|Year : 2017 | Volume
| Issue : 1 | Page : 107-111
Understanding depression: An overview
Department of Psychiatry, Father Muller Medical College, Mangalore, Karnataka, India
|Date of Web Publication||16-Jun-2017|
A T Safeekh
Department of Psychiatry, Father Muller Medical College, Mangalore, Karnataka
Source of Support: None, Conflict of Interest: None
Depression is a major mental health problem, cuts across sociocultural background of all genders and age groups worldwide. The prevalence of depression is rising in an alarming rate and predicted to become the second leading cause for disability worldwide. Multiple factors are found to influence the etiology, course and prognosis of depression and various models of depression have been explained. However, the heterogeneity of this disorder makes it too complicated to be understood by any single model or theory. The clinical features, course, treatment response, and outcome also are as diverse as its origin.
Keywords: Depression, depressive disorders, overview
|How to cite this article:|
Safeekh A T. Understanding depression: An overview. Arch Med Health Sci 2017;5:107-11
“I know that if anybody spoke to me
or looked at me too closely
the tears would fly out of my eyes
and the sob would fly out of my throat
And I'd cry for a week
I could feel the tears brimming and sloshing in me like water in a glass
That is unsteady and too full“
| Introduction|| |
Persons suffering from depression might not be able to express or communicate their agony and distress as vivid and clear as Silvia Plath; the renowned romantic poet of the past century, whose brief life and death was shadowed in the relentless fangs of depression. The word depression seems to be very easy and simple to understand. The dictionaries define depression as “feeling of severe despondency and dejection” with symptoms of melancholy, misery, sadness, unhappiness, sorrow, woe, gloominess, dejection, downheartedness, despondency, dispiritedness, low sprit, heavy-heartedness, moroseness, discouragement, despair, desolation, dolefulness, moodiness, pessimism, and hopelessness. Depression which was called as “melancholia” was first mentioned in the ancient Mesopotamian texts.
From a common man to many medical professionals; depression is just a normal passing feeling of sadness and is attributed to stressful life events, which is very much normal and hardly considered as a pathological and an illness which requires medical interventions. When somebody tries to talk about their depressive feelings, even the empathetic listeners (friends, relatives, teachers, priests, family physician, etc.) tend to minimize it by saying, it is normal and everyone goes through it and try to console them saying that it is the matter of time and you will get over it and efforts are made to cheer the person up with the philosophical quotes. It is an emotion we cannot live without. As Lord Byron said
“We know that tears are vain,
That death nor heeds nor hears distress
Will this unteach us to complain?
Or make one mourner weep the less?“
It is important to demarcate the normal feelings of sadness and depression from its pathological counterpart. To consider depression pathological, it should be severe enough and last long enough to produce significant distress in the various aspects of one's life. Although the common term used is depression, there are different types of depressive disorders.
| Burden of Depression|| |
The World Health Organization estimates that by 2020 depression will be the second leading caused for disability worldwide. The life time prevalence of depression is estimated to be the range of 1.5%–19% with higher prevalence among higher income countries than lower income. The proportion of global population suffering from depression in 2015 is estimated to be 4.45 with higher prevalence among females (5.1%) than males (3.6%). The prevalence of depression varies with age having higher rate among older adults (7.5% among females and 5.5% among males between the ages of 55 and 74 years). Depression does not spare even children and adolescents below the age of 15 years but with a lower rate. About 3022 million people in the world are living with depression. About half of this is in Southeast Asia region and Western specific regions, due to the large population of those two regions which include India and China. There is a rapid increase in the incidents of depression between 2005 and 2015 (18%).
Depression negatively affects education and often cause termination of education, marriage and stabilities and effects employment status, role performance, marital function, parenting functioning, and financial status.,,, It is a known fact that depression is associated with multiple medical disorders such as arthritis, asthma, cancer, cardiovascular disease, hypertension, diabetes, and pain disorder.,,, Its prevalence in India is 4.5% and that translates to 56,675,969 people who are suffering from depression. Realizing the suffering caused by depression and the enormous burden of depression; WHO is conducting a global campaign for depression in 2017. The goal of the campaign is to make people aware of depression and seek help.
| Etiology|| |
Hippocrates believed that melancholia (depression) was a medical illness and was caused excessive black bile in the spleen. But over the time, scientific thinking about the causes of mental illness and depression regressed, and people started believing that depressed patients are possessed by the devil, demons, or witches. During Renaissance which started in late 14th century, many doctors returned to the views of Hippocrates (biological causation as etiology). Robert Burton described the psychological and social causes as reasons for depression in his book “Anatomy of Melancholy,” in 1621. Late 19th century and early 20th century, psychoanalytical and psychodynamic causation were considered as etiological factors for depression. It was much easier and simple to say feeling depressed or sad is due to loss, but the current understanding of the etiology of depression doubtlessly proves the biological basis with the advances in molecular neurobiology and structural and functional brain imaging techniques. The theories of a biological causation of depression do not surpass the influence of environment.
Although various schools of thought such as psychoanalytical model and cognitive behavior model of the current psychology, Biopsychosocial model, Biomedical reductionism of medical model, humanistic model, and Existentialism have been put forward, the heterogeneity of depression makes it impossible for any single model to able explain all types of depression.,, The etiology of depression can be best understood as a prototypical genetic and environmental interaction and subsequent epigenetic modifications. Major 3 monoamine systems implicated in depression are Serotonin (5HT), norepinephrine (NE), and Dopamine (DA). The major serotonin system alterations seen in depression are low concentration of the major metabolic of serotonin, increased serotonin receptors in blood platelets and brain tissue, decreased serotonin transporters (SERT) binding sites density in midbrain and blood platelets, decreased plasma concentration of l-tryptophan (precursor to serotonin). Furthermore, it is found that depletion of serotonin reuptake inhibitors of depressed patients in remission provokes rapid relapse and also increased monoamine oxidase (MAO-A) activity is found in the central nervous system of depressed patients. The NE alterations seen in depression include low levels of NE metabolites found in the urine and cerebrospinal fluid (CSF), increased density of beta-adrenergic receptors in postmortem brain tissue, increased activity of NE circuits in the brain following stress, increased MAO-A activity, blunted growth Hormone response to D2 adrenergic agonist Clonidine and the effectiveness of NE reuptake inhibitors in depression. DA is a major neurotransmitter that mediates the ability to experience pleasure and “anhedonia” which is the inability to experience the pleasure from previously pleasurable activities is one of the cardinal symptoms seen in depression. Depression is common in Parkinson's disease where DA neuron degeneration occurs. Postmortem brain studies showed decreased dopamine transporters binding and increased postsynaptic D2/D3 receptors binding suggestive of reduced DA neurotransmission. CSF of depressed patients found to have reduction in the metabolites of DA and increased MAO-A activity is found in the CNS system of depressed patients. The antidepressant properties of MAO Inhibitors (MAOI's), DA reuptake blockers, and DA receptors agonists are also suggestive of alterations in DA system in depression.,,,
Structural brain imaging has shown reduction in hippocampal and caudate nuclear size and increase in pituitary volume, abnormalities in limbic system, cerebrocortical circuits, more significantly, reduced activity in frontal cortical areas and hyperactivity in amygdala and other limbic areas. The increased activity in the subgenual cingulate cortex which is seen in depression comes down following treatment with selective serotonin reuptake inhibitors (SSRI's) and electro convulsive therapy (ECT). The role of neuroendocrine system is one of the other important factors in the causation of depression. The hypersecretion of cortisol (the major adrino-cortical stress hormone) is a consistent finding in patients with depression. The chronic hypersecretion of Corticotrophin-releasing hormone in depression produces alteration in the hypothalamic-pituitary-adrenal (HPA) axis. Dexamethasone suppression test done in patients with depression suggest impaired feedback regulation and hyper activities of HPA axis. There is substantial evidence suggestive of the role of immune system and its chronic implication in the pathology of depression. Elevated levels of proinflammatory cytokines are found in depressive patients. Furthermore, high incidents of depression are reported in patients with chronic inflammatory medical disorders  Moreover, certain anti-inflammatory agents like celecoxib found to have antidepressant properties.
The interactions of genes and environmental influence are the most determining factors for depression. Various studies have found that stressful life in childhood is one of the risk factors for depression. There is a strong relationship between depression and trauma in the early life with the poor remission and recovery, prolonged course, and earlier onset. Although the stress in early life increases the risk for depression, it is more important how the individual responds to the events. The differences in the response to the stressful life event are determined and explained by various genetic factors. Family studies, adoption studies, and twin studies have found evidence for heritability in depressive disorders. If one parent has mood disorder, child has a risk of 10%–25% of developing mood disorders and if both parents have mood disorders, the risk doubles. The more the genetic loading (more number of family members who are affected), the greater is the risk to the offspring. The closer the relationship ( first degree relative than distant relatives), the greater is the risk. Advances and understanding in the molecular biology have found serotonin transporter gene and genes involved in the serotonergic system are candidate genes for susceptibility to depression. The tryptophan hydroxylase gene and the Val66Met polymorphism in the BDNF gene are also found to be associated with depression., The occurrence of a stressful life event found to be one of the most positive predictors of onset of a depressive episode. The stress often becomes a precipitating factor than a causative agent. Various psychodynamic factors also have been described as causative factors since the time of Sigmund Freud. Cognitive theories of depression focus on specific cognitive distortions present in a person which makes him susceptible for depression.
| Diagnosis|| |
According to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, depressive disorders include:
- Disruptive Mood Dysregulation Disorder
- Major Depressive Disorder
- Persistent Depressive Disorder (Dysthymia)
- Premenstrual Dysphoric Disorder
- Substance/Medication-induced Depressive Disorder.
The cardinal symptoms of depression include Persistently depressed or sad mood lasting for two or more weeks, profoundly decreased energy, decreased interest in activities, disrupted sleep (typically difficulty falling asleep and staying asleep, but also can be excessive sleep), decreased libido, difficulty concentrating, change in appetite (typically loss of appetite, but can also be increased appetite) often accompanied by weight loss/gain, persistently impaired self-esteem (feeling “worthless“), feeling hopeless, and thoughts of suicide. Other commonly reported symptoms include crying spells, feeling isolated, lack of motivation, increased the perception of pain, increased anxiety and irritability, and difficulty making simple decisions or indecisiveness. Depression can present with melancholic symptoms, neurotic symptoms, mixed symptoms or as pure depression. Many depressive patients will have predominant anxiety symptoms, while the patients with melancholic symptoms will present with severe psychomotor retardation, anhedonia, and absence of mood reactivity. The patients with mixed depressive symptoms are more common in bipolar disorder, but they are also seen frequently in major depressive disorder.
The presentation of depressive disorders largely varies with the type, time of presentation, duration and presence of comorbid psychiatric and medical disorders. In other words, “depression is not simply depression.” Depression presents in many varieties with different hues and colors in varying degree of severity. We might have to look way beyond depression to understand depression.
Although depressed mood is the hallmark of depressive disorder, it might not be out rightly present in many depressive disorders. The cultures where physical symptoms are more accepted than emotional symptoms, the depressive disorders present with various physical symptoms. In many cultures like Indian, people are not comfortable communicating their emotional distress to others and do not consider it as an illness. Hence, they present to physician with the other symptoms of depression, such as increased fatigability, tiredness, decreased sleep, decreased appetite, decreased libido, weight loss, and multiple aches and pains. Moreover, there might be no other illness that might have showed so much variation in the presentation of symptoms across the cultures. Western cultures where people are more vocal and communicative might be able to explain their psychological distress very effectively  like Silvia Plath. One might find her poetry overflowing with all the phenomenology of depression such as sorrow, despise, hopelessness, helplessness, and anhedonia. Even then in developed countries, it is reported that 2/3rd of the patients with depression primarily present with somatic symptoms. International Classification of Diseases-10 approves the diagnosis of depression even in the absence of depressed mood if other symptoms of depression are present. The risk of suicide in depression is well known and elevated risks of early death in depressive patients are often due to high risk of suicide. The clinical features and course of depression will widely wary in children and often goes unrecognized. Comorbidities in childhood depression are rather a rule than exception. It might appear like a trait than a state. Irritable mood rather than depressed mood is seen in many children with depressive disorders. Early onset depression will affect the overall development including physical (due lack of physical activity), skill development, and academics.
The most common psychiatric comorbidities seen in depression are Alcohol Dependence Syndrome and Anxiety Disorders. The presence of comorbid illness is an indicator of poor prognosis. It is not uncommon that primary depressive disorder gets masked with alcohol dependence and is often diagnosed while that person is undergoing treatment for alcohol dependence syndrome. Anxiety disorder on the other hand often coexists with depressive disorder.
Depression is a risk factor for the development of chronic illnesses such as diabetes and Coronary Heart Disease and adversely affects the course, complications, and management of chronic medical illness. The relationship between depression and chronic physical illnesses is often bidirectional as the behaviors and psychoneuroimmunological changes in depression can increase the risk for medical illness and can have a negative impact on existing medical illness, and the other hand, biological changes in chronic illness can precipitate depression., The association of depression with many types medical illness is the reason for the elevated risk for early death apart from suicide. The prevalence of major depressive episodes in physically ill patients varies from 5% to more than 40%. But as depression is often unrecognized among the medically ill, the actual prevalence could be much higher. Depression might start at any time in life and often begins as subthreshold depression in case of late onset. There could be a single episode or recurrent episodes or can run a chronic course depending on the type of depressive disorder, and many depressive patients might not achieve a complete remission.
Various tools used to assess depressive disorders are the Hamilton Rating Scale for Depression, Hospital Anxiety and Depression Scale, Beck Depression Inventory-II, Patient Health Questionnaire, Montgomery–Asberg Depression Rating Scale, Quick Inventory of Depressive Symptomatology, Zung Self-Rating Depression Scale, Geriatric Depression Scale, and Cornell Scale for Depression in Dementia. Center for Epidemiological Studies Depression Scale for Children, Revised Children's Anxiety and Depression Scale, Children's Depression Inventory, Children's Depression Scale, and Mood and Feelings Questionnaire are used to assess depression in children.
| Management|| |
A multimodal approach will be often necessary in the management of depressive disorders, the first line treatments being pharmacotherapy and psychological interventions. Physical treatments might be necessary in certain cases. Pharmacotherapy includes antidepressants from various classes such as tricycles, SSRI's serotonin and noradrenalin reuptake inhibitors, selective noradrenalin reuptake inhibitors, and MAOIs.
A report in JAMA says that SSRIs are no better than placebo in less severe cases of depression. Efficacy of antidepressants is different in children compared to adults. Cognitive behavior therapy and interpersonal therapy are found to be most effective in depression. The Sequenced Treatment Alternatives to Relieve Depression study found that no one treatment better than another. Other psychotherapies such as marital therapy and couple therapy are also found to be effective. There are reports that says combination of pharmacotherapy and psychotherapy is better than either treatment alone. ECT is the earliest modern treatment found to be effective in depression since the first half of the last century, but currently, it is indicated as an acute treatment only in severe depressive disorder with high suicidal risk and which is resistant to other modalities of treatment, patients with catatonia not responding to pharmacotherapy and for refractory depression. Even after ECT, pharmacotherapy has to be continued. Other physical treatments found to be useful in depression are light therapy (for Seasonal Affective Disorder), Repetitive Transcranial Magnetic Stimulation, Vagus Nerve Stimulation, and Deep brain Stimulation. Continuous, intermittent drug treatment and sequential treatment are all tried for prevention of recurrence in depression. Various alternative and complimentary therapies such as green tea, Saffron, St John's wort, Folate, Inositol, exercise, relaxation therapies, yoga, and acupuncture have been tried in depression.,
Misidentification of depression is reported more than the risk of missing diagnosis is reported which might have contributed to the exaggerated prevalence rate of depression worldwide. The marketing interests of pharmaceutical industry, their overzealous public awareness campaigns on depression and the close links between pharmaceutical industry and psychiatric academic establishments are pointed as another reason for reports of exaggerated rates of depression, reports of response to treatment with antidepressants and their prophylactic efficacy according to David Healy.
| Conclusion|| |
What is called as depression consists of a group of depressive disorders with different etiologies, presentation, course, and prognosis. The disorder could be primary or secondary to other psychiatric disorders or medical conditions. The presence of depression in any disorders negatively influences the course and outcome of that illness. Though multiple treatment modalities are available the outcome at its best is only moderate as complete remission is not achieved in about one-third of the patients with depressive disorders. Even with skeptic views from schools of thought like Existentialism which questions even the very validity of depression as a disease and people who attribute the increase in prevalence of depression to the influence of pharmaceutical industry on one side, depression found to cause the largest amount of nonfatal disability  and as the prevalence of depression is increasing in an alarming rate it becomes of prime importance to diagnose and treat depressive disorders in the early stages of depression. All medical professionals, apart from people working in the field of mental health also should be able to recognize and manage depression as it is a common comorbidity in physical illnesses and also often initially present with physical symptoms, without falling into the pitfall of “overdiagnosis” by labeling every person appearing sad as having a depressive disorder.
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