Anhedonia
Overview
Anhedonia is characterized by the diminished capacity to experience joy, pleasure, or show interest in activities that once were rewarding. This can be experienced throughout many domains, as anhedonia has recently become incorporated as a key defining symptom of many mental health conditions seen within society today.[1]
Although the term ‘anhedonia’ was first introduced to literature in 1896 by French philosopher Théodule Armand Ribot, it did not gain traction in modern-day psychoanalysis until 1980 when the American Psychological Association (APA) published the Diagnostic and Statistical Manual, 3rd edition (DSM-III) and included anhedonia as a defining characteristic of depression.[2]
Anhedonia continues to be an important component of psychopathology as remains a prominent diagnostic criterion for major depressive disorder and like conditions in the American Psychological Association’s 4th and 5th editions of the Diagnostic and Statistical Manual.
Causes
Anhedonia is a direct symptom observed in many mental health conditions.
While the exact cause of anhedonia can, at times, be uncertain (when there is no proper diagnosis), the inherent association between pleasure modulation, the brain’s reward system, and many neurobiological factors has led some researchers to further investigate whether anhedonia is a result of any of the following conditions:[3]
Reduced activity of the brain regions
Imbalances and deficits in neurotransmitters
Imbalances in the immune system
To best understand how these factors intersect, it is important to first be able to understand the brain’s reward system and how humans are biologically motivated by reward. Comprised of various structures in the brain, the reward system, also known as the mesolimbic system, is the system of signals in the brain responsible for the physiological and cognitive processing of reward.[4]
When an individual encounters a stimuli (substances, events, foods, activities, or behaviors) that our brain classifies as beneficial, pleasurable, or positive, the brain signals the mesolimbic system to release “feel good” neurotransmitters like dopamine as a reinforcer to the stimuli. As a result, the individual begins to associate their increased feeling of pleasure and joy with the stimuli, inherently reinforcing the positive stimuli by creating a reward system for their “positive” action. This ability to motivate and reinforce our actions is something that is not seen in those who experience anhedonia. Individuals who experience anhedonia are unable to experience the reward that our brains give us after completing something beneficial. As a consequence, individuals with anhedonia often trade things that once brought pleasure for quick fixes such as drugs, alcohol, and risky behaviors.[5]
The mesolimbic system is a complex dopaminergic neural pathway in the brain that plays an important role in the ability to process reward, pleasure, and motivation. When an individual recognizes a rewarding stimulus, an anticipatory response is activated and the brain begins to send signals to produce dopamine as the reward.[6]
This pathway begins in the ventral tegmental area (VTA), where a cluster of neurons (dopaminergic neurons) in the midbrain receive these external signals and as a result, produce the neurotransmitter dopamine. From here, the VTA sends dopamine to the nucleus acumbens (NAc), a region in the ventral striatum. The ventral striatum is known as the “pleasure center” and is another important component of how individuals process reward, pleasure, and motivation. Once dopamine has reached the NAc it binds to different types of dopamine receptors (D1 & D2), which activate a series of signaling pathways involved in experiencing pleasure and reward. Furthermore, this activates the release of other neurotransmitters such as glutamate, GABA, and serotonin, each of which facilitates communication between different brain regions. All together a pattern of communication is established and a reward circuit forms.[7-9]
Structural Features
Research by Arrondo (2015) suggests when there is reduced activity in the ventral striatum, the brain's ability to follow the plan outlined by the reward system disappears, resulting in a decline in task motivation and pleasure.[10] This produces a downstream effect and introduces the feeling of anhedonia. Individuals with anhedonia experience lower levels of dopamine observed inside the ventral striatum, specifically in the NAc.
Neurotransmitters
Dopamine, also known as the ‘feel-good’ hormone, is a neurotransmitter that is released in the brain when we do something that makes us feel good. It provides positive reinforcement to these ‘good’ behaviors and introduces a reward system to the brain to encourage similar behavior.[11-13]
When an individual completes a ‘good’ task whether easy or more complex, the body rewards them with a burst of pleasure-inducing signals, increasing their mood and providing motivation to repeat this behavior in the future. In this case, we can think of dopamine as the reward, as it provides motivation.
With this in consideration, a decrease in dopamine would mean there is a reduced sensation of pleasure, and without this positive reinforcer, there would also be a decrease in the effectiveness of the brain’s reward system.
The connection of dopamine deficiency to anhedonia is evident in the intersection of pleasure regulation.[14] In both cases, an individual loses interest in things that once brought joy and were of interest to them. This is seen by the decrease in motivation to engage in activities that were once rewarding, activities that we could say once made us feel good.
Immune System
When the body detects a harmful stimulus, such as damaged cells, toxic compounds, bacteria, or invasive species, it undergoes an inflammatory immune response to try and restore balance.[15] During this response, the body releases substances known as inflammatory mediators such as cytokines. These cause the blood vessels in tissues to swell, increasing blood flow and rate of repair. This understanding helps scientists better connect neurobiology and behavioral science, as cytokines are known to influence neurotransmitter metabolism, such as those discussed above.[16]
When investigating the immune system, researchers have noticed increased levels of inflammatory mediators such as the C-reactive protein (CRP) in those with depression. In other words, those who experience symptoms of depression also experience increased inflammation in the immune system. Research by Bekhbat (2022) and Felger (2015) found that when there are increased levels of CRP, there is also a decrease in neural connectivity in the brain regions contributing to motivation and reward (ventral striatum and ventromedial prefrontal cortex).[17,18] With all things considered, it is evident that functional cognitivity in the reward circuitry observed in those with anhedonia is diminished to the point that they are unable to experience satisfaction or pleasure. This discovery helps scientists better understand neurobiology, as cytokines are known to influence neurotransmitter metabolism, such as those discussed above.
Signs & Symptoms
Anhedonia is highly comorbid and is a common symptom experienced by individuals diagnosed with many different mental health conditions.
Anhedonia is primarily experienced in those diagnosed with:
Although anhedonia is most often correlated with these conditions, it is common to experience anhedonia with other depressive disorders, suicide-related events, neurodevelopmental disorders, neuropsychiatric disorders, or after experiencing traumatic or stressful events.[26,27]
When an individual experiences anhedonia, the loss of interest, joy, and pleasure, it can be felt in many different ways. It is important to note that anhedonia is not the same as the day-to-day experience of sadness, perceived laziness, or even apathy. These are characterized by a lack of energy or motivation to do things rather than an inability to feel pleasure when doing things. Moreover, those who experience anhedonia endure these symptoms in a more extreme and prolonged fashion.
Common symptoms can include but are not limited to:
Decreased pleasure from things of interest[28]
Less interest in engaging in activities[29]
Feeling empty, numb, and or sad[30]
Detaching from relationships and or social settings[31]
Increased boredom[32]
Negative outlook on life[33]
Loss of libido or interest in intimacy[34]
Lower appetite[35]
Poor physical health[36]
There has been a debate that anhedonia should be classified into two types; social and physical.[37]
Social Anhedonia: Relating to a decreased desire to engage in social settings, specifically in regard to maintaining relationships, (e.g., a person no longer feels joy when around their friends).[38]
Physical Anhedonia: Relating to a decrease in joy from physical touch, smells, or sounds, (e.g., no longer finding joy in listening to music, having sex, or eating favorite foods).[39]
Diagnosis
An evaluation from a doctor or medical professional is required in order to properly diagnose an individual with anhedonia. This can be measured in numerous ways; behavioral, electrophysiological, hemodynamic, interview-based measures, and through self-reports.[40] Although electrophysiological (EEG) and hemodynamic (cardiovascular function) approaches exist and are present in research, the most common way that anhedonia is diagnosed is through psychological and behavioral questionnaires and assessments as they hold greater predictive validity.[41]
This is seen by completing self-reported questionnaires administered by a clinician or by receiving an in-depth assessment from a mental health professional. One method of assessing anhedonia through a questionnaire is by using the diagnostic tool, the Snaith-Hamilton Pleasure Scale (SHPS), a quick 14-item self-questionnaire.[42] Some items from the SHPS include questions such as: whether I would enjoy my favorite television or radio program, I would enjoy being with family or close friends, and if I would find pleasure in my hobbies and pastimes. These results are then scored and evaluated.[43]
There are other instruments such as the 61-item Champam Physical Anhedonia Scale (PAS) and its revised form (R-PAS), as well as the Fawcett-Clark Pleasure Scale (FCPS), which both assess symptoms in the same manner as the SHAPS.[44] Although these are the primary mechanisms used to assess anhedonia, a doctor may also ask if the patient or their family has a history of substance use or excessive alcohol intake in case those could be factors impacting a person’s mental health and symptoms of anhedonia.
In some cases, a doctor may require a physical examination to rule out underlying health conditions or require a blood test to rule out possible causes which may include a vitamin deficiency (vitamin D) or a thyroid hormone imbalance (hypothyroidism) as they can add to symptoms of depression.[45,46]
Treatments
To properly treat anhedonia, a clinician must first understand the root cause of the symptom. Anhedonia is highly comorbid and experienced as a symptom of many mental health conditions. For these reasons, clinicians treat anhedonia in several ways, each of which is individualized to the patient.
Treatment plans can be complex requiring extensive medical attention or simply requiring an individual to practice mindfulness in their free time. The mechanism of treatment depends on conditions such as diagnosis or if there are any underlying medical conditions. For patients with a specific diagnosis, clinicians are likely to follow already-established treatment plans frequently employed for the condition. For instance, individuals experiencing anhedonia who have been diagnosed with a type of depressive disorder may be prescribed a form of antidepressant medication or talk therapy.
The following are reported forms of treatment used to treat symptoms of anhedonia:
Strength training and aerobic activities (to produce adrenaline and dopamine).[47]
Practice mindfulness, meditation, and self-care.[48]
Talk therapy (e.g., Cognitive Behavioral Therapy).[49]
Antidepressant medications such as Selective Serotonin Reuptake Inhibitors (SSRI).[50]
Dopamine agonists medications.[51]
Antipsychotic medications.[52]
Ketamine.[53]
Psychedelic micro-dosing (Psylocibin).[54]
Transcranial Magnetic Stimulation (TMS).[56]
Ultimately, anhedonia is a symptom that does not just disappear instantly following treatment. Anhedonia can come in waves and resurge in times of elevated distress, trauma, or change in lifestyle. Prioritizing well-being (both mentally and physically) is important to maintaining a stable and healthy lifestyle. Leaving anhedonia untreated can lead to a cascade of challenges or worsen current symptoms.
If you or someone you know is experiencing anhedonia, contact a health professional or call 988 (Suicide & Crisis Lifeline). If you are in immediate need of help, contact 911 or contact your local emergency line.
Contributed by: Meghan Callahan
Editor: Jennifer (Ghahari) Smith, Ph.D.
REFERENCES
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2 Ho, N., Sommers, M. (2013, June). Anhedonia: A concept analysis. Archives of psychiatric nursing. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3664836/#R30
3 Gorwood (2008)
4 Bekhbat, M., Li, Z., Mehta, N. D., Treadway, M. T., Lucido, M. J., Woolwine, B. J., Haroon, E., Miller, A. H., & Felger, J. C. (2022, October). Functional connectivity in reward circuitry and symptoms of anhedonia as therapeutic targets in depression with high inflammation: Evidence from a dopamine challenge study. Molecular psychiatry. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9718669/
5 Gorwood (2008)
6 Alcaro, A., Huber, R., & Panksepp, J. (2007). Behavioral functions of the mesolimbic dopaminergic system: an affective neuroethological perspective. Brain research reviews, 56(2), 283–321. https://doi.org/10.1016/j.brainresrev.2007.07.014
7 Gorwood (2008)
8 Arrondo, G., Segarra, N., Metastasio, A., Ziauddeen, H., Spencer, J., Reinders, N. R., Dudas, R. B., Robbins, T. W., Fletcher, P. C., & Murray, G. K. (2015, August 26). Reduction in ventral striatal activity when anticipating a reward in depression and schizophrenia: A replicated cross-diagnostic finding. Frontiers in psychology.
9 Luo, S. X., & Huang, E. J. (2016). Dopaminergic Neurons and Brain Reward Pathways: From Neurogenesis to Circuit Assembly. The American journal of pathology, 186(3), 478–488. https://doi.org/10.1016/j.ajpath.2015.09.023
10 Arrondo (2016)
11 Gorwood (2008)
12 Arrondo (2016)
13 Luo (2016)
14 Gorwood (2008)
15 Chen, L., Deng, H., Cui, H., Fang, J., Zuo, Z., Deng, J., Li, Y., Wang, X., & Zhao, L. (2017, December 14). Inflammatory responses and inflammation-associated diseases in organs. Oncotarget. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5805548/#:~:text=Inflammation%20is%20the%20immune%20system%27s,the%20healing%20process%20%5B2%5D
16 Miller, A. H., Haroon, E., Raison, C. L., & Felger, J. C. (2013, April). Cytokine targets in the brain: Impact on neurotransmitters and neurocircuits. Depression and anxiety. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4141874/#:~:text=Through%20their%20effects%20on%20neurotransmitter,as%20anxiety%2C%20arousal%20and%20alarm
17 Bekhbat (2022)
18 Felger, J. C., Li, Z., Haroon, E., Woolwine, B. J., Jung, M. Y., Hu, X., & Miller, A. H. (2015, November 10). Inflammation is associated with decreased functional connectivity within corticostriatal reward circuitry in depression. Nature News. https://www.nature.com/articles/mp2015168
19 American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). https://doi.org/10.1176/appi.books.9780890425596
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21 Martinotti, G., Andreoli, S., & Reina, D. (2011, June). Acetyl-l-carnitine in the treatment of anhedonia, melancholic, and negative symptoms in alcohol-dependent subjects. Progress in neuro-psychopharmacology & biological psychiatry. https://pubmed.ncbi.nlm.nih.gov/21256179/
22 Ho (2013)
23 Boehm, I., Flohr, L., & Steding, J. (2018, January). The trajectory of anhedonic and depressive symptoms in anorexia nervosa: A longitudinal and cross-sectional approach. European eating disorders review : the journal of the Eating Disorders Association. https://pubmed.ncbi.nlm.nih.gov/29168305/
24 Fujiwara, S. (2011, January). Anhedonia in Japanese patients with Parkinson’s Disease. Geriatrics & gerontology international. https://pubmed.ncbi.nlm.nih.gov/21241445/
25 Pittman, J., & Goldsmith, A. (2011, April). Post-traumatic stress disorder, depression, and health-related quality of life in OEF/OIF veterans. Quality of life research : an international journal of quality of life aspects of treatment, care and rehabilitation. https://pubmed.ncbi.nlm.nih.gov/21516356/
26 Kuba, T. (2011, April). Suicide-related events among child and adolescent patients during short-term antidepressant therapy. Psychiatry and clinical neurosciences. https://pubmed.ncbi.nlm.nih.gov/21507130/
27 Chevallier, C. (2012, July). Brief report: Selective social anhedonia in high-functioning autism. Journal of autism and developmental disorders. https://pubmed.ncbi.nlm.nih.gov/21986875/
28 Gorwood (2008)
29 Ibid.
30 Cleveland Clinic Medical Professional. What is anhedonia?. Cleveland Clinic. (2023, July). https://my.clevelandclinic.org/health/symptoms/25155-anhedonia
31 Wisner, W. (2023, August 22). Anhedonia: Symptoms, diagnosis & treatment. Talkspace. https://www.talkspace.com/blog/anhedonia-symptoms-signs-causes-what-is/
32 Cleveland Clinic Medical Professional (2023)
33 Ibid.
34 Pizzagalli, D. A., Jahn, A. L., & O’Shea, J. P. (2005, February 15). Toward an objective characterization of an ANHEDONIC phenotype: A signal-detection approach. Biological psychiatry. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2447922/
35 Mason, T. B., Dunton, G. F., Gearhardt, A. N., & Leventhal, A. M. (2020). Emotional disorder symptoms, anhedonia, and negative urgency as predictors of hedonic hunger in adolescents. Eating behaviors, 36, 101343. https://doi.org/10.1016/j.eatbeh.2019.101343
36 Cleveland Clinic Medical Professional (2023)
37 Kerns, J. (2008, November). Social and physical anhedonia and Valence and arousal aspects of emotional experience. Journal of abnormal psychology. https://pubmed.ncbi.nlm.nih.gov/19025222/
38 Barkus, E., & Badcock, J. C. (2019, April 24). A transdiagnostic perspective on social anhedonia. Frontiers in psychiatry. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6491888/
39 Cleveland Clinic Medical Professional (2023)
40 Frank, D. W., Stevens, E. M., & Versace, F. (2019, July). A neurophysiological measure of reward sensitivity and its association with anhedonia in psychiatrically healthy adolescents and young adults. International Journal of Psychophysiology : official journal of the International Organization of Psychophysiology. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6555656/
41 Gorwood (2008)
42 Franken, I. (2007, April). The assessment of anhedonia in clinical and non-clinical populations: Further validation of the snaith-hamilton pleasure scale (shaps). Journal of Affective Disorders. https://pubmed.ncbi.nlm.nih.gov/16996138/
43 Gorwood (2008)
44 Ibid.
45 Cleveland Clinic Medical Professional (2023)
46 Nuguru, S. P., Rachakonda, S., Sripathi, S., Khan, M. I., Patel, N., & Meda, R. T. (2022, August 20). Hypothyroidism and depression: A narrative review. Cureus. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9392461/
47 Costa, T. da. (2022, August 26). Effects of aerobic and strength training on depression, anxiety, and health self-perception levels during the COVID-19 pandemic. European review for medical and pharmacological sciences. https://pubmed.ncbi.nlm.nih.gov/35993659/
48 Edenfield, T. M. (2012, November). An update on mindfulness meditation as a self-help treatment for anxiety and depression. Psychology research and behavior management. https://pubmed.ncbi.nlm.nih.gov/23175619/
49 Vinney, C. (2023, May 8). Anhedonia: What to do when you can’t experience pleasure. Verywell Mind. https://www.verywellmind.com/what-is-anhedonia-i-dont-feel-pleasure-5680269
50 Cao, B. (2019, June). Pharmacological interventions targeting anhedonia in patients with major depressive disorder: A systematic review. Progress in neuro-psychopharmacology & biological psychiatry. https://pubmed.ncbi.nlm.nih.gov/30611836/
51 Ventorp, F., Lindahl, J., Westen, D., (2022, April 30). Preliminary evidence of efficacy and target engagement of pramipexole in Anhedonic depression. Psychiatric Research and Clinical Practice. https://prcp.psychiatryonline.org/doi/10.1176/appi.prcp.20210042#:~:text=Pramipexole%20is%20a%20dopamine%20receptor,motor%20symptom%20improvement%20(3)
52 Lambert, C., Da Silva, S., Ceniti, A. K., Rizvi, S. J., Foussias, G., & Kennedy, S. H. (2018, July). Anhedonia in depression and schizophrenia: A transdiagnostic challenge. CNS neuroscience & therapeutics. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6489811/
53 Nogo, D., & Jasrai, A. K. (2022, July). The effect of ketamine on anhedonia: Improvements in dimensions of anticipatory, consummatory, and motivation-related reward deficits. Psychopharmacology. https://pubmed.ncbi.nlm.nih.gov/35292831/
54 Lyons, A. (2022). Self-administration of psilocybin in the setting of treatment-resistant depression. Innovations in clinical neuroscience. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9507144/
55 Cano, M. (2022, September). Electroconvulsive therapy effects on anhedonia and reward circuitry anatomy: A dimensional structural neuroimaging approach. Journal of Affective Disorders. https://pubmed.ncbi.nlm.nih.gov/35764228/
56 Fukuda, A. M., Kang, J. W. D., Gobin, A. P., Tirrell, E., Kokdere, F., & Carpenter, L. L. (2021, September). Effects of transcranial magnetic stimulation on anhedonia in treatment-resistant major depressive disorder. Brain and behavior. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8442591/