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I can't see the point of singling out drug addiction as its own thing in the lead of an article about general addiction, especially before the part about the main topic. Can you?
Just another rewarding thing that people crave. I get that there's a specific subtopic article for it, and I'm not against Wikilinking it in the lead. Just should go with the others in Paragraph 2. Probably first in that list, since it's the most famous, but not bigger than addiction itself. InedibleHulk(talk) 19:22, October 20, 2014 (UTC)
Behavioral addiction and drug addiction are a dichotomy. Stop editing the lead sentence. Seppi333 (Insert 2¢ | Maintained) 19:36, 22 November 2014 (UTC)
Dichotomies are for opposites. There's a slight difference between compulsively seeking rewarding sex and compulsively seeking rewarding drugs, but only as much as between rewarding food and rewarding gambling. Not two different things.
Sorry for the delay in responding - didn't notice this until now.
All compulsions are pathologically reinforced behaviors, but the main difference between that paper and the characterizations used by the reviews in several sections of this article is that these reviews require that the behavior/drug be rewarding - i.e., activate the reward system, particularly the mesolimbic pathway/nucleus accumbens, in functional neuroimaging studies. The nucleus accumbens governs the response to positive reinforcement (the form of reinforcement that involves a reward), and it is there that ΔFosB overexpression has been shown to simultaneously occur with the appearance of addictive behavior and structural neurplasticity. It's a rather simple definition, but it actually has rather significant/profound implications for the neuropsychology and molecular neurobiology involving a drug or behavior. Seppi333 (Insert 2¢) 03:46, 19 June 2015 (UTC)
^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.
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