Approximately 70% of individuals diagnosed with Major Depressive Disorder (MDD) experience anhedonia, the progressive, pervasive loss of the capacity for pleasure, motivation, and connection that researchers now recognise as one of the most clinically significant and most persistently undertreated features of mood disorders worldwide (Serretti, 2023).
In Bipolar Disorder (BD), the figure reaches approximately 52%, with anhedonic symptoms frequently persisting even during periods of apparent clinical stability, when other depressive symptoms have remitted (Whitton & Pizzagalli, 2022). These are not minor or incidental findings. They point toward a symptom that sits at the very heart of mood disorder pathology, one that shapes illness severity, predicts treatment resistance, and independently elevates the risk of suicide, yet continues to be routinely overlooked in favour of targeting low mood alone.
For millions of people living with mood disorders, anhedonia is not an occasional bad day. It is the defining feature of their illness and one of the least understood, least targeted, and most persistently undertreated symptoms in modern psychiatry.
More Than Loss of Pleasure
Anhedonia is a Greek term that literally translates to not feeling pleasure, and it was officially defined in 1896 by French psychologist Théodule-Armand Ribot as the incapability to enjoy anything. For most of the twentieth century, it sat quietly in diagnostic manuals as a supporting symptom of depression, overshadowed by the more visible face of the disorder: sadness, tearfulness, withdrawal.
But science has advanced radically. Now, researchers realise that anhedonia has much more than a lack of ability to experience pleasure in the moment. It encompasses a continuum of failures to process rewards – to look forward to the experience of future pleasure, to be motivated to seek it, to learn when an experience is rewarding, and to make a choice that is reflective of our concerns (Serretti, 2023).
In what has become a landmark theoretical paper in the field, Treadway and Zald (2011) made a well-known distinction between two neurologically distinct systems: the wanting and the liking. An individual with anhedonia may still feel like taking a warm bath or responding to a kind word when already in the middle of it, but may not experience the motivation to seek them. The want has gone missing. The fondness, in other cases, persists. This difference is not just intellectual. It directs to entirely different brain processes, and thus entirely different treatment targets (Treadway & Zald, 2011).
What it Actually Feels Like
Clinical scales and brain scans can do nothing but part of the story. A more disturbing and more detailed image is produced when researchers are seated with depressed patients, and when they are asked to talk about how they felt in their own words. Respondents talk of not only the deprivation of pleasure but deprivation of connection – to friends, to meaning, to themselves (Whitton & Pizzagalli, 2022).
They talk of inertia: the lack of ability even to engage in things they know they love. They talk about seeing the world pass by them like through thick glass, being there physically and not spiritually. The loss of a sense of purpose is one of the themes that recurs with remarkable regularity: a silent existential displacement that cannot be properly described in terms of the general criteria used to define depression (Whitton & Pizzagalli, 2022).
This is important since it implies that when a clinician poses the question of whether a patient is enjoying things less, there may be much of what the patient is actually suffering that goes undetected. The experience of anhedonia, as lived, is wider and stranger and more philosophically disorienting than any checklist can describe it.
A Symptom that Shapes the Whole Illness
Anhedonia is not only unpleasant to live with. It proactively dictates the severity, duration and resistance to treatment of a mood disorder. Studies consistently indicate that the greater the anhedonia at the beginning of a depressive episode, the longer the episode, the higher the number of relapses, and the overall burden of illness throughout the lifespan of a person (Serretti, 2023).
In teens, the dulling of rewards in the brain pathways is predictive of depressive episodes in the future, as early as it is seen on brain scans before the onset of a depression (Whitton & Pizzagalli, 2022). In other words, anhedonia can be among the first warning signs that the brain can provide, way before an individual can find words to describe whatever it is they are experiencing.
Most urgently of all, anhedonia has been demonstrated to predict suicidal ideation and suicide attempts independently, even when the overall depth of depression is considered (Serretti, 2023). This observation, as observed in several studies and in populations, expresses a chilling clinical message: a patient who appears to be improving in general may still be carrying significant risk if their anhedonia remains unaddressed. It is not enough to lift the mood. The capacity for reward must be restored.
Depression and Bipolar Disorder: Different Engines, Same Symptom
Among the most significant new findings in the study of anhedonia is the discovery that not all anhedonias resemble each other even when they appear the same without looking inside. Neuroimaging studies in Major Depressive Disorder have consistently demonstrated that the ventral striatum of the brain, the main reward processing centre, is not properly engaged when the patient is in anticipation of a pleasurable stimulus (Whitton & Pizzagalli, 2022).
Essentially, the reward system has become silent. Such a trend is so regular that it is also present in individuals who have never experienced depression, but who are at risk due to family history, indicating it is a vulnerable response built into the brain structure, rather than a disease scar (Whitton & Pizzagalli, 2022).
Bipolar disorder narrates otherwise. Depressed bipolar disorder patients report anhedonia proportionately as often as patients with unipolar depression. About half of them fit clinical criteria for the symptom, but their brains present a different deviation (Whitton & Pizzagalli, 2022). Instead of mere underactivation, the bipolar reward system is dysregulated: it is overactivated by the orbitofrontal cortex, which can be observed even during the intervals of stability, and in healthy relatives (Rizvi et al., 2018).
The system does not go quiet. It goes haywire. This neurobiological deviation has far-reaching consequences: attempting to treat bipolar anhedonia in the same manner as unipolar anhedonia is arguably a deeply misinformed strategy, which may be one of the reasons why many of the patients still suffer despite treatment that seems clinically appropriate (Rizvi et al., 2018).
Why Conventional Therapies are Ineffective and Why Alternative Therapies are Better?
The study reveals a painful reality: the drugs most frequently used to treat depression, selective serotonin reuptake inhibitors (SSRIs), do not primarily treat anhedonia effectively (Serretti, 2023). There are studies indicating that they may, in fact, make it worse in some patients, creating a condition of emotional numbness which patients refer to as feeling flattened or switched off. This is an especially worrisome observation since the first and even sole offered pharmacological intervention is SSRIs.
The positive thing is that there are alternatives, and they are becoming better evidenced. The most pharmacologically promising therapeutic approach to directly work on anhedonia is agomelatine and vortioxetine, both of which interact with dopaminergic pathways in a manner largely inconsistent with SSRIs (Serretti, 2023). Clinicians use ketamine in the treatment of treatment-resistant depression. It shows rapid anti-anhedonic effects. Therefore, it provides new opportunities for patients in crisis (Serretti, 2023).
The use of transcranial magnetic stimulation targets prefrontal networks involved in reward processing. It has demonstrated significant practical value in large naturalistic studies (Serretti, 2023). Psychological therapies also have an important role to play. Cognitive behavioural therapy helps challenge the mental models that keep people disengaged from life. Behavioural activation is a simple but effective intervention. It encourages patients to actively participate in life. It has built up a strong evidence base in the treatment of anhedonia (Serretti, 2023).
What is emerging is that anhedonia needs a case-by-case treatment. It is important to identify the kind of anhedonia an individual has. It may be primarily motivational, consummatory, or social. And, it is also important to understand its biological signature. These factors must determine the choice of treatment (Treadway & Zald, 2011). Precision is the future of anhedonia care, not prescription pads.
Giving Colour Back to the World
Anhedonia has been a long-neglected footnote of the history of depression. The evidence is now unambiguous. It is not a secondary symptom. Sadness does not cause it as a side effect, nor does it resolve on its own once the mood improves (Serretti, 2023). Also, it is a central feature of mood disorders, neurobiologically distinct and prognostically critical. It carries its own clinical weight, predicting illness severity, treatment resistance, and even suicide risk independently of depression itself (Serretti, 2023; Whitton & Pizzagalli, 2022).
It manifests differently across diagnostic categories. Major depressive disorder (MDD) involves a dampened reward system, while bipolar disorder (BD) involves a dysregulated reward system. This difference means that clinicians must tailor clinical approaches accordingly and should not apply them uniformly (Rizvi et al., 2018). Standard first-line treatments such as SSRIs show limited benefit for anhedonia specifically. Emerging evidence supports the use of dopaminergic pharmacotherapies. It also supports ketamine, transcranial magnetic stimulation, and behavioural activation as more targeted alternatives (Serretti, 2023)
Furthermore, anhedonia persists beyond depressive episodes in a significant proportion of patients. This suggests that it may be a trait-level vulnerability. It is not just a state-dependent symptom alone (Whitton & Pizzagalli, 2022). For the individual whose world has gradually lost its colour, that recognition matters. Their experience is real, it is measurable, it has a name, and increasingly, it has a treatment. The world does not have to stay grey. Science is learning, slowly and surely, how to turn the colour back on.
References +
- Cleveland Clinic. (2023, July 26).Anhedonia. https://my.clevelandclinic.org/health/symptoms/23341-anhedonia
- Heininga, V. E., Dejonckheere, E., Houben, M., Obbels, J., Sienaert, P., Leroy, B., van Roy, J., & Kuppens, P. (2019). The dynamical signature of anhedonia in major depressive disorder: Positive emotion dynamics, reactivity, and recovery.BMC Psychiatry, 19, Article 59. https://doi.org/10.1186/s12888-018-1983-5
- Rizvi, S. J., Lambert, C., & Kennedy, S. (2018). Presentation and neurobiology of anhedonia in mood disorders: Commonalities and distinctions. Current Psychiatry Reports, 20, Article 13. https://doi.org/10.1007/s11920-018-0877-z
- Serretti, A. (2023). Anhedonia and depressive disorders. Clinical Psychopharmacology and Neuroscience, 21(3), 401–409. https://doi.org/10.9758/cpn.23.1086
- Treadway, M. T., & Zald, D. H. (2011). Reconsidering anhedonia in depression: Lessons from translational neuroscience. Neuroscience & Biobehavioral Reviews, 35(3), 537–555. https://doi.org/10.1016/j.neubiorev.2010.06.006
- Whitton, A. E., & Pizzagalli, D. A. (2022). Anhedonia in depression and bipolar disorder. Current Topics in Behavioural Neurosciences, 58, 111–127. https://doi.org/10.1007/7854_2022_323
