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^Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 15: Reinforcement and Addictive Disorders". In Sydor A, Brown RY. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 365–367. ISBN9780071481274.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. PMID26851575. 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.
^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 , 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 . 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 .
^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. PMC4541325. PMID26347716. 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.
Incentive salience / neurobiology reviews to add
^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. PMID27475769. 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
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.
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
^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.'
^"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.
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.
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)
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. Interpersonal traumas, such as child abuse and violent assaults, are particularly predictive of substance-related problems."
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)