The Neuroscience of Addiction
Addiction
According to the American Society of Addiction Medicine, addiction is defined as “a treatable, chronic medical disease involving complex interactions among brain circuits, genetics, the environment, and an individual’s life experiences” (American Society of Addiction Medicine). Drug addiction is a chronically relapsing disorder that has been characterized by a compulsion to seek and take the drug, loss of control in limiting intake, and emergence of a negative emotional state reflecting a motivational withdrawal syndrome when access to the drug is prevented (Koob & Volkow, 2010). According to the National Survey on Drug and Use and Health (NSDUH), 19.7 million American adults (aged 12 or over) battled a substance abuse disorder in 2017.
Addiction centers around alterations to a single pathway in the brain referred to as the “reward” circuit located in the limbic system. This circuit has been connected to addiction of all kinds including opioids, alcohol, tobacco, marijuana, and even caffeine. The addiction pathway is the same brain system that dictates motivated behaviors. Researchers refer to this system as the brain reward region and have confirmed its role in plenty of animal studies (rats and mice) as well as brain imaging studies on human addicts.
This pathway has been identified as the mesolimbic dopamine reward system. The reward pathway begins in the ventral tegmental area, where neurons release dopamine to make you feel pleasure (Volkow et al., 2012). The brain begins making connections between activity and pleasure, ensuring that we will repeat these behaviors. Drugs work by exploiting this same pathway that helps humans learn and survive. All addictive drugs modulate dopamine signaling in this pathway (Huang et al., 2009). Not everyone that uses drugs becomes addicted. When an individual first tries a drug, they experience a sense of euphoria without a natural award. Often, this unnatural feeling encourages individuals to take more of the drug. The drug target the ventral tegmental area to release dopamine into the nucleus accumbens. Endorphins, the primary natural opioid, are also released. The combined activation of dopamine and endorphins is what makes of the sensation of pleasure when using drugs. Research has also shown that the faster the dopamine levels increase in the brain, the stronger the reinforcing effects are.
Drug-evoked synaptic plasticity occurs after prolonged use of a drug and repetitive exposure (Lüscher & Malenka, 2011). The synaptic and neural circuit modifications caused by a drug experience often lay the foundation for more drug induced adaptations. Synapses in the reward pathway become more excitatory due to the strong increase in the frequency of action potentials during drug use. These synaptic changes can affect the amount of neurotransmitter released and the density of receptors in the synapse. Continued use of addictive drugs results in the decrease of natural dopamine and forces individual to feel less satisfied. Long-term drug use has been associated with decreased levels of dopamine receptors as well as natural dopamine. A tolerance develops because the individual requires more of the drug to feel anything and even more natural dopamine to feel normal. This is when a dependence on the drug is formed and withdrawal symptoms begin if the drug is not taken (See et al., 2003).
Addiction occurs because of drug induced modifications to the brain after repeated exposure. These changes create a cycle of dependency where the user needs drugs to feel normal. This is because the natural dopamine levels decrease and the individual no longer feels happy. This cycle can be broken with the help of trained professionals. If seeking help, please refer to some of the information towards the bottom of the page.
Neuroscience to Help Addiction
Some characteristics of addiction are similar to other chronic diseases because it changes the brain and impairs the way it works.
The above image is an example of a brain imaging technique that measures the function of the brain. The greater activity is shown in reds and yellows, wile reduced activity is identified by blues and purples. The healthy control shows a significant increase in function over the brains who struggled with a methamphetamine addiction. In drug addiction, the frontal cortex shows less activity which is important to recognize because it is responsible for judgement and decision making.
How the brain recovers from addiction is an emerging area of research. The image above shows a healthy brain on the left compared to two brains recovering from a methamphetamine addiction. It is clear that only after one month of abstinence, the brain looks very different from the healthy brain. After 14 months of abstinence, the dopamine transporter levels in the reward region of the brain return to nearly normal function. There is limited research on the brain’s recovery from drug use. One study found that adolescents that stopped using drugs had a significant recovery with respect to behavioral disinhibition and negative emotionality (Hicks et al., 2012). This would suggest that some recovery is occurring in the prefrontal cortex after a period of abstinence. Furthermore, more research suggests that a number of abstinent days shows improved executive function, larger cerebellar volumes, and improved short-term memory.
While promising, the study of neuroscience in help addiction is still in its infancy. What is clear is that damage causes by prolonged drug use can be reversed and cognitive function can be improved. There is little evidence to show how we can improve brain recovery from substance use, but physical exercise has been shown to improve brain health and neuroplasticity.
Functional imaging techniques allow scientists to measure the contributions of various structures to specific psychological processes. Functional images offer insight to the brain regions that are activated while performing a given task. In the image below, the right brain is an individual with a cocaine use disorder while the left brain is a control. This is a positron emission tomography (PET) scan that is tracking a radioactive tracer indicating activity in the brain. The red and yellow indicates areas of high activity while the blues and purples indicate areas of low activity.
Imaging techniques like positron emission tomography (PET), electroencephalography (EEG), functional near infrared spectroscopy (fNIRS), and functional magnetic resonance imaging (fMRI) offer information on the changes of brain structures after drug use. Imaging technology has already been used to investigate why some individuals are more vulnerable to drug addiction than others. Imaging studies suggest that pre-existing differences in the reward circuit could explain the variability in drug addiction. More research should be performed to understand the specific changes drugs make to the brain. More information on activity changes could lead to improved treatments and therapies for patients suffering from drug use disorders and addiction.
Imaging studies have already suggested a few methods of helping individuals who struggle from drug abuse disorders. One strategy suggests decreasing the reward value of the drug of choice and increasing the reward value of non-drug reinforcers. This would require adjusting dopamine levels when the drug is used compared to other stimuli. The second strategy is to weaken conditioned drug behaviors through extinction. Extinction is the gradual weakening of a conditioned response that results in the behavior disappearing or decreasing. The third strategy is weakening the motivational drive to take the drug of abuse. This would require altering neurotransmitter levels in the prefrontal cortex which is associated with motivation. It would also be important to observe the cerebellum, amygdala, and hippocampus. These are the learning structures of the brain that allow the addiction and dependence to occur. The final strategy is strengthening frontal inhibitory and executive control. Teaching individuals better control over their desires and needs could could help improve and drug seeking behaviors. This could occur through learning techniques as motivation is constantly studied.
Addiction Video Library
This video library consists of many resources that take a fresh perspective on the epidemic of addiction. Addiction is a serious disorder that requires the attention of researchers everywhere. One serious problem I learned while studying addiction is the lack of neuroscience that is being applied to addiction. Other brain disorders have been studied for years now compared to addiction. More knowledge on addiction will help end the epidemic and improve the condition anyone suffering.
Johann Hari: Everything you think you know about addiction is wrong. Hari discusses why we treat addicts the way we do and if there is a better way to do so. His questioning brought him around the world and introduced him to a hopeful way of viewing addiction.
Michael Botticelli: Addiction is a disease. We should treat it like one. Boticelli is a former director of the National Drug Control Policy who is working to end the addiction epidemic by treating people with kindness, compassion, and fairness.
Ethan Nadelmann: Why we need to end the War on Drugs. Nadelmann asks the question if the War on Drugs is doing more harm than good? He argues for a safe regulation of drugs instead of stamping out the drug trade.
For a better explanation on addiction and the brain from a professional neuroscientist check out this video below. Neuroscientist and former addict Marc Lewis makes his case to the Royal Institution that addiction isn’t a disease at all.
Take this quiz to test your knowledge on addiction and how it affects the brain.
Addiction is a disorder of the brain that can be studied and helped with the proper resources. If seeking help for addiction it is important to know that you are not alone, please contact SAMHSA national helpline at 1–800–662–4357. Help is available so speak with a counselor today.
Sources
Bevilacqua, L., & Goldman, D. (2009). Genes and Addictions. Clinical Pharmacology and Therapeutics, 85(4), 359–361. https://doi.org/10.1038/clpt.2009.6
Hicks, J. A., Friedman, 2R. S., Gable, P. A., & Davis, W. E. (2012). Interactive effects of approach motivational intensity and alcohol cues on the scope of perceptual attention. Addiction, 107(6), 1074–1080.
Huang, X., Gu, H. H., & Zhan, C.-G. (2009). Mechanism for Cocaine Blocking the Transport of Dopamine: Insights from Molecular Modeling and Dynamics Simulations. The Journal of Physical Chemistry. B, 113(45), 15057–15066. https://doi.org/10.1021/jp900963n
Koob, G. F., & Volkow, N. D. (2010). Neurocircuitry of Addiction. Neuropsychopharmacology, 35(1), 217–238. https://doi.org/10.1038/npp.2009.110
Ling, W., Mooney, L., & Wu, L.-T. (2012). Advances in Opioid Antagonist Treatment for Opioid Addiction. The Psychiatric Clinics of North America, 35(2), 297–308. https://doi.org/10.1016/j.psc.2012.03.002
Lüscher, C., & Malenka, R. C. (2011). Drug-evoked synaptic plasticity in addiction: From molecular changes to circuit remodeling. Neuron, 69(4), 650–663. https://doi.org/10.1016/j.neuron.2011.01.017
See, R. E., Fuchs, R. A., Ledford, C. C., & McLAUGHLIN, J. (2003). Drug Addiction, Relapse, and the Amygdala. Annals of the New York Academy of Sciences, 985(1), 294–307. https://doi.org/10.1111/j.1749-6632.2003.tb07089.x
Volkow, N. D., Wang, G.-J., Fowler, J. S., & Tomasi, D. (2012). Addiction Circuitry in the Human Brain. Annual Review of Pharmacology and Toxicology, 52, 321–336. https://doi.org/10.1146/annurev-pharmtox-010611-134625
Media Sources
