top of page

- the neurobiology of addiction -

Desk_edited.png

Many theories attempt to explain addiction. From a neurobiological perspective, addictive behaviors reflect a type of hyper-learning. Addictive substances trigger mammoth spikes in the biochemicals linked to learning, with researchers particularly focused on dopamine and glutamate. We learn by association. The more intensely or frequently that a behavior activates the biochemical expression of reward, the more that behavior is conditioned (i.e., learned).

Addictive substances trigger mammoth spikes in the biochemicals linked to learning - dopamine & glutamate.

Addictive substances exploit the brain’s plastic potential, the learning linked to addictive behaviors deeply anchored .

Think of addiction as a form of hyper-learning.

Therapy can also tap into the brain's plastic potential and help to reestablish a balance between the impulsive midbrain and executive forebrain. 

Addictive behaviors tend to activate both intense and frequent rewards. In fact, the surges in dopamine and glutamate associated with substances of misuse far exceed the levels released in normally rewarding experiences, like relationships, a career, a favorite hobby, and so forth. Such intense biochemical experiences condition the brain to become increasingly sensitive to the cues associated with drink and drug. Over time, the circuits in the brain linked to learning and motivation become primed to respond to a drug. Think of addiction as a form of hyper-learning.

Research has demonstrated that the mesolimbic circuit, as the reward system in the brain, becomes increasingly dedicated to an addiction over time; in the more severe cases of addiction, the reward system fires off almost exclusively in response to cues to use (places, persons, memories, certain emotions). As a result, people mired in addiction lose interest in their relationships, careers, academics, and other normally pleasurable experiences, those experiences unable to compete with the intense biochemical reactions that addictive substances trigger.

​The Nucleus Accumbens (NAc), as the epicenter of learning along the mesolimbic circuit, literally grows in size over the course of addictive use, with research in recent years discovering that the number and density of glutamate dendrites along the NAc increase in parallel to an addiction (Quintero 2013). That growth signals the brain’s plasticity at play. The NAc becomes something of a behemoth, as addictive substances exploit the brain’s plastic potential, the learning linked to addictive behaviors deeply anchored in the brain.

That’s why people continue to use and relapse, even as the consequences related to their addiction mount. Even after a third DUI, or near fatal overdose, or a termination, maybe after a separation from a loved-one, people continue to use and/or drink, seemingly oblivious to reality. That's because addictive behaviors change the brain, shaping neuroadaptations that propel people to act against their better judgement (Berridge, K, 2013).

​The brain’s plasticity normally promotes adaptive and pro-social behavior. In cases of addiction, however, that plasticity actually reinforces the drive to use or drink on a neurobiological (i.e., preconscious) level. If your loved one appears oblivious, it’s only because of the effect described here. Addictions prime the mesolimbic system to fire off more easily and for prolonged periods. Consequently, the midbrain – the more primitive part of the human brain – begins to dictate behavior. A dysregulated midbrain will overrun the executive areas of the frontal lobe and their ability to inhibit urges. As a result, those with addictive behaviors will become more impulsive, and less reflective.

Therapy can also tap into the brain's plastic potential (Porto, Oliveira, et al., 2009; Beauregard, 2014), and help to reestablish a balance between the impulsive midbrain and executive forebrain. Behavioral therapy strives to normalize the ebb and flow of neuro-impulses between the two areas. To use a car analogy, the midbrain represents the gas pedal, while the frontal area serves as the braking system; addictions produce a Ferrari with bad brakes. Behavioral therapy, then, essentially services  your braking system.

REFERENCES:

Alderman, BL, Olson, RL, Brush, CJ  and Shors, TJ. MAP training: combining meditation and aerobic exercise reduces depression and rumination while enhancing synchronized brain activity. Translational Psychiatry (2016), 6, e726

Beauregard, M. Functional neuroimaging studies of the effects of psychotherapy. Dialogues Clinical Neuroscience, 2014, Mar, 16(1), 75–81.

Blum, K., Femino, J., Teitelbaum, S., Giordano, J., Oscar-Berman, M., Gold, M. (2013). Molecular Neurobiology of Addiction Recovery: The 12 Steps Program and Fellowship. Springer Briefs in Neuroscience. Springer-Verlag New York. DOI 10.1007/978-1-4614-7230-8

Dempsey JP, Harris KS, Shumway ST, Kimball TG, Herrera JC, Dsauza CM, Bradshaw SD. Functional near infrared spectroscopy as a potential biological assessment of addiction recovery: preliminary findings. American Journal of Drug and Alcohol Abuse, 2015, Mar, 41(2), 119-26.

Feldstein Ewing SW, Chung T. Neuroimaging mechanisms of change in psychotherapy for addictive behaviors: emerging translational approaches that bridge biology and behavior. Psychology of Addictive Behaviors, 2013, Jun, 27 (2), 329-35.

Feldstein-Ewing, SW, Filbey, FM, et al. Proposed Model of the Neurobiological Mechanisms Underlying Psychosocial Alcohol Interventions: The Example of Motivational Interviewing. Journal of Studies on Alcohol and Drugs. 2011, Nov, 72(6), 903–916.

Goldapple K, Segal Z, Garson C, Lau M, Bieling P, Kennedy S, Mayberg H. Modulation of cortical-limbic pathways in major depression: treatment-specific effects of cognitive behavior therapy. Archives of General Psychiatry. 2004, Jan, 61(1), 34-41.

Goldstein RZ, Craig AD, Bechara A, Garavan H, Childress AR, Paulus MP, Volkow ND. The neurocircuitry of impaired insight in drug addiction. Trends in Cognitive Sciences, 2009, Sep, 13(9), 372-80

Goldstein RZ, Volkow ND. Dysfunction of the prefrontal cortex in addiction: neuroimaging findings and clinical implications. Nature Reviews Neuroscience, 2011, Oct 20, 12(11), 652-69

Holzschneider K & Mulert C. Neuroimaging in anxiety disorders. Dialogues Clinical Neuroscience, 2011, 13(4), 453-61.

Karlsson, H. How Psychotherapy Changes the Brain. August 11, 2011. http:// www.psychiatrictimes.com/ psychotherapy/how-psychotherapy-changes-brain

Koob, GF. Brain stress systems in the amygdala and addiction. Brain Research, 2009, October 13, 1293, 61–75.

 

Martin-Fardon R, Zorrilla EP, Ciccocioppo R, Weiss F. Role of innate and drug-induced dysregulation of brain stress and arousal systems in addiction. Brain Research, 2010, Feb, vol.16, 1314, 145-61

 

Nosen, E., et al., Treatment of co-occurring PTSD-AUD: Effect of exposure-based and non-trauma psychotherapy on alcohol and trauma cue reactivity. Behaviour Research and Therapy, Oct 2014, vol. 61. 

Porto PR, Oliveira L, Mari J, Volchan E, Figueira I, Ventura P. Does cognitive behavioral therapy change the brain? A systematic review of neuroimaging in anxiety disorders. Journal of Neuropsychiatry & Clinical  Neuroscience, 2009, Spring, 21(2), 114-25.

Quintero GC. Role of nucleus accumbens glutamatergic plasticity in drug addiction. Journal of Neuropsychiatric Disease and Treatment, 2013, 9, 1499-512

Thayer RE, Hutchison KE. Neuroimaging in clinical studies of craving: importance of reward and control networks. Psychology of Addictive Behaviors, 2013, Jun, 27(2), 543-6.

 

Torregrossa MM & Taylor JR. Learning to forget: manipulating extinction and reconsolidation processes to treat addiction. Psychopharmacology (Berl)., 2013, Apr, 226(4), 659-72.

 

Vollstädt-Klein S, Loeber S, Kirsch M, Bach P, Richter A, Buhler M, von der Goltz C, Hermann D, Mann K, Kiefer F. Effects of cue-exposure treatment on neural cue reactivity in alcohol dependence: a randomized trial. Biological Psychiatry, 2011, 69, 1060–1066

Weirs, CE, Stelzel, C, et al., (2014). Neural Correlates of Alcohol-Approach Bias in Alcohol Addiction: the Spirit is Willing but the Flesh is Weak for Spirits, Neuropsychopharmacology, 39, p.688-697

bottom of page