The Neuroscience of Recovery: Anhedonia (Dr. Noelle Jacquelin)

Like many other chronic diseases, Substance Use Disorder is treatable, but it is critical for individuals who are affected to explore how their neurobiology has been physiologically changed by their experiences. SUD is a complex condition in which “there is [or was] uncontrolled use of a substance despite harmful consequences” (American Psychiatric Association, 2024) whereby people keep using the substance even when they know it is causing or will cause problems. With SUD there are distinct modifications that occur within the structure and function of the brain. During recovery, it is essential to understand how the brain can and will heal after this kind of trauma. Understanding certain neuroscientific findings may provide resilience in the journey to long-term recovery and assist in the acknowledgement of SUD as a disease of the brain’s reward system.

            Anhedonia is generally defined as the lack of interest, enjoyment, or pleasure from life’s activities. It causes emotional detachment and emotional numbing. Individuals who suffer from it tend to isolate themselves, feel a sense of hollowness, and sometimes are tortured by a sense of overwhelming sadness and hopelessness. Anhedonia is common in addictive disorders (Garfield, et al., 2013). It is a key symptom deserving of attention in addictive disorders in general, and Cocaine Use Disorder in particular. Researchers have suggested that an approach to developing new treatments for CUD may be to investigate and target poor prognostic signs. Anhedonia is one such sign (i.e. a loss of pleasure or interest in non-drug dopamine rewards), as it predicts worse outcomes in existing CUD treatments (Fries, et al., 2018) and may suggest a more complicated path to wellness. Many people in recovery experience anhedonia as a co-occurring symptom with another psychiatric condition such as depression. Oftentimes, a history of depression or avoidant attachment styles due to childhood trauma or neglect precedes SUD. The withdrawal and recovery effort from a substance may trigger or worsen existing conditions. This is not a moral failing. Anhedonia should be targeted and treated to support effective recovery.

The recovering brain attempts to re-balance neurotransmitters, particularly dopamine. Human imaging studies have shown a reduction of dopamine receptors accompanied by a lesser release of endogenous dopamine in the ventral striatum of cocaine, heroin, and alcohol-dependent subjects, thereby offering visual proof of the “dopamine-impoverished” addicted human brain (Marco, 2011). During active substance use, addictive drugs artificially enhance the functioning of the reward circuitry of the brain. They interfere with the way the brain sends, receives, and processes messages. There is a chemically altered flow of dopamine that halts natural dopamine production. During recovery, there is a biochemical withdrawal in addition to a substance withdrawal. Dopamine levels do not return to pre-SUD levels until there is a passage of time and clearly sought out intervention. The prefrontal cortex which regulates our thoughts, actions, and emotions and also helps people to control their impulses and ignore distractions is affected. The limbic system, responsible for processing emotion and memory, motivation, stress response, reward-related events, sexual stimulation, and arousal is also deeply implicated in SUD and in its common aftermath partner, anhedonia. This part of the amygdala plays a role in stressful feelings like anxiety, irritability, and unease, which characterize long-term withdrawal months after the drug high fades and thus may motivate the person to seek the drug again as they descend into a sense of desperation and anhedonia. Over time, a person with substance use disorder in recovery may seek drugs to get temporary relief from this discomfort rather than to get high. It is critical for those in recovery to recognize that when they experience any of the signs of anhedonia that they understand these are neurobiological issues and not a personal weakness and that they seek immediate support and assistance from therapists, physicians, and loved ones.  

With such a systemic alteration of the brain, it has adapted. To understand the neurological features that promote successful abstinence, it is necessary to understand changes to the brain that result from SUD exposure. During active substance use, the brain becomes accustomed to the influx of artificially produced dopamine. Without it, even six to fourteen months after discontinuation of substances, the brain continues to strive to achieve a healthier baseline where dopamine transporter levels in the reward center of the brain can adjust to a nearly normal level of functioning. The body and the brain must take time and care to rebalance natural production.

The development of treatments to target individuals with SUD who have symptoms of anhedonia and low dopamine production has the potential to improve overall outcomes for those with this condition (Crits-Christoph, et al., 2018). The lasting reduction in physiological activity of the dopamine transmitter system leads to the idea that an increment in its activity, to restore pre-drug levels, may yield significant clinical improvements (reduction of craving, relapse, and drug-seeking/taking) (Marco, 2011). In theory, it may be achieved naturally through an increase in dietary protein and velvet beans and other foods rich in tyrosine that activate L-Dopa, vigorous exercise, long walks in natural settings, meditation, non-drug but high-risk activities (such as skydiving), and therapeutic conversations to process negative emotions; pharmacologically (although some research indicates that some popular depression medications may actually lead to additional emotional blunting, other recent research indicates that the medication levodopa may alleviate anhedonia symptoms); and/or with novel interventions such as transcranial magnetic stimulation (TMS) (Belujon and Grace, 2017; Goldsmith, et al, 2023; Lampariello, 2012; Marcus and Bruchas, 2021;Watson, 2021).

Restoring dopamine function may well be therapeutically advantageous during recovery and during related episodic anhedonia. Those in recovery may experience symptoms of anhedonia for two to three years after their last drug use, similar to the brain’s grief process whereby there continues to be grief bursts. However, it is important to note that symptoms subside with prolonged abstinence and this knowledge may help those in recovery to keep their lives going, knowing that the brain will heal and their lives will once again feel worth living.