Types of Depression

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Depression is not a single disease—it is a broad family of mood disorders that vary in course, severity, context, and required treatment. The ICD-11 and DSM-5 classifications distinguish over a dozen categories and specifiers. Understanding the different types of depression has direct clinical significance: it influences the choice of therapy, the assessment of relapse risk, and patient safety.

When someone says, “I have depression,” they may be describing very different experiences. One patient may live for years with a backdrop of chronic sadness that robs daily life of its color but does not completely paralyze them. Another experiences an acute episode marked by suicidal ideation, an inability to get out of bed, and the conviction that they are a burden to everyone around them. Yet another person, with mathematical regularity, withdraws into themselves every year as autumn arrives—and just as regularly returns to life in March. Someone else, the mother of a weeks-old infant, cannot understand why she feels emptiness and terror instead of happiness.

All of these individuals may be diagnosed with depression—and all may require completely different therapeutic approaches. This is why the concept of types of depression is important not just as an academic classification, but as a tool for precision in understanding and treating the disorder. This article systematically discusses all clinical types of depression according to ICD-10, ICD-11, and DSM-5, with references to current scientific research.

ICD and DSM Classifications: The Foundation of Depressive Typology

Before discussing individual types of depression, it is worth understanding the formal language used to describe them. In many European healthcare systems, ICD-10 remains the standard for coding diagnoses, with a gradual transition to ICD-11. In scientific and educational circles, DSM-5 and DSM-5-TR function in parallel. Both classifications organize the same clinical area but do so with slightly different logic: the ICD emphasizes the description of the course and severity, while the DSM focuses on precise symptomatic criteria and an extensive system of specifiers.

In ICD-10, mood disorders are coded in sections F30–F39. Key codes regarding types of depression include: bipolar affective disorder (F31), depressive episode (F32), recurrent depressive disorder (F33), cyclothymia (F34.0), dysthymia (F34.1), and mental disorders associated with the puerperium (F53.0) [1, 2]. ICD-11, implemented gradually since 2022, restructured this system: it separated depressive disorders into a category distinct from bipolar disorders, modernized the specifier system, and changed the classification of dysthymia and cyclothymia [3, 4].

The DSM-5 organizes depression around two main categories: major depressive disorder (MDD) and persistent depressive disorder (PDD). A key feature of the DSM-5 is its extensive system of specifiers—further clarifications such as “with melancholic features,” “with atypical features,” “with psychotic features,” “with seasonal pattern,” or “with catatonia” [5, 6]. Specifiers do not create separate diagnostic entities; they describe a variant of a given episode or course, which is highly significant for treatment planning and risk assessment.

Important for Clinicians: Common terms like “psychotic depression,” “seasonal depression,” or “catatonic depression” describe episode specifiers in DSM-5, not separate entities. This distinction prevents the error of treating these presentations as milder variants of depression rather than conditions requiring specific and often urgent intervention.

Depressive Episode and Recurrent (Unipolar) Depression

The basic diagnostic category in ICD-10 is the depressive episode (F32)—a state in which characteristic symptoms persist for at least two weeks: low mood, loss of interest and the ability to feel pleasure (anhedonia), and decreased energy. This may be accompanied by sleep disturbances, changes in appetite and weight, difficulty concentrating, feelings of guilt or worthlessness, and in more severe cases, suicidal thoughts or actions. When these symptoms appear for the first time, without a prior history of mania, a depressive episode is diagnosed [1].

When episodes recur in a patient’s history and no manic episode has ever occurred, recurrent depressive disorder (F33) is diagnosed. This distinction has far-reaching clinical consequences: a recurrent course is associated with a higher risk of subsequent episodes, the need for longer maintenance treatment, and different preventive planning. Research indicates that after the first episode of depression, the risk of relapse is approximately 50%; after two episodes, it rises to approximately 70%; and after three, it exceeds 90% [29]. This means that every relapse should prompt an extension of treatment and a deeper analysis of risk factors.

In the DSM-5, the equivalent is major depressive disorder, marked as “single episode” or “recurrent” with a set of specifiers. It is worth noting that MDD can be diagnosed at the very first episode—the “recurrent” label appears in the description of the course and is not a condition for the diagnosis itself. In clinical practice, this means that from the very first episode, it is worth discussing the risk of relapse, protective factors, and the importance of regular maintenance therapy with the patient—before another crisis occurs.

ICD-11 clarifies this division by introducing a clear distinction between “single episode depressive disorder” and “recurrent depressive disorder,” allowing for more detailed coding of the current episode’s features, including severity, the presence of psychotic symptoms, and seasonal patterns [3]. This change reflects a growing awareness that the description of the course is clinically just as important as the description of the current state.

Severity of Depression: Mild, Moderate, Severe

Both ICD-10 and DSM-5 distinguish degrees of severity for a depressive episode. These are not arbitrary; they are linked to specific consequences for treatment selection and risk assessment. ICD-10 distinguishes: mild episode (F32.0), moderate episode (F32.1), severe without psychotic symptoms (F32.2), and severe with psychotic symptoms (F32.3) [1]. DSM-5 uses an analogous three-stage division: mild, moderate, and severe, with the option to add a psychotic specifier.

In a mild episode, the patient usually retains the ability to function daily, though with marked effort and reduced efficiency. Symptoms are distressing and noticeable but do not prevent work, social contact, or basic self-care. In a moderate episode, functioning is significantly impaired—work, relationships, and daily duties require disproportionate effort or are partially impossible. A severe episode is characterized by profound anhedonia, significant psychomotor retardation or agitation, intense feelings of worthlessness and guilt, an inability to function, and most often, the presence of suicidal thoughts or actions.

The severity of the episode directly translates to recommended treatment. Clinical guidelines indicate that in a mild episode, psychotherapy may be the first choice; in a moderate episode, a combination of psychotherapy and pharmacotherapy is recommended; and in a severe episode, pharmacotherapy is essential and should be implemented immediately [18]. In clinical practice, structured tools are used to assess severity: the Hamilton Rating Scale for Depression (HDRS), the Montgomery–Åsberg Depression Rating Scale (MADRS), and the PHQ-9 (Patient Health Questionnaire), the validity of which is well-documented in meta-analyses [30].

For Patients: The severity of depression is not a judgment of “strength of character” or a measure of how much someone is “truly” suffering. It is a description of a clinical state that helps the doctor choose the right treatment. Both mild and severe episodes deserve help—the difference lies in the type and intensity of intervention, not in whether help is needed.

Endogenous Depression: A Traditional Term and Modern Caveats

The term “endogenous depression” originates from the 19th and 20th-century traditions of descriptive psychiatry. It suggests that the cause of depression lies primarily “inside” the body—in neurobiological mechanisms—rather than as a reaction to external life events. Historically, it was contrasted with “reactive depression,” triggered by a clear stressor. The clinical picture of endogenous depression emphasized a distinct circadian rhythm of symptoms (worse in the morning, improving in the evening), early morning awakening, deep anhedonia, psychomotor inhibition, and a lack of mood reactivity to positive external stimuli.

Modern psychiatry is cautious about this division for several important reasons. First, depression is a multifactorial phenomenon—biological, psychological, and environmental factors coexist and interact in most patients. The absence of an identifiable life stressor does not prove a purely “biological” cause for the episode; it may simply mean the stressor was subtle, long-term, or internal (e.g., chronic self-criticism). Second, the term does not function as a formal diagnostic entity in the ICD or DSM, which leads to communication misunderstandings between clinicians and patients [5, 6].

Nevertheless, the clinical description of a phenotype with a predominance of biological symptoms remains useful. In DSM-5, the equivalent of this clinical observation is largely the “with melancholic features” specifier, which clarifies the characteristic features of an episode without suggesting a single cause. This description may indicate a higher risk of relapse, a need for more intensive pharmacological treatment, and a potentially good response to ECT. Therefore, it is safer and more precise to speak of an episode “with melancholic features” or “with clear neurobiological symptoms” rather than assigning a single biological cause to depression using the “endogenous” label.

Depression in Bipolar Disorder: A Distinct and Often Misidentified Type

In common parlance, the term “bipolar depression” is used, but it is clinically crucial to understand that depression in the course of bipolar affective disorder (BD) is not just another type of unipolar depression—it is part of a different mood regulation disorder in which a history of mania or hypomania plays a significant role. In ICD-10, it is coded as F31, and the diagnosis is based on the history of the illness, not just the current mood [1, 7]. Depressive episodes in BD are often longer and more debilitating than manic ones, and the first episodes of the illness are almost always depressive—meaning that at the beginning, BD may be indistinguishable from unipolar depression.

The distinction is not purely academic. Antidepressant monotherapy in bipolar depression can destabilize mood, trigger (hypo)manic episodes, mixed states, or accelerate rapid cycling. Treatment typically requires mood stabilizers or atypical antipsychotics as a foundation; the addition of antidepressants—if used at all—should be cautious and closely monitored [18]. Literature indicates that the delay in a correct BD diagnosis averages several years—during which time patients often receive a diagnosis of recurrent depression and suboptimal treatment [7].

Clinical red flags suggesting bipolarity in a depressive presentation include: onset before age 25, a family history of BD or psychosis, previous episodes with significantly elevated energy and decreased need for sleep, rapid cycling (≥4 episodes per year), poor response to or destabilization from antidepressants, and mixed features in the current episode (agitation, racing thoughts alongside low mood). Any of these signs should prompt an in-depth interview for BD—ideally using standardized tools like the Mood Disorder Questionnaire (MDQ).

It is important to distinguish between Bipolar I (with full manic episodes) and Bipolar II (with hypomania, but no full mania). Both involve significant functional impairment and increased suicide risk, particularly in the mixed or depressive phases [7]. Bipolar disorder is a condition requiring long-term psychiatric care, not just the treatment of individual episodes. Proper diagnosis is the first and most important step toward stability.

Cyclothymia: Chronic Mood Instability as a Distinct Disorder

Cyclothymia (ICD-10: F34.0) describes chronic mood fluctuations where periods of low mood alternate with short episodes of elevated energy and improved well-being—however, none of these states reach the severity required for a full depressive or manic episode [1, 2]. Symptoms persist for at least two years (one year in children and adolescents per DSM-5), without long periods of stability. In daily life, this looks like a characteristic “rhythm” of changes in mood, energy, and motivation that can be misunderstood by both the individual and those around them.

Clinically, the difficulty lies in the fact that some people with cyclothymia describe these fluctuations as part of their temperament or personality rather than an illness. Meanwhile, they can be a source of real suffering: difficulties in long-term relationships, professional instability, impulsive financial or sexual decisions during elevated phases, and withdrawal or procrastination during low phases. The “better” phases are often short-lived and can lead to commitments that cannot be kept during the “worse” phase. Over the years, this pattern can erode relationships and self-esteem.

ICD-11 and many contemporary studies place cyclothymia on the spectrum of affective disorders, closer to bipolar than unipolar disorders [4]. The risk of progression to full BD is estimated at approximately 15–50% over decades of observation—a significant argument for monitoring these patients even in seemingly mild cases. Treatment for cyclothymia includes psychoeducation (understanding the pattern of fluctuations and its impact on life), psychotherapy (particularly Interpersonal and Social Rhythm Therapy—IPSRT), and, in justified cases, mood stabilizers.

Dystymia and Persistent Depressive Disorder: Depression That Isn’t Always Acute, but Can Be Debilitating

Dystymia (ICD-10: F34.1) is a chronic low mood persisting for at least two years (one year in children and adolescents), usually of lower intensity than an acute depressive episode, but with a significant and long-lasting impact on quality of life [2]. DSM-5 and DSM-5-TR replaced the concept of dystymia with the broader category of Persistent Depressive Disorder (PDD), which combines former dystymia with chronic major depression [5, 8]. Criteria include a long-term low mood and at least two typical symptoms: sleep disturbances, low energy, low self-esteem, difficulty concentrating, feelings of hopelessness, or changes in appetite. Crucially, during this time, the mood is never symptom-free for more than two consecutive months.

Patients with dystymia can function “at half mast” for years—sometimes decades. Without a dramatic crisis to prompt them to seek help, they often view their state as a character trait: “I’m just a pessimist,” or “That’s just how I am.” However, the chronicity of symptoms leads to profound secondary consequences: social withdrawal, a decline in professional and educational achievements, the entrenchment of negative thinking patterns, and often problems in intimate relationships. A person with dystymia rarely cries out for help—they quietly withdraw from one area of life after another.

Treatment for dystymia is possible and effective, though it requires patience. A meta-analysis by Cuijpers et al. showed that both psychotherapy (particularly CBT and Interpersonal Therapy) and pharmacotherapy bring improvement—though effects may be smaller than in acute episodes, and treatment time longer [31]. Research suggests that a combination of psychotherapy and pharmacotherapy is more effective than either approach alone, which is particularly important given the long-term nature of the disorder. An essential element of therapy is psychoeducation: understanding that dystymia is a health disorder, not a personality trait, can be the beginning of change in itself.

Double Depression: When Dystymia and Acute Episodes Overlap

The concept of “double depression” describes a clinically common and diagnostically significant phenomenon where an acute episode of major depression is superimposed on a chronic dysthymic background. After the acute episode, a patient with double depression does not return to full health—they only return to their “baseline” state of low mood that existed before. This means they remain ill the entire time between episodes, even if they do not currently meet the criteria for a major depressive episode.

This presentation has serious practical consequences. First, the patient and their surroundings may interpret the worsening as just “another bad period,” delaying the diagnosis of a full-blown episode and the implementation of appropriate treatment. Second, after the acute episode subsides, the patient is still ill—they have dystymia—and requires continued care, not “completion of treatment.” A scenario where pharmacotherapy is discontinued after improvement, only for the patient to return months later with another episode, is very common and largely predictable in this group.

Studies indicate that individuals with double depression have a poorer prognosis and a higher risk of relapse than those with major depression alone without a dystymic background [31]. Response to treatment is slower, and the risk of chronicity is higher. From a clinical perspective, it is key to recognize both layers: the current episode and the chronic background. Treatment should be planned with both in mind—and should not end when the acute episode resolves but should continue long-term, including both maintenance pharmacotherapy and psychotherapy aimed at changing deeper schemas.

Perinatal and Postpartum Depression: An Underappreciated and Often Late-Diagnosed Type

Pregnancy and the first year after childbirth are associated with an increased risk of mood disorders. Literature increasingly uses the term perinatal depression, covering both the prenatal and postpartum periods—since symptoms can begin during pregnancy, not just after birth [4, 10]. DSM-5 and ICD-11 use the “with peripartum onset” specifier, which can be applied to a depressive episode or an episode in the course of BD. The global prevalence of postpartum depression is estimated at approximately 17–18% in large meta-analyses, with significant differences between populations and measurement methods [9, 10]. Newer reviews show that symptoms can persist beyond 12 months—their frequency in the second year after birth remains clinically significant [11].

Clinically distinguishing between three states is key to proper intervention:

1. Baby blues: Mild, short-term (3–5 days) mood fluctuations in the first week after birth, resulting from rapid hormonal changes—it is common and resolves spontaneously without treatment.
2. Postpartum depression: Symptoms of depression persisting longer than two weeks that impair functioning and the bond with the child; it requires clinical assessment and usually treatment.
3. Postpartum psychosis: Rare (1–2 cases per 1,000 births) but severe and requiring urgent psychiatric hospitalization; it involves delusions, hallucinations, and disorganized thinking.

Risk factors for perinatal depression include: prior episodes of depression or anxiety (the strongest predictor), lack of partner and social support, financial difficulties, complicated delivery or high-risk pregnancy, unplanned pregnancy, and biological susceptibility to hormonal fluctuations. Prenatal depression (during pregnancy) may be even more common than postpartum depression but is particularly underdiagnosed—it is often masked by natural pregnancy discomforts and social pressure to “be happy about the pregnancy.”

Untreated perinatal depression has consequences beyond the mother’s well-being. Research points to a negative impact on the mother–child bond, the infant’s emotional and cognitive development, and the risk of mood disorders in the partner. Postpartum depression is not a mother’s weakness or proof that she loves her child less—it is a recognizable health problem with effective treatment methods. If intrusive thoughts about harming the child or oneself appear, or if there is intense helplessness or psychotic symptoms, an urgent psychiatric consultation is necessary.

Seasonal Affective Disorder (SAD): A Course Specifier with Important Therapeutic Implications

Seasonal Affective Disorder (SAD) refers to recurrent depressive episodes linked to the time of year—most often worsening in autumn and winter and resolving in spring or summer. In DSM-5, it is described as a “with seasonal pattern” specifier, which can be assigned to major depressive disorder or bipolar disorders if criteria for recurrence and the dominance of seasonal episodes are met [12, 13]. Formally, SAD is not a separate disease entity—it is a pattern of depressive course, which does not diminish its reality or the burden it can place on a patient.

Winter SAD is characterized by an atypical symptom profile: excessive sleepiness (hypersomnia), increased appetite with a characteristic craving for carbohydrates, marked weight gain in winter months, low energy, and social withdrawal. This profile contrasts sharply with the classic insomnia and anorexia of “typical” depressive episodes [13, 14]. A less commonly described summer form of SAD involves insomnia, agitation, and irritability. While the mechanisms are not fully understood, the roles of daylight deficiency, circadian rhythm changes, and dysregulation of melatonin and the serotonergic system are well-documented.

Light therapy (phototherapy) is the first-line treatment for winter SAD: its effectiveness in randomized trials is comparable to pharmacotherapy, and its side-effect profile is much more favorable [13]. Lamps with an intensity of 10,000 lux are used for about 20–30 minutes in the morning throughout the winter season. Pharmacotherapy (particularly SSRIs) is effective as a second-line treatment or in combination with phototherapy. Regular sleep rituals, physical activity, and limiting social isolation in winter have proven preventive value.

Clinically, it is important to distinguish SAD from low mood due solely to psychosocial reasons (winter isolation, holiday stress) and from other causes of low energy in autumn—including hypothyroidism and Vitamin D deficiency. Particular caution is advised when seasonality overlaps with a presentation suggesting BD: winter depressive episodes and spring periods of increased energy in one person may indicate Bipolar II with a seasonal pattern, not “regular SAD” [12]. The distinction has serious therapeutic implications—light therapy and antidepressants used without a mood stabilizer can destabilize the course of BD.

Psychotic Depression: A Severe and Often Hidden Type

Depression with psychotic features is a depressive episode in which delusions and/or hallucinations occur. Most often, these are mood-congruent—revolving around guilt, punishment, catastrophe, financial ruin, hopelessness, or nihilism (the conviction that internal organs are “rotting”—Cotard’s syndrome). They can also be mood-incongruent, which is clinically significant and may suggest a psychotic spectrum requiring different management [6, 15]. It is estimated that approximately 14–18% of major depressive episodes have psychotic features, with the frequency increasing with age and episode severity [16].

This condition is often unrecognized or diagnosed late for several reasons. First, patients actively hide psychotic content—out of shame, fear of hospitalization, or a lack of insight into the pathological nature of their beliefs. Second, in a brief diagnostic contact, the patient may appear to have “simple depression,” maintaining appropriate contact and not revealing delusional thoughts. Third, depressive delusions are sometimes misinterpreted as extreme pessimistic thinking or excessive guilt—without recognizing their delusional, fixed nature. A standard psychiatric interview should include direct questions about beliefs regarding guilt, illness, ruin, and punishment.

The treatment of psychotic depression differs fundamentally from depression without psychosis. Clinical literature has long indicated that antidepressant monotherapy is insufficient—effective methods include a combination of an antidepressant with an atypical antipsychotic or electroconvulsive therapy (ECT), which shows particularly high efficacy in this patient group [17, 18]. Suicide risk in psychotic depression is higher than in non-psychotic depression, requiring careful safety assessment and consideration of hospitalization.

For Loved Ones and Patients: Psychosis in depression does not mean a permanent loss of contact with reality or a “different personality.” It is a symptom of an active illness episode that resolves with proper treatment. It is crucial to seek specialist help immediately—do not wait for it to “go away on its own.”

Catatonic Depression: A Rare but Critical Clinical Picture

Catatonia is most commonly associated with schizophrenia; however, modern data indicate that the most common cause of catatonia is mood disorders—depression and bipolar disorder—rather than psychosis [21]. DSM-5 treats catatonia as a specifier accompanying depression, BD, or psychotic disorders, but it can also occur as a condition directly related to another medical state [19, 20]. The clinical picture may include: mutism, extreme negativism (active resistance to instructions or contact), immobility, stupor, unusual postures or grimacing, waxy flexibility (flexibilitas cerea), echolalia (repeating words), or echopraxia (repeating movements). Because the patient may refuse food and drink or remain immobile for long periods, catatonia is a potentially life-threatening condition and requires urgent diagnosis and treatment.

A 2024 review in the Journal of Clinical Medicine emphasizes that catatonic depression is often unrecognized because psychomotor symptoms typical of severe depression—slowness, inhibition, poverty of movement and speech—can overlap with catatonic symptoms and blur the diagnostic line [21]. Motor inhibition may be misinterpreted as extreme apathy rather than catatonia requiring specific treatment. The Bush–Francis Catatonia Rating Scale (BFCRS) is helpful in diagnosis, and the catatonic nature of symptoms can be confirmed by a lorazepam challenge—temporary improvement after the administration of a benzodiazepine.

Treatment of catatonia, regardless of its cause, relies on benzodiazepines as the first-line method and ECT in case of non-response or life-threatening situations [21]. Traditional antipsychotics are contraindicated or used with extreme caution in catatonia, as they can worsen symptoms or lead to neuroleptic malignant syndrome. From a social education perspective, it is worth emphasizing: “freezing” and “falling silent” in severe depression is not always a metaphor—it can have a real, medical dimension requiring an immediate response from those around the patient.

Atypical and Masked Depression: Diagnosis vs. Phenotype

In the DSM-5, the “with atypical features” specifier describes a depressive episode whose central feature is mood reactivity—the ability to experience temporary, significant improvement in response to positive external events. This is usually accompanied by: excessive sleepiness (hypersomnia), increased appetite or weight gain, a feeling of “leaden paralysis” (heavy limbs), and marked interpersonal rejection sensitivity—the latter is considered particularly characteristic and can persist between depressive episodes, shaping a chronic relational pattern [6].

Mood reactivity in atypical depression is often mistaken by patients, families, and sometimes even clinicians as proof of a lack of “real” depression: “If they can smile at a good movie, they’re not really sick.” However, in atypical depression, this very possibility of temporary improvement is a defining feature, not evidence of its absence. Patients with this profile may function seemingly normally in short windows yet still meet the criteria for a full-blown episode when looking at their overall functioning over time. Atypical depression is also associated with an earlier age of onset and a higher frequency of comorbid social anxiety [6].

From a pharmacotherapeutic perspective, atypical depression shows a better response to MAO inhibitors (MAOIs) than to tricyclic antidepressants (TCAs)—one of the few examples in psychiatry where a specific phenotype indicates a preference for a particular class of drugs. In practice, SSRIs are used as first-line treatment due to safety and availability, with MAOIs as an option for inadequate response. Psychotherapy focusing on emotion regulation and rejection-related schemas is an important part of holistic treatment.

“Masked depression” is not a formal entity in ICD-10 or DSM-5—it is a clinical term describing a situation where the patient primarily reports somatic complaints: headaches, back pain, stomach aches, heart palpitations, chronic fatigue, or sleep disturbances, while low mood is poorly articulated or viewed by the patient as secondary. Such individuals often see multiple somatic specialists before depression is recognized. The risk of missing the diagnosis is real and costly—for the patient seeking a diagnosis for years and for the healthcare system generating numerous unnecessary tests. Today, this presentation is described as depression with predominant somatic symptoms or depression comorbid with somatization disorders.

Melancholic Depression: A Classic and Clinically Vital Phenotype

The “with melancholic features” specifier in DSM-5 describes a depressive episode dominated by deep anhedonia of a specific nature: there is no mood reactivity—even clearly positive events (visits from loved ones, good news) bring no relief. This is accompanied by: a marked worsening of symptoms in the morning, early morning awakening (at least two hours before the normal time), significant psychomotor retardation or agitation, marked weight loss or loss of appetite, and excessive or inappropriate guilt, often taking on ruminative or delusional qualities [6].

Melancholia is the phenotype with the longest descriptive history in psychiatry—its clinical picture was recognized as early as Hippocrates. Modern neuroendocrinological studies indicate more frequent HPA axis overactivity (elevated cortisol) and greater circadian rhythm disruptions than in depression without melancholic features [3]. From a clinical perspective, melancholia is associated with a more severe course, higher relapse risk, and a poorer prognosis without pharmacological treatment.

Melancholic depression shows a better response to pharmacotherapy—particularly TCAs and venlafaxine at higher doses—than to psychotherapy as a standalone treatment in the acute phase. ECT is an exceptionally well-documented method for this group, especially when melancholia co-occurs with psychotic features or life-threatening symptoms. Psychotherapy has an important place in maintenance treatment and relapse prevention, but in the acute phase of severe melancholia, it does not replace biological treatment. It is also worth noting that it is difficult to identify melancholia based solely on questionnaire results (e.g., PHQ-9); it requires a careful clinical interview.

Substance- and Medication-Induced Depression

In DSM-5 and ICD-11, there is a distinct category for substance/medication-induced depressive disorder, where depressive symptoms are directly related to intoxication, withdrawal, or pharmacological exposure [22, 23]. The key criterion is the temporal link: symptoms appear during substance use, shortly after its initiation or dose escalation, or during withdrawal, and their severity and nature are not better explained by an independent depressive disorder. The distinction is important—not to “deny” the patient a depression diagnosis, but because treatment may require a different approach, often involving the discontinuation or change of the inducing substance.

Alcohol is the most common substance linked to depression. Many people turn to alcohol to alleviate depressive symptoms—while it may bring short-term relief, long-term alcohol is a central nervous system depressant: it deepens mood dysregulation, disrupts sleep (reducing REM phase), worsens anxiety symptoms, and complicates treatment. Alcohol dependence and depression create a self-perpetuating feedback loop that is difficult to break without addressing both problems simultaneously. Among medications, a documented depressive effect is seen with: Interferon-alpha (used in Hepatitis C and some cancers), long-term corticosteroid use, benzodiazepines (paradoxically, with chronic use or withdrawal), and to a lesser extent, beta-blockers and certain hormonal contraceptives [22].

In clinical practice, a mixed picture is common: depression was present earlier, and the substance became a form of “self-medication,” which subsequently worsened symptoms. In such a setup, distinguishing cause and effect is difficult, and treatment must address both issues in parallel—attempts to “fix” only one rarely bring lasting improvement. It is also important that patients do not independently discontinue medications “suspected” of causing depression; the decision to modify therapy should be made with a doctor who assesses the risk-benefit balance.

Depression in the Course of Somatic Illnesses

Somatic illnesses and depression share a close, bidirectional relationship. On one hand, chronic illness—through pain, limited mobility, anxiety about the future, isolation, and the need for long-term treatment—significantly increases the risk of depression. On the other hand, depression worsens the prognosis of somatic illness: it lowers treatment adherence, intensifies pain perception, impairs immune function, and is associated with higher mortality in cardiovascular diseases and cancer. The diagnosis of “depressive disorder due to another medical condition” in DSM-5 requires demonstrating a direct physiopathological link, though in clinical practice, the boundary can be hard to define precisely [5].

Diseases with particularly high risk and well-documented mechanisms:

• Hypothyroidism: Symptoms overlap with depression; TSH testing is a mandatory part of differential diagnosis for every depressive episode.
• Parkinson’s Disease: Depression affects about 40% of patients and can be both a psychological reaction and part of the illness’s neurobiology (dopamine and serotonin deficit).
• Multiple Sclerosis: Prevalence of depression is around 50%, involving inflammatory and neurodegenerative factors.
• Diabetes: Meta-analyses point to a twofold higher risk of depression, with shared inflammatory pathways and glucose dysregulation affecting the brain.
• Cancer: Depression is the most common mental disorder in oncological patients; its treatment improves quality of life and can influence prognosis.

Depression in the context of chronic illness is too often treated as a “natural reaction you have to learn to live with.” However, it is a clinically significant disorder requiring treatment—and one that, with the right intervention, can be treated effectively.

Depression and Age: Childhood, Adolescence, Old Age

Depression in Children and Adolescents

Depression in children and teens presents differently than in adults. The central symptom may not be sadness; irritable mood is more common: the child or teen may be explosive, impatient, or easily angered. Somatic symptoms—headaches, stomach aches, fatigue without an apparent cause—can dominate. There is also a visible drop in school performance, withdrawal from peer relationships, and abandonment of previous interests. The WHO estimates that depression is one of the leading causes of disability among adolescents globally [28].

Depression in the Elderly

Depression in seniors is one of the most underdiagnosed disorders in this age group. Symptoms are often masked by somatic complaints or mistaken for natural aging or dementia—so-called depressive pseudodementia, where cognitive impairment is a dominant symptom of depression rather than dementia. Risk factors include multimorbidity, chronic pain, polypharmacy, social isolation, loss of loved ones and mobility, and neurological changes associated with brain aging (e.g., vascular depression).

Depression and Genetics: Polygenicity and the Limits of Simple Labels

Genetic studies of depression show its architecture is complex and multigenic. There is no “depression gene”—no single mutation determines the illness. Hundreds of risk loci have been identified, each contributing a small individual effect [26, 27]. Heritability for major depressive disorder is estimated at around 37%—genetics explains less than half of the risk variation; the rest is explained by experience and environment [29].

For patients, this means: family history increases risk but does not determine it; a lack of family history does not protect if strong environmental factors exist. Biological and psychological dimensions of depression should not be opposed—they are two perspectives on the same phenomenon.

Summary: Table of Depressive Types

Type of Depression	ICD-10 / DSM-5 Code	Key Features	Clinical Notes
Depressive Episode	F32 / MDD	Low mood ≥2 weeks, anhedonia, sleep/appetite/energy changes	Severity assessment is vital for treatment choice
Recurrent Depression	F33 / MDD recurrent	≥2 episodes, no history of mania	Relapse risk >90% after 3 episodes; maintenance is key
Dystymia / PDD	F34.1 / PDD	Chronic (≥2 years) low mood	Often unrecognized; risk of double depression
Double Depression	F33 + F34.1 / MDD + PDD	Acute episode on a dystymic background	Poorer prognosis; do not stop treatment after acute phase
Bipolar Depression	F31 / Bipolar MDE	Depressive episodes + history of mania/hypomania	Antidepressant monotherapy is risky; mood stabilizers needed
Cyclothymia	F34.0 / Cyclothymia	Chronic fluctuations ≥2 years, below episode threshold	15–50% risk of progression to BD
Perinatal Depression	F53.0 / MDD + specifier	Episode during pregnancy or up to 12 months postpartum	Assessment of risk for both mother and child is vital
Seasonal Affective Disorder	DSM-5/ICD-11 specifier	Seasonal recurrence, hypersomnia, carb cravings	Light therapy is effective; rule out Bipolar II
Psychotic Depression	F32.3 / MDD + specifier	Episode + delusions/hallucinations	Requires AD + antipsychotic or ECT; high suicide risk
Catatonic Depression	DSM-5 specifier	Mutism, stupor, negativism, immobility	Life-threatening; BZDs and ECT are first-line
Atypical Depression	DSM-5 specifier	Mood reactivity, hypersomnia, rejection sensitivity	Better response to MAOIs; reactivity ≠ no depression
Melancholic Depression	DSM-5 specifier	Deep anhedonia, morning worsening, early awakening	Better response to TCAs and ECT; meds essential
Substance-Induced	F1x.8 / SUD-induced	Symptoms temporally linked to substance/medication	Mixed picture common; do not stop meds without consult
Somatic Disease-Linked	F06.3 / due to medical condition	Depression as part of/sequel to somatic illness	Requires treatment; monitor drug interactions

Knowing the types of depression and being able to differentiate between them is the foundation of precise diagnosis and effective treatment.

Bibliography and Sources

1. WHO, ICD-10 (2019) – kody F31–F34: icd.who.int
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