual and a loss of control over the intake of such drugs (American Psychiatric Association, 2013). From a neurobiologic perspective, addiction represents maladaptive neural plasticity in response to drugs of abuse, which involves long-term molecular alterations in key brain regions that control reward (Fig. 48.1), leading to potentially lifelong behavioral abnormalities (reviewed in Nestler (2014)). ...

These risk factors include adverse early life experiences and other environmental stimuli that "prime" an individual to be more vulnerable to addiction (Pena et al., 2014). Indeed, without exposure to drugs (an environmental factor itself ), the addicted phenotype would not be detected, thus highlighting the complex interplay between genes and environmental factors involved in the initiation and maintenance of the addicted phenotype (Fig. 48.2). ...

In its broadest definition, epigenetics describes changes in gene expression that do not arise from changes to the DNA sequence; this generally involves alterations in histone modifications, DNA methylation, and noncoding RNAs (microRNAs (miRNAs) and long noncoding RNAs (lncRNAs); see Chapter 5). Each of these mechanisms can be altered in response to internal and external signals and provides a mechanism by which environmental stimuli can interact with an individual's genome to influence cellular responses and function, including neuroplasticity. The differing temporal effects of each mechanism are, in part, the result of their varying levels of stability – e.g., most histone modifications are exceptionally dynamic, whereas DNA methylation is generally less so (Jaenisch and Bird, 2003). ...

It remains unknown whether such transgenerational transmission of addiction-like vulnerability is mediated behaviorally, through epigenetic modifications in sperm, or through chemical changes in seminal fluid, among other possibilities. In any event, these data raise the possibility that an individual's risk for addiction is mediated not just by genes and environment but also by additional factors that are transmitted across generations. 

While there are difficulties associated with adoption studies (reviewed in Hall et al. (2013)), they have been instrumental in recognizing genetic contributions to the development of addiction by identifying a link between substance abuse in the biologic parent and adopted offspring. Adoption studies have also highlighted environmental factors important for the development of addiction by linking abuse in the adopted offspring to characteristics in the adopted parents. In particular, parental divorce or parental psychiatric disorders were identified as risk factors for the development of substance abuse in offspring (Cadoret et al., 1986, 1995, 1996). ... Evidence from twin studies consistently estimates that the genetic contribution to substance abuse disorders is 50% for alcoholism (Heath et al., 1993; Prescott and Kendler, 1999; True et al., 1999) and ranges from 30% to 80% for other drugs of abuse (Tsuang et al., 1996; Kendler et al., 2000, 2006; Agrawal et al., 2005; Pergadia et al., 2006). Interestingly, evidence suggests that genetic factors play a greater role in the severity of substance abuse (i.e., the development of addiction) than in earlier stages of drug use, which are seemingly influenced to a greater extent by environmental factors (Tsuang et al., 1996; Kendler and Prescott, 1998; Rhee et al., 2003; Fowler et al., 2007), highlighting the multi-factorial nature of the addiction phenotype.

EPIGENETIC MECHANISMS OF ADDICTION
Because of the strong influence of external risk factors on the development of addiction, it has been proposed that epigenetic mechanisms regulate the long-term changes associated with phenotypic priming and the subsequent addicted phenotype. To date, a majority of the work on the epigenetic mechanisms involved in addiction has focused on the effects of drugs of abuse in animal models of addiction, with a concentration on the effects of stimulants in the nucleus accumbens (NAc), a key brain region involved in reward. Recently, work has expanded to other brain regions in the reward circuitry (Fig. 48.1), including the ventral tegmental area (VTA), prefrontal cortex (PFC), basolateral amygdala (BLA), and hippocampus (HC), as well as to other drugs of abuse. ...

While there is substantial evidence that genetic factors contribute roughly half of the risk for an addicted phenotype, specific genes and other genomic regions that mediate this risk have been very difficult to identify with certainty. More powerful experimental methods and associated bioinformatic approaches that are agnostic in nature – e.g., GWAS with whole-exome or whole-genome sequencing – are now enabling far more penetrating studies which should reveal gene networks that underlie addiction risk. On the other hand, environmental risk factors are also important and a few vague factors (e.g., child abuse, adverse life experiences) are known, but their mechanisms remain poorly understood, particularly in humans.
— From [1]

  2. United States Surgeon General's report on addiction (published November 2016).[2]
  3. Review of the neurobiology of addiction[3]
Other content to add

Epigenetic effects of drugs

Neuropsychology


Seppi333 (Insert 2¢) 21:35, 28 January 2017 (UTC); updated 01:57, 21 July 2018 (UTC)

References

  1. ^ 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.
  2. ^ "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.
  3. ^ 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
  4. ^ 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].
  5. ^ 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.
  6. ^ 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.
  7. ^ 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[edit]

Reflist

References

  1. ^ Nora Volkow (31 March 2016). "A Major Step Forward for Addiction Medicine". National Institute on Drug Abuse. National Institutes of Health. Retrieved 3 April 2016. Only about 10 percent of the 21 million Americans who meet the need for care for an alcohol or drug use disorder receive any form of treatment, and much of the treatment available does not meet standards for evidence-based care. There are many attitudinal and systemic reasons for this treatment gap, including stigma against treating people with addictions and institutional barriers to providing or funding addiction treatment. ... A major milestone was reached on March 14, 2016, when the American Board of Medical Specialties (ABMS) formally announced recognition of the field of Addiction Medicine as a medical subspecialty. ... In a statement issued to mark this milestone, ABAM President Robert J. Sokol summed up its significance: 'This landmark event, more than any other, recognizes addiction as a preventable and treatable disease, helping to shed the stigma that has long plagued it. It sends a strong message to the public that American medicine is committed to providing expert care for this disease and services designed to prevent the risky substance use that precedes it.'
  2. ^ "AMERICAN BOARD OF MEDICAL SPECIALTIES RECOGNIZES THE NEW SUBSPECIALTY OF ADDICTION MEDICINE" (PDF). American Board of Addiction Medicine. 14 March 2016. Retrieved 3 April 2016. Sixteen percent of the non-institutionalized U.S. population age 12 and over – more than 40 million Americans – meets medical criteria for addiction involving nicotine, alcohol or other drugs. This is more than the number of Americans with cancer, diabetes or heart conditions. In 2014, 22.5 million people in the United States needed treatment for addiction involving alcohol or drugs other than nicotine, but only 11.6 percent received any form of inpatient, residential, or outpatient treatment. Of those who do receive treatment, few receive evidence-based care. (There is no information available on how many individuals receive treatment for addiction involving nicotine.)
    Risky substance use and untreated addiction account for one-third of inpatient hospital costs and 20 percent of all deaths in the United States each year, and cause or contribute to more than 100 other conditions requiring medical care, as well as vehicular crashes, other fatal and non-fatal injuries, overdose deaths, suicides, homicides, domestic discord, the highest incarceration rate in the world and many other costly social consequences. The economic cost to society is greater than the cost of diabetes and all cancers combined. Despite these startling statistics on the prevalence and costs of addiction, few physicians have been trained to prevent or treat it.

Reward system[edit]

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. Face-tongue.svg 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[edit]

I haven't read through these papers yet, so I'm just putting these links here for now.

Seppi333 (Insert 2¢) 07:13, 9 October 2016 (UTC)

Environmental enrichment-based behavioral therapy[edit]

  • 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]

    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.

    Seppi333 (Insert 2¢) 22:20, 13 December 2016 (UTC)

References

  1. ^ 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]

Facing Addiction: A National Summit - November 21, 2016[edit]

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

  1. ^ [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)

External links modified[edit]

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Study or review?[edit]

See edit here.

An addiction to loud music is seen more often in non-professional musicians than in non-musician control subjects.[1]

References

  1. ^ 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[edit]

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)
Something to think about. InedibleHulk (talk) 19:14, 20 June 2018 (UTC)
Here's a few to start (mostly historical):

Changes[edit]

Hello, Today I am going to be revising this article for a neutral tone, checking for grammar and mechanical errors, watching for concise language, making sure the article has a strong lead, organizing the paragraphs, checking sites, and finally I will be summarizing.

Courtneymfoster (talk) 03:01, 27 September 2018 (UTC) Courtney Foster

Criticism Section ?[edit]

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[edit]

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[edit]

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. 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. 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. 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 Nine-teenth-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. 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. Fortschritte der Neurologie, Psychiatrie, 74(9), 511-521.

THIS! MY GOD, THIS! Robshort (talk) 00:36, 9 November 2019 (UTC)

Evaluate an Article[edit]

https://en.wikipedia.org/wiki/User:Lilbitkait — Preceding unsigned comment added by Lilbitkait (talk • contribs) 03:48, 21 January 2020 (UTC)

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