major depression essay

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Biological, Psychological, and Social Determinants of Depression: A Review of Recent Literature

Olivia remes.

1 Institute for Manufacturing, University of Cambridge, Cambridge CB3 0FS, UK

João Francisco Mendes

2 NOVA Medical School, Universidade NOVA de Lisboa, 1099-085 Lisbon, Portugal; ku.ca.mac@94cfj

Peter Templeton

3 IfM Engage Limited, Institute for Manufacturing, University of Cambridge, Cambridge CB3 0FS, UK; ku.ca.mac@32twp

4 The William Templeton Foundation for Young People’s Mental Health (YPMH), Cambridge CB2 0AH, UK

Associated Data

Depression is one of the leading causes of disability, and, if left unmanaged, it can increase the risk for suicide. The evidence base on the determinants of depression is fragmented, which makes the interpretation of the results across studies difficult. The objective of this study is to conduct a thorough synthesis of the literature assessing the biological, psychological, and social determinants of depression in order to piece together the puzzle of the key factors that are related to this condition. Titles and abstracts published between 2017 and 2020 were identified in PubMed, as well as Medline, Scopus, and PsycInfo. Key words relating to biological, social, and psychological determinants as well as depression were applied to the databases, and the screening and data charting of the documents took place. We included 470 documents in this literature review. The findings showed that there are a plethora of risk and protective factors (relating to biological, psychological, and social determinants) that are related to depression; these determinants are interlinked and influence depression outcomes through a web of causation. In this paper, we describe and present the vast, fragmented, and complex literature related to this topic. This review may be used to guide practice, public health efforts, policy, and research related to mental health and, specifically, depression.

1. Introduction

Depression is one of the most common mental health issues, with an estimated prevalence of 5% among adults [ 1 , 2 ]. Symptoms may include anhedonia, feelings of worthlessness, concentration and sleep difficulties, and suicidal ideation. According to the World Health Organization, depression is a leading cause of disability; research shows that it is a burdensome condition with a negative impact on educational trajectories, work performance, and other areas of life [ 1 , 3 ]. Depression can start early in the lifecourse and, if it remains unmanaged, may increase the risk for substance abuse, chronic conditions, such as cardiovascular disease, and premature mortality [ 4 , 5 , 6 , 7 , 8 ].

Treatment for depression exists, such as pharmacotherapy, cognitive behavioural therapy, and other modalities. A meta-analysis of randomized, placebo-controlled trials of patients shows that 56–60% of people respond well to active treatment with antidepressants (selective serotonin reuptake inhibitors, tricyclic antidepressants) [ 9 ]. However, pharmacotherapy may be associated with problems, such as side-effects, relapse issues, a potential duration of weeks until the medication starts working, and possible limited efficacy in mild cases [ 10 , 11 , 12 , 13 , 14 ]. Psychotherapy is also available, but access barriers can make it difficult for a number of people to get the necessary help.

Studies on depression have increased significantly over the past few decades. However, the literature remains fragmented and the interpretation of heterogeneous findings across studies and between fields is difficult. The cross-pollination of ideas between disciplines, such as genetics, neurology, immunology, and psychology, is limited. Reviews on the determinants of depression have been conducted, but they either focus exclusively on a particular set of determinants (ex. genetic risk factors [ 15 ]) or population sub-group (ex. children and adolescents [ 16 ]) or focus on characteristics measured predominantly at the individual level (ex. focus on social support, history of depression [ 17 ]) without taking the wider context (ex. area-level variables) into account. An integrated approach paying attention to key determinants from the biological, psychological, and social spheres, as well as key themes, such as the lifecourse perspective, enables clinicians and public health authorities to develop tailored, person-centred approaches.

The primary aim of this literature review: to address the aforementioned challenges, we have synthesized recent research on the biological, psychological, and social determinants of depression and we have reviewed research from fields including genetics, immunology, neurology, psychology, public health, and epidemiology, among others.

The subsidiary aim: we have paid special attention to important themes, including the lifecourse perspective and interactions between determinants, to guide further efforts by public health and medical professionals.

This literature review can be used as an evidence base by those in public health and the clinical setting and can be used to inform targeted interventions.

2. Materials and Methods

We conducted a review of the literature on the biological, psychological, and social determinants of depression in the last 4 years. We decided to focus on these determinants after discussions with academics (from the Manchester Metropolitan University, University of Cardiff, University of Colorado, Boulder, University of Cork, University of Leuven, University of Texas), charity representatives, and people with lived experience at workshops held by the University of Cambridge in 2020. In several aspects, we attempted to conduct this review according to PRISMA guidelines [ 18 ].

The inclusion and exclusion criteria are the following:

• - We included documents, such as primary studies, literature reviews, systematic reviews, meta-analyses, reports, and commentaries on the determinants of depression. The determinants refer to variables that appear to be linked to the development of depression, such as physiological factors (e.g., the nervous system, genetics), but also factors that are further away or more distal to the condition. Determinants may be risk or protective factors, and individual- or wider-area-level variables.
• - We focused on major depressive disorder, treatment-resistant depression, dysthymia, depressive symptoms, poststroke depression, perinatal depression, as well as depressive-like behaviour (common in animal studies), among others.
• - We included papers regardless of the measurement methods of depression.
• - We included papers that focused on human and/or rodent research.
• - This review focused on articles written in the English language.
• - Documents published between 2017–2020 were captured to provide an understanding of the latest research on this topic.
• - Studies that assessed depression as a comorbidity or secondary to another disorder.
• - Studies that did not focus on rodent and/or human research.
• - Studies that focused on the treatment of depression. We made this decision, because this is an in-depth topic that would warrant a separate stand-alone review.
• Next, we searched PubMed (2017–2020) using keywords related to depression and determinants. Appendix A contains the search strategy used. We also conducted focused searches in Medline, Scopus, and PsycInfo (2017–2020).
• Once the documents were identified through the databases, the inclusion and exclusion criteria were applied to the titles and abstracts. Screening of documents was conducted by O.R., and a subsample was screened by J.M.; any discrepancies were resolved through a communication process.
• The full texts of documents were retrieved, and the inclusion and exclusion criteria were again applied. A subsample of documents underwent double screening by two authors (O.R., J.M.); again, any discrepancies were resolved through communication.
• a. A data charting form was created to capture the data elements of interest, including the authors, titles, determinants (biological, psychological, social), and the type of depression assessed by the research (e.g., major depression, depressive symptoms, depressive behaviour).
• b. The data charting form was piloted on a subset of documents, and refinements to it were made. The data charting form was created with the data elements described above and tested in 20 studies to determine whether refinements in the wording or language were needed.
• c. Data charting was conducted on the documents.
• d. Narrative analysis was conducted on the data charting table to identify key themes. When a particular finding was noted more than once, it was logged as a potential theme, with a review of these notes yielding key themes that appeared on multiple occasions. When key themes were identified, one researcher (O.R.) reviewed each document pertaining to that theme and derived concepts (key determinants and related outcomes). This process (a subsample) was verified by a second author (J.M.), and the two authors resolved any discrepancies through communication. Key themes were also checked as to whether they were of major significance to public mental health and at the forefront of public health discourse according to consultations we held with stakeholders from the Manchester Metropolitan University, University of Cardiff, University of Colorado, Boulder, University of Cork, University of Leuven, University of Texas, charity representatives, and people with lived experience at workshops held by the University of Cambridge in 2020.

We condensed the extensive information gleaned through our review into short summaries (with key points boxes for ease of understanding and interpretation of the data).

Through the searches, 6335 documents, such as primary studies, literature reviews, systematic reviews, meta-analyses, reports, and commentaries, were identified. After applying the inclusion and exclusion criteria, 470 papers were included in this review ( Supplementary Table S1 ). We focused on aspects related to biological, psychological, and social determinants of depression (examples of determinants and related outcomes are provided under each of the following sections.

3.1. Biological Factors

The following aspects will be discussed in this section: physical health conditions; then specific biological factors, including genetics; the microbiome; inflammatory factors; stress and hypothalamic–pituitary–adrenal (HPA) axis dysfunction, and the kynurenine pathway. Finally, aspects related to cognition will also be discussed in the context of depression.

3.1.1. Physical Health Conditions

Studies on physical health conditions—key points:

• The presence of a physical health condition can increase the risk for depression
• Psychological evaluation in physically sick populations is needed
• There is large heterogeneity in study design and measurement; this makes the comparison of findings between and across studies difficult

A number of studies examined the links between the outcome of depression and physical health-related factors, such as bladder outlet obstruction, cerebral atrophy, cataract, stroke, epilepsy, body mass index and obesity, diabetes, urinary tract infection, forms of cancer, inflammatory bowel disorder, glaucoma, acne, urea accumulation, cerebral small vessel disease, traumatic brain injury, and disability in multiple sclerosis [ 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 , 46 , 47 , 48 , 49 , 50 , 51 , 52 , 53 , 54 , 55 , 56 , 57 , 58 , 59 , 60 , 61 , 62 , 63 , 64 , 65 , 66 , 67 , 68 , 69 , 70 , 71 ]. For example, bladder outlet obstruction has been linked to inflammation and depressive behaviour in rodent research [ 24 ]. The presence of head and neck cancer also seemed to be related to an increased risk for depressive disorder [ 45 ]. Gestational diabetes mellitus has been linked to depressive symptoms in the postpartum period (but no association has been found with depression in the third pregnancy trimester) [ 50 ], and a plethora of other such examples of relationships between depression and physical conditions exist. As such, the assessment of psychopathology and the provision of support are necessary in individuals of ill health [ 45 ]. Despite the large evidence base on physical health-related factors, differences in study methodology and design, the lack of standardization when it comes to the measurement of various physical health conditions and depression, and heterogeneity in the study populations makes it difficult to compare studies [ 50 ].

The next subsections discuss specific biological factors, including genetics; the microbiome; inflammatory factors; stress and hypothalamic–pituitary–adrenal (HPA) axis dysfunction, and the kynurenine pathway; and aspects related to cognition.

3.1.2. Genetics

Studies on genetics—key points:

There were associations between genetic factors and depression; for example:

• The brain-derived neurotrophic factor (BDNF) plays an important role in depression
• Links exist between major histocompatibility complex region genes, as well as various gene polymorphisms and depression
• Single nucleotide polymorphisms (SNPs) of genes involved in the tryptophan catabolites pathway are of interest in relation to depression

A number of genetic-related factors, genomic regions, polymorphisms, and other related aspects have been examined with respect to depression [ 61 , 72 , 73 , 74 , 75 , 76 , 77 , 78 , 79 , 80 , 81 , 82 , 83 , 84 , 85 , 86 , 87 , 88 , 89 , 90 , 91 , 92 , 93 , 94 , 95 , 96 , 97 , 98 , 99 , 100 , 101 , 102 , 103 , 104 , 105 , 106 , 107 , 108 , 109 , 110 , 111 , 112 , 113 , 114 , 115 , 116 , 117 , 118 , 119 , 120 , 121 , 122 , 123 , 124 , 125 , 126 , 127 , 128 , 129 , 130 , 131 , 132 , 133 , 134 , 135 , 136 , 137 , 138 , 139 , 140 ]. The influence of BDNF in relation to depression has been amply studied [ 117 , 118 , 141 , 142 , 143 ]. Research has shown associations between depression and BDNF (as well as candidate SNPs of the BDNF gene, polymorphisms of the BDNF gene, and the interaction of these polymorphisms with other determinants, such as stress) [ 129 , 144 , 145 ]. Specific findings have been reported: for example, a study reported a link between the BDNF rs6265 allele (A) and major depressive disorder [ 117 ].

Other research focused on major histocompatibility complex region genes, endocannabinoid receptor gene polymorphisms, as well as tissue-specific genes and gene co-expression networks and their links to depression [ 99 , 110 , 112 ]. The SNPs of genes involved in the tryptophan catabolites pathway have also been of interest when studying the pathogenesis of depression.

The results from genetics studies are compelling; however, the findings remain mixed. One study indicated no support for depression candidate gene findings [ 122 ]. Another study found no association between specific polymorphisms and major depressive disorder [ 132 ]. As such, further research using larger samples is needed to corroborate the statistically significant associations reported in the literature.

3.1.3. Microbiome

Studies on the microbiome—key points:

• The gut bacteria and the brain communicate via both direct and indirect pathways called the gut-microbiota-brain axis (the bidirectional communication networks between the central nervous system and the gastrointestinal tract; this axis plays an important role in maintaining homeostasis).
• A disordered microbiome can lead to inflammation, which can then lead to depression
• There are possible links between the gut microbiome, host liver metabolism, brain inflammation, and depression

The common themes of this review have focused on the microbiome/microbiota or gut metabolome [ 146 , 147 , 148 , 149 , 150 , 151 , 152 , 153 , 154 , 155 , 156 , 157 , 158 , 159 , 160 , 161 ], the microbiota-gut-brain axis, and related factors [ 152 , 162 , 163 , 164 , 165 , 166 , 167 ]. When there is an imbalance in the intestinal bacteria, this can interfere with emotional regulation and contribute to harmful inflammatory processes and mood disorders [ 148 , 151 , 153 , 155 , 157 ]. Rodent research has shown that there may be a bidirectional association between the gut microbiota and depression: a disordered gut microbiota can play a role in the onset of this mental health problem, but, at the same time, the existence of stress and depression may also lead to a lower level of richness and diversity in the microbiome [ 158 ].

Research has also attempted to disentangle the links between the gut microbiome, host liver metabolism, brain inflammation, and depression, as well as the role of the ratio of lactobacillus to clostridium [ 152 ]. The literature has also examined the links between medication, such as antibiotics, and mood and behaviour, with the findings showing that antibiotics may be related to depression [ 159 , 168 ]. The links between the microbiome and depression are complex, and further studies are needed to determine the underpinning causal mechanisms.

3.1.4. Inflammation

Studies on inflammation—key points:

• Pro-inflammatory cytokines are linked to depression
• Pro-inflammatory cytokines, such as the tumour necrosis factor (TNF)-alpha, may play an important role
• Different methods of measurement are used, making the comparison of findings across studies difficult

Inflammation has been a theme in this literature review [ 60 , 161 , 164 , 169 , 170 , 171 , 172 , 173 , 174 , 175 , 176 , 177 , 178 , 179 , 180 , 181 , 182 , 183 , 184 ]. The findings show that raised levels of inflammation (because of factors such as pro-inflammatory cytokines) have been associated with depression [ 60 , 161 , 174 , 175 , 178 ]. For example, pro-inflammatory cytokines, such as tumour necrosis factor (TNF)-alpha, have been linked to depression [ 185 ]. Various determinants, such as early life stress, have also been linked to systemic inflammation, and this can increase the risk for depression [ 186 ].

Nevertheless, not everyone with elevated inflammation develops depression; therefore, this is just one route out of many linked to pathogenesis. Despite the compelling evidence reported with respect to inflammation, it is difficult to compare the findings across studies because of different methods used to assess depression and its risk factors.

3.1.5. Stress and HPA Axis Dysfunction

Studies on stress and HPA axis dysfunction—key points:

• Stress is linked to the release of proinflammatory factors
• The dysregulation of the HPA axis is linked to depression
• Determinants are interlinked in a complex web of causation

Stress was studied in various forms in rodent populations and humans [ 144 , 145 , 155 , 174 , 176 , 180 , 185 , 186 , 187 , 188 , 189 , 190 , 191 , 192 , 193 , 194 , 195 , 196 , 197 , 198 , 199 , 200 , 201 , 202 , 203 , 204 , 205 , 206 , 207 , 208 , 209 , 210 , 211 ].

Although this section has some overlap with others (as is to be expected because all of these determinants and body systems are interlinked), a number of studies have focused on the impact of stress on mental health. Stress has been mentioned in the literature as a risk factor of poor mental health and has emerged as an important determinant of depression. The effects of this variable are wide-ranging, and a short discussion is warranted.

Stress has been linked to the release of inflammatory factors, as well as the development of depression [ 204 ]. When the stress is high or lasts for a long period of time, this may negatively impact the brain. Chronic stress can impact the dendrites and synapses of various neurons, and may be implicated in the pathway leading to major depressive disorder [ 114 ]. As a review by Uchida et al. indicates, stress may be associated with the “dysregulation of neuronal and synaptic plasticity” [ 114 ]. Even in rodent studies, stress has a negative impact: chronic and unpredictable stress (and other forms of tension or stress) have been linked to unusual behaviour and depression symptoms [ 114 ].

The depression process and related brain changes, however, have also been linked to the hyperactivity or dysregulation of the HPA axis [ 127 , 130 , 131 , 182 , 212 ]. One review indicates that a potential underpinning mechanism of depression relates to “HPA axis abnormalities involved in chronic stress” [ 213 ]. There is a complex relationship between the HPA axis, glucocorticoid receptors, epigenetic mechanisms, and psychiatric sequelae [ 130 , 212 ].

In terms of the relationship between the HPA axis and stress and their influence on depression, the diathesis–stress model offers an explanation: it could be that early stress plays a role in the hyperactivation of the HPA axis, thus creating a predisposition “towards a maladaptive reaction to stress”. When this predisposition then meets an acute stressor, depression may ensue; thus, in line with the diathesis–stress model, a pre-existing vulnerability and stressor can create fertile ground for a mood disorder [ 213 ]. An integrated review by Dean and Keshavan [ 213 ] suggests that HPA axis hyperactivity is, in turn, related to other determinants, such as early deprivation and insecure early attachment; this again shows the complex web of causation between the different determinants.

3.1.6. Kynurenine Pathway

Studies on the kynurenine pathway—key points:

• The kynurenine pathway is linked to depression
• Indolamine 2,3-dioxegenase (IDO) polymorphisms are linked to postpartum depression

The kynurenine pathway was another theme that emerged in this review [ 120 , 178 , 181 , 184 , 214 , 215 , 216 , 217 , 218 , 219 , 220 , 221 ]. The kynurenine pathway has been implicated not only in general depressed mood (inflammation-induced depression) [ 184 , 214 , 219 ] but also postpartum depression [ 120 ]. When the kynurenine metabolism pathway is activated, this results in metabolites, which are neurotoxic.

A review by Jeon et al. notes a link between the impairment of the kynurenine pathway and inflammation-induced depression (triggered by treatment for various physical diseases, such as malignancy). The authors note that this could represent an important opportunity for immunopharmacology [ 214 ]. Another review by Danzer et al. suggests links between the inflammation-induced activation of indolamine 2,3-dioxegenase (the enzyme that converts tryptophan to kynurenine), the kynurenine metabolism pathway, and depression, and also remarks about the “opportunities for treatment of inflammation-induced depression” [ 184 ].

3.1.7. Cognition

Studies on cognition and the brain—key points:

• Cognitive decline and cognitive deficits are linked to increased depression risk
• Cognitive reserve is important in the disability/depression relationship
• Family history of cognitive impairment is linked to depression

A number of studies have focused on the theme of cognition and the brain. The results show that factors, such as low cognitive ability/function, cognitive vulnerability, cognitive impairment or deficits, subjective cognitive decline, regression of dendritic branching and hippocampal atrophy/death of hippocampal cells, impaired neuroplasticity, and neurogenesis-related aspects, have been linked to depression [ 131 , 212 , 222 , 223 , 224 , 225 , 226 , 227 , 228 , 229 , 230 , 231 , 232 , 233 , 234 , 235 , 236 , 237 , 238 , 239 ]. The cognitive reserve appears to act as a moderator and can magnify the impact of certain determinants on poor mental health. For example, in a study in which participants with multiple sclerosis also had low cognitive reserve, disability was shown to increase the risk for depression [ 63 ]. Cognitive deficits can be both causal and resultant in depression. A study on individuals attending outpatient stroke clinics showed that lower scores in cognition were related to depression; thus, cognitive impairment appears to be associated with depressive symptomatology [ 226 ]. Further, Halahakoon et al. [ 222 ] note a meta-analysis [ 240 ] that shows that a family history of cognitive impairment (in first degree relatives) is also linked to depression.

In addition to cognitive deficits, low-level cognitive ability [ 231 ] and cognitive vulnerability [ 232 ] have also been linked to depression. While cognitive impairment may be implicated in the pathogenesis of depressive symptoms [ 222 ], negative information processing biases are also important; according to the ‘cognitive neuropsychological’ model of depression, negative affective biases play a central part in the development of depression [ 222 , 241 ]. Nevertheless, the evidence on this topic is mixed and further work is needed to determine the underpinning mechanisms between these states.

3.2. Psychological Factors

Studies on psychological factors—key points:

• There are many affective risk factors linked to depression
• Determinants of depression include negative self-concept, sensitivity to rejection, neuroticism, rumination, negative emotionality, and others

A number of studies have been undertaken on the psychological factors linked to depression (including mastery, self-esteem, optimism, negative self-image, current or past mental health conditions, and various other aspects, including neuroticism, brooding, conflict, negative thinking, insight, cognitive fusion, emotional clarity, rumination, dysfunctional attitudes, interpretation bias, and attachment style) [ 66 , 128 , 140 , 205 , 210 , 228 , 235 , 242 , 243 , 244 , 245 , 246 , 247 , 248 , 249 , 250 , 251 , 252 , 253 , 254 , 255 , 256 , 257 , 258 , 259 , 260 , 261 , 262 , 263 , 264 , 265 , 266 , 267 , 268 , 269 , 270 , 271 , 272 , 273 , 274 , 275 , 276 , 277 , 278 , 279 , 280 , 281 , 282 , 283 , 284 , 285 , 286 , 287 , 288 , 289 , 290 ]. Determinants related to this condition include low self-esteem and shame, among other factors [ 269 , 270 , 275 , 278 ]. Several emotional states and traits, such as neuroticism [ 235 , 260 , 271 , 278 ], negative self-concept (with self-perceptions of worthlessness and uselessness), and negative interpretation or attention biases have been linked to depression [ 261 , 271 , 282 , 283 , 286 ]. Moreover, low emotional clarity has been associated with depression [ 267 ]. When it comes to the severity of the disorder, it appears that meta-emotions (“emotions that occur in response to other emotions (e.g., guilt about anger)” [ 268 ]) have a role to play in depression [ 268 ].

A determinant that has received much attention in mental health research concerns rumination. Rumination has been presented as a mediator but also as a risk factor for depression [ 57 , 210 , 259 ]. When studied as a risk factor, it appears that the relationship of rumination with depression is mediated by variables that include limited problem-solving ability and insufficient social support [ 259 ]. However, rumination also appears to act as a mediator: for example, this variable (particularly brooding rumination) lies on the causal pathway between poor attention control and depression [ 265 ]. This shows that determinants may present in several forms: as moderators or mediators, risk factors or outcomes, and this is why disentangling the relationships between the various factors linked to depression is a complex task.

The psychological determinants are commonly researched variables in the mental health literature. A wide range of factors have been linked to depression, such as the aforementioned determinants, but also: (low) optimism levels, maladaptive coping (such as avoidance), body image issues, and maladaptive perfectionism, among others [ 269 , 270 , 272 , 273 , 275 , 276 , 279 , 285 , 286 ]. Various mechanisms have been proposed to explain the way these determinants increase the risk for depression. One of the underpinning mechanisms linking the determinants and depression concerns coping. For example, positive fantasy engagement, cognitive biases, or personality dispositions may lead to emotion-focused coping, such as brooding, and subsequently increase the risk for depression [ 272 , 284 , 287 ]. Knowing the causal mechanisms linking the determinants to outcomes provides insight for the development of targeted interventions.

3.3. Social Determinants

Studies on social determinants—key points:

• Social determinants are the conditions in the environments where people are born, live, learn, work, play, etc.; these influence (mental) health [ 291 ]
• There are many social determinants linked to depression, such as sociodemographics, social support, adverse childhood experiences
• Determinants can be at the individual, social network, community, and societal levels

Studies also focused on the social determinants of (mental) health; these are the conditions in which people are born, live, learn, work, play, and age, and have a significant influence on wellbeing [ 291 ]. Factors such as age, social or socioeconomic status, social support, financial strain and deprivation, food insecurity, education, employment status, living arrangements, marital status, race, childhood conflict and bullying, violent crime exposure, abuse, discrimination, (self)-stigma, ethnicity and migrant status, working conditions, adverse or significant life events, illiteracy or health literacy, environmental events, job strain, and the built environment have been linked to depression, among others [ 52 , 133 , 235 , 236 , 239 , 252 , 269 , 280 , 292 , 293 , 294 , 295 , 296 , 297 , 298 , 299 , 300 , 301 , 302 , 303 , 304 , 305 , 306 , 307 , 308 , 309 , 310 , 311 , 312 , 313 , 314 , 315 , 316 , 317 , 318 , 319 , 320 , 321 , 322 , 323 , 324 , 325 , 326 , 327 , 328 , 329 , 330 , 331 , 332 , 333 , 334 , 335 , 336 , 337 , 338 , 339 , 340 , 341 , 342 , 343 , 344 , 345 , 346 , 347 , 348 , 349 , 350 , 351 , 352 , 353 , 354 , 355 , 356 , 357 , 358 , 359 , 360 , 361 , 362 , 363 , 364 , 365 , 366 , 367 , 368 , 369 , 370 , 371 ]. Social support and cohesion, as well as structural social capital, have also been identified as determinants [ 140 , 228 , 239 , 269 , 293 , 372 , 373 , 374 , 375 , 376 , 377 , 378 , 379 ]. In a study, part of the findings showed that low levels of education have been shown to be linked to post-stroke depression (but not severe or clinical depression outcomes) [ 299 ]. A study within a systematic review indicated that having only primary education was associated with a higher risk of depression compared to having secondary or higher education (although another study contrasted this finding) [ 296 ]. Various studies on socioeconomic status-related factors have been undertaken [ 239 , 297 ]; the research has shown that a low level of education is linked to depression [ 297 ]. Low income is also related to depressive disorders [ 312 ]. By contrast, high levels of education and income are protective [ 335 ].

A group of determinants touched upon by several studies included adverse childhood or early life experiences: ex. conflict with parents, early exposure to traumatic life events, bullying and childhood trauma were found to increase the risk of depression (ex. through pathways, such as inflammation, interaction effects, or cognitive biases) [ 161 , 182 , 258 , 358 , 362 , 380 ].

Gender-related factors were also found to play an important role with respect to mental health [ 235 , 381 , 382 , 383 , 384 , 385 ]. Gender inequalities can start early on in the lifecourse, and women were found to be twice as likely to have depression as men. Gender-related factors were linked to cognitive biases, resilience and vulnerabilities [ 362 , 384 ].

Determinants can impact mental health outcomes through underpinning mechanisms. For example, harmful determinants can influence the uptake of risk behaviours. Risk behaviours, such as sedentary behaviour, substance abuse and smoking/nicotine exposure, have been linked to depression [ 226 , 335 , 355 , 385 , 386 , 387 , 388 , 389 , 390 , 391 , 392 , 393 , 394 , 395 , 396 , 397 , 398 , 399 , 400 , 401 ]. Harmful determinants can also have an impact on diet. Indeed, dietary aspects and diet components (ex. vitamin D, folate, selenium intake, iron, vitamin B12, vitamin K, fiber intake, zinc) as well as diet-related inflammatory potential have been linked to depression outcomes [ 161 , 208 , 236 , 312 , 396 , 402 , 403 , 404 , 405 , 406 , 407 , 408 , 409 , 410 , 411 , 412 , 413 , 414 , 415 , 416 , 417 , 418 , 419 , 420 , 421 , 422 , 423 , 424 , 425 , 426 , 427 , 428 ]. A poor diet has been linked to depression through mechanisms such as inflammation [ 428 ].

Again, it is difficult to constrict diet to the ‘social determinants of health’ category as it also relates to inflammation (biological determinants) and could even stand alone as its own category. Nevertheless, all of these factors are interlinked and influence one another in a complex web of causation, as mentioned elsewhere in the paper.

Supplementary Figure S1 contains a representation of key determinants acting at various levels: the individual, social network, community, and societal levels. The determinants have an influence on risk behaviours, and this, in turn, can affect the mood (i.e., depression), body processes (ex. can increase inflammation), and may negatively influence brain structure and function.

3.4. Others

Studies on ‘other’ determinants—key points:

• A number of factors are related to depression
• These may not be as easily categorized as the other determinants in this paper

A number of factors arose in this review that were related to depression; it was difficult to place these under a specific heading above, so this ‘other’ category was created. A number of these could be sorted under the ‘social determinants of depression’ category. For example, being exposed to deprivation, hardship, or adversity may increase the risk for air pollution exposure and nighttime shift work, among others, and the latter determinants have been found to increase the risk for depression. Air pollution could also be regarded as an ecologic-level (environmental) determinant of mental health.

Nevertheless, we have decided to leave these factors in a separate category (because their categorization may not be as immediately clear-cut as others), and these factors include: low-level light [ 429 ], weight cycling [ 430 ], water contaminants [ 431 ], trade [ 432 ], air pollution [ 433 , 434 ], program-level variables (ex. feedback and learning experience) [ 435 ], TV viewing [ 436 ], falls [ 437 ], various other biological factors [ 116 , 136 , 141 , 151 , 164 , 182 , 363 , 364 , 438 , 439 , 440 , 441 , 442 , 443 , 444 , 445 , 446 , 447 , 448 , 449 , 450 , 451 , 452 , 453 , 454 , 455 , 456 , 457 , 458 , 459 , 460 , 461 , 462 , 463 , 464 , 465 , 466 , 467 , 468 , 469 ], mobile phone use [ 470 ], ultrasound chronic exposure [ 471 ], nighttime shift work [ 472 ], work accidents [ 473 ], therapy enrollment [ 226 ], and exposure to light at night [ 474 ].

4. Cross-Cutting Themes

4.1. lifecourse perspective.

Studies on the lifecourse perspective—key points:

• Early life has an importance on mental health
• Stress has been linked to depression
• In old age, the decline in social capital is important

Trajectories and life events are important when it comes to the lifecourse perspective. Research has touched on the influence of prenatal or early life stress on an individual’s mental health trajectory [ 164 , 199 , 475 ]. Severe stress that occurs in the form of early-life trauma has also been associated with depressive symptoms [ 362 , 380 ]. It may be that some individuals exposed to trauma develop thoughts of personal failure, which then serve as a catalyst of depression [ 380 ].

At the other end of the life trajectory—old age—specific determinants have been linked to an increased risk for depression. Older people are at a heightened risk of losing their social networks, and structural social capital has been identified as important in relation to depression in old age [ 293 ].

4.2. Gene–Environment Interactions

Studies on gene–environment interactions—key points:

• The environment and genetics interact to increase the risk of depression
• The etiology of depression is multifactorial
• Adolescence is a time of vulnerability

A number of studies have touched on gene–environment interactions [ 72 , 77 , 82 , 119 , 381 , 476 , 477 , 478 , 479 , 480 , 481 ]. The interactions between genetic factors and determinants, such as negative life events (ex. relationship and social difficulties, serious illness, unemployment and financial crises) and stressors (ex. death of spouse, minor violations of law, neighbourhood socioeconomic status) have been studied in relation to depression [ 82 , 135 , 298 , 449 , 481 ]. A study reported an interaction of significant life events with functional variation in the serotonin-transporter-linked polymorphic region (5-HTTLPR) allele type (in the context of multiple sclerosis) and linked this to depression [ 361 ], while another reported an interaction between stress and 5-HTTLPR in relation to depression [ 480 ]. Other research reported that the genetic variation of HPA-axis genes has moderating effects on the relationship between stressors and depression [ 198 ]. Another study showed that early-life stress interacts with gene variants to increase the risk for depression [ 77 ].

Adolescence is a time of vulnerability [ 111 , 480 ]. Perceived parental support has been found to interact with genes (GABRR1, GABRR2), and this appears to be associated with depressive symptoms in adolescence [ 480 ]. It is important to pay special attention to critical periods in the lifecourse so that adequate support is provided to those who are most vulnerable.

The etiology of depression is multifactorial, and it is worthwhile to examine the interaction between multiple factors, such as epigenetic, genetic, and environmental factors, in order to truly understand this mental health condition. Finally, taking into account critical periods of life when assessing gene–environment interactions is important for developing targeted interventions.

5. Discussion

Depression is one of the most common mental health conditions, and, if left untreated, it can increase the risk for substance abuse, anxiety disorders, and suicide. In the past 20 years, a large number of studies on the risk and protective factors of depression have been undertaken in various fields, such as genetics, neurology, immunology, and epidemiology. However, there are limitations associated with the extant evidence base. The previous syntheses on depression are limited in scope and focus exclusively on social or biological factors, population sub-groups, or examine depression as a comorbidity (rather than an independent disorder). The research on the determinants and causal pathways of depression is fragmentated and heterogeneous, and this has not helped to stimulate progress when it comes to the prevention and intervention of this condition—specifically unravelling the complexity of the determinants related to this condition and thus refining the prevention and intervention methods.

The scope of this paper was to bring together the heterogeneous, vast, and fragmented literature on depression and paint a picture of the key factors that contribute to this condition. The findings from this review show that there are important themes when it comes to the determinants of depression, such as: the microbiome, dysregulation of the HPA axis, inflammatory reactions, the kynurenine pathway, as well as psychological and social factors. It may be that physical factors are proximal determinants of depression, which, in turn, are acted on by more distal social factors, such as deprivation, environmental events, and social capital.

The Marmot Report [ 291 ], the World Health Organization [ 482 ], and Compton et al. [ 483 ] highlight that the most disadvantaged segments of society are suffering (the socioeconomic context is important), and this inequality in resources has translated to inequality in mental health outcomes [ 483 ]. To tackle the issue of egalitarianism and restore equality in the health between the groups, the social determinants need to be addressed [ 483 ]. A wide range of determinants of mental health have been identified in the literature: age, gender, ethnicity, family upbringing and early attachment patterns, social support, access to food, water and proper nutrition, and community factors. People spiral downwards because of individual- and societal-level circumstances; therefore, these circumstances along with the interactions between the determinants need to be considered.

Another important theme in the mental health literature is the lifecourse perspective. This shows that the timing of events has significance when it comes to mental health. Early life is a critical period during the lifespan at which cognitive processes develop. Exposure to harmful determinants, such as stress, during this period can place an individual on a trajectory of depression in adulthood or later life. When an individual is exposed to harmful determinants during critical periods and is also genetically predisposed to depression, the risk for the disorder can be compounded. This is why aspects such as the lifecourse perspective and gene–environment interactions need to be taken into account. Insight into this can also help to refine targeted interventions.

A number of interventions for depression have been developed or recommended, addressing, for example, the physical factors described here and lifestyle modifications. Interventions targeting various factors, such as education and socioeconomic status, are needed to help prevent and reduce the burden of depression. Further research on the efficacy of various interventions is needed. Additional studies are also needed on each of the themes described in this paper, for example: the biological factors related to postpartum depression [ 134 ], and further work is needed on depression outcomes, such as chronic, recurrent depression [ 452 ]. Previous literature has shown that chronic stress (associated with depression) is also linked to glucocorticoid receptor resistance, as well as problems with the regulation of the inflammatory response [ 484 ]. Further work is needed on this and the underpinning mechanisms between the determinants and outcomes. This review highlighted the myriad ways of measuring depression and its determinants [ 66 , 85 , 281 , 298 , 451 , 485 ]. Thus, the standardization of the measurements of the outcomes (ex. a gold standard for measuring depression) and determinants is essential; this can facilitate comparisons of findings across studies.

5.1. Strengths

This paper has important strengths. It brings together the wide literature on depression and helps to bridge disciplines in relation to one of the most common mental health problems. We identified, selected, and extracted data from studies, and provided concise summaries.

5.2. Limitations

The limitations of the review include missing potentially important studies; however, this is a weakness that cannot be avoided by literature reviews. Nevertheless, the aim of the review was not to identify each study that has been conducted on the risk and protective factors of depression (which a single review is unable to capture) but rather to gain insight into the breadth of literature on this topic, highlight key biological, psychological, and social determinants, and shed light on important themes, such as the lifecourse perspective and gene–environment interactions.

6. Conclusions

We have reviewed the determinants of depression and recognize that there are a multitude of risk and protective factors at the individual and wider ecologic levels. These determinants are interlinked and influence one another. We have attempted to describe the wide literature on this topic, and we have brought to light major factors that are of public mental health significance. This review may be used as an evidence base by those in public health, clinical practice, and research.

This paper discusses key areas in depression research; however, an exhaustive discussion of all the risk factors and determinants linked to depression and their mechanisms is not possible in one journal article—which, by its very nature, a single paper cannot do. We have brought to light overarching factors linked to depression and a workable conceptual framework that may guide clinical and public health practice; however, we encourage other researchers to continue to expand on this timely and relevant work—particularly as depression is a top priority on the policy agenda now.

Acknowledgments

Thank you to Isla Kuhn for the help with the Medline, Scopus, and PsycInfo database searches.

Supplementary Materials

The following are available online at https://www.mdpi.com/article/10.3390/brainsci11121633/s1 , Figure S1: Conceptual framework: Determinants of depression, Table S1: Data charting—A selection of determinants from the literature.

Appendix A.1. Search Strategy

Search: ((((((((((((((((“Gene-Environment Interaction”[Majr]) OR (“Genetics”[Mesh])) OR (“Genome-Wide Association Study”[Majr])) OR (“Microbiota”[Mesh] OR “Gastrointestinal Microbiome”[Mesh])) OR (“Neurogenic Inflammation”[Mesh])) OR (“genetic determinant”)) OR (“gut-brain-axis”)) OR (“Kynurenine”[Majr])) OR (“Cognition”[Mesh])) OR (“Neuronal Plasticity”[Majr])) OR (“Neurogenesis”[Mesh])) OR (“Genes”[Mesh])) OR (“Neurology”[Majr])) OR (“Social Determinants of Health”[Majr])) OR (“Glucocorticoids”[Mesh])) OR (“Tryptophan”[Mesh])) AND (“Depression”[Mesh] OR “Depressive Disorder”[Mesh]) Filters: from 2017—2020.

Ovid MEDLINE(R) and Epub Ahead of Print, In-Process, In-Data-Review & Other Non-Indexed Citations, Daily and Versions(R)

• exp *Depression/
• exp *Depressive Disorder/
• exp *”Social Determinants of Health”/
• exp *Tryptophan/
• exp *Glucocorticoids/
• exp *Neurology/
• exp *Genes/
• exp *Neurogenesis/
• exp *Neuronal Plasticity/
• exp *Kynurenine/
• exp *Genetics/
• exp *Neurogenic Inflammation/
• exp *Gastrointestinal Microbiome/
• exp *Genome-Wide Association Study/
• exp *Gene-Environment Interaction/
• exp *Depression/et [Etiology]
• exp *Depressive Disorder/et
• or/4-16   637368
• limit 22 to yr = “2017–Current”
• “cause* of depression”.mp.
• “cause* of depression”.ti.
• (cause adj3 (depression or depressive)).ti.
• (caus* adj3 (depression or depressive)).ti.

Appendix A.2. PsycInfo

(TITLE ( depression OR “ Depressive Disorder ”) AND TITLE (“ Social Determinants of Health ” OR tryptophan OR glucocorticoids OR neurology OR genes OR neurogenesis OR “ Neuronal Plasticity ” OR kynurenine OR genetics OR “ Neurogenic Inflammation ” OR “ Gastrointestinal Microbiome ” OR “ Genome-Wide Association Study ” OR “ Gene-Environment Interaction ” OR aetiology OR etiology )) OR TITLE ( cause* W/3 ( depression OR depressive )).

Author Contributions

O.R. was responsible for the design of the study and methodology undertaken. Despite P.T.’s involvement in YPMH, he had no role in the design of the study; P.T. was responsible for the conceptualization of the study. Validation was conducted by O.R. and J.F.M. Formal analysis (data charting) was undertaken by O.R. O.R. and P.T. were involved in the investigation, resource acquisition, and data presentation. The original draft preparation was undertaken by O.R. The writing was conducted by O.R., with review and editing by P.T. and J.F.M. Funding acquisition was undertaken by O.R. and P.T. All authors have read and agreed to the published version of the manuscript.

This research was funded by The William Templeton Foundation for Young People’s Mental Health, Cambridge Philosophical Society, and the Aviva Foundation.

Conflicts of Interest

The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, or in the decision to publish the results.

Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations.

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• Depression (major depressive disorder)
• What is depression? A Mayo Clinic expert explains.

Learn more about depression from Craig Sawchuk, Ph.D., L.P., clinical psychologist at Mayo Clinic.

Hi, I'm Dr. Craig Sawchuk, a clinical psychologist at Mayo Clinic. And I'm here to talk with you about depression. Whether you're looking for answers for yourself, a friend, or loved one, understanding the basics of depression can help you take the next step.

Depression is a mood disorder that causes feelings of sadness that won't go away. Unfortunately, there's a lot of stigma around depression. Depression isn't a weakness or a character flaw. It's not about being in a bad mood, and people who experience depression can't just snap out of it. Depression is a common, serious, and treatable condition. If you're experiencing depression, you're not alone. It honestly affects people of all ages and races and biological sexes, income levels and educational backgrounds. Approximately one in six people will experience a major depressive episode at some point in their lifetime, while up to 16 million adults each year suffer from clinical depression. There are many types of symptoms that make up depression. Emotionally, you may feel sad or down or irritable or even apathetic. Physically, the body really slows down. You feel tired. Your sleep is often disrupted. It's really hard to get yourself motivated. Your thinking also changes. It can just be hard to concentrate. Your thoughts tend to be much more negative. You can be really hard on yourself, feel hopeless and helpless about things. And even in some cases, have thoughts of not wanting to live. Behaviorally, you just want to pull back and withdraw from others, activities, and day-to-day responsibilities. These symptoms all work together to keep you trapped in a cycle of depression. Symptoms of depression are different for everyone. Some symptoms may be a sign of another disorder or medical condition. That's why it's important to get an accurate diagnosis.

While there's no single cause of depression, most experts believe there's a combination of biological, social, and psychological factors that contribute to depression risk. Biologically, we think about genetics or a family history of depression, health conditions such as diabetes, heart disease or thyroid disorders, and even hormonal changes that happen over the lifespan, such as pregnancy and menopause. Changes in brain chemistry, especially disruptions in neurotransmitters like serotonin, that play an important role in regulating many bodily functions, including mood, sleep, and appetite, are thought to play a particularly important role in depression. Socially stressful and traumatic life events, limited access to resources such as food, housing, and health care, and a lack of social support all contribute to depression risk. Psychologically, we think of how negative thoughts and problematic coping behaviors, such as avoidance and substance use, increase our vulnerability to depression.

The good news is that treatment helps. Effective treatments for depression exist and you do have options to see what works best for you. Lifestyle changes that improve sleep habits, exercise, and address underlying health conditions can be an important first step. Medications such as antidepressants can be helpful in alleviating depressive symptoms. Therapy, especially cognitive behavioral therapy, teaches skills to better manage negative thoughts and improve coping behaviors to help break you out of cycles of depression. Whatever the cause, remember that depression is not your fault and it can be treated.

To help diagnose depression, your health care provider may use a physical exam, lab tests, or a mental health evaluation. These results will help identify various treatment options that best fit your situation.

Help is available. You don't have to deal with depression by yourself. Take the next step and reach out. If you're hesitant to talk to a health care provider, talk to a friend or loved one about how to get help. Living with depression isn't easy and you're not alone in your struggles. Always remember that effective treatments and supports are available to help you start feeling better. Want to learn more about depression? Visit mayoclinic.org. Do take care.

Depression is a mood disorder that causes a persistent feeling of sadness and loss of interest. Also called major depressive disorder or clinical depression, it affects how you feel, think and behave and can lead to a variety of emotional and physical problems. You may have trouble doing normal day-to-day activities, and sometimes you may feel as if life isn't worth living.

More than just a bout of the blues, depression isn't a weakness and you can't simply "snap out" of it. Depression may require long-term treatment. But don't get discouraged. Most people with depression feel better with medication, psychotherapy or both.

Depression care at Mayo Clinic

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Although depression may occur only once during your life, people typically have multiple episodes. During these episodes, symptoms occur most of the day, nearly every day and may include:

• Feelings of sadness, tearfulness, emptiness or hopelessness
• Angry outbursts, irritability or frustration, even over small matters
• Loss of interest or pleasure in most or all normal activities, such as sex, hobbies or sports
• Sleep disturbances, including insomnia or sleeping too much
• Tiredness and lack of energy, so even small tasks take extra effort
• Reduced appetite and weight loss or increased cravings for food and weight gain
• Anxiety, agitation or restlessness
• Slowed thinking, speaking or body movements
• Feelings of worthlessness or guilt, fixating on past failures or self-blame
• Trouble thinking, concentrating, making decisions and remembering things
• Frequent or recurrent thoughts of death, suicidal thoughts, suicide attempts or suicide
• Unexplained physical problems, such as back pain or headaches

For many people with depression, symptoms usually are severe enough to cause noticeable problems in day-to-day activities, such as work, school, social activities or relationships with others. Some people may feel generally miserable or unhappy without really knowing why.

Depression symptoms in children and teens

Common signs and symptoms of depression in children and teenagers are similar to those of adults, but there can be some differences.

• In younger children, symptoms of depression may include sadness, irritability, clinginess, worry, aches and pains, refusing to go to school, or being underweight.
• In teens, symptoms may include sadness, irritability, feeling negative and worthless, anger, poor performance or poor attendance at school, feeling misunderstood and extremely sensitive, using recreational drugs or alcohol, eating or sleeping too much, self-harm, loss of interest in normal activities, and avoidance of social interaction.

Depression symptoms in older adults

Depression is not a normal part of growing older, and it should never be taken lightly. Unfortunately, depression often goes undiagnosed and untreated in older adults, and they may feel reluctant to seek help. Symptoms of depression may be different or less obvious in older adults, such as:

• Memory difficulties or personality changes
• Physical aches or pain
• Fatigue, loss of appetite, sleep problems or loss of interest in sex — not caused by a medical condition or medication
• Often wanting to stay at home, rather than going out to socialize or doing new things
• Suicidal thinking or feelings, especially in older men

When to see a doctor

If you feel depressed, make an appointment to see your doctor or mental health professional as soon as you can. If you're reluctant to seek treatment, talk to a friend or loved one, any health care professional, a faith leader, or someone else you trust.

When to get emergency help

If you think you may hurt yourself or attempt suicide, call 911 in the U.S. or your local emergency number immediately.

Also consider these options if you're having suicidal thoughts:

• Call your doctor or mental health professional.
• Contact a suicide hotline.
• In the U.S., call or text 988 to reach the 988 Suicide & Crisis Lifeline, available 24 hours a day, seven days a week. Or use the Lifeline Chat . Services are free and confidential.
• U.S. veterans or service members who are in crisis can call 988 and then press “1” for the Veterans Crisis Line . Or text 838255. Or chat online .
• The Suicide & Crisis Lifeline in the U.S. has a Spanish language phone line at 1-888-628-9454 (toll-free).
• Reach out to a close friend or loved one.
• Contact a minister, spiritual leader or someone else in your faith community.

If you have a loved one who is in danger of suicide or has made a suicide attempt, make sure someone stays with that person. Call 911 or your local emergency number immediately. Or, if you think you can do so safely, take the person to the nearest hospital emergency room.

More Information

Depression (major depressive disorder) care at Mayo Clinic

• Male depression: Understanding the issues
• Nervous breakdown: What does it mean?
• Pain and depression: Is there a link?

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It's not known exactly what causes depression. As with many mental disorders, a variety of factors may be involved, such as:

• Biological differences. People with depression appear to have physical changes in their brains. The significance of these changes is still uncertain, but may eventually help pinpoint causes.
• Brain chemistry. Neurotransmitters are naturally occurring brain chemicals that likely play a role in depression. Recent research indicates that changes in the function and effect of these neurotransmitters and how they interact with neurocircuits involved in maintaining mood stability may play a significant role in depression and its treatment.
• Hormones. Changes in the body's balance of hormones may be involved in causing or triggering depression. Hormone changes can result with pregnancy and during the weeks or months after delivery (postpartum) and from thyroid problems, menopause or a number of other conditions.
• Inherited traits. Depression is more common in people whose blood relatives also have this condition. Researchers are trying to find genes that may be involved in causing depression.
• Marijuana and depression
• Vitamin B-12 and depression

Risk factors

Depression often begins in the teens, 20s or 30s, but it can happen at any age. More women than men are diagnosed with depression, but this may be due in part because women are more likely to seek treatment.

Factors that seem to increase the risk of developing or triggering depression include:

• Certain personality traits, such as low self-esteem and being too dependent, self-critical or pessimistic
• Traumatic or stressful events, such as physical or sexual abuse, the death or loss of a loved one, a difficult relationship, or financial problems
• Blood relatives with a history of depression, bipolar disorder, alcoholism or suicide
• Being lesbian, gay, bisexual or transgender, or having variations in the development of genital organs that aren't clearly male or female (intersex) in an unsupportive situation
• History of other mental health disorders, such as anxiety disorder, eating disorders or post-traumatic stress disorder
• Abuse of alcohol or recreational drugs
• Serious or chronic illness, including cancer, stroke, chronic pain or heart disease
• Certain medications, such as some high blood pressure medications or sleeping pills (talk to your doctor before stopping any medication)

Complications

Depression is a serious disorder that can take a terrible toll on you and your family. Depression often gets worse if it isn't treated, resulting in emotional, behavioral and health problems that affect every area of your life.

Examples of complications associated with depression include:

• Excess weight or obesity, which can lead to heart disease and diabetes
• Pain or physical illness
• Alcohol or drug misuse
• Anxiety, panic disorder or social phobia
• Family conflicts, relationship difficulties, and work or school problems
• Social isolation
• Suicidal feelings, suicide attempts or suicide
• Self-mutilation, such as cutting
• Premature death from medical conditions
• Depression and anxiety: Can I have both?

There's no sure way to prevent depression. However, these strategies may help.

• Take steps to control stress, to increase your resilience and boost your self-esteem.
• Reach out to family and friends, especially in times of crisis, to help you weather rough spells.
• Get treatment at the earliest sign of a problem to help prevent depression from worsening.
• Consider getting long-term maintenance treatment to help prevent a relapse of symptoms.
• Brown AY. Allscripts EPSi. Mayo Clinic, Rochester, Minn. Nov. 17, 2016.
• Research report: Psychiatry and psychology, 2016-2017. Mayo Clinic. http://www.mayo.edu/research/departments-divisions/department-psychiatry-psychology/overview?_ga=1.199925222.939187614.1464371889. Accessed Jan. 23, 2017.
• Depressive disorders. In: Diagnostic and Statistical Manual of Mental Disorders DSM-5. 5th ed. Arlington, Va.: American Psychiatric Association; 2013. http://www.psychiatryonline.org. Accessed Jan. 23, 2017.
• Depression. National Institute of Mental Health. https://www.nimh.nih.gov/health/topics/depression/index.shtml. Accessed Jan. 23, 2017.
• Depression. National Alliance on Mental Illness. http://www.nami.org/Learn-More/Mental-Health-Conditions/Depression/Overview. Accessed Jan. 23, 2017.
• Depression: What you need to know. National Institute of Mental Health. https://www.nimh.nih.gov/health/publications/depression-what-you-need-to-know/index.shtml. Accessed Jan. 23, 2017.
• What is depression? American Psychiatric Association. https://www.psychiatry.org/patients-families/depression/what-is-depression. Accessed Jan. 23, 2017.
• Depression. NIH Senior Health. https://nihseniorhealth.gov/depression/aboutdepression/01.html. Accessed Jan. 23, 2017.
• Children’s mental health: Anxiety and depression. Centers for Disease Control and Prevention. https://www.cdc.gov/childrensmentalhealth/depression.html#depression. Accessed. Jan. 23, 2017.
• Depression and complementary health approaches: What the science says. National Center for Complementary and Integrative Health. https://nccih.nih.gov/health/providers/digest/depression-science. Accessed Jan. 23, 2017.
• Depression. Natural Medicines. https://naturalmedicines.therapeuticresearch.com/databases/medical-conditions/d/depression.aspx. Accessed Jan. 23, 2017.
• Natural medicines in the clinical management of depression. Natural Medicines. http://naturaldatabase.therapeuticresearch.com/ce/CECourse.aspx?cs=naturalstandard&s=ND&pm=5&pc=15-111. Accessed Jan. 23, 2017.
• The road to resilience. American Psychological Association. http://www.apa.org/helpcenter/road-resilience.aspx. Accessed Jan. 23, 2017.
• Simon G, et al. Unipolar depression in adults: Choosing initial treatment. http://www.uptodate.com/home. Accessed Jan. 23, 2017.
• Stewart D, et al. Risks of antidepressants during pregnancy: Selective serotonin reuptake inhibitors (SSRIs). http://www.uptodate.com/home. Accessed Jan. 23, 2017.
• Kimmel MC, et al. Safety of infant exposure to antidepressants and benzodiazepines through breastfeeding. http://www.uptodate.com/home. Accessed Jan. 23, 2017.
• Bipolar and related disorders. In: Diagnostic and Statistical Manual of Mental Disorders DSM-5. 5th ed. Arlington, Va.: American Psychiatric Association; 2013. http://www.psychiatryonline.org. Accessed Jan. 23, 2017.
• Hirsch M, et al. Monoamine oxidase inhibitors (MAOIs) for treating depressed adults. http://www.uptodate.com/home. Accessed Jan. 24, 2017.
• Hall-Flavin DK (expert opinion). Mayo Clinic, Rochester, Minn. Jan. 31, 2017.
• Krieger CA (expert opinion). Mayo Clinic, Rochester, Minn. Feb. 2, 2017.
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Home — Essay Samples — Nursing & Health — Psychiatry & Mental Health — Depression

Essays About Depression

Depression essay topic examples.

Explore topics like the impact of stigma on depression, compare it across age groups or in literature and media, describe the emotional journey of depression, discuss how education can help, and share personal stories related to it. These essay ideas offer a broad perspective on depression, making it easier to understand and engage with this important subject.

Argumentative Essays

Argumentative essays require you to analyze and present arguments related to depression. Here are some topic examples:

• 1. Argue whether mental health stigma contributes to the prevalence of depression in society.
• 2. Analyze the effectiveness of different treatment approaches for depression, such as therapy versus medication.

Example Introduction Paragraph for an Argumentative Essay: Depression is a pervasive mental health issue that affects millions of individuals worldwide. This essay delves into the complex relationship between mental health stigma and the prevalence of depression in society, examining the barriers to seeking help and the consequences of this stigma.

Example Conclusion Paragraph for an Argumentative Essay: In conclusion, the analysis of mental health stigma's impact on depression underscores the urgent need to challenge and dismantle the stereotypes surrounding mental health. As we reflect on the far-reaching consequences of stigma, we are called to create a society that fosters empathy, understanding, and open dialogue about mental health.

Compare and Contrast Essays

Compare and contrast essays enable you to examine similarities and differences within the context of depression. Consider these topics:

• 1. Compare and contrast the symptoms and risk factors of depression in adolescents and adults.
• 2. Analyze the similarities and differences between the portrayal of depression in literature and its depiction in modern media.

Example Introduction Paragraph for a Compare and Contrast Essay: Depression manifests differently in various age groups and mediums of expression. This essay embarks on a journey to compare and contrast the symptoms and risk factors of depression in adolescents and adults, shedding light on the unique challenges faced by each demographic.

Example Conclusion Paragraph for a Compare and Contrast Essay: In conclusion, the comparison and contrast of depression in adolescents and adults highlight the importance of tailored interventions and support systems. As we contemplate the distinct challenges faced by these age groups, we are reminded of the need for age-appropriate mental health resources and strategies.

Descriptive Essays

Descriptive essays allow you to vividly depict aspects of depression, whether it's the experience of the individual or the societal impact. Here are some topic ideas:

• 1. Describe the emotional rollercoaster of living with depression, highlighting the highs and lows of the experience.
• 2. Paint a detailed portrait of the consequences of untreated depression on an individual's personal and professional life.

Example Introduction Paragraph for a Descriptive Essay: Depression is a complex emotional journey that defies easy characterization. This essay embarks on a descriptive exploration of the emotional rollercoaster that individuals with depression experience, delving into the profound impact it has on their daily lives.

Example Conclusion Paragraph for a Descriptive Essay: In conclusion, the descriptive portrayal of the emotional rollercoaster of depression underscores the need for empathy and support for those grappling with this condition. Through this exploration, we are reminded of the resilience of the human spirit and the importance of compassionate understanding.

Persuasive Essays

Persuasive essays involve arguing a point of view related to depression. Consider these persuasive topics:

• 1. Persuade your readers that incorporating mental health education into the school curriculum can reduce the prevalence of depression among students.
• 2. Argue for or against the idea that employers should prioritize the mental well-being of their employees to combat workplace depression.

Example Introduction Paragraph for a Persuasive Essay: The prevalence of depression underscores the urgent need for proactive measures to address mental health. This persuasive essay asserts that integrating mental health education into the school curriculum can significantly reduce the prevalence of depression among students, offering them the tools to navigate emotional challenges.

Example Conclusion Paragraph for a Persuasive Essay: In conclusion, the persuasive argument for mental health education in schools highlights the potential for early intervention and prevention. As we consider the well-being of future generations, we are called to prioritize mental health education as an essential component of a holistic education system.

Narrative Essays

Narrative essays offer you the opportunity to tell a story or share personal experiences related to depression. Explore these narrative essay topics:

• 1. Narrate a personal experience of overcoming depression or supporting a loved one through their journey.
• 2. Imagine yourself in a fictional scenario where you advocate for mental health awareness and destigmatization on a global scale.

Example Introduction Paragraph for a Narrative Essay: Personal experiences with depression can be transformative and enlightening. This narrative essay delves into a personal journey of overcoming depression, highlighting the challenges faced, the support received, and the lessons learned along the way.

Example Conclusion Paragraph for a Narrative Essay: In conclusion, the narrative of my personal journey through depression reminds us of the resilience of the human spirit and the power of compassion and understanding. As we reflect on our own experiences, we are encouraged to share our stories and contribute to the ongoing conversation about mental health.

A Narrative About Depression: Navigating The Abyss

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Depression: Understanding The Silent Epidemic

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Overview of Biological Predispositions and Risk Factors Associated with Depression

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The Issue of Depression: Mental Battle

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Depression, known as major depressive disorder or clinical depression, is a psychological condition characterized by enduring feelings of sadness and a significant loss of interest in activities. It is a mood disorder that affects a person's emotional state, thoughts, behaviors, and overall well-being.

Its origin can be traced back to ancient civilizations, where melancholia was described as a state of sadness and melancholy. In the 19th century, depression began to be studied more systematically, and terms such as "melancholic depression" and "nervous breakdown" emerged. The understanding and classification of depression have evolved over time. In the early 20th century, Sigmund Freud and other psychoanalysts explored the role of unconscious conflicts in the development of depression. In the mid-20th century, the Diagnostic and Statistical Manual of Mental Disorders (DSM) was established, providing a standardized criteria for diagnosing depressive disorders.

Biological Factors: Genetic predisposition plays a role in depression, as individuals with a family history of the disorder are at a higher risk. Psychological Factors: These may include a history of trauma or abuse, low self-esteem, pessimistic thinking patterns, and a tendency to ruminate on negative thoughts. Environmental Factors: Adverse life events, such as the loss of a loved one, financial difficulties, relationship problems, or chronic stress, can increase the risk of depression. Additionally, living in a socioeconomically disadvantaged area or lacking access to social support can be contributing factors. Health-related Factors: Chronic illnesses, such as cardiovascular disease, diabetes, and chronic pain, are associated with a higher risk of depression. Substance abuse and certain medications can also increase vulnerability to depression. Developmental Factors: Certain life stages, including adolescence and the postpartum period, bring about unique challenges and changes that can contribute to the development of depression.

Depression is characterized by a range of symptoms that affect an individual's emotional, cognitive, and physical well-being. These characteristics can vary in intensity and duration but generally include persistent feelings of sadness, hopelessness, and a loss of interest or pleasure in activities once enjoyed. One prominent characteristic of depression is a noticeable change in mood, which can manifest as a constant feeling of sadness or emptiness. Individuals may also experience a significant decrease or increase in appetite, leading to weight loss or gain. Sleep disturbances, such as insomnia or excessive sleepiness, are common as well. Depression can impact cognitive functioning, causing difficulties in concentration, decision-making, and memory recall. Negative thoughts, self-criticism, and feelings of guilt or worthlessness are also common cognitive symptoms. Furthermore, physical symptoms may arise, including fatigue, low energy levels, and a general lack of motivation. Physical aches and pains, without an apparent medical cause, may also be present.

The treatment of depression typically involves a comprehensive approach that addresses both the physical and psychological aspects of the condition. It is important to note that the most effective treatment may vary for each individual, and a personalized approach is often necessary. One common form of treatment is psychotherapy, which involves talking to a mental health professional to explore and address the underlying causes and triggers of depression. Cognitive-behavioral therapy (CBT) is a widely used approach that helps individuals identify and change negative thought patterns and behaviors associated with depression. In some cases, medication may be prescribed to help manage depressive symptoms. Antidepressant medications work by balancing neurotransmitters in the brain that are associated with mood regulation. It is crucial to work closely with a healthcare provider to find the right medication and dosage that suits an individual's needs. Additionally, lifestyle changes can play a significant role in managing depression. Regular exercise, a balanced diet, sufficient sleep, and stress reduction techniques can all contribute to improving mood and overall well-being. In severe cases of depression, when other treatments have not been effective, electroconvulsive therapy (ECT) may be considered. ECT involves administering controlled electric currents to the brain to induce a brief seizure, which can have a positive impact on depressive symptoms.

1. According to the World Health Organization (WHO), over 264 million people worldwide suffer from depression, making it one of the leading causes of disability globally. 2. Depression can affect people of all ages, including children and adolescents. In fact, the prevalence of depression in young people is increasing, with an estimated 3.3 million adolescents in the United States experiencing at least one major depressive episode in a year. 3. Research has shown that there is a strong link between depression and other physical health conditions. People with depression are more likely to experience chronic pain, cardiovascular diseases, and autoimmune disorders, among other medical conditions.

The topic of depression holds immense significance and should be explored through essays due to its widespread impact on individuals and society as a whole. Understanding and raising awareness about depression is crucial for several reasons. Firstly, depression affects a significant portion of the global population, making it a pressing public health issue. Exploring its causes, symptoms, and treatment options can contribute to better mental health outcomes and improved quality of life for individuals affected by this condition. Additionally, writing an essay about depression can help combat the stigma surrounding mental health. By promoting open discussions and providing accurate information, essays can challenge misconceptions and foster empathy and support for those experiencing depression. Furthermore, studying depression allows for a deeper examination of its complex nature, including its psychological, biological, and sociocultural factors. Lastly, essays on depression can highlight the importance of early detection and intervention, promoting timely help-seeking behaviors and reducing the burden of the condition on individuals and healthcare systems. By shedding light on this critical topic, essays have the potential to educate, inspire action, and contribute to the overall well-being of individuals and society.

1. American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). American Psychiatric Publishing. 2. World Health Organization. (2017). Depression and other common mental disorders: Global health estimates. World Health Organization. 3. Kessler, R. C., Bromet, E. J., & Quinlan, J. (2013). The burden of mental disorders: Global perspectives from the WHO World Mental Health Surveys. Cambridge University Press. 4. Beck, A. T., Rush, A. J., Shaw, B. F., & Emery, G. (1979). Cognitive therapy of depression. Guilford Press. 5. Nierenberg, A. A., & DeCecco, L. M. (2001). Definitions and diagnosis of depression. The Journal of Clinical Psychiatry, 62(Suppl 22), 5-9. 6. Greenberg, P. E., Fournier, A. A., Sisitsky, T., Pike, C. T., & Kessler, R. C. (2015). The economic burden of adults with major depressive disorder in the United States (2005 and 2010). Journal of Clinical Psychiatry, 76(2), 155-162. 7. Cuijpers, P., Berking, M., Andersson, G., Quigley, L., Kleiboer, A., & Dobson, K. S. (2013). A meta-analysis of cognitive-behavioural therapy for adult depression, alone and in comparison with other treatments. Canadian Journal of Psychiatry, 58(7), 376-385. 8. Hirschfeld, R. M. A. (2014). The comorbidity of major depression and anxiety disorders: Recognition and management in primary care. Primary Care Companion for CNS Disorders, 16(2), PCC.13r01611. 9. Rush, A. J., Trivedi, M. H., Wisniewski, S. R., Nierenberg, A. A., Stewart, J. W., Warden, D., ... & Fava, M. (2006). Acute and longer-term outcomes in depressed outpatients requiring one or several treatment steps: A STAR*D report. American Journal of Psychiatry, 163(11), 1905-1917. 10. Kendler, K. S., Kessler, R. C., Walters, E. E., MacLean, C., Neale, M. C., Heath, A. C., & Eaves, L. J. (1995). Stressful life events, genetic liability, and onset of an episode of major depression in women. American Journal of Psychiatry, 152(6), 833-842.

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Conclusion depression.

Depression is one of the most common conditions in primary care, but is often unrecognized, undiagnosed, and untreated. Depression has a high rate of morbidity and mortality when left untreated. Most patients suffering from depression do not complain of feeling depressed, but rather anhedonia or vague unexplained symptoms. All physicians should remain alert to effectively screen for depression in their patients. There are several screening tools for depression that are effective and feasible in primary care settings. An appropriate history, physical, initial basic lab evaluation, and mental status examination can assist the physician in diagnosing the patient with the correct depressive spectrum disorder (including bipolar disorder). Primary care physicians should carefully assess depressed patients for suicide. Depression in the elderly is not part of the normal aging process. Patients who are elderly when they have their first episode of depression have a relatively higher likelihood of developing chronic and recurring depression. The prognosis for recovery is equal in young and old patients, although remission may take longer to achieve in older patients. Elderly patients usually start antidepressants at lower doses than their younger counterparts.

Most primary care physician can successfully treat uncomplicated mild or moderate forms of major depression in their settings with careful psychiatric management (e.g., close monitoring of symptoms, side effects, etc.); maintaining a therapeutic alliance with their patient; pharmacotherapy (acute, continuation, and maintenance phases); and / or referral for psychotherapy. The following situations require referral to psychiatrist: suicide risk, bipolar disorder or a manic episode, psychotic symptoms, severe decrease in level of functioning, recurrent depression and chronic depression, depression that is refractory to treatment, cardiac disease that requires tricyclic antidepressants treatment, need for electroconvulsive therapy (ECT), lack of available support system, and any diagnostic or treatment questions.

Antidepressant medications’ effectiveness is generally comparable across classes and within classes of medications.  The medications differ in side effect profiles, drug-drug interactions, and cost.  The history of a positive response to a particular drug for an individual or a family member, as well as patient preferences, should also be taken into account.  Most psychiatrists agree that an SSRI should be the first line choice.  The dual action reuptake inhibitors venlafaxine and bupropion are generally regarded as second line agents.  Tricyclics and other mixed or dual action inhibitors are third line, and MAOI’s (monoamine oxidase inhibitors) are usually medications of last resort for patients who have not responded to other medications, due to their low tolerability, dietary restrictions, and drug-drug interactions.  Most primary care physicians would prefer that a psychiatrist manage patients requiring MAOI’s.

Psychotherapy may be a first line therapy choice for mild depression particularly when associated with psychosocial stress, interpersonal problems, or with concurrent developmental or personality disorders. Psychotherapy in mild to moderate depression is most effective in the acute phase, and in preventing relapse during continuation phase treatment. Psychotherapy is not appropriate alone for severe depression, psychosis, and bipolar disorders. For more severe depression, psychotherapy may be appropriate in combination with the use of medications. The most effective forms of psychotherapy are those with structured and brief approaches such as cognitive behavioral therapy, interpersonal therapy, and certain problem solving therapies. Regardless of the psychotherapy initiated, “psychiatric management” must be integrated at the same time.

Patients, who live with depression, and their family and friends, have enormous challenges to overcome. Primary care physicians can provide compassionate care, important education, psychiatric monitoring, social support, reassurance, and advocacy for these patients and their loved ones.

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7 Depression Research Paper Topic Ideas

Nancy Schimelpfening, MS is the administrator for the non-profit depression support group Depression Sanctuary. Nancy has a lifetime of experience with depression, experiencing firsthand how devastating this illness can be.

Cara Lustik is a fact-checker and copywriter.

In psychology classes, it's common for students to write a depression research paper. Researching depression may be beneficial if you have a personal interest in this topic and want to learn more, or if you're simply passionate about this mental health issue. However, since depression is a very complex subject, it offers many possible topics to focus on, which may leave you wondering where to begin.

If this is how you feel, here are a few research titles about depression to help inspire your topic choice. You can use these suggestions as actual research titles about depression, or you can use them to lead you to other more in-depth topics that you can look into further for your depression research paper.

What Is Depression?

Everyone experiences times when they feel a little bit blue or sad. This is a normal part of being human. Depression, however, is a medical condition that is quite different from everyday moodiness.

Your depression research paper may explore the basics, or it might delve deeper into the  definition of clinical depression  or the  difference between clinical depression and sadness .

What Research Says About the Psychology of Depression

Studies suggest that there are biological, psychological, and social aspects to depression, giving you many different areas to consider for your research title about depression.

Types of Depression

There are several different types of depression  that are dependent on how an individual's depression symptoms manifest themselves. Depression symptoms may vary in severity or in what is causing them. For instance, major depressive disorder (MDD) may have no identifiable cause, while postpartum depression is typically linked to pregnancy and childbirth.

Depressive symptoms may also be part of an illness called bipolar disorder. This includes fluctuations between depressive episodes and a state of extreme elation called mania. Bipolar disorder is a topic that offers many research opportunities, from its definition and its causes to associated risks, symptoms, and treatment.

Causes of Depression

The possible causes of depression are many and not yet well understood. However, it most likely results from an interplay of genetic vulnerability  and environmental factors. Your depression research paper could explore one or more of these causes and reference the latest research on the topic.

For instance, how does an imbalance in brain chemistry or poor nutrition relate to depression? Is there a relationship between the stressful, busier lives of today's society and the rise of depression? How can grief or a major medical condition lead to overwhelming sadness and depression?

Who Is at Risk for Depression?

This is a good research question about depression as certain risk factors may make a person more prone to developing this mental health condition, such as a family history of depression, adverse childhood experiences, stress , illness, and gender . This is not a complete list of all risk factors, however, it's a good place to start.

The growing rate of depression in children, teenagers, and young adults is an interesting subtopic you can focus on as well. Whether you dive into the reasons behind the increase in rates of depression or discuss the treatment options that are safe for young people, there is a lot of research available in this area and many unanswered questions to consider.

Depression Signs and Symptoms

The signs of depression are those outward manifestations of the illness that a doctor can observe when they examine a patient. For example, a lack of emotional responsiveness is a visible sign. On the other hand, symptoms are subjective things about the illness that only the patient can observe, such as feelings of guilt or sadness.

An illness such as depression is often invisible to the outside observer. That is why it is very important for patients to make an accurate accounting of all of their symptoms so their doctor can diagnose them properly. In your depression research paper, you may explore these "invisible" symptoms of depression in adults or explore how depression symptoms can be different in children .

How Is Depression Diagnosed?

This is another good depression research topic because, in some ways, the diagnosis of depression is more of an art than a science. Doctors must generally rely upon the patient's set of symptoms and what they can observe about them during their examination to make a diagnosis. 

While there are certain  laboratory tests that can be performed to rule out other medical illnesses as a cause of depression, there is not yet a definitive test for depression itself.

If you'd like to pursue this topic, you may want to start with the Diagnostic and Statistical Manual of Mental Disorders (DSM). The fifth edition, known as DSM-5, offers a very detailed explanation that guides doctors to a diagnosis. You can also compare the current model of diagnosing depression to historical methods of diagnosis—how have these updates improved the way depression is treated?

Treatment Options for Depression

The first choice for depression treatment is generally an antidepressant medication. Selective serotonin reuptake inhibitors (SSRIs) are the most popular choice because they can be quite effective and tend to have fewer side effects than other types of antidepressants.

Psychotherapy, or talk therapy, is another effective and common choice. It is especially efficacious when combined with antidepressant therapy. Certain other treatments, such as electroconvulsive therapy (ECT) or vagus nerve stimulation (VNS), are most commonly used for patients who do not respond to more common forms of treatment.

Focusing on one of these treatments is an option for your depression research paper. Comparing and contrasting several different types of treatment can also make a good research title about depression.

A Word From Verywell

The topic of depression really can take you down many different roads. When making your final decision on which to pursue in your depression research paper, it's often helpful to start by listing a few areas that pique your interest.

From there, consider doing a little preliminary research. You may come across something that grabs your attention like a new study, a controversial topic you didn't know about, or something that hits a personal note. This will help you narrow your focus, giving you your final research title about depression.

Remes O, Mendes JF, Templeton P. Biological, psychological, and social determinants of depression: A review of recent literature . Brain Sci . 2021;11(12):1633. doi:10.3390/brainsci11121633

National Institute of Mental Health. Depression .

American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition . American Psychiatric Association.

National Institute of Mental Health. Mental health medications .

Ferri, F. F. (2019). Ferri's Clinical Advisor 2020 E-Book: 5 Books in 1 . Netherlands: Elsevier Health Sciences.

By Nancy Schimelpfening Nancy Schimelpfening, MS is the administrator for the non-profit depression support group Depression Sanctuary. Nancy has a lifetime of experience with depression, experiencing firsthand how devastating this illness can be.  

The Biology of Depression

Reviewed by Psychology Today Staff

Depression makes deep inroads on biology to bring about the many symptoms of depression, from sleep disruption and an inability to experience pleasure to lack of motivation and feelings of guilt. Many factors influence how a person reacts to stressful events, whether an individual gets depressed, and how the disorder manifests. These include genetic inheritance, life experience, temperament, personality traits, social supports, and beliefs.

Still, exactly how biological changes give rise to depressive symptoms is not well understood. Because of its complexity—and because the disorder contributes so much to human suffering—the biology of depression is a major subject of ongoing research.

On This Page

• What is the role of genetics in depression?
• Can genes for depression be modified?
• What happens in the brain with depression?
• How does lack of sleep alter brain function?
• How does the brain regulate mood?
• What role does serotonin play in depression?
• Does dopamine play a role in depression?
• How does nerve cell communication go awry in depression?
• How does stress affect the brain
• How does childhood stress affect adult brain function?
• What areas of the brain play a role in depression?
• What does brain imaging look at in depression?
• How does depresson itself change the brain?
• Can talk therapy change the way the brain functions?
• Why is nerve cell growth, or neuroplasticity, important?
• What are ways of stimulating neuroplasticity?

The inheritance of risk for depression is considered, at best, polygenetic—that is, a number of unknown genes each contributes a tiny risk under certain environmental conditions. None of them makes depression inevitable. The baseline risk of depression in the population is 10 percent; having a first-degree relative (parent or sibling) with depression doubles or triples an individual’s risk, to 20 to 30 percent over the course of a lifetime.

There are many non-genetic factors that contribute to risk of onset of major depression, and there are some inherited factors as well. To make matters a bit more complex, some non-genetic factors, including certain kinds of adverse childhood experience—such as repeated child abuse or neglect—can have a lasting impact on the function of genes (such as those that activate the stress system) to increase the risk of depression later on.

Variation of one gene associated with the serotonin system ( the serotonin transporter gene ) has been most linked to depression susceptibility—it is thought to moderate the impact of stressful life events—but the evidence has been disappointing. Life experience and lifestyle factors are believed to play more significant roles in depression risk.

Scientists know that the expression and function of many genes can be altered without doing the near-impossible—making any changes to the gene structure itself. Such changes are known as epigenetic modifications. Some life experiences can create vulnerability to depression through epigenetic changes. For example, in rat pups, lack of maternal care can permanently reset the sensitivity of receptors to stress hormones. If their mothers fail to lick and groom them, they grow up to display an exaggerated response to stress hormones and develop depression-like behavior in response to stress.

But there are also ways to strategically induce epigenetic changes to reverse symptoms of depression. For example, the nutritional supplement SAM-e , a synthetic version of a compound found in the body, contains a substance that chemically augments the activation and deactivation of genes. Some studies show it is effective against symptoms of depression.

Overexcitability of the stress response system, shifts in activity of various neurochemicals in the brain, diminished efficiency of nerve circuitry and nerve generation, disturbances in energy use nerve cells, the intrusion of inflammatory substances in the brain, upsets in the brain’s 24-hour (circadian) clock—all play a role in depression onset or progression and influence the kind and severity of symptoms.

Two major areas of the brain—the hippocampus (seat of memory) and the cortex (the thinking part of the brain)— undergo shrinkage . Both the size of nerve cells and the number of their connections with other neurons are reduced. At the same time, depressive behavior is linked to overactivation of the hypothalamus, which coordinates the stress response, and overactivity of the amygdala, which signals threat and generates negative emotions.

Reduced activity in the prefrontal cortex, which interprets and regulates emotional signals coming from the amygdala, accounts for the difficulties in decision-making and the cognitive fog that depressed people experience.

The human brain may be unique in its ability to generate new nerve connections, called neuroplasticity ; this is what underlies all adaptation and learning. In depression, neuroplasticity is impaired, especially in the hippocampus. In addition, reward centers of the brain shrink and fail to activate in response to stimulation. There are changes in sensitivity to the hormones that regulate feeding behavior, resulting in changes in appetite.

Disruption of the sleep-wake cycle is one of the hallmarks of depression and is a major source the mood disturbance in major depression. Lack of sleep upsets the body’s circadian clock that orchestrates the natural daily rhythm of most biological functions, including patterns of secretion, release, and activity of many neurochemicals in the brain.

Sleep deprivation is thought to impede the transmission of neural signals. One result is that sleep deprivation makes people emotionally reactive , increasing activity in the amygdala and decreasing it in the emotion regulation center of the prefrontal cortex. Sleep deprivation impairs the brain’s ability to control negative thoughts.

Mistimed light input resulting from sleep disturbance also disrupts the dopamine-sensitive nucleus accumbens. Studies show that people with mood disorders benefit from maintaining a strict sleep/wake routine, rising in the morning and going to sleep at night at the same time every day.

Emotions are fleeting responses to stimuli; mood is a more sustained state of emotion. Like emotions, mood probably originates with activity of the amygdala, where emotions are coded. But it also involves the prefrontal cortex, which, through bundles of two-way circuitry with the amygdala, helps regulate emotional response and influences the general state of reactivity of the amygdala.

Under normal conditions, moods are relatively stable. But the persistence of negative mood in major depression suggests something is amiss in the nerve pathways between the amygdala and cortex.

Another important influence on mood is the circadian rhythm that governs the timing of much physiological activity, most prominently the sleep-wake cycle . Disturbances in biological rhythms are known to disrupt mood, and studies of depressed patients find that they exhibit abnormal patterns of many body functions, from temperature regulation to hormone secretion.

The neurotransmitter serotonin is one of many signaling chemicals in the brain associated with depressive symptoms. Under normal conditions, serotonin inhibits pain, influences the processing of various emotions, and mediates many mental capacities important in social life .

But like the other neurotransmitters involved in depression, its production and activity are affected by the hormones the body secretes in response to threat or stress, such as cortisol. One result is a functional lack of serotonin, which, among other things, disrupts the circuitry that regulates moral emotions. Growing evidence suggest that is why those who are depressed are haunted by excessive self-blame and a sense of guilt.

The neurotransmitter dopamine, which mediates motivation and desire, is one of several brain signaling chemicals that are implicated in depression . It is associated with two of the most prominent features of depression—anhedonia, or the inability to experience pleasure, and appetite alterations.

Many neurons that use dopamine to relay signals are sensitive to the effects of stress, which can alter their excitability and activity. Studies have also shown that reward-generating areas of the brain—such as the nucleus accumbens, where dopamine signals originate—may be underactive in depression.

Where once researchers and clinicians focused on the role of neurotransmitters such as serotonin in depression, they now know that neurotransmitters are only one part of a much larger story of how nerve cells function in circuits to relay messages from one part of the brain to another. In fact, many experts see depression as a nerve circuit disorder, marked by a power failure in the brain’s wiring, affecting communication between one area of the brain and another.

The nerve cell connections between the amygdala and the prefrontal cortex (PFC) are sometimes called the “depression circuit;” depression results when emotion-laden signals from the amygdala overpower the ability of the PFC to regulate the signals. The prolonged or excessive release of stress hormones can lead to a failure of activation of key nodes in neural networks or impair the strength of signals between them, especially when processing emotion-related or reward stimuli.

It’s important that depression is now seen as a nerve circuit disorder, because that influences the search for effective treatments.

Stress can be beneficial to the brain, depending on how intense and long-lasting the stressor is. In brief bursts, stress fosters alertness, learning, and adaptation. Severe or prolonged stress, however, can disrupt many aspects of brain function and lead to depression .

Such stress dysregulates the normal stress response through the overproduction of cortisol. Cortisol is especially toxic to cells in the brain’s hippocampus, and one consequence of uncontrolled stress is shrinkage of the hippocampus, manifest in the impaired memory and learning that are characteristic of depression.

Cortisol also turns off the generation of new nerve cells in some areas of the brain, affecting the circuitry of the brain. In addition, prolonged cortisol exposure affects production of the insulating myelin sheath surrounding nerve cells, diminishing the overall efficiency or nerve signaling.

Severe or sustained early life adversity shifts the course of brain development and can lastingly impair emotion regulation and cognitive development. Excessive or prolonged activation of the stress response in childhood, studies show, can sensitize the stress response system so that it overresponds to minimal levels of threat, making people feel easily overwhelmed by life’s normal difficulties.

Severe or prolonged childhood adversity can affect the function of genes important for the wiring of the brain, so that emotional control is difficult—overproducing neural connections in regions such as the amygdala that signal threat and other negative emotions while underendowing neural connectivity in brain areas responsible for behavioral control, reasoning, and planning.

Nevertheless, adult brains retain the capacity for neuroplasticity. Although it takes effort, and often the guidance of psychotherapy, people can learn to overcome many of the ill effects of early adversity.

Many areas of the brain contribute to the symptoms of depression, such as the hippocampus, which is the seat of memory and learning, and the superchiasmatic nucleus, which is the “body clock” that paces all physiologic activity, notably the sleep-wake cycle. But brain imaging studies suggest that there is a primary “depression circuit,” consisting of the amygdala, which flags emotion-related stimuli; the prefrontal cortex, which analyzes and interprets experience, modulates emotional reactivity, and controls attention; and the two-way network of nerve fibers that connect them.

In this model of depression, the amygdala becomes hyperactive, sending out a constant flood of emotions, and the PFC becomes hypoactive, unable to regulate the stream of emotional input. Through feedback loops, the failure of the PFC further dysregulates the amygdala and leaves unchecked its inherent bias toward negative emotions.

Some types of brain imaging, such as CT scans and magnetic resonance imaging (MRI), take static pictures of the brain to determine whether any specific structures are larger or smaller than normal in depressed patients. Positron emission tomography (PET) scans and functional magnetic resonance imaging (fMRI) look at the brain in action, to see whether and where there are problems in the way the brain processes specific types of information .

In fMRI studies, normal controls and depressed patents are typically given some task to perform in the scanner. For example, subjects may be asked to look at a series of pictures, some of them with emotionally disturbing content, to see how the brain handles negative stimuli. The brain scanners measure blood flow or metabolic activity, based on the concentration of agents earlier injected into the bloodstream. Comparison of hot spots and dead spots of activity between controls and depressed patients highlight areas of the brain that malfunction in response to challenging stimuli.

The longer an episode of depression lasts, the greater the likelihood of a recurrence of depression. That is because depression changes the brain in ways that are only now yielding to understanding. If left untreated, depression can become a progressive disease leading to neurodegeneration.

The sustained stress that triggers depression releases a cascade of hormones linked to shrinkage of the hippocampus, a part of the brain essential for learning and storing and retrieving memories. Prominent changes to other brain areas, including the amygdala, create a sustained tendency to generate negatively coded emotions.

Untreated depression also changes the activity of substances that help regulate the mitochondria, the energy factories of all cells, especially critical to function of the brain because it is such a metabolically active organ. Depression also causes changes in the network of brain areas involved in processing physical pain , and the degree of hyperactivity in such areas as seen on brain scans correlates with the severity of depression that patients experience.

Recent studies show that like other neurodegenerative conditions, longstanding depression increases levels of inflammatory substances in the brain that further impair its function , affecting many brain regions and circuits of connectivity.

The most studied form of psychotherapy—cognitive behavioral therapy (CBT)—has been shown to produces long-lasting changes in emotion, cognition, behavior, and somatic symptoms of patients with depression and other mental health conditions. Using functional magnetic resonance imaging (fMRI), researchers find that CBT alters patterns of connections between brain regions, notably in circuits related to the processing of emotions.

Images show decreased reactivity of the brain’s amygdala, which processes emotion, and increased activity in the prefrontal cortex, the thinking and executive control center of the brain, indicating more control over emotional reactions and memories, and greater flexibility in finding solutions to problems . The changes in cognition power help reduce negative emotionality by increasing people’s ability to calmly manage experiences and thoughts that stir emotions.

Throughout life, the growth of new nerve cell connections, or neuroplasticity, is the major way brains adapt to new or challenging circumstances. It’s called learning, and it’s the brain’s major means of problem-solving. Depression is characterized by a loss of plasticity—negative neuroplasticity; patients feel imprisoned in their own repetitive negative thoughts.

It’s long been known that prolonged or excessive outpouring of stress hormones curbs the growth of nerve cells, particularly in the hippocampus, seat of memory and learning.Such changes are reflected in a smaller size hippocampus and impaired memory in depressed patients.

Changes also occur in the prefrontal cortex, undermining regulation of emotional experience, limiting the ability to set goals, and much more. All effective treatments of depression restore the capacity for mental and behavioral change and are known to stimulate the growth of new nerve cells —they enable the brain to rewire itself.

All known therapies for depression stimulate the growth of new nerve cell connections. But the growth of new nerve cell connections is not dependent on antidepressant drugs. Researchers find that there are many ways to bring about neuroplasticity.

One of the most effective ways is aerobic exercise. And it doesn’t have to be intense to have an effect. In fact, all physical activity is linked to the generation of neurotrophic factors, chemicals that stimulate the growth and recovery of brain cells.

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Major Depressive Disorder (MDD) Research Paper

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Introduction

Literature studies, management of mdd.

MDD is a cluster of syndromes that comprises a mental disorder, which is marked by declined moods, followed by a decline in self-esteem and not being interested in pleasurable tasks. Its features involve a clinical course, marked by major depressive periods. These take like a fortnight, marked by low moods and displeasure. The condition is also referred to as major depression, unipolar depression and clinical depression.

The disorder is disabling and comprises an individual’s lifestyle and family, loss of appetite and sleep distractions, which compromises one’s health (Greden, 2001). The patients of this medical condition end up committing suicide. The reason as to why I chose the topic is because it affects my life and many people around me in school and at home.

Having the condition has affected my lifestyle, school work, social life and has compromised my career since I lose pleasure in all activities. I even devalue life as I find my self contemplating on suicide during the phases of depression.

MDD affects people differently with different symptoms such as weight loss, pessimism, feeling guilty, loss of concentration, insomnia or hypersomnia, sleeping disorders, fatigue, hopelessness, irritability, loss of self-worth, disinterest in life and in severe cases, delusions and hallucinations may result.

The disorder affects more of females as compared to males (Deb & Bhattacharjee, 2009). The occurrence of the disorder may be linked to other medical close to 20.0 % to 25.0% of patients with conditions related to cancer, prolonged pain, diabetes, stroke, hypothyroidism, medications e.g. sedatives as well as myocardial infarction, which worsens these conditions (Deb & Bhattacharjee, 2009).

Health conditions that accompany MDD include drug abuse, panic, anxiety, obsessive-compulsive disorder, anorexia nervosa, Bulimia Nervosa and borderline personality disorder (Deb & Bhattacharjee, 2009).

According to one study dubbed the ‘ epidemiology of Major Depressive Disorder’ aimed at determining the prevalence of MDD. The study design used face to face research in 48 homes in the U.S by interviewing individuals over eighteen years. From the study, the MDD prevalence for a lifetime was 16.2% and that over one year was 6.6% and stated to be “10.4% mild, 38.6% moderate, 38.0% severe, and 12.9% very severe” (Kessler et al, 2003).

Role impairment showed 59.3% over a year where 51.6% of the cases sought medical attention and were being treated for MDD. Treatment proved enough for 41.9% of the cases, adding up to 21.7% MDD treatment annually. The study concludes that MDD was a common condition with its distribution being extensive in the population. It is linked to severe symptoms and role impairment.

There has been a rise in treating MDD, which offers hope for its management although lack of enough treatment is still a critical issue. The study maintains that “Emphasis on screening and expansion of treatment needs to be accompanied by a parallel emphasis on treatment quality improvement” (Kessler et al, 2003)

Another study regarding MDD on 3,258 adults is presented. According to the study, “MDD was found to affect women more than men by a ratio of nearly 2 to 1. The lifetime prevalence rate for both sexes combined was 8.6%. The period prevalence rates for both sexes combined were 3.2% and 4.6%, for 6 mo and 1 yr, respectively.

The age of onset for MDD showed a wide range, with over 75% of cases having an onset prior to age 30 yrs. The presence of a recurrent MDD was associated with an increased risk of substance abuse, panic disorder, and dysthymia, whereas a single MDD episode was not associated with increased comorbidity” (Spaner et al, 1994).

The prevalence of MDD according to Culture, sex and age is obvious. Culture for instance affects the communication and experiences regarding MDD where it is mostly experienced as somatic in nature and not by guilt of low moods. Some complain of nerves as well as headaches particularly for Latinos as well as those from Mediterranean origin.

Others complain of weakness or fatigue especially the Chinese and Asian people while other talk of heart problems such as those in the Middle East to refer to the depressive feeling. MDD occurs twice as many times as in adolescents and mature women as compared to adolescents and mature males (Deb & Bhattacharjee, 2009).

The prevalence of MDD is high for individuals aged 25 to 44 years of all genders and lower for those aged 65 and above. Its onset may be at any age but is mostly notable during mid twenties.

Studies related to MDD have shown a broad rage of outcomes for the population assessment of the condition. The lifetime risk for MDD in population samples vary from 10.0% to 25.0% for males while the point prevalence of MDD in adult population samples varies from 2.0 to 3.0 % for males.

MDD is 1.5 to 3 times greater for 1 st degree relatives of patients with MDD as compared to the general population. Besides, it has been indicated that alcohol dependence is high in mature 1 st degree relatives as well as a higher rate of hyperactivity disorder for children of patients with MDD (Deb & Bhattacharjee, 2009).

MDD has been attributed to various fatalities where approximately fifteen percent of patients end up committing suicide. Epidemiological studies points that the fatalities of those aged over fifty five years with MDD have risen by four times in the recent years.

Treatment of MDD may involve use of antidepressants such as Selective serotonin re-uptake inhibitors (SSRIs) or Serotonin norepinephrine reuptake inhibitors (SNRIs). Antipsychotic medications are recommended for the ones with severe psychotic symptoms. These drugs needs to be taken for an extensive period and may be combined with supplements like Lithium & thyroid hormone for their efficiency of antidepressants, to prevent recurrence of the condition and avoid situations of treatment-resistant depression (Herrman, 2009).

Additionally, talk therapy is very efficient and may involve counseling on one’s thoughts and behaviors. Cognitive Behavioral Therapy is one such procedure, which utilize the modeling of thoughts and feelings as reflected in the behavior of an individual. This method repels negative thoughts. Psychotherapy is essential in the understanding of the causes of the problem in relation to their behavior, thinking and feelings.

Patients may also be put under Electroconvulsive therapy (ECT) especially ones contemplating suicide in order to enhance their moods, for ones with treatment-resistant depression and ones those with psychotic symptoms. Besides, Transcranial magnetic stimulation (TMS) utilizes magnetic pulses directed towards affected brain sections and may be done after carrying out an ECT (Greden, 2001).

The cause of MDD is not proven though many studies indicate it could result from chemical instability in the brain. This may be as a result of genetic predisposition and interaction with the environment. The factors that are known to trigger MDD include drug use, socio-economic constrains and medical conditions.

MDD is known to result to several fatalities and therefore it requires to be managed through pharmacological or talk therapies. Open communication is also essential for patients to gain assistance before the disorder destroys a person completely. Such patients needs to be well monitored without being left alone, else they contemplate of suicide.

Deb, S. and Bhattacharjee, A. (2009). Mental Depression: The Silent Killer . New Delhi: Concept Publishing Company.

Greden, J. F. (2001). Treatment of Recurrent Depression, Volume 20, Issue 5 . Washington, DC: American Psychiatric Publishing, Inc.

Herrman, H., Maj, M, and Sartorius, N. (2009). Depressive Disorders . New York: John Wiley and Sons.

Kessler, C. R. et al. (2003). “ The epidemiology of Major Depressive Disorder: Results from Comorbidity Survey Replication (NCS-R). ” The Journal of the American Medical Association, 289(23):3095-3105. Web.

Spaner, D., Bland, R. C. and Newman, S. C. (1994). “ Major Depressive Disorder .” Acta Psychiatrica Scandinavica , Vol 89(376, Suppl), 7-15. Web.

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IvyPanda. (2018, May 30). Major Depressive Disorder (MDD). https://ivypanda.com/essays/major-depressive-disorder-mdd/

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1. IvyPanda . "Major Depressive Disorder (MDD)." May 30, 2018. https://ivypanda.com/essays/major-depressive-disorder-mdd/.

Bibliography

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Everyone experiences sadness at times. But depression is something more. Depression is extreme sadness or despair that lasts more than days. It interferes with the activities of daily life and can cause physical symptoms such as pain, weight loss or gain, sleeping pattern disruptions, or lack of energy.

People with depression may also experience an inability to concentrate, feelings of worthlessness or excessive guilt, and recurrent thoughts of death or suicide.

Depression is the most common mental disorder. Fortunately, depression is treatable. A combination of therapy and antidepressant medication can help ensure recovery.

Adapted from the Encyclopedia of Psychology

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The Phenomenology of Major Depression and the Representativeness and Nature of DSM Criteria

• Kenneth S. Kendler , M.D.

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How should DSM criteria relate to the disorders they are designed to assess? To address this question empirically, the author examines how well DSM-5 symptomatic criteria for major depression capture the descriptions of clinical depression in the post-Kraepelin Western psychiatric tradition as described in textbooks published between 1900 and 1960. Eighteen symptoms and signs of depression were described, 10 of which are covered by the DSM criteria for major depression or melancholia. For two symptoms (mood and cognitive content), DSM criteria are considerably narrower than those described in the textbooks. Five symptoms and signs (changes in volition/motivation, slowing of speech, anxiety, other physical symptoms, and depersonalization/derealization) are not present in the DSM criteria. Compared with the DSM criteria, these authors gave greater emphasis to cognitive, physical, and psychomotor changes, and less to neurovegetative symptoms. These results suggest that important features of major depression are not captured by DSM criteria. This is unproblematic as long as DSM criteria are understood to index rather than constitute psychiatric disorders. However, since DSM-III, our field has moved toward a reification of DSM that implicitly assumes that psychiatric disorders are actually just the DSM criteria. That is, we have taken an index of something for the thing itself. For example, good diagnostic criteria should be succinct and require minimal inference, but some critical clinical phenomena are subtle, difficult to assess, and experienced in widely varying ways. This conceptual error has contributed to the impoverishment of psychopathology and has affected our research, clinical work, and teaching in some undesirable ways.

The tower of Babel never yielded such confusion of tongues, as the chaos of melancholy doth variety of symptoms.

—Robert Burton, Anatomy of Melancholia , 6th edition, 1651 ( 1 , p. 456)

The introduction of operationalized diagnostic criteria in DSM-III has had many benefits for psychiatric practice and research. However, its wide use has produced an unanticipated side effect—the reification of the DSM criteria ( 2 ). In our training, clinical work, and research, we typically evaluate only DSM criteria, as if they constituted all anyone would want to know about the disorder in question ( 3 ). Focusing solely on the symptoms and signs in DSM risks producing an impoverished view of psychopathology ( 4 ) and has encouraged the rise of diagnostic literalism ( 5 ).

In this article, I first evaluate these claims empirically for one of the most common and important of psychiatric disorders: major depression. In this historical inquiry, I ask: How well do the A criteria for major depression used in DSM-III through DSM-5 capture the descriptive approach taken to clinical depression in the post-Kraepelin Western psychiatric tradition circa 1900–1960? (I chose this period because the clinical features associated with what we now call depression were considerably more diverse in earlier epochs [ 6 ]). I focus initially on textbooks as the best place to obtain expert opinion about the important symptoms and signs of depression. I next review the phenomenology of depression described by Aubrey Lewis in what is the most detailed survey of the phenomenology of depression written in the 20th century ( 7 ). I then evaluate how well our clinical descriptive tradition for depressive illness is represented in the DSM criteria.

Then, in light of this historical analysis, I review the question: How should DSM criteria relate to the disorders they are designed to assess? I suggest that U.S. psychiatry, as a field, has tended to reify DSM criteria. This approach reflects a conceptual error—a category mistake. That mistake is taking an index of a thing for the thing itself . The criteria proposed in DSM-III and subsequent DSM editions are practical means to identify disorders with what are hoped to be good reliability, sensitivity, and specificity. They do not constitute the disorders they seek to identify. This conceptual error is central to the problem of psychopathologic impoverishment. Its correction has important implications for the ways in which the DSM criteria are used in research, clinical care, and especially teaching.

I identified textbooks of psychiatry or psychological medicine published from ∼1900 to 1960, and written or translated into English, from three major sources: Amazon.com, the National Library of Medicine, and Forgotten Books (forgottenbooks.com). Textbooks were rejected if they did not adopt the Kraepelinian diagnostic perspective on affective illness or if the information they contained on the symptoms and signs of major depression was too sparse to be useful. When multiple editions were available, I reviewed the earliest edition. In total, 19 textbooks, published from 1899 to 1956 from five countries (nine from the United States, seven from the United Kingdom, and one each from Germany, France, and Switzerland), met inclusion criteria.

I reviewed the relevant sections of text in historical order starting with the 6th edition of Kraepelin’s Psychiatry textbook ( 8 ), creating categories for signs and symptoms as needed as I progressed through the textbooks. After going through all the texts, developing and testing the categories, I went back over them a second time to ensure consistent application of the categories. In the key table, I included short quotations or paraphrases to give a sense of the authors’ “turn of phrase” in their descriptions.

Nine issues arose during this process. First, I focused on the general descriptions of what the author termed either “depression” or (for many of the earlier authors who did not use this category) “melancholia” (terms included depression, melancholia, depressive states, state(s) of depression, depressed type, types of depression, depressive phase, depressive psychosis, and depressed reaction). For the purposes of this essay, I refer to this syndrome as major depression. Second, I never accepted symptoms or signs only described in case reports. Third, if the author described depressive subtypes, I generally took representative symptoms from those of mild to moderate severity. I did not include symptoms or signs only noted for severe or stuporous depression. Fourth, I did not accept symptoms or signs that were described only for “involutional melancholy,” as most authors considered it distinct from “depression” or more typical “melancholia.” Fifth, I did not include signs or symptoms that were present in “mixed states.”

Sixth, I did not describe the delusions or hallucinations associated with major depression, as these are not part of the DSM A criteria. Seventh, none of these authors separately described the symptoms and signs of depression occurring in the course of unipolar versus bipolar illness, so I could not make that distinction. Eighth, many authors described a brief set of symptoms or signs that they judged to be central or primary to the depressive syndrome: I noted these by an asterisk in the table. Ninth, several authors provided rather long lists of associated somatic symptoms. In these situations, I summarized those that seemed most prominent.

Textbooks’ Descriptions of Symptoms and Signs

Mood disturbances in the course of major depression were described by all 19 textbook authors ( Table 1 ). However, a number of them were broader than the “feels sad, empty, hopeless” described in DSM-5 criterion A1. Common additional terms included “gloomy,” “painful,” “misery,” “worried,” “wretched,” “blue”, and “lonesome.” Twelve of the authors commented on loss of interest using language broadly similar to DSM-5 criterion A2, often using terms indicating apathy or indifference.

TABLE 1. Symptoms and Signs of Depression as Described by Authors of 19 Textbooks of Psychiatry Published Circa 1900–1960

a An asterisk (*) indicates that the symptom or sign was judged by the author to be prominent. “Depression” is described variously by these authors as depressive states, state(s) of depression, types of depression, depressed type, melancholia, depressive phase, depressive psychosis, and depressed reaction.

TABLE 1. Symptoms and Signs of Depression as Described by Authors of 19 Textbooks of Psychiatry Published Circa 1900–1960 a

All authors described specific cognitive content as characteristic of depressed patients. While guilt and worthlessness were frequently noted, other common descriptors included hopelessness, pessimism, self-accusation, self-derogation, feelings of inadequacy and of being a failure, and a specific focus on prior moral shortcomings, often of a sexual nature. The depressive cognitive content was therefore considerably broader than that incorporated in the relevant DSM criterion A7: “Feelings of worthlessness or excessive or inappropriate guilt.”

All but one author described changes in cognitive functioning, most typically of slowness of thought and difficulty with concentration, consistent with major depression criterion A8, “diminished ability to think or concentrate.”

Depression-related changes in volition and motivation were described by 15 authors and were typically distinguished both from the more physical feelings of fatigue and the difficulty in decision making. Most commonly, this was described as lack of initiative, loss of will, or inability to work. This symptomatic domain is not included in the DSM-5 A criteria for major depression.

Difficulties with decision making were noted by seven authors and are well captured by part of criterion A8, “indecisiveness.” Anhedonia was described by seven authors, most commonly as a loss of feeling of affection for loved ones and natural enjoyment. This symptom is relatively well represented by the relevant part of criterion A2: “markedly diminished pleasure.”

Psychomotor changes were reported by all but one author, 12 of whom described only aspects of psychomotor retardation and six of whom also commented on agitation. These signs are well presented in DSM-5 criterion A5. Fatigue, exhaustion, and feelings of being tired out, symptoms well captured by DSM criterion A6, were described by only eight authors. Speech that was slow, hesitant, indistinct, and/or monosyllabic was described by all but two authors. This symptom is not included in DSM-5.

Disturbed sleep was noted by 14 authors, most typically described as insomnia or disturbed or unrefreshing sleep. Early morning awakening was described by three authors. This symptom is well covered by “insomnia” in criterion A4. However, “hypersomnia,” also noted in this criterion, was not described as a symptom of depression by any of the authors.

Various aspects of anxiety, including panic attacks and obsessive fears, were noted by 14 authors, but anxiety is not included in the DSM criteria for major depression. Poor appetite and weight loss were described by, respectively, 10 and nine textbook authors, consistent with DSM criterion A3. However, none of the authors noted increased appetite and weight gain, which are also described in this DSM criterion.

Other physical symptoms and signs, noted by 17 authors, was the most difficult symptom category to summarize. Most commonly described were gastrointestinal complaints, but diminished libido, amenorrhea, and headaches were also often noted. Also frequently described were changes in facial expression and posture. These phenomena are not captured by any part of the A criterion in DSM-5 major depression.

Suicidal thoughts and ruminations were described by 13 of the authors, and this symptom area is well covered by DSM criterion A9, which includes “recurrent thoughts of death,” “recurrent suicidal ideation,” or suicide attempt or plan. Seven authors described circadian shifts in depressive symptoms, all noting that the symptoms were more severe in the morning. This is not in the DSM A criteria for major depression but is reflected in specifier criterion B2 for “melancholic features.”

Depression-associated depersonalization and derealization were noted in 12 of the textbooks. A number of descriptions were provided, including everything feeling changed or unreal, seeing the world through a mist, and perplexity. No DSM-5 criteria for major depression describe this kind of depressive symptomatology.

Prominent Symptoms and Signs

Fifteen authors noted a subset of symptoms and signs of major depression they regarded as of particular importance or centrality to the syndrome. As seen in Table 1 (bottom row), this analysis indicated that these authors, in aggregate, strongly endorsed three symptoms/signs of depression as being of special diagnostic importance: lowered mood, impairment in cognitive function, and psychomotor changes. All three of these are well reflected in the DSM criteria for major depression. The next most common central symptom, volitional changes, was noted by only 20% of these authors and is not described in DSM-5 criteria. Of note, only one author described neurovegetative changes in sleep, appetite, or weight as a central symptom of depression.

Criteria for Depression Proposed by Muncie

One of the authors—Muncie ( 22 ), in a 1939 textbook—proposed a relatively complete set of diagnostic criteria for depression, which for historical interest is presented in Table 2 . Compared with the DSM-5 criteria, Muncie’s criteria included symptoms of depersonalization and derealization and gave greater emphasis to physiological symptoms and changes in facial expression and posture.

TABLE 2. Criteria for Depression Proposed by Muncie in 1939

a From Muncie’s Psychobiology and Psychiatry ( 22 ).

b “In some cases at least, the expression of depersonalization … [may result from] … the fact that the misery is of such a degree as to beggar description in positive terms.”

TABLE 2. Criteria for Depression Proposed by Muncie in 1939 a

Lewis’s Monograph

In 1934 Aubrey Lewis ( 7 ) described the “clinical features” of 61 cases of “depressive state,” all examined and treated by Lewis in 1928–1929 in the Maudsley Hospital, London. This 102-page monograph provides considerably greater details of depressive symptoms and signs than any of the textbooks consulted. I can only hope to capture some relevant main themes of this rich paper. First, Lewis comments on all but two of the symptoms and signs that I developed from the textbook review, so there is a high degree of consilience between these two sources of information ( Table 3 ). Second, as with the texts, his descriptions of the mood changes are much richer than those provided by DSM-5. Third, he strongly emphasizes the importance and diversity of changes in cognitive content, demonstrating even more clearly than the textbooks the relative narrowness of the “worthlessness and guilt” description provided in DSM criterion A7. Fourth, he comments on but does not emphasize the depression-related changes in volition. Fifth, he highlights the close relationship between depressive and anxious symptoms, and he specifically notes the relatively high frequency of episode-related obsessions and compulsions. Sixth, he comments prominently on the depression-related signs of change in posture and facial expression. Finally, in accord with the textbook writers, he notes in considerable detail the relatively frequent symptoms of depersonalization and derealization.

TABLE 3. Symptoms and Signs of Depression as Described by Lewis in 1934

a From Lewis’s monograph “Melancholia: A Clinical Survey of Depressive States” ( 7 ).

TABLE 3. Symptoms and Signs of Depression as Described by Lewis in 1934 a

Quantitative Analysis

Finally, I took each of the 18 symptoms and signs developed in the textbook review and divided them into three categories: well covered by DSM criteria, partly covered by DSM criteria, and not at all covered by DSM criteria. As seen in Table 4 , ten of the 18 symptoms and signs were well described by the DSM A criteria for major depression and one by a criterion for melancholia. Two symptoms and signs (mood changes and changes in cognitive content) were partly covered by DSM criteria. Five symptoms and signs were not reflected in the DSM criteria for major depression.

TABLE 4. The Degree of Coverage by DSM-5 Criteria for Major Depression of the 18 Symptoms and Signs of Depression Assessed by Textbook Authors

TABLE 4. The Degree of Coverage by DSM-5 Criteria for Major Depression of the 18 Symptoms and Signs of Depression Assessed by Textbook Authors

Empirical Conclusions

The goal of the historical portion of this essay was to determine how well the phenomenology of depressive illness described in the post-Kraepelinian Western psychiatric tradition is captured by the current DSM symptomatic criteria for major depression. I begin by reviewing the nine major conclusions of this investigation.

First, the description of the core mood symptom for major depression in DSM-5, “depressed … sad, empty, hopeless,” was narrower than that provided by the textbook authors and by Lewis. Terms like “painful,” “miserable,” “wretched,” “dull,” “broken-hearted,” and “in agony” were used by various authors to reflect the diverse subjective manifestations of the dysphoric mood that is widely agreed to be central to the depressive syndrome.

Second, the descriptive literature placed greater relative emphasis on the cognitive and attitudinal changes associated with depression than do the DSM criteria, where these features constitute only one criterion, characterized solely by worthlessness and guilt. In agreement with Beck ( 27 ), the classical authors consistently emphasized the importance and diversity of cognitive changes in depression. In addition to worthlessness and guilt, other cognitive content was emphasized, including hopelessness, gloom, and a range of diverse self-accusatory and self-derogatory themes.

Third, second to mood changes, the most frequently noted key symptom of major depression was changes in cognitive functioning, typically characterized by difficulties in thinking and concentrating. These symptoms, while noted in the clinical and neuropsychological literature ( 28 ), have rarely, in the post-DSM-III world, been regarded as central to the clinical presentation of major depression.

Fourth, these authors describe a range of somatic symptoms and signs in depressed patients that receive little attention in DSM. Gastrointestinal changes, especially constipation, was commonly observed, as were menstrual and libidinal changes. Observations of dried skin and characteristic changes in facial expressions and posture were also frequently noted. Somatic symptoms of major depression may be more common in non-Western cultures, especially China, and it has been claimed that this is due to a “mentalization” of depression in Western culture ( 29 ). The widespread use of DSM criteria for major depression, which exclude consideration of somatic symptoms, may have contributed to this trend.

Fifth, the textbook authors gave less importance to the neurovegetative features of depression—changes in sleep, appetite, and weight—than the DSM criteria do. No author noted them as key depressive symptoms.

Sixth, consistent with recent work ( 30 ), these authors gave greater prominence to changes in psychomotor functioning, especially psychomotor retardation, than is our current practice. This was noted as a key depressive sign by over two-thirds of authors who listed such symptoms. However, only five of the 19 textbook authors described psychomotor agitation as a common symptom of depression or melancholia. In addition, several others referred to sections on “mixed” states where they described such cases.

The typical affect is that of sadness, but has been described as being qualitatively … different to that normally experienced … the typical depressed mood thus shades into depersonalization in which the patient feels changes—strange, lifeless, detached, automatic. Sometimes, instead of feeling that they themselves have changed, the patients lay emphasis on a change in the outer world which seems dead or macabre ( 24 , p. 157).

It was as if the whatness of each thing … the essence of each thing in the sense of the tableness of the table or the chairness of the chair … was gone. There was a mute and indifferent object in that place. Its availability to human living … in the world was drained out of it. Its identity as a familiar object that we live with each day was gone … the world had lost its welcoming quality ( 31 , pp. 212–213).

Some pathological experiences in depression may not be best understood as “symptoms that a person has” (e.g., sore throat, insomnia) but rather a fundamental change in a person’s “being in the world” ( 32 ). That is, hopelessness or guilt can become an “existential state” rather than a “symptom.”

Eighth, nearly all authors commented on changes in the speech of depressed patients, most typically describing it as slow, low in volume, with long pauses. This sign is not in DSM-5.

Finally, the symptomatology of atypical depression—particularly the “reverse” vegetative features of increased eating/weight and hypersomnia—was not described in the classical literature. One of these symptoms (hypersomnia) was introduced into the Feighner criteria (although it was not in the two earlier sets of diagnostic criteria for depression that influenced the Feighner criteria [ 33 , 34 ]). Increased eating and weight gain were introduced into the Research Diagnostic Criteria ( 35 ) for major depression and carried over into all subsequent editions of DSM.

Conceptual Issues With Our Current Approach to DSM Criteria

This historical inquiry provides a useful framework in which to reflect on the way to answer the following question: How should DSM criteria relate to the disorders they are designed to assess? I wish to argue that many in our field have made a serious category mistake in the ways in which we have understood and used the DSM criteria. Put succinctly, we have confused an index of a thing with the thing itself .

Let me explain. As in all diagnostic systems, DSM criteria were designed to index (i.e., measure or assess) syndromes—to describe signs and symptoms that permit the clinician to classify individuals as being affected or unaffected, with good efficiency, reliability, sensitivity, and specificity. To use major depression as an example, if the criteria work well, then individuals who meet the criteria for major depression have a high likelihood of really having depression and being neither psychiatrically well nor having another syndrome, such as panic disorder. But meeting the DSM criteria for major depression is not the same thing as having major depression. The DSM criteria do not constitute clinically significant depression.

Second, the Apgar score ( 37 , 38 ) was proposed in 1953 by Virginia Apgar as a rapid way to assess immediate postpartum neonatal health. It contains five items (heart rate, respiratory effort, reflex irritability, muscle tone, and color) that can be evaluated quickly in the delivery room ( 38 ). The Apgar score is practical, reliable, and valid in that it robustly predicts neonatal survival and risk of future cognitive impairment ( 38 ). But would anyone wish to argue that a healthy baby is just having a baby with a high Apgar score, or, to phrase it differently, that the construct of infant health can be reduced to an Apgar score?

Third, the intelligence quotient (IQ) originated with Alfred Binet in 1905. Its major function was to predict school performance, and it is still widely used (for example, as the Stanford-Binet Intelligence Scale) as a broad measure of intellectual functioning. Despite its wide popularity and entry into the general vocabulary, it would be a confusion to assert that being intelligent is just having a high IQ measured by constructs such as fluid reasoning, knowledge, quantitative reasoning, visual-spatial processing, and working memory.

There is, of course, a common core to these three examples. We have a latent concept or process that we cannot easily directly assess: MI, general health of a newborn, and intelligence. We develop a method to assess that construct which is practical to apply and is a good predictor of that latent concept. But then we are at risk of a misstep. As pointed out by John Locke, the great English philosopher (and physician), “Another great abuse of words is taking them for things.… How much names taken for things are apt to mislead the understanding” ( 39 , pp. 442–443). Once we have a name—MI, Apgar, IQ, or DSM major depression—we are at risk of confusing our index with the thing itself, that is, what it was developed to measure.

Following from Locke’s observation, we can reframe our concept of a category mistake into a more concrete and semantic form: the meaning of the sentence “Mary suffers from depression” is reduced to “Mary meets the DSM-V criteria for major depression.” This would be the same error as claiming that “Roger has had a heart attack” is reducible to “Roger meets the WHO criteria for MI” and claiming that “April is a healthy baby” is just the same as saying “April had a high Apgar score.”

Illustrations of the Problems Associated With Our Category Mistake

Why is it a bad idea to conflate our DSM criteria with the disorders themselves? Our historical review of symptoms of major depression presents three illustrative problems. First, for most diagnostic criteria, rapidity and reliability of assessment is critical. The developers of DSM-III explicitly preferred criteria that required low levels of inference, because these are typically more reliable ( 40 ). Many of the symptomatic criteria for major depression—such as changes in appetite, weight, psychomotor performance, and sleep—can be quickly and reliably assessed.

But some important features of psychiatric disorders may not be like that. They may be subtle, and time-consuming to evaluate. Does this mean that such symptoms should be disregarded? If DSM criteria for major depression constitute depression, that would be a logical conclusion.

But many of our classical textbook authors believed that derealization was an important clinical feature of major depression. We can understand why this did not make it into DSM: It is a subtle concept, time-consuming to evaluate, and perhaps of limited reliability. Yet, senior clinicians of earlier generations thought it was a critical feature of the depressive syndrome that reflected their patients’ lived experiences. Should we not evaluate it or teach it to our students because it is not in DSM?

Second, developers of diagnostic criteria are also appropriately concerned about specificity. A symptom could be quite clinically important, but if it is shared by many other syndromes, it would likely not make a good diagnostic criterion. Most of our textbook writers considered anxiety to be a prominent and clinically important part of the presentation of major depression. If we conflate our criteria with our disorders, we are then in the awkward position of suggesting that anxiety is not important in major depression because it is not in our criteria.

Third, to be practical, diagnostic criteria need to be succinct. For the key major depression criteria A1 and A7, DSM-5 lists three and two descriptors, respectively. As illustrated by our textbook writers, these lists are too short to capture adequately the range of human experience of the mood state of depression and the range of self-derogatory/pessimistic depressive cognitions.

Consequences of Our Category Mistake

Reification has many meanings, but in this context it reflects the process whereby we have taken DSM criteria as too sacrosanct. Hyman trenchantly writes, “Unfortunately, the disorders within these classifications [DSM and ICD] are not generally treated as heuristic, but to a great degree have become reified” ( 2 , p. 156). Many of us have become diagnostic literalists with respect to DSM, stymied by an excessive respect for own creation. DSM criteria are imperfect approximations created by a very human process that, although scientifically informed, could not be claimed by any knowledgeable individual to be infallible. These criteria have been enshrined in our diagnostic algorithms and structured interviews, and are so often required by journal and grant reviewers that they approach the tokens of an orthodox faith. By losing sight of the indexical function of our diagnostic criteria and confounding the criteria with the disorders themselves, we open the door to reification.

Furthermore, if meeting DSM criteria constitutes a psychiatric disorder, why should we evaluate anything but the DSM criteria? This view is deeply problematic. Psychiatry is the inheritor of the richest tradition of description in all of medicine because the features of the disordered mind/brain system that is the subject of our discipline are so diverse, so innately fascinating and profound in the degree to which they illuminate the human condition. Part of the process of good clinical care is to explore the experiences of our patients. This helps us better understand their experiences, and this sense of shared understanding can be directly therapeutic. This cannot be done without knowledge of the world of psychopathology outside of DSM. DSM might provide a guide to but can hardly be a replacement for our rich psychopathological tradition.

From a historical perspective, psychiatry has been appropriately proud of the “DSM revolution.” However, we still lack gold-standard validators like coronary angiography. The presence of such validators helps illustrate the difference between indexing and constituting a disorder. Given our pride in our diagnosis and our lack of definitive validators, it is understandable that our field has had undergone a “conceptual creep” in which our criteria have mistakenly become our disorder.

Potential Limitations

My historical review of symptoms and signs of major depression should be interpreted in the context of three potentially important methodological limitations. First, the nature of psychiatric practice changed during the 20th century, with outpatient care constituting a larger proportion of our work, especially after 1960. Many of the classical textbook writers were seeing severely depressed patients in hospitals. By the time DSM-III was published in 1980, the majority of depressed patients were being seen in ambulatory settings and were often more mildly ill. Second, none of these authors distinguished between depressions occurring in bipolar illness and those occurring in unipolar illness. It is possible, although unlikely given modest symptomatic differences seen for depression in major depression as compared with bipolar illness ( 37 ), that some of the differences between the symptoms described and those listed in the DSM-5 criteria result from admixture of patients with bipolar illness. Third, as noted above, the goals of those who develop diagnostic criteria are not the same as those of the textbook writers, with the former being much more concerned with brevity, reliability (and hence low inferential content), and specificity.

All you have done is pointed out the difference between diagnostic criteria and clinical evaluation. Since DSM-III, DSM has contained an “associated features” section that describes common symptoms and signs of the disorder not included as diagnostic criteria. We use diagnostic criteria for referral or treatment decisions but then put them aside and do our complete clinical evaluation.

Conclusions

The DSM symptomatic criteria for major depression do a reasonable but incomplete job of assessing the prominent clinical symptoms and signs of depressive illness as described in the Western post-Kraepelinian psychiatric tradition. In their use as diagnostic criteria, this is unproblematic because, across all of medicine, diagnostic criteria are designed to index rather than exhaustively describe a clinical syndrome. That is, criteria need only to identify true cases with sufficient sensitivity and specificity, and not to reflect complete catalogs of important symptoms and signs. But it is problematic when we focus our teaching, our clinical work, and our research solely around DSM criteria. In our teaching, our trainees need to understand that the DSM criteria for depression, while a good place to start a diagnostic evaluation, do not represent all the relevant symptoms and signs that merit evaluation. In our clinical work, we should make an effort to explore the diversity of the depressive experiences of our patients, some of which clearly lie beyond the bounds of the DSM criteria. For our research, if we focus only on DSM criteria for major depression, how can we further improve on our current criteria?

I suggest that, to many intents and purposes, we have been misusing the DSM diagnostic criteria because we have confused them with the diagnostic entities they are designed to assess. To be explicit, our DSM criteria for major depression are a good index of the clinical syndrome of depression. But, as my historical survey suggests, this depressive syndrome is not entirely constituted by the DSM criteria. Recognizing and correcting this approach to DSM should help us enjoy the many benefits our increasingly research-based criteria can afford to our field while diminishing its negative effects of reduced interest in our rich descriptive heritage and of excessive diagnostic literalism and reification.

The author reports no financial relationships with commercial interests.

Denny Borsboom, Ph.D., and Paul Appelbaum, M.D., provided helpful comments on earlier versions of the manuscript.

1 Burton R : The Anatomy of Melancholia . London, Bell and Sons, 1893 Google Scholar

2 Hyman SE : The diagnosis of mental disorders: the problem of reification . Annu Rev Clin Psychol 2010 ; 6:155–179 Crossref , Medline ,  Google Scholar

3 Kendler KS : DSM issues: incorporation of biological tests, avoidance of reification, and an approach to the “box canyon problem” . Am J Psychiatry 2014 ; 171:1248–1250 Link ,  Google Scholar

4 Andreasen NC : DSM and the death of phenomenology in America: an example of unintended consequences . Schizophr Bull 2007 ; 33:108–112 Crossref , Medline ,  Google Scholar

5 Zachar P : A Metaphysics of Psychopathology . Cambridge, Mass, MIT Press, 2014 Crossref ,  Google Scholar

6 Berrios GE : The History of Mental Symptoms: Descriptive Psychopathology Since the Nineteenth Century . New York, Cambridge University Press, 1996 Crossref ,  Google Scholar

7 Lewis AJ : Melancholia: a clinical survey of depressive states . J Ment Sci 1934 ; 80:277–378 Crossref ,  Google Scholar

8 Kraepelin E: Psychiatry: A Textbook for Students and Physicians, vol 2, Clinical Psychiatry. Translated by Sabine Ayed, edited by Jacques Quen. Canton, Mass, Science History Publications, 1990 (originally published 1899) Google Scholar

9 De Fursac R: Manual of Psychiatry. London, Forgotten Books, 2013 (originally published 1905) Google Scholar

10 Paton S: Psychiatry: A Text-Book for Students and Physicians. London, Forgotten Books, 2014 (originally published 1905) Google Scholar

11 Dana CL : Text-Book of Nervous Diseases and Psychiatry: For the Use of Students and Practitioners of Medicine , 6th rev and enlarged ed. New York, William Wood, 1904 Google Scholar

12 Craig M: Psychological Medicine: A Manual on Mental Diseases for Practitioners and Students. London, Forgotten Books, 2013 (originally published 1912) Google Scholar

13 White WA : Outlines of Psychiatry: Nervous and Mental Disease Monograph Series No 1 , 4th ed. New York, Journal of Nervous and Mental Disease Publishing Company, 1913 Google Scholar

14 Cole RH : Mental Diseases: A Text-Book of Psychiatry for Medical Students and Practitioners . London, University of London Press, 1913 Google Scholar

15 Buckley AC: The Basis of Psychiatry (Psychological Medicine): A Guide to the Study of Mental Disorders, for Students and Practitioners. London, Forgotten Books, 1920 (originally published 1920) Google Scholar

16 Jelliffe SE, White WA : Diseases of the Nervous System: A Text-Book of Neurology and Psychiatry , 4th ed, revised, rewritten, and enlarged ed. Philadelphia and New York, Lea & Febiger, 1923 . Google Scholar

17 Bleuler E : Textbook of Psychiatry . New York, Arno Press, 1976 Google Scholar

18 Yellowlees H : Clinical Lectures on Psychological Medicine . Baltimore, J & A Churchill, 1932 Google Scholar

19 Sadler WS : Theory and Practice of Psychiatry . St Louis, Mosby, 1936 Crossref ,  Google Scholar

20 Noyes AP : A Textbook of Psychiatry , 2nd ed. New York, Macmillan, 1936 Google Scholar

21 Gordon RG, Harris NG, Rees JR : An Introduction to Psychological Medicine . London, Oxford University Press, Oxford Medical Publications, 1936 Google Scholar

22 Muncie W : Psychobiology and Psychiatry: A Textbook of Normal and Abnormal Human Behavior . St Louis, Mosby, 1939 Google Scholar

23 Henderson DK, Gillespie RD : A Text-Book of Psychiatry for Students and Practitioners , 6th ed. London, Oxford University Press, Oxford Medical Publications, 1944 Google Scholar

24 Curran D, Guttmann E : Psychological Medicine: A Short Introduction to Psychiatry , 2nd ed. Edinburgh, UK, Livingstone, 1945 Google Scholar

25 Mayer-Gross W, Slater E, Roth M : Clinical Psychiatry . London, Cassell, 1954 Google Scholar

26 Ulett GA, Goodrich DW : A Synopsis of Contemporary Psychiatry . St Louis, Mosby, 1956 Crossref ,  Google Scholar

27 Beck AT, Alford BA : Depression: Causes and Treatment , 2nd ed. Philadelphia, University of Pennsylvania Press, 2008 Google Scholar

28 Trivedi MH, Greer TL : Cognitive dysfunction in unipolar depression: implications for treatment . J Affect Disord 2014 ; 152–154:19–27 Crossref , Medline ,  Google Scholar

29 Kleinman A, Kleinman J: Somatization: the interconnections in Chinese society among culture, depressive experiences, and the meanings of pain, in Culture and Depression: Studies in the Anthropology and Cross-Cultural Psychiatry of Affect and Disorder. Edited by Kleinman A, Good B. Berkeley, University of California Press, 1985, pp 429–490 Google Scholar

30 Parker G, Hadzi-Pavlovic D, Austin MP, et al. : Sub-typing depression, I: is psychomotor disturbance necessary and sufficient to the definition of melancholia? Psychol Med 1995 ; 25:815–823 Crossref , Medline ,  Google Scholar

31 Hornstein G : Agnes’s Jacket: A Psychologist’s Search for the Meanings of Madness . New York, Rodale Books, 2009 Google Scholar

32 Ratcliffe M : Experiences of Depression: A Study in Phenomenology . Oxford, UK, Oxford University Press, 2015 Google Scholar

33 Cassidy WL, Flanagan NB, Spellman M, et al. : Clinical observations in manic-depressive disease: a quantitative study of one hundred manic-depressive patients and fifty medically sick controls . J Am Med Assoc 1957 ; 164:1535–1546 Crossref , Medline ,  Google Scholar

34 Stone TT, Burris BC : Melancholia; clinical study of 50 selected cases . JAMA 1950 ; 142:165–168 Crossref , Medline ,  Google Scholar

35 Spitzer RL, Endicott J, Robins E : Research Diagnostic Criteria for a Selected Group of Functional Disorders , 2nd ed. New York, New York Psychiatric Institute, 1975 Google Scholar

36 Anonymous : Nomenclature and criteria for diagnosis of ischemic heart disease: Report of the Joint International Society and Federation of Cardiology/World Health Organization task force on standardization of clinical nomenclature . Circulation 1979 ; 59:607–609 Crossref , Medline ,  Google Scholar

37 Apgar V : A proposal for a new method of evaluation of the newborn infant . Curr Res Anesth Analg 1953 ; 32:260–267 Crossref , Medline ,  Google Scholar

38 Finster M, Wood M : The Apgar score has survived the test of time . Anesthesiology 2005 ; 102:855–857 Crossref , Medline ,  Google Scholar

39 Locke J : An Essay Concerning Human Understanding . Oxford, UK, Oxford University Press, 1979 Google Scholar

40 Decker HS : The Making of DSM-III: A Diagnostic Manual’s Conquest of American Psychiatry . New York, Oxford University Press, 2013 Google Scholar

• Impact of depersonalization on the course of depression: longitudinal observations from the gutenberg health study 8 March 2024 | BMC Psychiatry, Vol. 24, No. 1
• Longitudinal studies of bipolar patients and their families: translating findings to advance individualized risk prediction, treatment and research 12 April 2024 | International Journal of Bipolar Disorders, Vol. 12, No. 1
• Multidimensional behavioral profiles associated with resilience and susceptibility after inescapable stress 27 April 2024 | Scientific Reports, Vol. 14, No. 1
• Philosophy of psychiatry: theoretical advances and clinical implications 10 May 2024 | World Psychiatry, Vol. 23, No. 2
• A revisionist model for treatment-resistant and difficult-to-treat depression 27 March 2024 | Australian & New Zealand Journal of Psychiatry, Vol. 58, No. 6
• The Miami Framework for ALS and related neurodegenerative disorders: an integrated view of phenotype and biology 20 May 2024 | Nature Reviews Neurology, Vol. 20, No. 6
• Intersubjectivity and psychiatric diagnosis Minerva Psychiatry, Vol. 65, No. 2
• A Comparative Study on Mental Disorder Conceptualization: A Cross-Disciplinary Analysis 6 February 2024 | Community Mental Health Journal, Vol. 60, No. 4
• Joseph Guislain's writings on melancholia from 1835 and 1852 Journal of Affective Disorders, Vol. 351
• The Case of the Many Messiahs: Narrative Competence and Religious Symptoms 5 July 2023 | Academic Psychiatry, Vol. 48, No. 2
• Do enteric glial cells play a role in the pathophysiology of major depression? 28 April 2024 | Exploration of Neuroscience, Vol. 3, No. 2
• Clinical Features of Depressive Disorders
• Emotional Blunting in Depression in the PREDDICT Clinical Trial: Inflammation-Stratified Augmentation of Vortioxetine With Celecoxib 5 March 2024 | International Journal of Neuropsychopharmacology, Vol. 27, No. 3
• Depression, professional self-efficacy, and job performance as predictors of life satisfaction: the mediating role of work engagement in nurses 1 February 2024 | Frontiers in Public Health, Vol. 12
• Systematic Review and Meta-Synthesis: How Is Depression Experienced by Adolescents? A Synthesis of the Qualitative Literature Journal of the American Academy of Child & Adolescent Psychiatry, Vol. 10
• Assessment of Depression in Adults and Youth 20 April 2023 | Assessment, Vol. 31, No. 1
• Characterizing depression after traumatic brain injury using a symptom-oriented approach Journal of Affective Disorders, Vol. 345
• What Do We Know About Depression Among Youth and How Can We Make Progress Toward Improved Understanding and Reducing Distress? A New Hope 7 June 2023 | Clinical Child and Family Psychology Review, Vol. 26, No. 4
• Prototypes of People With Depression 3 November 2023 | Psychological Science, Vol. 34, No. 12
• Distinct neurofunctional alterations during motivational and hedonic processing of natural and monetary rewards in depression – a neuroimaging meta-analysis 24 November 2023 | Psychological Medicine, Vol. 372
• Too sad to be true: hypo- and hyperreality in experiences of depression 28 August 2023 | Philosophical Psychology, Vol. 36, No. 7
• Anxiolytic-like effects of extremely low frequency electric field in stressed rats: involvement of 5-HT2C receptors 20 June 2022 | International Journal of Radiation Biology, Vol. 99, No. 9
• Predictors of Depressive Symptoms Among Parents of Children With Cancer in Ethiopia 26 October 2023 | Journal of Pediatric Hematology/Oncology Nursing, Vol. 40, No. 5
• Phenomenology and therapeutic potential of patient experiences during oral esketamine treatment for treatment-resistant depression: an interpretative phenomenological study 24 May 2023 | Psychopharmacology, Vol. 240, No. 7
• Specificity of polygenic signatures across symptom dimensions in bipolar disorder: an analysis of UK Bipolar Disorder Research Network data The Lancet Psychiatry, Vol. 152
• Psychiatric comorbidity: a concept in need of a theory 2 June 2023 | Psychological Medicine, Vol. 143
• Epidemiology of Depression and Suicide Ideation in Patients With Psoriasis: A Meta-analysis of Prospective Cohort Studies 29 June 2023 | International Journal of Dermatology and Venereology, Vol. 6, No. 2
• The genetic basis of major depressive disorder 26 January 2023 | Molecular Psychiatry, Vol. 28, No. 6
• Adolescent depression beyond DSM definition: a network analysis 2 December 2021 | European Child & Adolescent Psychiatry, Vol. 32, No. 5
• Precision behavioral phenotyping as a strategy for uncovering the biological correlates of psychopathology 10 May 2023 | Nature Mental Health, Vol. 1, No. 5
• Dimensions of the Hamilton Depression Rating Scale Correlate with Impulsivity and Personality Traits among Youth Patients with Depression 22 February 2023 | Journal of Clinical Medicine, Vol. 12, No. 5
• Neurobiology of depression in Parkinson’s disease: Insights into epidemiology, molecular mechanisms and treatment strategies Ageing Research Reviews, Vol. 85
• Introducing a depression-like syndrome for translational neuropsychiatry: a plea for taxonomical validity and improved comparability between humans and mice 14 September 2022 | Molecular Psychiatry, Vol. 28, No. 1
• Phenomenology and psychiatry: Shaping the diagnosis Theoria, Beograd, Vol. 66, No. 1
• A critical evaluation of dynamical systems models of bipolar disorder 28 September 2022 | Translational Psychiatry, Vol. 12, No. 1
• Studying Mental Health Problems as Systems, Not Syndromes 6 October 2022 | Current Directions in Psychological Science, Vol. 31, No. 6
• Chronic stress-induced depression requires the recruitment of peripheral Th17 cells into the brain 14 July 2022 | Journal of Neuroinflammation, Vol. 19, No. 1
• Neural correlations between cognitive deficits and emotion regulation strategies: understanding emotion dysregulation in depression from the perspective of cognitive control and cognitive biases 10 November 2022 | Psychoradiology, Vol. 2, No. 3
• A call for renewed attention to construct validity and measurement in psychopathology research 21 October 2022 | Psychological Medicine, Vol. 3
• Network structure of time‐varying depressive symptoms through dynamic time warp analysis in late‐life depression 5 August 2022 | International Journal of Geriatric Psychiatry, Vol. 37, No. 9
• More phenomenology in psychiatry? Applied ontology as a method towards integration The Lancet Psychiatry, Vol. 9, No. 9
• Contemporary Genome-Wide Association Studies in Depression: The Critical Role of Phenotyping 26 October 2022 | Neuroscience and Behavioral Physiology, Vol. 52, No. 6
• Effects of COVID-19 pandemic and lockdown on lifestyle and mental health of students: A retrospective study from Karachi, Pakistan Annales Médico-psychologiques, revue psychiatrique, Vol. 180, No. 6
• The structure of the symptoms of major depression: Factor analysis of a lifetime worst episode of depressive symptoms in a large general population sample Journal of Affective Disorders, Vol. 307
• ECT is evidence-based – a commentary on depression: why drugs and electricity are not the answer 8 June 2022 | Psychological Medicine, Vol. 52, No. 8
• The Development of GABAergic Network in Depression in Recent 17 Years: A Visual Analysis Based on CiteSpace and VOSviewer 18 May 2022 | Frontiers in Psychiatry, Vol. 13
• Major Depression and Its Recurrences: Life Course Matters Annual Review of Clinical Psychology, Vol. 18, No. 1
• General and Specific Dimensions of Mood Symptoms Are Associated With Impairments in Common Executive Function in Adolescence and Young Adulthood 14 April 2022 | Frontiers in Human Neuroscience, Vol. 16
• Increased global integration in the brain after psilocybin therapy for depression 11 April 2022 | Nature Medicine, Vol. 28, No. 4
• Digital phenotyping in depression diagnostics: Integrating psychiatric and engineering perspectives World Journal of Psychiatry, Vol. 12, No. 3
• Cognitive Considerations in Major Depression: Evaluating the Effects of Pharmacotherapy and ECT on Mood and Executive Control Deficits 4 March 2022 | Brain Sciences, Vol. 12, No. 3
• Vigor, Effort-Related Aspects of Motivation and Anhedonia 4 May 2022
• At the Core of Depression: A Diagnostic Interview of the Core Features of Depression 11 March 2022 | Psychopathology, Vol. 55, No. 3-4
• Contemporary GWAS studies of depression: the critical role of phenotyping Zhurnal nevrologii i psikhiatrii im. S.S. Korsakova, Vol. 122, No. 1
• Delirium disorder: Unity in diversity General Hospital Psychiatry, Vol. 74
• Clinical depression: the fault not in our stars? 14 June 2021 | Australasian Psychiatry, Vol. 29, No. 6
• Validation of the Oxford Depression Questionnaire: Sensitivity to change, minimal clinically important difference, and response threshold for the assessment of emotional blunting Journal of Affective Disorders, Vol. 294
• The characteristic signs and symptoms of mania and depression according to Kraepelin circa 1905: a comparison with DSM-III 4 May 2020 | Psychological Medicine, Vol. 51, No. 15
• Public epistemic trustworthiness and the integration of patients in psychiatric classification 5 September 2018 | Synthese, Vol. 198, No. S19
• Decline of depressive symptoms in Europe: differential trends across the lifespan 12 November 2020 | Social Psychiatry and Psychiatric Epidemiology, Vol. 56, No. 7
• Profile of a short-acting κ-antagonist, LY2795050, on self-grooming behaviors, forced swim test and locomotor activity: sex comparison in mice 26 March 2021 | Journal of Psychopharmacology, Vol. 35, No. 5
• Extending the usefulness of the verbal memory test: The promise of machine learning Psychiatry Research, Vol. 297
• Potential Applications of Mobile and Wearable Devices for Psychological Support During the COVID-19 Pandemic: A Review IEEE Sensors Journal, Vol. 21, No. 6
• Memantine in neurological disorders – schizophrenia and depression 14 January 2021 | Journal of Molecular Medicine, Vol. 99, No. 3
• Kraepelin's final views on manic-depressive Illness Journal of Affective Disorders, Vol. 282
• A closer look at the nosological status of the highs (hypomanic symptoms) in the postpartum period 7 February 2020 | Archives of Women's Mental Health, Vol. 24, No. 1
• The Study of Depression in the Frame of the New Research Paradigm in Psychiatry 1 January 2022
• Delusional Depression and Melancholia
• Introduction
• Pain and suffering
• How can we know what is true, then?
• Using network analysis to examine links between individual depressive symptoms, inflammatory markers, and covariates 28 October 2019 | Psychological Medicine, Vol. 50, No. 16
• Recovering from depression with repetitive transcranial magnetic stimulation (rTMS): a systematic review and meta-analysis of preclinical studies 10 November 2020 | Translational Psychiatry, Vol. 10, No. 1
• Pre-pubertal bipolar disorder: origins and current status of the controversy 20 April 2020 | International Journal of Bipolar Disorders, Vol. 8, No. 1
• Increasing the Role of Phenomenology in Psychiatric Diagnosis–The Clinical Staging Approach 23 October 2020 | The Journal of Medicine and Philosophy: A Forum for Bioethics and Philosophy of Medicine, Vol. 45, No. 6
• Questionable Agreement: The Experience of Depression and DSM-5 Major Depressive Disorder Criteria 18 November 2020 | The Journal of Medicine and Philosophy: A Forum for Bioethics and Philosophy of Medicine, Vol. 45, No. 6
• The relationship between demoralization and depressive symptoms among patients from the general hospital: network and exploratory graph analysis Journal of Affective Disorders, Vol. 276
• Test-retest & familial concordance of MDD symptoms Psychiatry Research, Vol. 292
• Psychedelic Treatments for Psychiatric Disorders: A Systematic Review and Thematic Synthesis of Patient Experiences in Qualitative Studies 17 August 2020 | CNS Drugs, Vol. 34, No. 9
• Beyond pathology: women’s lived experiences of melancholy and mourning in infertility treatment 6 June 2019 | Medical Humanities, Vol. 46, No. 3
• The Origin of Our Modern Concept of Depression—The History of Melancholia From 1780-1880 JAMA Psychiatry, Vol. 77, No. 8
• The one and the many: a case highlighting comorbidity and complexity in psychiatry 19 March 2020 | BJPsych Bulletin, Vol. 44, No. 4
• Tracing the Roots of Dementia Praecox: The Emergence of Verrücktheit as a Primary Delusional-Hallucinatory Psychosis in German Psychiatry From 1860 to 1880 9 June 2020 | Schizophrenia Bulletin, Vol. 46, No. 4
• The proportion of non-depressed subjects in a study sample strongly affects the results of psychometric analyses of depression symptoms 6 July 2020 | PLOS ONE, Vol. 15, No. 7
• The Impact of Faculty Psychology and Theories of Psychological Causation on the Origins of Modern Psychiatric Nosology
• Adi Maron-Katz , Ph.D. ,
• Yu Zhang , Ph.D. ,
• Manjari Narayan , Ph.D. ,
• Wei Wu , Ph.D. ,
• Russell T. Toll , Ph.D. ,
• Sharon Naparstek , Ph.D. ,
• Carlo De Los Angeles , M.S. ,
• Parker Longwell , B.A. ,
• Emmanuel Shpigel , B.A. ,
• Jennifer Newman , Ph.D. ,
• Duna Abu-Amara , M.P.H. ,
• Charles Marmar , M.D. ,
• Amit Etkin , M.D., Ph.D.
• Direction of Dependence Between Specific Symptoms of Depression: A Non-Gaussian Approach 22 November 2019 | Clinical Psychological Science, Vol. 8, No. 2
• Préface à l’édition française
• Anhedonia in Depressive Disorder: A Narrative Review 15 July 2020 | Psychopathology, Vol. 53, No. 5-6
• Epistemic Injustice and Psychiatric Classification 1 January 2022 | Philosophy of Science, Vol. 86, No. 5
• The Dimensionality of Proposed DSM-5 PTSD Symptoms in Trauma-Exposed Young Children 6 June 2019 | Journal of Abnormal Child Psychology, Vol. 47, No. 11
• The future of rodent models in depression research 2 October 2019 | Nature Reviews Neuroscience, Vol. 20, No. 11
• Trait anhedonia is a transdiagnostic correlate of internalizing problems during adolescence Journal of Research in Personality, Vol. 81
• Experience versus diagnosis as the appropriate basis for assessment of depression: A reply to the commentary from Kirmayer et al. (2017) Social Science & Medicine, Vol. 232
• Advance in Diagnosis of Depressive Disorder 30 November 2019
• Psychological Medicine, Vol. 49, No. 16
• Perspectives on Science, Vol. 27, No. 2
• Brexanolone, a neurosteroid antidepressant, vindicates the GABAergic deficit hypothesis of depression and may foster resilience 29 May 2019 | F1000Research, Vol. 8
• Historical precedents for the DSM-III bereavement exclusion criteria for major depression 20 March 2018 | Psychological Medicine, Vol. 48, No. 16
• Lower levels of brain‐derived neurotrophic factor are associated with melancholic psychomotor retardation among depressed inpatients 8 March 2018 | Bipolar Disorders, Vol. 20, No. 8
• Hanna Keren , Ph.D. ,
• Georgia O’Callaghan , Ph.D. ,
• Pablo Vidal-Ribas , M.Sc. ,
• George A. Buzzell , Ph.D. ,
• Melissa A. Brotman , Ph.D. ,
• Ellen Leibenluft , M.D. ,
• Pedro M. Pan , M.D. , Ph.D ,
• Liana Meffert , B.Sc. ,
• Ariela Kaiser , B.A. ,
• Selina Wolke , M.Sc. ,
• Daniel S. Pine , M.D. ,
• Argyris Stringaris , M.D. , Ph.D.
• Signes et symptômes en psychiatrie au xxie siècle : une nouvelle frontière… ? French Journal of Psychiatry, Vol. 1
• Evaluation of Prioritization Methods of Extrinsic Apoptotic Signaling Pathway Genes for Retrieval of the New Candidates Associated with Major Depressive Disorder 19 November 2018 | Russian Journal of Genetics, Vol. 54, No. 11
• Imaging genetics paradigms in depression research: Systematic review and meta-analysis Progress in Neuro-Psychopharmacology and Biological Psychiatry, Vol. 86
• The benefits of antidepressants: news or fake news? 20 July 2018 | The British Journal of Psychiatry, Vol. 213, No. 2
• The challenge of psychiatric diagnosis: Looking beyond the symptoms to the company that they keep 15 July 2018 | Bipolar Disorders, Vol. 20, No. 5
• The genealogy of the clinical syndrome of mania: signs and symptoms described in psychiatric texts from 1880 to 1900 11 October 2017 | Psychological Medicine, Vol. 48, No. 10
• When Checklists Were New: The Prototype of DSM’s Operational Criteria 1 September 2018 | Ethical Human Psychology and Psychiatry, Vol. 20, No. 1
• Patient reported outcome measures (PROMs): examination of the psychometric properties of two measures for burden of symptoms and quality of life in patients with depression or anxiety 16 March 2018 | Nordic Journal of Psychiatry, Vol. 72, No. 4
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• Guest Editorial 18 June 2018 | Psychoanalytic Psychotherapy, Vol. 32, No. 2
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• Letter to the Editor: Measuring and defining: the double role of the DSM criteria for psychiatric disorders 17 July 2017 | Psychological Medicine, Vol. 48, No. 5
• The centrality of DSM and non-DSM depressive symptoms in Han Chinese women with major depression Journal of Affective Disorders, Vol. 227
• Commentary: Bipolar disorder in youth – what is it and where is it? – a commentary on Parry et al. (2018) 24 January 2018 | Child and Adolescent Mental Health, Vol. 23, No. 1
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• Behavioural Brain Research, Vol. 344
• Journal of Affective Disorders, Vol. 225
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• BMC Psychiatry, Vol. 18, No. 1
• Revista Latinoamericana de Psicopatologia Fundamental, Vol. 21, No. 1
• Psychopathological dimensions and the clinician's subjective experience Psychiatry Research, Vol. 258
• Editorial: What is depression? 17 November 2017 | Journal of Child Psychology and Psychiatry, Vol. 58, No. 12
• The genealogy of major depression: symptoms and signs of melancholia from 1880 to 1900 8 August 2017 | Molecular Psychiatry, Vol. 22, No. 11
• Persistent increase in TNF and IL‐1 markers in severe mental disorders suggests trait‐related inflammation: a one year follow‐up study 16 August 2017 | Acta Psychiatrica Scandinavica, Vol. 136, No. 4
• Epidemiology of anxiety disorders: from surveys to nosology and back 1 April 2022 | Dialogues in Clinical Neuroscience, Vol. 19, No. 2
• The Philosophy of Nosology Annual Review of Clinical Psychology, Vol. 13, No. 1
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• Mood Disorders 17 April 2017
• Targeting and transforming major depression 16 December 2016 | Acta Psychiatrica Scandinavica, Vol. 135, No. 4
• Biological Psychiatry: Cognitive Neuroscience and Neuroimaging, Vol. 2, No. 4
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• Psychological Medicine, Vol. 47, No. 6
• Psychological Medicine, Vol. 47, No. 12
• Psychological Medicine, Vol. 47, No. 16
• Evidence Based Mental Health, Vol. 20, No. 3
• BMC Medicine, Vol. 15, No. 1
• PLOS ONE, Vol. 12, No. 6
• Frontiers in Psychiatry, Vol. 8
• The Clinical Features of Paranoia in the 20th Century and Their Representation in Diagnostic Criteria From DSM-III Through DSM-5 21 December 2016 | Schizophrenia Bulletin
• Frontiers in Psychiatry, Vol. 7

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