Linking Depressive Symptoms & Academic Achievement in UK Adolescents

Research Paper Title

Depressive symptoms and academic achievement in UK adolescents: a cross-lagged analysis with genetic covariates.

Background

The relationship between adolescent depressive symptoms and academic achievement remains poorly understood. The aim of this study was to help clarify the nature and directionality of this association.

Methods

The researchers used a sample of 13,599 British adolescents (main sample of N=3,809 participants). They fitted cross-lagged panel models using four repeated measures of self-reported depressive symptoms and four measures of academic achievement based on British national records between 11-18 years, separately for male and female adolescents and considering polygenic risk scores (PRS) for educational attainment and depression, alongside other child and parental covariates.

Observational design, variation around measurement times, missing data.

Results

The researchers found evidence of an overall negative association that was stronger in boys (R=-0.21, 95% CI -0.31 to -0.11) than in girls (-0.13, -0.31 to 0.05). Higher depressive symptoms were associated with lower academic achievement at a later stage up to the end of compulsory education (16 years), when the direction of the association reversed, although girls with lower achievement also appeared vulnerable to depressive symptoms at previous stages. The genetic variables derived for this study showed stronger associations for academic achievement, but the PRS for depression also showed a negative association with academic achievement in girls. Child intelligence quotient and peer victimisation also showed relevant associations.

Conclusions

Depressive symptoms and academic achievement should be considered jointly when designing school-based programmes for children and adolescents, alongside gender, child ability and school experience. Including genetic information in research can help to disentangle average from time-varying effects.

Reference

Lopez-Lopez, J.A., Kwong, A.S.F., Washbrook, L., Tilling, K., Fazel, M.S. & Pearson, R.M. (2021) Depressive symptoms and academic achievement in UK adolescents: a cross-lagged analysis with genetic covariates. Journal of Affective Disorders. 284, pp.104-113. doi: 10.1016/j.jad.2021.01.091. Online ahead of print.

Linking Depression & Internet Gaming Disorder

Research Paper Title

Depressive symptoms and depression in individuals with internet gaming disorder: A systematic review and meta-analysis.

Background

Although depression has frequently been associated with Internet Gaming Disorder (IGD), its epidemiological impact on this emerging condition has not been systematically assessed. In this study, the researchers aimed to synthesize the available evidence focusing on depression and depressive symptoms in individuals with IGD.

Methods

The researchers searched PubMed, Embase, PsycINFO, GreyLit, OpenGrey, and ProQuest up to March 2020 for observational studies focusing on depression-related outcomes in IGD. They conducted random-effects meta-analyses on 1) rate of comorbid depression in IGD; 2) severity of depressive symptoms in IGD participants without depression.

Results

The researchers identified 92 studies from 25 different countries including 15,148 participants. 21 studies (n = 5025 participants) provided data for the first analysis, resulting in a pooled event rate of depression of 0.32 (95% Confidence Interval 0.21-0.43). The pooled Beck Depression Inventory scores in individuals without depression were suggestive of mild severity (13 studies, n = 508; 10.3, 95% Confidence Interval 8.3-12.4).

Conclusions

The considerable inconsistency of methods employed across studies limits the transferability of these findings to clinical practice.

The prevalence of depression in individuals with IGD varied considerably across studies, affecting approximately one out of three participants overall. Furthermore, a globally major severity of depressive symptoms was found in those without a clinical diagnosis of depression, compared to the general population.

These findings confirm a relevant impact of mood disturbances in IGD.

Reference

Ostinelli, E.G., Zangani, C., Giordano, B., Maestri, D., Gambini, O., D’Agostino, A., Furukawa, T.A. & Purgato, M. (2021) Depressive symptoms and depression in individuals with internet gaming disorder: A systematic review and meta-analysis. Journal of Affective Disorders. doi: 10.1016/j.jad.2021.02.014. Online ahead of print.

What is the Zung Self-Rating Depression Scale?

Introduction

The Zung Self-Rating Depression Scale (SDS) was designed by Duke University psychiatrist William W.K. Zung MD (1929-1992) to assess the level of depression for patients diagnosed with depressive disorder.

The Levels

  • 20-44: Normal Range.
  • 45-59: Mildly Depressed.
  • 60-69: Moderately Depressed.
  • 70 and above Severely Depressed.

The SDS has been translated into many languages, including Arabic, Azerbaijani, Dutch, German, Portuguese, and Spanish.

You can find an online version of the SDS here.

Refer to Zung Self-Rating Anxiety Scale.

Reference

Zung, W.A.K. (1965) A Self-Rating Depression Scale. Archives of General Psychiatry. 12(1), pp63-70.

Aromatherapy & Mental Health

Research Paper Title

The effects of Lavender and Chamomile essential oil inhalation aromatherapy on depression, anxiety and stress in older community-dwelling people: A randomised controlled trial.

Background

Considering the prevalence of mental health problems in older adults, this study aims to investigate the effect of inhalation aromatherapy using lavender and chamomile essential oils on depression, anxiety, and stress of community-dwelling older people.

Methods

A three-armed, parallel, randomised, and controlled trial design was used in this study. 183 participants were enrolled and randomly assigned to three groups (n = 61): the lavender, chamomile, and control groups. The participants in the experimental groups inhaled three drops of 1.5% lavender and chamomile essential oils for 30 nights. The participants in the control group inhaled only distilled water in a similar fashion. Data were collected using the Depression, Anxiety, and Stress-Scale (DASS) at baseline, immediately after the intervention, and one month after the intervention. Chi-square, Fisher’s exact, one-way ANOVA, and repeated measures ANOVA were used for data analysis.

Results

Statistically significant improvement occurred in depression, anxiety, and stress levels immediately and one month after the intervention in lavender and chamomile groups compared to the control group (p < 0.01).

Conclusions

Inhalation aromatherapy with both lavender and chamomile essential oils helped decrease depression, anxiety, and stress levels in community-dwelling older adults.

Reference

Ebrahimi, H., Mardani, A., Basirinezhad, M.H., Hamidzadeh, A. & Eskandari, F. (2021) The effects of Lavender and Chamomile essential oil inhalation aromatherapy on depression, anxiety and stress in older community-dwelling people: A randomized controlled trial. Explore (New York, N.Y.). doi: 10.1016/j.explore.2020.12.012. Online ahead of print.

What are Rating Scales for Depression?

Introduction

A depression rating scale is a psychiatric measuring instrument having descriptive words and phrases that indicate the severity of depression for a time period.

When used, an observer may make judgements and rate a person at a specified scale level with respect to identified characteristics. Rather than being used to diagnose depression, a depression rating scale may be used to assign a score to a person’s behaviour where that score may be used to determine whether that person should be evaluated more thoroughly for a depressive disorder diagnosis. Several rating scales are used for this purpose.

Between 1918 and 2009, more than 280 measures of depressive severity were developed and published (Santor, Gregus & Welch, 2009).

What is the Purpose of a Rating Scale?

To determine degree of depression.

Who Can Complete Rating Scales?

Scales Completed by Researchers

Some depression rating scales are completed by researchers. For example, the Hamilton Depression Rating Scale includes 21 questions with between 3 and 5 possible responses which increase in severity. The clinician must choose the possible responses to each question by interviewing the patient and by observing the patient’s symptoms. Designed by psychiatrist Max Hamilton in 1960, the Hamilton Depression Rating Scale is one of the two most commonly used among those completed by researchers assessing the effects of drug therapy. Alternatively, the Montgomery-Åsberg Depression Rating Scale has ten items to be completed by researchers assessing the effects of drug therapy and is the other of the two most commonly used among such researchers. Another scale is the Raskin Depression Rating Scale; which rates the severity of the patients symptoms in three areas: verbal reports, behaviour, and secondary symptoms of depression.

Scales Completed by Patients

Some depression rating scales are completed by patients. The Beck Depression Inventory, for example, is a 21-question self-report inventory that covers symptoms such as irritability, fatigue, weight loss, lack of interest in sex, and feelings of guilt, hopelessness or fear of being punished. The scale is completed by patients to identify the presence and severity of symptoms consistent with the DSM-IV diagnostic criteria. The Beck Depression Inventory was originally designed by psychiatrist Aaron T. Beck in 1961.

The Geriatric Depression Scale (GDS) is another self-administered scale, but in this case it is used for older patients, and for patients with mild to moderate dementia. Instead of presenting a five-category response set, the GDS questions are answered with a simple “yes” or “no”. The Zung Self-Rating Depression Scale is similar to the Geriatric Depression Scale in that the answers are preformatted. In the Zung Self-Rating Depression Scale, there are 20 items: ten positively worded and ten negatively worded. Each question is rated on a scale of 1 through 4 based on four possible answers: “a little of the time”, “some of the time”, “good part of the time”, and “most of the time”.

The Patient Health Questionnaire (PHQ) sets are self-reported depression rating scales. For example, the Patient Health Questionnaire-9 (PHQ-9) is a self-reported, 9-question version of the Primary Care Evaluation of Mental Disorders. The Patient Health Questionnaire-2 (PHQ-2) is a shorter version of the PHQ-9 with two screening questions to assess the presence of a depressed mood and a loss of interest or pleasure in routine activities; a positive response to either question indicates further testing is required.

The two questions on the Patient Health Questionnaire-2 (PHQ-2):

During the past month, have you often been bothered by feeling down, depressed, or hopeless?

During the past month, have you often been bothered by little interest or pleasure in doing things?

Scales Completed by Patients and Researchers

The Primary Care Evaluation of Mental Disorders (PRIME-MD) is completed by the patient and a researcher. This depression rating scale includes a 27-item screening questionnaire and follow-up clinician interview designed to facilitate the diagnosis of common mental disorders in primary care. Its lengthy administration time has limited its clinical usefulness; it has been replaced by the Patient Health Questionnaire.

What is the Validity and Usefulness of Rating Scales?

How Useful are Rating Scales?

Screening programmes using rating scales to search for candidates for a more in-depth evaluation have been advocated to improve detection of depression, but there is evidence that they do not improve detection rates, treatment, or outcome. There is also evidence that a consensus on the interpretation of rating scales, in particular the Hamilton Rating Scale for Depression, is largely missing, leading to misdiagnosis of the severity of a patient’s depression. However, there is evidence that portions of rating scales, such as the somatic section of the PHQ-9, can be useful in predicting outcomes for subgroups of patients like coronary heart disease patients.

How Valid are Rating Scales?

Several research articles have come out in the past several years that question the validity of sum-score rating scales for depression.

Fried, E.I. (2017) The 52 Symptoms of Major Depression: Lack of Content Overlap Among Seven Common Depression Scales. Journal of Affective Disorders. 208, pp.191-197. https://doi.org/10.1016/j.jad.2016.10.019.

Santor, D.A., Gregus, M. & Welch, A. (2009) Eight Decades of Measurement in Depression. Measurement: Interdisciplinary Research and Perspectives. 4(3), pp.135-155. https://doi.org/10.1207/s15366359mea0403_1.

Copyrighted vs. Public Domain Rating Scales

The Beck Depression Inventory is copyrighted, a fee must be paid for each copy used, and photocopying it is a violation of copyright. There is no evidence that the BDI-II is more valid or reliable than other depression scales, and public domain scales such as the Centre for Epidemiological Studies Depression Scale (CES-D), the Zung Depression scale and Patient Health Questionnaire – Nine Item (PHQ-9) has been studied as a useful tool.

Other copyrighted scales allow individual clinicians and researchers to make copies for their own use, but require licenses for electronic versions or large-scale redistribution, including:

  • The Clinically Useful Depression Outcome Scale (CUDOS).
  • The Inventory of Depressive Symptomatology (IDS).
  • The Mood and Feelings Questionnaire (MFQ).
  • The Quick Inventory of Depressive Symptoms (QIDS).
  • The Patient Health Questionnaire (PHQ).
    • Research in process – Banner University Medical Centre.
  • Hamilton Rating Scale (HRSDD, HDRS, Ham-D).
  • Columbia Suicide Severity Rating Scale (C-SSRS).
  • Depression and Anxiety Stress Scales (DASS).
  • Depression Self-Rating Scale for Children.
  • Brief Psychiatric Rating Scale (BPRS).
  • Geriatric Depression Scale (GDS).
  • Beck’s Depression Inventory (BDI).
  • HEADS-ED, used in hospital emergency departments.
  • Children’s Depression Rating Scale (CDRS).
  • Behavioural Activation for Depression Scale (BADS-SF).
  • Edinburgh Postnatal Depression Scale.
  • Quick Inventory of Depressive Symptomatology Clinician (QIDS-C).
  • Quick Inventory of Depressive Symptomatology Self Report (QIDS-SR).
  • Kutcher Adolescent Depression Scale (KADS-11).
  • Montgomery-Asberg Depression Scale (MADRS).
  • Clinically Useful Depression Outcome Scale (CUDOS).
  • Hospital Anxiety and Depression Scale.
  • Primary Care Evaluation of Mental Disorders (PRIME-MD).
  • Children’s Depression Inventory (CDI).

What is the Prevalence & Risk Factors of Perinatal Depression Among Women in Rural Bihar?

Research Paper Title

Prevalence and risk factors of perinatal depression among women in rural Bihar: A community-based cross-sectional study.

Background

Perinatal depression (PND) is one of the most common mental disorders occurring during the perinatal period among women. Few studies examined prevalence and risk factors of PND from rural settings in India. This study aimed to estimate the prevalence of perinatal depression and identify social risk factors for it among women from rural Bihar.

Methods

A cross sectional study was conducted in a community setting in rural areas of Bihar. All perinatal women were screened through a door to door survey and recruited after obtaining informed consent. A semi-structured proforma was used to collect sociodemographic characteristics and family related variables. Edinburgh postnatal depression scale (EPDS) was used to screen for perinatal depression.

Results

A total of 564 perinatal women were recruited into the study. The estimated prevalence of PND was 23.9 % (95 % CI: 20.6,27.6). Multivariate analysis showed perinatal depression was associated with physical illness in the mother, previous history of abortion, poor financial status and ill-treatment by in-laws.

Conclusions

Prevalence of perinatal depression among women is high in rural settings of North India. A multitude of factors ranging from physical, obstetric, economic and family related confer a high risk for PND. Comprehensive interventions are needed to address these risk factors of perinatal depression.

Reference

Raghavan, V., Khan, H.A., Seshu, U., Rai, S.P., Durairaj, J., Aarthi, G., Sangeetha, C., John, S. & Thara, R. (2021) Prevalence and risk factors of perinatal depression among women in rural Bihar: A community-based cross-sectional study. Asian Journal of Psychiatry. doi: 10.1016/j.ajp.2021.102552. Online ahead of print.

What is Major Depressive Disorder?

Introduction

Major depressive disorder (MDD), also known simply as depression, is a mental disorder characterised by at least two weeks of pervasive low mood. Low self-esteem, loss of interest in normally enjoyable activities, low energy, and pain without a clear cause are common symptoms. Those affected may also occasionally have delusions or hallucinations. Some people have periods of depression separated by years, while others nearly always have symptoms present. Major depression is more severe and lasts longer than sadness, which is a normal part of life.

The diagnosis of MDD is based on the person’s reported experiences and a mental status examination. There is no laboratory test for the disorder, but testing may be done to rule out physical conditions that can cause similar symptoms. Those with MDD are typically treated with counselling and antidepressant medication. Medication appears to be effective, but the effect may only be significant in the most severely depressed. Types of counselling used include cognitive behavioural therapy (CBT) and interpersonal therapy, and electroconvulsive therapy (ECT) may be considered if other measures are not effective. Hospitalisation may be necessary in cases with a risk of harm to self and may occasionally occur against a person’s wishes.

The most common time of onset is in a person’s 20s and 30s, with females affected about twice as often as males. MDD affected approximately 163 million people (2% of the world’s population) in 2017. The percentage of people who are affected at one point in their life varies from 7% in Japan to 21% in France. Lifetime rates are higher in the developed world (15%) compared to the developing world (11%). The disorder causes the second-most years lived with disability, after lower back pain.

The term MDD was introduced by a group of US clinicians in the mid-1970s. The cause of MDD is believed to be a combination of genetic, environmental, and psychological factors, with about 40% of the risk related to genetics. Risk factors include a family history of the condition, major life changes, certain medications, chronic health problems, and substance abuse. It can negatively affect a person’s personal life, work life, or education as well as sleeping, eating habits, and general health. Those currently or previously affected with the disorder may be stigmatised.

Not to be confused with Depression (Mood).

Brief History

The Ancient Greek physician Hippocrates described a syndrome of melancholia as a distinct disease with particular mental and physical symptoms; he characterised all “fears and despondencies, if they last a long time” as being symptomatic of the ailment. It was a similar but far broader concept than today’s depression; prominence was given to a clustering of the symptoms of sadness, dejection, and despondency, and often fear, anger, delusions and obsessions were included.

The term depression itself was derived from the Latin verb deprimere, “to press down”. From the 14th century, “to depress” meant to subjugate or to bring down in spirits. It was used in 1665 in English author Richard Baker’s Chronicle to refer to someone having “a great depression of spirit”, and by English author Samuel Johnson in a similar sense in 1753. The term also came into use in physiology and economics. An early usage referring to a psychiatric symptom was by French psychiatrist Louis Delasiauve in 1856, and by the 1860s it was appearing in medical dictionaries to refer to a physiological and metaphorical lowering of emotional function. Since Aristotle, melancholia had been associated with men of learning and intellectual brilliance, a hazard of contemplation and creativity. The newer concept abandoned these associations and through the 19th century, became more associated with women.

Although melancholia remained the dominant diagnostic term, depression gained increasing currency in medical treatises and was a synonym by the end of the century; German psychiatrist Emil Kraepelin may have been the first to use it as the overarching term, referring to different kinds of melancholia as depressive states.

Sigmund Freud likened the state of melancholia to mourning in his 1917 paper Mourning and Melancholia. He theorized that objective loss, such as the loss of a valued relationship through death or a romantic break-up, results in subjective loss as well; the depressed individual has identified with the object of affection through an unconscious, narcissistic process called the libidinal cathexis of the ego. Such loss results in severe melancholic symptoms more profound than mourning; not only is the outside world viewed negatively but the ego itself is compromised. The patient’s decline of self-perception is revealed in his belief of his own blame, inferiority, and unworthiness. He also emphasized early life experiences as a predisposing factor. Adolf Meyer put forward a mixed social and biological framework emphasizing reactions in the context of an individual’s life, and argued that the term depression should be used instead of melancholia. The first version of the DSM (DSM-I, 1952) contained depressive reaction and the DSM-II (1968) depressive neurosis, defined as an excessive reaction to internal conflict or an identifiable event, and also included a depressive type of manic-depressive psychosis within Major affective disorders.

In the mid-20th century, researchers theorised that depression was caused by a chemical imbalance in neurotransmitters in the brain, a theory based on observations made in the 1950s of the effects of reserpine and isoniazid in altering monoamine neurotransmitter levels and affecting depressive symptoms. The chemical imbalance theory has never been proven.

The term unipolar (along with the related term bipolar) was coined by the neurologist and psychiatrist Karl Kleist, and subsequently used by his disciples Edda Neele and Karl Leonhard.

The term Major depressive disorder was introduced by a group of US clinicians in the mid-1970s as part of proposals for diagnostic criteria based on patterns of symptoms (called the “Research Diagnostic Criteria”, building on earlier Feighner Criteria), and was incorporated into the DSM-III in 1980. The American Psychiatric Association added “major depressive disorder” to the Diagnostic and Statistical Manual of Mental Disorders (DSM-III), as a split of the previous depressive neurosis in the DSM-II, which also encompassed the conditions now known as dysthymia and adjustment disorder with depressed mood. To maintain consistency the ICD-10 used the same criteria, with only minor alterations, but using the DSM diagnostic threshold to mark a mild depressive episode, adding higher threshold categories for moderate and severe episodes. The ancient idea of melancholia still survives in the notion of a melancholic subtype.

The new definitions of depression were widely accepted, albeit with some conflicting findings and views. There have been some continued empirically based arguments for a return to the diagnosis of melancholia. There has been some criticism of the expansion of coverage of the diagnosis, related to the development and promotion of antidepressants and the biological model since the late 1950s.

Epidemiology

MDD affected approximately 163 million people in 2017 (2% of the global population). The percentage of people who are affected at one point in their life varies from 7% in Japan to 21% in France. In most countries the number of people who have depression during their lives falls within an 8-18% range. In North America, the probability of having a major depressive episode within a year-long period is 3-5% for males and 8-10% for females. Major depression is about twice as common in women as in men, although it is unclear why this is so, and whether factors unaccounted for are contributing to this. The relative increase in occurrence is related to pubertal development rather than chronological age, reaches adult ratios between the ages of 15 and 18, and appears associated with psychosocial more than hormonal factors. As of 2017, depression is the third most common worldwide cause of disability among both sexes, following low back pain and headache.

People are most likely to develop their first depressive episode between the ages of 30 and 40, and there is a second, smaller peak of incidence between ages 50 and 60. The risk of major depression is increased with neurological conditions such as stroke, Parkinson’s disease, or multiple sclerosis, and during the first year after childbirth. It is also more common after cardiovascular illnesses, and is related more to those with a poor cardiac disease outcome than to a better one. Studies conflict on the prevalence of depression in the elderly, but most data suggest there is a reduction in this age group. Depressive disorders are more common in urban populations than in rural ones and the prevalence is increased in groups with poorer socioeconomic factors, e.g. homelessness.

Signs and Symptoms

Major depression significantly affects a person’s family and personal relationships, work or school life, sleeping and eating habits, and general health. Its impact on functioning and well-being has been compared to that of other chronic medical conditions, such as diabetes.

A person having a major depressive episode usually exhibits a low mood, which pervades all aspects of life, and an inability to experience pleasure in previously enjoyable activities. Depressed people may be preoccupied with – or ruminate over – thoughts and feelings of worthlessness, inappropriate guilt or regret, helplessness or hopelessness. In severe cases, depressed people may have symptoms of psychosis. These symptoms include delusions or, less commonly, hallucinations, usually unpleasant. Other symptoms of depression include poor concentration and memory (especially in those with melancholic or psychotic features), withdrawal from social situations and activities, reduced sex drive, irritability, and thoughts of death or suicide. Insomnia is common among the depressed. In the typical pattern, a person wakes very early and cannot get back to sleep. Hypersomnia, or oversleeping, can also happen. Some antidepressants may also cause insomnia due to their stimulating effect.

A depressed person may report multiple physical symptoms such as fatigue, headaches, or digestive problems; physical complaints are the most common presenting problem in developing countries, according to the World Health Organisation’s (WHO’s) criteria for depression. Appetite often decreases, with resulting weight loss, although increased appetite and weight gain occasionally occur. Family and friends may notice that the person’s behaviour is either agitated or lethargic. Older depressed people may have cognitive symptoms of recent onset, such as forgetfulness, and a more noticeable slowing of movements.

Depressed children may often display an irritable mood rather than a depressed one, and show varying symptoms depending on age and situation. Most lose interest in school and show a decline in academic performance. They may be described as clingy, demanding, dependent, or insecure. Diagnosis may be delayed or missed when symptoms are interpreted as “normal moodiness.”

Associated Conditions

Major depression frequently co-occurs with other psychiatric problems. The 1990-1992 National Comorbidity Survey (US) reports that half of those with major depression also have lifetime anxiety and its associated disorders such as generalised anxiety disorder. Anxiety symptoms can have a major impact on the course of a depressive illness, with delayed recovery, increased risk of relapse, greater disability and increased suicide attempts. There are increased rates of alcohol and drug abuse and particularly dependence, and around a third of individuals diagnosed with attention deficit hyperactivity disorder (ADHD) develop comorbid depression. Post-traumatic stress disorder and depression often co-occur. Depression may also coexist with ADHD, complicating the diagnosis and treatment of both. Depression is also frequently comorbid with alcohol abuse and personality disorders. Depression can also be exacerbated during particular months (usually winter) for those with seasonal affective disorder. While overuse of digital media has been associated with depressive symptoms, digital media may also be utilised in some situations to improve mood.

Depression and pain often co-occur. One or more pain symptoms are present in 65% of depressed patients, and anywhere from 5 to 85% of patients with pain will be suffering from depression, depending on the setting; there is a lower prevalence in general practice, and higher in specialty clinics. The diagnosis of depression is often delayed or missed, and the outcome can worsen if the depression is noticed but completely misunderstood.

Depression is also associated with a 1.5- to 2-fold increased risk of cardiovascular disease, independent of other known risk factors, and is itself linked directly or indirectly to risk factors such as smoking and obesity. People with major depression are less likely to follow medical recommendations for treating and preventing cardiovascular disorders, which further increases their risk of medical complications. In addition, cardiologists may not recognise underlying depression that complicates a cardiovascular problem under their care.

Depression often coexists with physical disorders common among the elderly, such as stroke, other cardiovascular diseases, Parkinson’s disease, and chronic obstructive pulmonary disease.

Cause(s)

The biopsychosocial model proposes that biological, psychological, and social factors all play a role in causing depression. The diathesis-stress model specifies that depression results when a pre-existing vulnerability, or diathesis, is activated by stressful life events. The pre-existing vulnerability can be either genetic, implying an interaction between nature and nurture, or schematic, resulting from views of the world learned in childhood.

Childhood abuse, either physical, sexual or psychological, are all risk factors for depression, among other psychiatric issues that co-occur such as anxiety and drug abuse. Childhood trauma also correlates with severity of depression, lack of response to treatment and length of illness. However, some are more susceptible to developing mental illness such as depression after trauma, and various genes have been suggested to control susceptibility.

Genetics

Family and twin studies find that nearly 40% of individual differences in risk for major depressive disorder can be explained by genetic factors. Like most psychiatric disorders, major depressive disorder is likely to be influenced by many individual genetic changes. In 2018, a genome-wide association study discovered 44 variants in the genome linked to risk for major depression. This was followed by a 2019 study that found 102 variants in the genome linked to depression.

The 5-HTTLPR, or serotonin transporter promoter gene’s short allele has been associated with increased risk of depression. However, since the 1990s, results have been inconsistent, with three recent reviews finding an effect and two finding none. Other genes that have been linked to a gene-environment interaction include CRHR1, FKBP5 and BDNF, the first two of which are related to the stress reaction of the HPA axis, and the latter of which is involved in neurogenesis. There is no conclusive effects of candidate gene on depression, either alone or in combination with life stress. Research focusing on specific candidate genes has been criticised for its tendency to generate false positive findings. There are also other efforts to examine interactions between life stress and polygenic risk for depression.

Other Health Problems

Depression may also come secondary to a chronic or terminal medical condition, such as HIV/AIDS or asthma, and may be labelled “secondary depression.” It is unknown whether the underlying diseases induce depression through effect on quality of life, of through shared aetiologies (such as degeneration of the basal ganglia in Parkinson’s disease or immune dysregulation in asthma). Depression may also be iatrogenic (the result of healthcare), such as drug-induced depression. Therapies associated with depression include interferons, beta-blockers, isotretinoin, contraceptives, cardiac agents, anticonvulsants, antimigraine drugs, antipsychotics, and hormonal agents such as gonadotropin-releasing hormone agonist. Drug abuse in early age is also associated with increased risk of developing depression later in life. Depression that occurs as a result of pregnancy is called postpartum depression, and is thought to be the result of hormonal changes associated with pregnancy. Seasonal affective disorder, a type of depression associated with seasonal changes in sunlight, is thought to be the result of decreased sunlight.

Pathophysiology

The pathophysiology of depression is not yet understood, but the current theories centre around monoaminergic systems, the circadian rhythm, immunological dysfunction, HPA axis dysfunction and structural or functional abnormalities of emotional circuits.

The monoamine theory, derived from the efficacy of monoaminergic drugs in treating depression, was the dominant theory until recently. The theory postulates that insufficient activity of monoamine neurotransmitters is the primary cause of depression. Evidence for the monoamine theory comes from multiple areas. Firstly, acute depletion of tryptophan, a necessary precursor of serotonin, a monoamine, can cause depression in those in remission or relatives of depressed patients; this suggests that decreased serotonergic neurotransmission is important in depression. Secondly, the correlation between depression risk and polymorphisms in the 5-HTTLPR gene, which codes for serotonin receptors, suggests a link. Third, decreased size of the locus coeruleus, decreased activity of tyrosine hydroxylase, increased density of alpha-2 adrenergic receptor, and evidence from rat models suggest decreased adrenergic neurotransmission in depression. Furthermore, decreased levels of homovanillic acid, altered response to dextroamphetamine, responses of depressive symptoms to dopamine receptor agonists, decreased dopamine receptor D1 binding in the striatum, and polymorphism of dopamine receptor genes implicate dopamine, another monoamine, in depression. Lastly, increased activity of monoamine oxidase, which degrades monoamines, has been associated with depression. However, this theory is inconsistent with the fact that serotonin depletion does not cause depression in healthy persons, the fact that antidepressants instantly increase levels of monoamines but take weeks to work, and the existence of atypical antidepressants which can be effective despite not targeting this pathway. One proposed explanation for the therapeutic lag, and further support for the deficiency of monoamines, is a desensitisation of self-inhibition in raphe nuclei by the increased serotonin mediated by antidepressants. However, disinhibition of the dorsal raphe has been proposed to occur as a result of decreased serotonergic activity in tryptophan depletion, resulting in a depressed state mediated by increased serotonin. Further countering the monoamine hypothesis is the fact that rats with lesions of the dorsal raphe are not more depressive than controls, the finding of increased jugular 5-HIAA in depressed patients that normalised with SSRI treatment, and the preference for carbohydrates in depressed patients. Already limited, the monoamine hypothesis has been further oversimplified when presented to the general public.

Immune system abnormalities have been observed, including increased levels of cytokines involved in generating sickness behaviour (which shares overlap with depression). The effectiveness of nonsteroidal anti-inflammatory drugs (NSAIDs) and cytokine inhibitors in treating depression, and normalization of cytokine levels after successful treatment further suggest immune system abnormalities in depression.

HPA axis abnormalities have been suggested in depression given the association of CRHR1 with depression and the increased frequency of dexamethasone test non-suppression in depressed patients. However, this abnormality is not adequate as a diagnosis tool, because its sensitivity is only 44%. These stress-related abnormalities have been hypothesized to be the cause of hippocampal volume reductions seen in depressed patients. Furthermore, a meta-analysis yielded decreased dexamethasone suppression, and increased response to psychological stressors. Further abnormal results have been obscured with the cortisol awakening response, with increased response being associated with depression.

Theories unifying neuroimaging findings have been proposed. The first model proposed is the “Limbic Cortical Model”, which involves hyperactivity of the ventral paralimbic regions and hypoactivity of frontal regulatory regions in emotional processing. Another model, the “Corito-Striatal model”, suggests that abnormalities of the prefrontal cortex in regulating striatal and subcortical structures results in depression. Another model proposes hyperactivity of salience structures in identifying negative stimuli, and hypoactivity of cortical regulatory structures resulting in a negative emotional bias and depression, consistent with emotional bias studies.

Diagnosis

Clinical Assessment

A diagnostic assessment may be conducted by a suitably trained general practitioner, or by a psychiatrist or psychologist, who records the person’s current circumstances, biographical history, current symptoms, family history, and alcohol and drug use. The assessment also includes a mental state examination, which is an assessment of the person’s current mood and thought content, in particular the presence of themes of hopelessness or pessimism, self-harm or suicide, and an absence of positive thoughts or plans. Specialist mental health services are rare in rural areas, and thus diagnosis and management is left largely to primary-care clinicians. This issue is even more marked in developing countries. Rating scales are not used to diagnose depression, but they provide an indication of the severity of symptoms for a time period, so a person who scores above a given cut-off point can be more thoroughly evaluated for a depressive disorder diagnosis. Several rating scales are used for this purpose; these include the Hamilton Rating Scale for Depression, the Beck Depression Inventory[90] or the Suicide Behaviours Questionnaire-Revised.

Primary-care physicians and other non-psychiatrist physicians have more difficulty with under-recognition and undertreatment of depression compared to psychiatric physicians, in part because of the physical symptoms that often accompany depression, in addition to many potential patient, provider, and system barriers. A review found that non-psychiatrist physicians miss about two-thirds of cases, though this has improved somewhat in more recent studies.

Before diagnosing major depressive disorder, a doctor generally performs a medical examination and selected investigations to rule out other causes of symptoms. These include blood tests measuring TSH and thyroxine to exclude hypothyroidism; basic electrolytes and serum calcium to rule out a metabolic disturbance; and a full blood count including ESR to rule out a systemic infection or chronic disease. Adverse affective reactions to medications or alcohol misuse are often ruled out, as well. Testosterone levels may be evaluated to diagnose hypogonadism, a cause of depression in men. Vitamin D levels might be evaluated, as low levels of vitamin D have been associated with greater risk for depression.

Subjective cognitive complaints appear in older depressed people, but they can also be indicative of the onset of a dementing disorder, such as Alzheimer’s disease. Cognitive testing and brain imaging can help distinguish depression from dementia. A CT scan can exclude brain pathology in those with psychotic, rapid-onset or otherwise unusual symptoms. No biological tests confirm major depression. In general, investigations are not repeated for a subsequent episode unless there is a medical indication.

DSM and ICD Criteria

The most widely used criteria for diagnosing depressive conditions are found in the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders (DSM) and the WHO’s International Statistical Classification of Diseases and Related Health Problems (ICD) which uses the name depressive episode for a single episode and recurrent depressive disorder for repeated episodes. The latter system is typically used in European countries, while the former is used in the US and many other non-European nations, and the authors of both have worked towards conforming one with the other.

Both DSM-5 and ICD-10 mark out typical (main) depressive symptoms. ICD-10 defines three typical depressive symptoms (depressed mood, anhedonia, and reduced energy), two of which should be present to determine the depressive disorder diagnosis. According to DSM-5, there are two main depressive symptoms- a depressed mood and loss of interest/pleasure in activities (anhedonia). These symptoms, as well as five out of the nine more specific symptoms listed, must frequently occur for more than two weeks (to the extent in which it impairs functioning) for the diagnosis.

MDD is classified as a mood disorder in DSM-5. The diagnosis hinges on the presence of single or recurrent major depressive episodes. Further qualifiers are used to classify both the episode itself and the course of the disorder. The category Unspecified Depressive Disorder is diagnosed if the depressive episode’s manifestation does not meet the criteria for a major depressive episode. The ICD-10 system does not use the term major depressive disorder but lists very similar criteria for the diagnosis of a depressive episode (mild, moderate or severe); the term recurrent may be added if there have been multiple episodes without mania.

Major Depressive Episode

A major depressive episode (MDE) is characterised by the presence of a severely depressed mood that persists for at least two weeks.

Episodes may be isolated or recurrent and are categorised as mild (few symptoms in excess of minimum criteria), moderate, or severe (marked impact on social or occupational functioning). An episode with psychotic features – commonly referred to as psychotic depression – is automatically rated as severe. If the patient has had an episode of mania or markedly elevated mood, a diagnosis of bipolar disorder is made instead. Depression without mania is sometimes referred to as unipolar because the mood remains at one emotional state or “pole”.

DSM-IV-TR excludes cases where the symptoms are a result of bereavement, although it is possible for normal bereavement to evolve into a depressive episode if the mood persists and the characteristic features of a MDE develop. The criteria were criticised because they do not take into account any other aspects of the personal and social context in which depression can occur. In addition, some studies have found little empirical support for the DSM-IV cut-off criteria, indicating they are a diagnostic convention imposed on a continuum of depressive symptoms of varying severity and duration. Bereavement is no longer an exclusion criterion in DSM-5, and it is now up to the clinician to distinguish between normal reactions to a loss and MDD. Excluded are a range of related diagnoses, including:

  • Dysthymia, which involves a chronic but milder mood disturbance;
  • Recurrent brief depression, consisting of briefer depressive episodes;
  • Minor depressive disorder, whereby only some symptoms of major depression are present; and
  • Adjustment disorder with depressed mood, which denotes low mood resulting from a psychological response to an identifiable event or stressor.

Three new depressive disorders were added to the DSM-5:

  • Disruptive mood dysregulation disorder, classified by significant childhood irritability and tantrums;
  • Premenstrual dysphoric disorder (PMDD), causing periods of anxiety, depression, or irritability in the week or two before a woman’s menstruation, and
  • Persistent depressive disorder.

Subtypes

The DSM-5 recognises six further subtypes of MDD, called specifiers, in addition to noting the length, severity and presence of psychotic features:

  • Melancholic depression:
    • This is characterised by a loss of pleasure in most or all activities, a failure of reactivity to pleasurable stimuli, a quality of depressed mood more pronounced than that of grief or loss, a worsening of symptoms in the morning hours, early-morning waking, psychomotor retardation, excessive weight loss (not to be confused with anorexia nervosa), or excessive guilt.
  • Atypical depression:
    • This is characterised by mood reactivity (paradoxical anhedonia) and positivity, significant weight gain or increased appetite (comfort eating), excessive sleep or sleepiness (hypersomnia), a sensation of heaviness in limbs known as leaden paralysis, and significant social impairment as a consequence of hypersensitivity to perceived interpersonal rejection.
  • Catatonic depression:
    • This is a rare and severe form of major depression involving disturbances of motor behaviour and other symptoms.
    • Here, the person is mute and almost stuporous, and either remains immobile or exhibits purposeless or even bizarre movements.
    • Catatonic symptoms also occur in schizophrenia or in manic episodes, or may be caused by neuroleptic malignant syndrome.
  • Depression with anxious distress:
    • This was added into the DSM-V as a means to emphasize the common co-occurrence between depression or mania and anxiety, as well as the risk of suicide of depressed individuals with anxiety.
    • Specifying in such a way can also help with the prognosis of those diagnosed with a depressive or bipolar disorder.
  • Depression with peri-partum onset:
    • This refers to the intense, sustained and sometimes disabling depression experienced by women after giving birth or while a woman is pregnant.
    • DSM-IV-TR used the classification “postpartum depression,” but this was changed in order to not exclude cases of depressed woman during pregnancy.
    • Depression with peripartum onset has an incidence rate of 10-15% among new mothers.
    • The DSM-V mandates that, in order to qualify as depression with peripartum onset, onset occur during pregnancy or within one month of delivery.
    • It has been said that postpartum depression can last as long as three months.
  • Seasonal affective disorder (SAD):
    • This is a form of depression in which depressive episodes come on in the autumn or winter, and resolve in spring.
    • The diagnosis is made if at least two episodes have occurred in colder months with none at other times, over a two-year period or longer.

Differential Diagnosis

Refer to Differential Diagnoses of Depression.

To confirm MDD as the most likely diagnosis, other potential diagnoses must be considered, including dysthymia, adjustment disorder with depressed mood, or bipolar disorder. Dysthymia is a chronic, milder mood disturbance in which a person reports a low mood almost daily over a span of at least two years. The symptoms are not as severe as those for major depression, although people with dysthymia are vulnerable to secondary episodes of major depression (sometimes referred to as double depression). Adjustment disorder with depressed mood is a mood disturbance appearing as a psychological response to an identifiable event or stressor, in which the resulting emotional or behavioural symptoms are significant but do not meet the criteria for a MDE. Bipolar disorder, also known as manic–depressive disorder, is a condition in which depressive phases alternate with periods of mania or hypomania. Although depression is currently categorised as a separate disorder, there is ongoing debate because individuals diagnosed with major depression often experience some hypomanic symptoms, indicating a mood disorder continuum. Further differential diagnoses involve chronic fatigue syndrome.

Other disorders need to be ruled out before diagnosing major depressive disorder. They include depressions due to physical illness, medications, and substance abuse. Depression due to physical illness is diagnosed as a mood disorder due to a general medical condition. This condition is determined based on history, laboratory findings, or physical examination. When the depression is caused by a medication, drug of abuse, or exposure to a toxin, it is then diagnosed as a specific mood disorder (previously called substance-induced mood disorder in the DSM-IV-TR).

Screening and Prevention

Since 2016, the United States Preventive Services Task Force (USPSTF) has recommended screening for depression among those over the age 12; a 2005 Cochrane review found that the routine use of screening questionnaires has little effect on detection or treatment.

Preventive efforts may result in decreases in rates of the condition of between 22 and 38%. Eating large amounts of fish may also reduce the risk.

Behavioural interventions, such as interpersonal therapy and cognitive-behavioural therapy, are effective at preventing new onset depression. Because such interventions appear to be most effective when delivered to individuals or small groups, it has been suggested that they may be able to reach their large target audience most efficiently through the Internet.

However, an earlier meta-analysis found preventive programmes with a competence-enhancing component to be superior to behaviour-oriented programmes overall, and found behavioural programmes to be particularly unhelpful for older people, for whom social support programmes were uniquely beneficial. In addition, the programs that best prevented depression comprised more than eight sessions, each lasting between 60 and 90 minutes, were provided by a combination of lay and professional workers, had a high-quality research design, reported attrition rates, and had a well-defined intervention.

The Netherlands mental health care system provides preventive interventions, such as the “Coping with Depression” course (CWD) for people with sub-threshold depression. The course is claimed to be the most successful of psychoeducational interventions for the treatment and prevention of depression (both for its adaptability to various populations and its results), with a risk reduction of 38% in major depression and an efficacy as a treatment comparing favourably to other psychotherapies.

Management

The three most common treatments for depression are psychotherapy, medication, and electroconvulsive therapy. Psychotherapy is the treatment of choice (over medication) for people under 18. The UK National Institute for Health and Care Excellence (NICE) 2004 guidelines indicate that antidepressants should not be used for the initial treatment of mild depression because the risk-benefit ratio is poor. The guidelines recommend that antidepressants treatment in combination with psychosocial interventions should be considered for:

  • People with a history of moderate or severe depression.
  • Those with mild depression that has been present for a long period.
  • As a second line treatment for mild depression that persists after other interventions.
  • As a first line treatment for moderate or severe depression.

The guidelines further note that antidepressant treatment should be continued for at least six months to reduce the risk of relapse, and that SSRIs are better tolerated than tricyclic antidepressants.

American Psychiatric Association treatment guidelines recommend that initial treatment should be individually tailored based on factors including severity of symptoms, co-existing disorders, prior treatment experience, and patient preference. Options may include pharmacotherapy, psychotherapy, exercise, electroconvulsive therapy (ECT), transcranial magnetic stimulation (TMS) or light therapy. Antidepressant medication is recommended as an initial treatment choice in people with mild, moderate, or severe major depression, and should be given to all patients with severe depression unless ECT is planned. There is evidence that collaborative care by a team of health care practitioners produces better results than routine single-practitioner care.

Treatment options are much more limited in developing countries, where access to mental health staff, medication, and psychotherapy is often difficult. Development of mental health services is minimal in many countries; depression is viewed as a phenomenon of the developed world despite evidence to the contrary, and not as an inherently life-threatening condition. A 2014 Cochrane review found insufficient evidence to determine the effectiveness of psychological versus medical therapy in children.

Lifestyle

Physical exercise is recommended for management of mild depression, and has a moderate effect on symptoms. Exercise has also been found to be effective for (unipolar) major depression. It is equivalent to the use of medications or psychological therapies in most people. In older people it does appear to decrease depression. Exercise may be recommended to people who are willing, motivated, and physically healthy enough to participate in an exercise programme as treatment.

There is a small amount of evidence that skipping a night’s sleep may improve depressive symptoms, with the effects usually showing up within a day. This effect is usually temporary. Besides sleepiness, this method can cause a side effect of mania or hypomania.

In observational studies, smoking cessation has benefits in depression as large as or larger than those of medications.

Besides exercise, sleep and diet may play a role in depression, and interventions in these areas may be an effective add-on to conventional methods.

Talking Therapies

Talking therapy (psychotherapy) can be delivered to individuals, groups, or families by mental health professionals. A 2017 review found that cognitive behavioural therapy appears to be similar to antidepressant medication in terms of effect. A 2012 review found psychotherapy to be better than no treatment but not other treatments. With more complex and chronic forms of depression, a combination of medication and psychotherapy may be used. There is moderate-quality evidence that psychological therapies are a useful addition to standard antidepressant treatment of treatment-resistant depression in the short term.

Psychotherapy has been shown to be effective in older people. Successful psychotherapy appears to reduce the recurrence of depression even after it has been stopped or replaced by occasional booster sessions.

Cognitive Behavioural Therapy

Cognitive behavioural therapy (CBT) currently has the most research evidence for the treatment of depression in children and adolescents, and CBT and interpersonal psychotherapy (IPT) are preferred therapies for adolescent depression. In people under 18, according to the National Institute for Health and Clinical Excellence, medication should be offered only in conjunction with a psychological therapy, such as CBT, interpersonal therapy, or family therapy. CBT has also been shown to reduce the number of sick days taken by people with depression, when used in conjunction with primary care.

The most-studied form of psychotherapy for depression is CBT, which teaches clients to challenge self-defeating, but enduring ways of thinking (cognitions) and change counter-productive behaviours. Research beginning in the mid-1990s suggested that CBT could perform as well as or better than antidepressants in patients with moderate to severe depression. CBT may be effective in depressed adolescents, although its effects on severe episodes are not definitively known. Several variables predict success for cognitive behavioural therapy in adolescents: higher levels of rational thoughts, less hopelessness, fewer negative thoughts, and fewer cognitive distortions. CBT is particularly beneficial in preventing relapse.

CBT and occupational programmes (including modification of work activities and assistance) have been shown to be effective in reducing sick days taken by workers with depression.

Variants

Several variants of CBT have been used in those with depression, the most notable being rational emotive behaviour therapy (REBT), and mindfulness-based cognitive therapy. Mindfulness-based stress reduction programmes may reduce depression symptoms. Mindfulness programmes also appear to be a promising intervention in youth.

Psychoanalysis

Psychoanalysis is a school of thought, founded by Sigmund Freud, which emphasizes the resolution of unconscious mental conflicts. Psychoanalytic techniques are used by some practitioners to treat clients presenting with major depression. A more widely practiced therapy, called psychodynamic psychotherapy, is in the tradition of psychoanalysis but less intensive, meeting once or twice a week. It also tends to focus more on the person’s immediate problems, and has an additional social and interpersonal focus. In a meta-analysis of three controlled trials of Short Psychodynamic Supportive Psychotherapy, this modification was found to be as effective as medication for mild to moderate depression.

Antidepressants

Conflicting results have arisen from studies that look at the effectiveness of antidepressants in people with acute, mild to moderate depression. Stronger evidence supports the usefulness of antidepressants in the treatment of depression that is chronic (dysthymia) or severe.

While small benefits were found, researchers Irving Kirsch and Thomas Moore state they may be due to issues with the trials rather than a true effect of the medication. In a later publication, Kirsch concluded that the overall effect of new-generation antidepressant medication is below recommended criteria for clinical significance. Similar results were obtained in a meta-analysis by Fornier.

A review commissioned by the National Institute for Health and Care Excellence (UK) concluded that there is strong evidence that selective serotonin reuptake inhibitors (SSRIs), such as escitalopram, paroxetine, and sertraline, have greater efficacy than placebo on achieving a 50% reduction in depression scores in moderate and severe major depression, and that there is some evidence for a similar effect in mild depression. Similarly, a Cochrane systematic review of clinical trials of the generic tricyclic antidepressant amitriptyline concluded that there is strong evidence that its efficacy is superior to placebo.

A 2019 Cochrane review on the combined use of antidepressants plus benzodiazepines demonstrated improved effectiveness when compared to antidepressants alone; however, these effects were not maintained in the acute or continuous phase. The benefits of adding a benzodiazepine should be balanced against possible harms and other alternative treatment strategies when antidepressant mono-therapy is considered inadequate.

In 2014, the US Food and Drug Administration published a systematic review of all antidepressant maintenance trials submitted to the agency between 1985 and 2012. The authors concluded that maintenance treatment reduced the risk of relapse by 52% compared to placebo, and that this effect was primarily due to recurrent depression in the placebo group rather than a drug withdrawal effect.

To find the most effective antidepressant medication with minimal side-effects, the dosages can be adjusted, and if necessary, combinations of different classes of antidepressants can be tried. Response rates to the first antidepressant administered range from 50 to 75%, and it can take at least six to eight weeks from the start of medication to improvement. Antidepressant medication treatment is usually continued for 16 to 20 weeks after remission, to minimise the chance of recurrence, and even up to one year of continuation is recommended. People with chronic depression may need to take medication indefinitely to avoid relapse.

SSRIs are the primary medications prescribed, owing to their relatively mild side-effects, and because they are less toxic in overdose than other antidepressants. People who do not respond to one SSRI can be switched to another antidepressant, and this results in improvement in almost 50% of cases. Another option is to switch to the atypical antidepressant bupropion. Venlafaxine, an antidepressant with a different mechanism of action, may be modestly more effective than SSRIs. However, venlafaxine is not recommended in the UK as a first-line treatment because of evidence suggesting its risks may outweigh benefits, and it is specifically discouraged in children and adolescents.

For children, some research has supported the use of the SSRI antidepressant fluoxetine. The benefit however appears to be slight in children, while other antidepressants have not been shown to be effective. Medications are not recommended in children with mild disease. There is also insufficient evidence to determine effectiveness in those with depression complicated by dementia. Any antidepressant can cause low blood sodium levels; nevertheless, it has been reported more often with SSRIs. It is not uncommon for SSRIs to cause or worsen insomnia; the sedating atypical antidepressant mirtazapine can be used in such cases.

Irreversible monoamine oxidase inhibitors, an older class of antidepressants, have been plagued by potentially life-threatening dietary and drug interactions. They are still used only rarely, although newer and better-tolerated agents of this class have been developed. The safety profile is different with reversible monoamine oxidase inhibitors, such as moclobemide, where the risk of serious dietary interactions is negligible and dietary restrictions are less strict.

It is unclear whether antidepressants affect a person’s risk of suicide. For children, adolescents, and probably young adults between 18 and 24 years old, there is a higher risk of both suicidal ideations and suicidal behaviour in those treated with SSRIs. For adults, it is unclear whether SSRIs affect the risk of suicidality. One review found no connection; another an increased risk; and a third no risk in those 25-65 years old and a decreased risk in those more than 65. A black box warning was introduced in the United States in 2007 on SSRIs and other antidepressant medications due to the increased risk of suicide in patients younger than 24 years old. Similar precautionary notice revisions were implemented by the Japanese Ministry of Health.

Other Medications

There is some evidence that omega-3 fatty acids fish oil supplements containing high levels of eicosapentaenoic acid (EPA) to docosahexaenoic acid (DHA) are effective in the treatment of, but not the prevention of major depression. However, a Cochrane review determined there was insufficient high quality evidence to suggest omega-3 fatty acids were effective in depression. There is limited evidence that vitamin D supplementation is of value in alleviating the symptoms of depression in individuals who are vitamin D-deficient. There is some preliminary evidence that COX-2 inhibitors, such as celecoxib, have a beneficial effect on major depression. Lithium appears effective at lowering the risk of suicide in those with bipolar disorder and unipolar depression to nearly the same levels as the general population. There is a narrow range of effective and safe dosages of lithium thus close monitoring may be needed. Low-dose thyroid hormone may be added to existing antidepressants to treat persistent depression symptoms in people who have tried multiple courses of medication. Limited evidence suggests stimulants, such as amphetamine and modafinil, may be effective in the short term, or as adjuvant therapy. Also, it is suggested that folate supplements may have a role in depression management. There is tentative evidence for benefit from testosterone in males.

Electroconvulsive Therapy

Electroconvulsive therapy (ECT) is a standard psychiatric treatment in which seizures are electrically induced in patients to provide relief from psychiatric illnesses. ECT is used with informed consent as a last line of intervention for major depressive disorder.

A round of ECT is effective for about 50% of people with treatment-resistant major depressive disorder, whether it is unipolar or bipolar. Follow-up treatment is still poorly studied, but about half of people who respond relapse within twelve months.

Aside from effects in the brain, the general physical risks of ECT are similar to those of brief general anaesthesia. Immediately following treatment, the most common adverse effects are confusion and memory loss. ECT is considered one of the least harmful treatment options available for severely depressed pregnant women.

A usual course of ECT involves multiple administrations, typically given two or three times per week, until the patient is no longer suffering symptoms. ECT is administered under anaesthesia with a muscle relaxant. Electroconvulsive therapy can differ in its application in three ways: electrode placement, frequency of treatments, and the electrical waveform of the stimulus. These three forms of application have significant differences in both adverse side effects and symptom remission. After treatment, drug therapy is usually continued, and some patients receive maintenance ECT.

ECT appears to work in the short term via an anticonvulsant effect mostly in the frontal lobes, and longer term via neurotrophic effects primarily in the medial temporal lobe.

Transcranial Magnetic Stimulation

Transcranial magnetic stimulation (TMS) or deep transcranial magnetic stimulation is a non-invasive method used to stimulate small regions of the brain. TMS was approved by the FDA for treatment-resistant major depressive disorder (trMDD) in 2008 and as of 2014 evidence supports that it is probably effective. The American Psychiatric Association the Canadian Network for Mood and Anxiety Disorders, and the Royal Australia and New Zealand College of Psychiatrists have endorsed TMS for trMDD.

Transcranial Direct Current Stimulation

Transcranial direct current stimulation (tDCS) is another non-invasive method used to stimulate small regions of the brain with the help of a weak electric current. Increasing evidence has been gathered for its efficiency as a depression treatment. A meta-analysis was published in 2020 summarising results across nine studies (572 participants) concluded that active tDCS was significantly superior to sham for response (30.9% vs. 18.9%, respectively), remission (19.9% vs. 11.7%) and depression improvement. According to a 2016 meta analysis, 34% of tDCS-treated patients showed at least 50% symptom reduction compared to 19% sham-treated across 6 randomised controlled trials.

Light Therapy

Bright light therapy reduces depression symptom severity, with benefit for both seasonal affective disorder and for non-seasonal depression, and an effect similar to those for conventional antidepressants. For non-seasonal depression, adding light therapy to the standard antidepressant treatment was not effective. For non-seasonal depression, where light was used mostly in combination with antidepressants or wake therapy, a moderate effect was found, with response better than control treatment in high-quality studies, in studies that applied morning light treatment, and with people who respond to total or partial sleep deprivation. Both analyses noted poor quality, short duration, and small size of most of the reviewed studies.

Other

There is insufficient evidence for Reiki and dance movement therapy in depression.

As of 2019 cannabis is specifically not recommended as a treatment.

Prognosis

Major depressive episodes often resolve over time whether or not they are treated. Outpatients on a waiting list show a 10-15% reduction in symptoms within a few months, with approximately 20% no longer meeting the full criteria for a depressive disorder. The median duration of an episode has been estimated to be 23 weeks, with the highest rate of recovery in the first three months.

Studies have shown that 80% of those suffering from their first major depressive episode will have at least one more depression during their life, with a lifetime average of 4 episodes. Other general population studies indicate that around half those who have an episode recover (whether treated or not) and remain well, while the other half will have at least one more, and around 15% of those experience chronic recurrence. Studies recruiting from selective inpatient sources suggest lower recovery and higher chronicity, while studies of mostly outpatients show that nearly all recover, with a median episode duration of 11 months. Around 90% of those with severe or psychotic depression, most of whom also meet criteria for other mental disorders, experience recurrence.

A high proportion of people who experience full symptomatic remission still have at least one not fully resolved symptom after treatment. Recurrence or chronicity is more likely if symptoms have not fully resolved with treatment. Current guidelines recommend continuing antidepressants for four to six months after remission to prevent relapse. Evidence from many randomised controlled trials indicate continuing antidepressant medications after recovery can reduce the chance of relapse by 70% (41% on placebo vs. 18% on antidepressant). The preventive effect probably lasts for at least the first 36 months of use.

People experiencing repeated episodes of depression require ongoing treatment in order to prevent more severe, long-term depression. In some cases, people must take medications for the rest of their lives.

Cases when outcome is poor are associated with inappropriate treatment, severe initial symptoms including psychosis, early age of onset, previous episodes, incomplete recovery after one year of treatment, pre-existing severe mental or medical disorder, and family dysfunction.

Depressed individuals have a shorter life expectancy than those without depression, in part because depressed patients are at risk of dying of suicide. They also have a higher rate of dying from other causes, being more susceptible to medical conditions such as heart disease. Up to 60% of people who die of suicide have a mood disorder such as major depression, and the risk is especially high if a person has a marked sense of hopelessness or has both depression and borderline personality disorder. About 2-8% of adults with major depression die by suicide, and about 50% of people who die by suicide had depression or another mood disorder. The lifetime risk of suicide associated with a diagnosis of major depression in the US is estimated at 3.4%, which averages two highly disparate figures of almost 7% for men and 1% for women (although suicide attempts are more frequent in women). The estimate is substantially lower than a previously accepted figure of 15%, which had been derived from older studies of hospitalised patients.

Major depression is currently the leading cause of disease burden in North America and other high-income countries, and the fourth-leading cause worldwide. In the year 2030, it is predicted to be the second-leading cause of disease burden worldwide after HIV, according to the WHO. Delay or failure in seeking treatment after relapse and the failure of health professionals to provide treatment are two barriers to reducing disability.

Depression may affect people’s ability to work. The combination of usual clinical care and support with return to work (like working less hours or changing tasks) probably reduces sick leave by 15%, and leads to fewer depressive symptoms and improved work capacity, reducing sick leave by an annual average of 25 days per year. Helping depressed people return to work without a connection to clinical care has not been shown to have an effect on sick leave days. Additional psychological interventions (such as online CBT) leads to fewer sick days compared to standard management only. Streamlining care or adding specific providers for depression care may help to reduce sick leave.

Society and Culture

Terminology

The term “depression” is used in a number of different ways. It is often used to mean this syndrome but may refer to other mood disorders or simply to a low mood. People’s conceptualisations of depression vary widely, both within and among cultures. “Because of the lack of scientific certainty,” one commentator has observed, “the debate over depression turns on questions of language. What we call it – ‘disease,’ ‘disorder,’ ‘state of mind’ – affects how we view, diagnose, and treat it.” There are cultural differences in the extent to which serious depression is considered an illness requiring personal professional treatment, or is an indicator of something else, such as the need to address social or moral problems, the result of biological imbalances, or a reflection of individual differences in the understanding of distress that may reinforce feelings of powerlessness, and emotional struggle.

The diagnosis is less common in some countries, such as China. It has been argued that the Chinese traditionally deny or somatise emotional depression (although since the early 1980s, the Chinese denial of depression may have modified). Alternatively, it may be that Western cultures reframe and elevate some expressions of human distress to disorder status. Australian professor Gordon Parker and others have argued that the Western concept of depression “medicalises” sadness or misery. Similarly, Hungarian-American psychiatrist Thomas Szasz and others argue that depression is a metaphorical illness that is inappropriately regarded as an actual disease. There has also been concern that the DSM, as well as the field of descriptive psychiatry that employs it, tends to reify abstract phenomena such as depression, which may in fact be social constructs. American archetypal psychologist James Hillman writes that depression can be healthy for the soul, insofar as “it brings refuge, limitation, focus, gravity, weight, and humble powerlessness.” Hillman argues that therapeutic attempts to eliminate depression echo the Christian theme of resurrection, but have the unfortunate effect of demonising a soulful state of being.

Stigma

Historical figures were often reluctant to discuss or seek treatment for depression due to social stigma about the condition, or due to ignorance of diagnosis or treatments. Nevertheless, analysis or interpretation of letters, journals, artwork, writings, or statements of family and friends of some historical personalities has led to the presumption that they may have had some form of depression. People who may have had depression include English author Mary Shelley, American-British writer Henry James, and American president Abraham Lincoln. Some well-known contemporary people with possible depression include Canadian songwriter Leonard Cohen and American playwright and novelist Tennessee Williams. Some pioneering psychologists, such as Americans William James and John B. Watson, dealt with their own depression.

There has been a continuing discussion of whether neurological disorders and mood disorders may be linked to creativity, a discussion that goes back to Aristotelian times. British literature gives many examples of reflections on depression. English philosopher John Stuart Mill experienced a several-months-long period of what he called “a dull state of nerves”, when one is “unsusceptible to enjoyment or pleasurable excitement; one of those moods when what is pleasure at other times, becomes insipid or indifferent”. He quoted English poet Samuel Taylor Coleridge’s “Dejection” as a perfect description of his case: “A grief without a pang, void, dark and drear, / A drowsy, stifled, unimpassioned grief, / Which finds no natural outlet or relief / In word, or sigh, or tear.” English writer Samuel Johnson used the term “the black dog” in the 1780s to describe his own depression, and it was subsequently popularised by depression sufferer former British Prime Minister Sir Winston Churchill.

Social stigma of major depression is widespread, and contact with mental health services reduces this only slightly. Public opinions on treatment differ markedly to those of health professionals; alternative treatments are held to be more helpful than pharmacological ones, which are viewed poorly. In the UK, the Royal College of Psychiatrists and the Royal College of General Practitioners conducted a joint Five-year Defeat Depression campaign to educate and reduce stigma from 1992 to 1996; a MORI study conducted afterwards showed a small positive change in public attitudes to depression and treatment.

Elderly

Depression is especially common among those over 65 years of age and increases in frequency beyond this age. In addition, the risk of depression increases in relation to the frailty of the individual. Depression is one of the most important factors which negatively impact quality of life in adults, as well as the elderly. Both symptoms and treatment among the elderly differ from those of the rest of the population.

As with many other diseases, it is common among the elderly not to present with classical depressive symptoms. Diagnosis and treatment is further complicated in that the elderly are often simultaneously treated with a number of other drugs, and often have other concurrent diseases. Treatment differs in that studies of SSRIs have shown lesser and often inadequate effects among the elderly, while other drugs, such as duloxetine (a serotonin-norepinephrine reuptake inhibitor), with more clear effects have adverse effects, such as dizziness, dryness of the mouth, diarrhoea and constipation, which can be especially difficult to handle among the elderly.

Problem solving therapy was, as of 2015, the only psychological therapy with proven effect, and can be likened to a simpler form of CBT. However, elderly with depression are seldom offered any psychological treatment, and the evidence proving other treatments effective is incomplete. ECT has been used in the elderly, and register-studies suggest it is effective, although less so as compared to the rest of the population. The risks involved with treatment of depression among the elderly as opposed to benefits are not entirely clear.

Research

MRI scans of patients with depression have revealed a number of differences in brain structure compared to those who are not depressed. Meta-analyses of neuroimaging studies in major depression reported that, compared to controls, depressed patients had increased volume of the lateral ventricles and adrenal gland and smaller volumes of the basal ganglia, thalamus, hippocampus, and frontal lobe (including the orbitofrontal cortex and gyrus rectus). Hyperintensities have been associated with patients with a late age of onset, and have led to the development of the theory of vascular depression.

Trials are looking at the effects of botulinum toxins on depression. The idea is that the drug is used to make the person look less frowning and that this stops the negative facial feedback from the face. In 2015 results showed, however, that the partly positive effects that had been observed until then could have been due to placebo effects.

In 2018-2019, the US Food and Drug Administration (FDA) granted Breakthrough therapy designation to Compass Pathways and, separately, Usona Institute. Compass is a for-profit company studying psilocybin for treatment-resistant depression; Usona is a non-profit organisation studying psilocybin for major depressive disorder more broadly.

Animals Models

Models of depression in animals for the purpose of study include iatrogenic depression models (such as drug-induced), forced swim tests, tail suspension test, and learned helplessness models. Criteria frequently used to assess depression in animals include expression of despair, neurovegetative changes, and anhedonia, as many other criteria for depression are untestable in animals, such as guilt and suicidality.

What is Learned Helplessness?

Introduction

Learned helplessness is behaviour exhibited by a subject after enduring repeated aversive stimuli beyond their control. It was initially thought to be caused from the subject’s acceptance of their powerlessness: discontinuing attempts to escape or avoid the aversive stimulus, even when such alternatives are unambiguously presented. Upon exhibiting such behaviour, the subject was said to have acquired learned helplessness.

Over the past few decades, neuroscience has provided insight into learned helplessness and shown that the original theory actually had it backwards: the brain’s default state is to assume that control is not present, and the presence of “helpfulness” is what is actually learned.

In humans, learned helplessness is related to the concept of self-efficacy; the individual’s belief in their innate ability to achieve goals. Learned helplessness theory is the view that clinical depression and related mental illnesses may result from such real or perceived absence of control over the outcome of a situation.

Refer to Learned Optimism.

Foundation of Research and Theory

Early Experiments

American psychologist Martin Seligman initiated research on learned helplessness in 1967 at the University of Pennsylvania as an extension of his interest in depression. This research was later expanded through experiments by Seligman and others. One of the first was an experiment by Seligman & Maier:

  • In Part 1 of this study, three groups of dogs were placed in harnesses.
    • Group 1 dogs were simply put in a harness for a period of time and were later released.
    • Groups 2 and 3 consisted of “yoked pairs”.
    • Dogs in Group 2 were given electric shocks at random times, which the dog could end by pressing a lever.
    • Each dog in Group 3 was paired with a Group 2 dog; whenever a Group 2 dog got a shock, its paired dog in Group 3 got a shock of the same intensity and duration, but its lever did not stop the shock.
    • To a dog in Group 3, it seemed that the shock ended at random, because it was their paired dog in Group 2 that was causing it to stop.
    • Thus, for Group 3 dogs, the shock was “inescapable”.
  • In Part 2 of the experiment the same three groups of dogs were tested in a shuttle-box apparatus (a chamber containing two rectangular compartments divided by a barrier a few inches high).
    • All of the dogs could escape shocks on one side of the box by jumping over a low partition to the other side.
    • The dogs in Groups 1 and 2 quickly learned this task and escaped the shock.
    • Most of the Group 3 dogs – which had previously learned that nothing they did had any effect on shocks – simply lay down passively and whined when they were shocked.

In a second experiment later that year with new groups of dogs, Overmier and Seligman ruled out the possibility that, instead of learned helplessness, the Group 3 dogs failed to avert in the second part of the test because they had learned some behaviour that interfered with “escape”. To prevent such interfering behaviour, Group 3 dogs were immobilised with a paralysing drug (curare), and underwent a procedure similar to that in Part 1 of the Seligman and Maier experiment. When tested as before in Part 2, these Group 3 dogs exhibited helplessness as before. This result serves as an indicator for the ruling out of the interference hypothesis.

From these experiments, it was thought that there was to be only one cure for helplessness. In Seligman’s hypothesis, the dogs do not try to escape because they expect that nothing they do will stop the shock. To change this expectation, experimenters physically picked up the dogs and moved their legs, replicating the actions the dogs would need to take in order to escape from the electrified grid. This had to be done at least twice before the dogs would start wilfully jumping over the barrier on their own. In contrast, threats, rewards, and observed demonstrations had no effect on the “helpless” Group 3 dogs.

Later Experiments

Later experiments have served to confirm the depressive effect of feeling a lack of control over an aversive stimulus. For example, in one experiment, humans performed mental tasks in the presence of distracting noise. Those who could use a switch to turn off the noise rarely bothered to do so, yet they performed better than those who could not turn off the noise. Simply being aware of this option was enough to substantially counteract the noise effect. In 2011, an animal study found that animals with control over stressful stimuli exhibited changes in the excitability of certain neurons in the prefrontal cortex. Animals that lacked control failed to exhibit this neural effect and showed signs consistent with learned helplessness and social anxiety.

Expanded Theories

Research has found that a human’s reaction to feeling a lack of control differs both between individuals and between situations, i.e. learned helplessness sometimes remains specific to one situation but at other times generalises across situations. Such variations are not explained by the original theory of learned helplessness, and an influential view is that such variations depend on an individual’s attributional or explanatory style. According to this view, how someone interprets or explains adverse events affects their likelihood of acquiring learned helplessness and subsequent depression. For example, people with pessimistic explanatory style tend to see negative events as permanent (“it will never change”), personal (“it’s my fault”), and pervasive (“I can’t do anything correctly”), and are likely to suffer from learned helplessness and depression.

Bernard Weiner proposed a detailed account of the attributional approach to learned helplessness. His attribution theory includes the dimensions of globality/specificity, stability/instability, and internality/externality:

  • A global attribution occurs when the individual believes that the cause of negative events is consistent across different contexts.
    • A specific attribution occurs when the individual believes that the cause of a negative event is unique to a particular situation.
  • A stable attribution occurs when the individual believes the cause to be consistent across time.
    • An unstable attribution occurs when the individual thinks that the cause is specific to one point in time.
  • An external attribution assigns causality to situational or external factors,
    • while an internal attribution assigns causality to factors within the person.

Research has shown that those with an internal, stable, and global attributional style for negative events can be more at risk for a depressive reaction to failure experiences.

Neurobiological Perspective

Research has shown that increased 5-HT (serotonin) activity in the dorsal raphe nucleus plays a critical role in learned helplessness. Other key brain regions that are involved with the expression of helpless behaviour include the basolateral amygdala, central nucleus of the amygdala and bed nucleus of the stria terminalis. Activity in medial prefrontal cortex, dorsal hippocampus, septum and hypothalamus has also been observed during states of helplessness.

In the article, “Exercise, Learned Helplessness, and the Stress-Resistant Brain”, Benjamin N. Greenwood and Monika Fleshner discuss how exercise might prevent stress-related disorders such as anxiety and depression. They show evidence that running wheel exercise prevents learned helplessness behaviours in rats. They suggest that the amount of exercise may not be as important as simply exercising at all. The article also discusses the neurocircuitry of learned helplessness, the role of serotonin (or 5-HT), and the exercise-associated neural adaptations that may contribute to the stress-resistant brain. However, the authors finally conclude that:

“The underlying neurobiological mechanisms of this effect, however, remain unknown. Identifying the mechanisms by which exercise prevents learned helplessness could shed light on the complex neurobiology of depression and anxiety and potentially lead to novel strategies for the prevention of stress-related mood disorders”.

Health Implications

People who perceive events as uncontrollable show a variety of symptoms that threaten their mental and physical well-being. They experience stress, they often show disruption of emotions demonstrating passivity or aggressiveness, and they can also have difficulty performing cognitive tasks such as problem-solving. They are less likely to change unhealthy patterns of behaviour, causing them, for example, to neglect diet, exercise, and medical treatment.

Depression

Abnormal and cognitive psychologists have found a strong correlation between depression-like symptoms and learned helplessness in laboratory animals.

Young adults and middle-aged parents with a pessimistic explanatory style often suffer from depression. They tend to be poor at problem-solving and cognitive restructuring, and also tend to demonstrate poor job satisfaction and interpersonal relationships in the workplace. Those with a pessimistic style also tend to have weakened immune systems, having not only increased vulnerability to minor ailments (e.g. cold, fever) and major illness (e.g. heart attack, cancers), but also poorer recovery from health problems.

Social Impact

Learned helplessness can be a factor in a wide range of social situations.

  • In emotionally abusive relationships, the victim often develops learned helplessness.
    • This occurs when the victim confronts or tries to leave the abuser only to have the abuser dismiss or trivialise the victim’s feelings, pretend to care but not change, or impede the victim from leaving.
  • The motivational effect of learned helplessness is often seen in the classroom.
    • Students who repeatedly fail may conclude that they are incapable of improving their performance, and this attribution keeps them from trying to succeed, which results in increased helplessness, continued failure, loss of self-esteem and other social consequences.
  • Child abuse by neglect can be a manifestation of learned helplessness.
    • For example, when parents believe they are incapable of stopping an infant’s crying, they may simply give up trying to do anything for the child.
  • Those who are extremely shy or anxious in social situations may become passive due to feelings of helplessness.
    • Gotlib and Beatty (1985) found that people who cite helplessness in social settings may be viewed poorly by others, which tends to reinforce the passivity.
  • Aging individuals may respond with helplessness to the deaths of friends and family members, the loss of jobs and income, and the development of age-related health problems.
    • This may cause them to neglect their medical care, financial affairs, and other important needs.
  • According to Cox et al., Abramson, Devine, and Hollon (2012), learned helplessness is a key factor in depression that is caused by inescapable prejudice (i.e. “deprejudice”).
    • Thus: “Helplessness born in the face of inescapable prejudice matches the helplessness born in the face of inescapable shocks.”
  • According to Ruby K. Payne’s book A Framework for Understanding Poverty, treatment of the poor can lead to a cycle of poverty, a culture of poverty, and generational poverty.
    • This type of learned helplessness is passed from parents to children.
    • People who embrace this mentality feel there is no way to escape poverty and so one must live in the moment and not plan for the future, trapping families in poverty.

Social problems resulting from learned helplessness may seem unavoidable to those entrenched. However, there are various ways to reduce or prevent it. When induced in experimental settings, learned helplessness has been shown to resolve itself with the passage of time. People can be immunized against the perception that events are uncontrollable by increasing their awareness of previous experiences, when they were able to effect a desired outcome. Cognitive therapy can be used to show people that their actions do make a difference and bolster their self-esteem.

Extensions

Cognitive scientist and usability engineer Donald Norman used learned helplessness to explain why people blame themselves when they have a difficult time using simple objects in their environment.

The UK educationalist Phil Bagge describes it as a learning avoidance strategy caused by prior failure and the positive reinforcement of avoidance such as asking teachers or peers to explain and consequently do the work. It shows itself as sweet helplessness or aggressive helplessness often seen in challenging problem solving contexts, such as learning to use a new computer programming language.

The US sociologist Harrison White has suggested in his book Identity and Control that the notion of learned helplessness can be extended beyond psychology into the realm of social action. When a culture or political identity fails to achieve desired goals, perceptions of collective ability suffer.

Emergence under Torture

Studies on learned helplessness served as the basis for developing enhanced interrogation techniques. In CIA interrogation manuals, learned helplessness is characterised as “apathy” which may result from prolonged use of coercive techniques which result in a “debility-dependency-dread” state in the subject, “If the debility-dependency-dread state is unduly prolonged, however, the arrestee may sink into a defensive apathy from which it is hard to arouse him.”

Is the Mental Wellbeing of Doctors Becoming an Increasing Concern?

Research Paper Title

Depressive symptoms in residents of a tertiary training hospital in Malaysia: The prevalence and associated factors.

Background

The mental wellbeing of doctors is becoming an increasing concern in the world today.

In Malaysia, residency is a challenging period in a doctor’s life, with many changes professionally and possibly in their personal lives as well.

This study aims to determine the prevalence of depressive symptoms and the socio-demographic correlates among residents in a tertiary training hospital in Malaysia.

It is a cross sectional study and all residents were approached to participate in the study.

Methods

The instruments used were a socio-demographic questionnaire and the Patient Health Questionnaire 9 (PHQ-9).

Chi-square test was used to explore the association between the socio-demographic correlates, and those that were found to have significant associations were further tested using multivariate logistic regression.

Results

The prevalence of depression among residents was 25.1 %. Longer working hours, missing meals, and working in Department of Surgery and Department of Anaesthesia was significantly positively associated while having protected study time, CME/lectures, leisure/hobbies and exercise were negatively associated with depression.

The Department of Rehabilitation Medicine had a significantly negative association with depression. After logistic regression, longer working hours and a lack of protected study time was significantly associated with depression in the respective departments.

Conclusions

In summary, the prevalence of depression among residents is high and is associated with longer working hours, missing meals and a lack of protected study time are significantly associated with depression.

Remedial steps should be taken to improve the mental health among residents.

Reference

Nair, N., Ng, C.G. & Sulaiman, A.H. (2021) Depressive symptoms in residents of a tertiary training hospital in Malaysia: The prevalence and associated factors. Asian Journal of Psychiatry. doi: 10.1016/j.ajp.2021.102548. Online ahead of print.

What is Dispossession, Oppression, and Depression?

Introduction

Supplementing the medical model of depression, many researchers have begun to conceptualise ways in which the historical legacies of racism and colonialism create depressive conditions. Given the lived experiences of marginalised peoples, ranging from conditions of migration, class stratification, cultural genocide, labour exploitation, and social immobility, depression can be seen as a “rational response to global conditions”, according to Ann Cvetkovich.

Background

Psychogeographical depression overlaps somewhat with the theory of “deprejudice”, a portmanteau of depression and prejudice proposed by Cox, Abramson, Devine, and Hollon in 2012, who argue for an integrative approach to studying the often comorbid experiences. Cox, Abramson, Devine, and Hollon are concerned with the ways in which social stereotypes are often internalised, creating negative self-stereotypes that then produce depressive symptoms.

Unlike the theory of “deprejudice”, a psychogeographical theory of depression attempts to broaden study of the subject beyond an individual experience to one produced on a societal scale, seeing particular manifestations of depression as rooted in dispossession; historical legacies of genocide, slavery, and colonialism are productive of segregation, both material and psychic material deprivation, and concomitant circumstances of violence, systemic exclusion, and lack of access to legal protections. The demands of navigating these circumstances compromise the resources available to a population to seek comfort, health, stability, and sense of security. The historical memory of this trauma conditions the psychological health of future generations, making psychogeographical depression an intergenerational experience as well.

This work is supported by recent studies in genetic science which has demonstrated an epigenetic link between the trauma suffered by Holocaust survivors and the genetic reverberations for subsequent generations. Likewise, research by scientists at Emory University suggests that memories of trauma can be inherited, rendering offspring vulnerable to psychological predispositions for stress disorders, schizophrenia, and PTSD.

Vacant Lot Greening and Mood

A 2018 study asked low income residents of Philadelphia “how often they felt nervous, hopeless, restless, depressed and worthless.” As an experimental mental health intervention, trash was removed from vacant lots. Some of the vacant lots were “greened”, with plantings of trees, grass, and small fences. Residents near the “greened” lots who had incomes below the poverty line reported a decrease in feelings of depression of 68%, while residents with incomes above the poverty line reported a decrease of 41%. Removing trash from vacant lots without installing landscaping did not have an observable mental health impact.