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I'm asking this from a purely psychological and biological viewpoint, mainly why a drug addict is said to always remain one, even after sobering up.

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closed as primarily opinion-based by queenslug, Robin Kramer, Keno, Seanny123, Arnon Weinberg Mar 17 '17 at 5:46

Many good questions generate some degree of opinion based on expert experience, but answers to this question will tend to be almost entirely based on opinions, rather than facts, references, or specific expertise. If this question can be reworded to fit the rules in the help center, please edit the question.

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    $\begingroup$ Great question. The "Always an addict" mantra has struck me sometimes as more of a political statement than a scientific one as it represents a fundamentally cynical/hopeless view and is often cited by behavior modification type people with an agenda. E.g. "You can't be cured, so you have to keep paying for therapy from me for life. This month will be $89.95." It would be great to have a theoretical or empirical basis for understanding why cures to addiction just don't happen. $\endgroup$ – Robert Columbia Mar 13 '17 at 2:57
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    $\begingroup$ For empirical background, see "relapse": en.wikipedia.org/wiki/Relapse; for theoretical background, see "renewal effect", and "rapid reacquisition": en.wikipedia.org/wiki/… (both articles have sections on drug addiction) - basically, reconditioning is much faster than initial conditioning. $\endgroup$ – Arnon Weinberg Mar 13 '17 at 3:48
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    $\begingroup$ Addiction can be treated, but not cured $\endgroup$ – Dhruv Saxena Mar 14 '17 at 19:48
  • $\begingroup$ It's worth noting that not everyone thinks that this is true. $\endgroup$ – EJoshuaS Mar 21 '17 at 23:00
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Short answer, which is one of many:

One interesting hypothesis about this is the "reward hijacking" model. Essentially, when somebody becomes addicted their reward circuits become hypersensitive to drug-related cues and lack sensitivity to other rewards. Specifically, areas like their orbitofrontal cortex, which has to do with representing reward, and their ventral striatum, which has to do with dopamine and motivation, start to function strangely. So even when they replace the drug with new habits they still display heightened sensitivity to the drug. See Wrase et al, 2007 for one of many imaging studies on this. There are many neurobiological theories that explain why the reward sensitization occurs in response to addictive drugs.

The way this translates to function is that drugs appeal more and more to somebody with an addiction, while alternative habits appeal less and less. This contributes to the very high relapse rate. Interestingly, deep brain stimulation of the ventral striatum has helped curb alcohol cravings for some alcoholics. (See Knapp 2009 for rats, and Muller 2016 for a pilot study in humans.)

I hope this helps! The question you're asking is a very broad one, so you have a wide range of answers to explore.

Wrase, J., Schlagenhauf, F., Kienast, T., Wüstenberg, T., Bermpohl, F., Kahnt, T., ... & Heinz, A. (2007). Dysfunction of reward processing correlates with alcohol craving in detoxified alcoholics. Neuroimage, 35(2), 787-794.

Knapp, C. M., Tozier, L., Pak, A., Ciraulo, D. A., & Kornetsky, C. (2009). Deep brain stimulation of the nucleus accumbens reduces ethanol consumption in rats. Pharmacology Biochemistry and Behavior, 92(3), 474-479.

Müller, U. J., Sturm, V., Voges, J., Heinze, H. J., Galazky, I., Büntjen, L., ... & Bogerts, B. (2016). Nucleus Accumbens Deep Brain Stimulation for Alcohol Addiction–Safety and Clinical Long-term Results of a Pilot Trial. Pharmacopsychiatry, 49(04), 170-173.

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