Case Example: Tina
Tina is a 21-year-old single mother of two children (a newborn and a 3-year-old). She began using alcohol and smoking cannabis when she was around 14 years old but did not experience many problems as a result of her substance use at that time. When Tina was a senior in high school, she began dating a guy that she really fell in love with and hoped that one day they would get married and start a life together. Although she and her boyfriend, Josh, did not plan to start having children until they both graduated high school and had steady jobs, Tina became pregnant with her first child. She was able to abstain from alcohol and cannabis throughout the time she was pregnant. Josh was unable to find work, so he joined the National Guard as a way to earn money and hopefully pay for college. Unfortunately,Josh’s battalion was deployed to Afghanistan and during his second deployment he was killed when his Humvee was hit by a rocket-propelled grenade (RPG). Tina had just given birth to their second child. Because her parents were against Tina getting married, she rarely spoke with them. She found herself isolated, alone and depressed. She began drinking and smoking cannabis
Biological Models of Addiction 107 again, only this time on a daily basis after the kids were in bed for the night. Tina would often wake up feeling hungover and even more depressed, feeling that she couldn’t face another day. After a neighbor called Child Protective Services on Tina for leaving her children unattended, she tried to stop drinking and smoking but found it very difficult. She reports that she would begin to experience “shakiness and sweats” which are common symptoms of alcohol withdrawal. She would eventually give in to drinking and smoking again.
Case Conceptualization
Tina is struggling with both depression as well as alcohol and cannabis use disorders. Although initially Tina felt that drinking and smoking pot would relax her and help her unwind from the stress of taking care of her children, she soon found that her drinking and smoking made her feel worse. This was most likely the result of dopamine and serotonin depletions that she began to experience as a result of several months of continuous substance use. Even when Tina tried to stop using, she would find herself feeling worse, initially because of acute withdrawal and then, after a few days or weeks, she would begin to experience post-acute withdrawal (often characterized by anxiety, lethargy, depressed affect, anhedonia, irritability, impatience and low frustration tolerance.) Post-acute withdrawal is thought to come about as a result of dopamine and serotonin depletions in the brain and often results in high relapse rates during the initial weeks/months of sobriety.
Boxed Item 5.3 Post-Acute Withdrawal (PAW)
Each of the various mood-altering substances that result in substance use disorders produce “substance-specific” withdrawal symptoms. Generally, the withdrawal symptoms for CNS depressant substances (e.g. alcohol, benzodiazepines, opioids) tend to produce withdrawal symptoms that are opposite to the depressant impact of these substances, which in this case is agitation, restlessness and overstimulation. Stimulant drugs of abuse (e.g. cocaine, methamphetamine, amphetamines), on the other hand, tend to produce withdrawal symptoms of depression, lethargy and malaise. All of the aforementioned withdrawal symptoms comprise what we know as “acute withdrawal,” which generally lasts for a few days; at most, several days. However, there is also a phenomena called post-acute withdrawal, which is thought to be the result of dopamine depletions in the brain.The thinking is that during the time a person is using mood-altering substances, they are essentially flooding their brain with dopamine. However, because of tolerance, the brain adapts and eventually stops producing dopamine on its own. It’s hypothesized that it takes several months (sometimes 6 to 12 months of total abstinence) before the brain begins to produce its own dopamine again. Not surprisingly, PAW is characterized by anhedonia (an inability to experience pleasure), lethargy and lack of motivation to accomplish things.
Boxed Item 5.4 Can Brain Scans Predict Relapse?
Recent research being conducted at Stanford University is seeking to predict who will relapse and who won’t by using fMRI brain scans. Researchers MacNiven, Knutson and colleagues were able to accurately predict those individuals who would relapse in 75% of the cases they studied.Their sample was composed of veterans who had completed a 28-day residential treatment program for stimulant use disorders (cocaine and methamphetamines.) This research is based, in part, on the findings that while self-reported drug craving is often not an effective predictor of relapse, brain activity as measured by fMRI scans does predict relapse. In this study, participants were shown several images of everyday objects like food and office supplies, but interspersed were images of drugs and drug paraphernalia. Those participants who experienced more intense brain activity in the mesolimbic (reward) center of the brain, and especially in the area known as the nucleus accumbens, were found to have relapsed within three months.
Collins, N. (2018, Dec. 28). Brain scans help predict drug relapse, Stanford researchers find. Stanford News. http://news.stanford.edu
Boxed Item 5.5 Chemical Imbalances
Many mental health and substance use disorders are thought to be the result of chemical imbalances in the brain. However, according to author Kelli Maria Korducki (2019) and Harvard Medical historian Anne Harrington (2018), this type of oversimplified thinking may have resulted in “the wholesale failure of mental health care in America,” which has become “a rigid and restrictive system that leaves even the reasonably privileged ... with little to work with and so many others with nothing” (Korducki, 2019, p. 4). Too much emphasis seems to have been placed on searching for biological answers to mental health and substance use disorders at the expense of other forms of “talk therapy.” In today’s world, psychiatrists have become medication managers who rarely spend more than 15 minutes with patients discussing their response to medications and side effects. Korducki does concede, however, that, for many, psychotropic medications are necessary and do provide relief. Yet she also points out that for many with complicated mental health and co-occurring disorders, simplified medication management solutions do not work.
Harrington, A. (2018). Mind fixers: Psychiatry’s troubled search for the biology of mental illness.
Korducki, K.M. (2019,July 28). It’s not just a chemical imbalance. New York Times, Sunday Review.
Boxed Item 5.6 The Epigenetics of Chronic Cocaine Use
Chronic cocaine use or cocaine addiction often results in strong associations between cocaine use and environmental triggers (e.g. using with certain people or in particular places, drug paraphernalia such as mirrors, razor blades, etc.). This type of associative learning is thought to occur as a result of classical conditioning, by pairing an unconditioned stimulus (UCS) or cocaine with a conditioned stimulus (CS) such as people, places or things (mirrors, razor blades). Recent research indicates that this type of associative learning actually results in changes in gene expression in the region of the brain known as the hippocampus. The hippocampus is involved in learning and memory Researchers Gajewski, Eagle et al. (2019) have demonstrated that chronic cocaine exposure in mice resulted in modifications in the epigenetic profile of the FosB in the hippocampus, which was hypothesized to account for the associative learning of cocaine triggers. Also, when the researchers blocked the changes made to the FosB in the hippocampus, the mice were unable to form associations between cocaine use and environmental triggers! This research has important implications for relapse prevention for those with cocaine use disorders.
Gajewski, P.A., Eagle, A.L., Williams, E.S., Manning, C.E., Lynch, H., McCornack, C., Maze, I. et al. (2019, Sept. 2). Epigenetic regulation of hippocampal FosB expression controls behavioral responses to cocaine. Journal of Neuroscience, doi: 10:1523/JNEUROSCI.0800-19.2019
Society for Neuroscience (2019, Sept. 2). Chronic cocaine use modifies gene expression. Retrieved from https://medicalexpress.com/news/2019-09-chronic-cocaine-gene. html
