Essay on Major Depressive Disorder


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Essay on Major Depressive Disorder

Major Depressive Disorder Essay: Introduction

The paper examines the major depressive disorder in detail and concentrates on topics such as DSM-5 criteria, PDD, studies in this field and advances in therapy. Besides, it correlates Major Depressive Disorder with PDD, presents genetic, molecular, and neuropathic findings, and addresses psychotherapy and pharmacology. The article shows that major depressive disorder can be treated with the right diagnosis and therapy.

Definition of Major Depressive Disorder

Many psychobiological syndromes have a large number of depressed mood characteristics and cognitive and somatic loss of interest associated with major depressive disorder (MDD). This causes significant functional impairment (Moussavi & Ustun, 2007). Depressive disorders are classified as a mood disorder, and the absence of manic episodes distinguishes them from bipolar disorders.

Wide-ranging epidemiological surveys have found that the most severe depressive disorder is prevalent with a lifetime prevalence of 16.6%, which is almost two times higher in women than in males. MDD is aggregated among families; it is 1.5 to 3 times higher in individuals with primary biological family members affected by MDD relative to the general population (Moussavi & Ustun, 2007). The score prevalence of MDD in primary care was 10%, in nursing home patients between 15% and 20%, and among medically ill patients between 22% and 33%.

MDD disorder has been traditionally linked with neurotransmitters or defects in the brain. Cerebrospinal fluid composition, neuroreceptor and transporter, as well as therapeutic reactions to monoaminergic drugs, findings indicate that MDD could be a misnomer for serotonergic, noradrenergic-related, neurotransmitter-related and neuropeptide processes. However, the interplay of environmental factors with genetic and neuroendocrine systems and the involvement of intracellular signalling pathways has been more focused (Moussavi & Ustun, 2007). The hypothalamic-hypophysis-adrenal axis mediates environmental stress and contributes to neuronal atrophy.

DSM-5 Criteria of Major Depressive Disorder

The following five (or more) signs occur over the same two week period and represent a change from previous symptoms; either depressed or loss of interest or pleasure is at least one (Hasin & Grant, 2018).

  1. It depressed most of the day, almost regularly according to subjective assessment (e.g. felt depressed, hollow, hopeless) or other experiences (e.g. being tearful).

  2. Significant weight loss by not eating or losing weight, or decline or increase in appetite nearly daily, e.g. by more than 5 percent in your weight.

  3. Almost every day, fatigue or energy loss.

  4. Feelings of insignificance or excessive or unreasonable (which can be delusional) almost daily (not merely self-reproach or guilt over being sick).

  5. Decreased ability, almost every day-through subject accounts or observing to think or concentrate or become indecisive.

  6. 1. Recurring death (not just fear of death), recurrent suicidal thinking without a specific plan, suicide attempt, or suicide plan.

Comparison with Persistent Depressive Disorder

PDD describes a person with long-term, clinically significant depression. Depression levels are usually not sufficiently severe to meet MDD criteria. Therefore, their relationship to time is one of the main distinctions between these two conditions: people with MDD have a regular mood while not experiencing depression. Those with PDD suffer persistent sadness and do not remember — or know — whether they look when they're not sad. The diagnosis of two conditions also involves time: symptoms need to last a minimum of 2 weeks to determine MDD (Rhebergen & Graham, 2014). Symptoms must have existed for at least two years for PDD to be diagnosed.

In general, the signs of MDD and PDD vary, often in severity. Including feeling sad, empty, tearful or desperate, reacting to even small issues with anger or frustration, losing interest in ordinary daily activities such as sports, sex or hobbies, sleeping with little or too much energy, losing appetite or increasing cravings for your food, losing weight, feeling guilty or worthless; Having difficulties making decisions, thinking, focusing, and remembering (Rhebergen & Graham, 2014). To make it easier, PDD symptoms may be less intense or weaker, but they will be permanent and lasting.

Genetic, Molecular, and Neuroimaging Studies

Genetic, molecular, and neuroimaging studies continue to help us understand the neurobiological basis of major depression disease. However, it is unclear how much neurobiological discoveries will continue to enhance individuals' health and behavioural outcomes with the condition (Mill & Petronis, 2007). In the past five years, therefore, neurobiological research has been induced in two directions: understanding the disease's pathophysiology and identifying neurobiological steps to guide the choices of treatment.

Genetic Studies

Owing to the possibility, complex psychological disorders are under the polygenic control of genetic variations associated with environmental factors. They are not easy to classify single candidate genes linked with severe depression. To try to discover a causal link, one strategy has been to move past the traditional emphasis on monoamines. In the NR3C1, monoamine oxidase A gene, 26 Glycogen Synthesis Gene, which is a significant factor in phosphorylation, metabolic and many transcript factors (which has a substantial role for phosphorylation and metabolic enzymes regulation, for instance) the major depressive disorder has been associated with polymorphism and a metabotropic GRM3 (Group-2) receptor gene (Uher, 2009). The success of candidate genes correlated with established biological processes and metabolic pathways for antifreeze drugs has been higher, and will, in effect, help to predict the response from the treatment of antidepressants.

Molecular Studies

At least three major peripheral hormone-type factors with which genetic mutations are related to severe depression disorders are implicated in disease pathophysiology: neurotrophic factors and other growth factors, like BDNF, endothelial growth factor vascular and growth factor insulin-like factor-1; proinflammatory cytokines, like interleukin-1β, interleukin-6 and other variables (Mill & Petronis, 2007). For example, in individuals with severe depression, serum BDNF decreases, and this decrease reverses antidepressant therapy.

Proinflammatory cytokines are more secreted and generated in people who are anxious and distressed and may restore concentrations or inhibit their production in the event of significant antidepressant medications (Mill & Petronis, 2007). Impaired HPA axis function has long been recorded in an acute episode of depression. The publication has demonstrated attenuation of the neuroendocrine sensitivity to the combination hormone test release by dexamethasone corticotrophin is a critical indicator of impaired HPA system modulation in antidepressant care.

Neuroimaging Studies

Neural mechanisms important for recognizing the highest depressive condition include those that facilitate cognitive regulation, reward-seeking and control the emotion (Philips & Drevet, 2008). Such networks include subcortical structures involved in the law, regulation of emotions (e.g. amygdala, ventral striatum), media prefrontal and pre-current cingulate cortical regions which affect emotion production and the automatic or implied management of emotions.

Figure 1. Neural systems of relevance to major depressive disorder (Philips & Drevet, 2008)

Essay on Major Depressive Disorder

Studies in neuroimages on the central depression disorder revealed that these neural systems in adults are functionally abnormal. Converging studies indicate that the amygdala, ventral stria, and medial prefrontal cortex activation are abnormally enhanced, particularly negative emotional stimuli such as fearful faces (Philips & Drevet, 2008). Abnormally decreased ventralized behaviour with constructive emotional stimulation and was also recorded in adults and young people with depression when earning and expecting a reward. Such results lead to negative emotional responses in people with extreme depression and do not promote constructive emotional and reward-related stimulation.

Advances in Treatment

Pharmacotherapy and depression-specific manual-driven psychotherapy are also thriving, either as monotherapies or in combination treatments for unipolar depression. Although comparable effects for behavioural psychotherapy are recorded in primary care trials, fewer published studies than in clinical samples are available in this sector (Davidson, 2010). Such findings show that psychological or pharmacotherapy psychotherapy alone is useful in the acute management of depression.

Depression-Specific Psychotherapies

For patients with depression, the response rate of interpersonal (modified) and pharmacotherapy participants was higher than for the participants who obtained pharmacotherapy alone in a clinical study. The results can be maintained well after recovery from acute interpersonal psychotherapy (Davidson, 2010). Similarly, several studies in the United States and Europe continue to support the critical effectiveness and use of cognitive therapy as an intervention to complete remission and reduce the risk of recurrence.

Antidepressant Pharmacotherapy

Although there is a significant rise in antidepressant care in the US, racial and ethnic groups continue at low rates. In clinic and hospital-based outpatient care services in 2005, antidepressants became the most prescribed class of medications. Some lists show antidepressants approved by the United States Food and Drug Administration (FDA) and the proposed mechanisms for the action of different antidepressants classes (Davidson, 2010). The American Psychiatric Association guidelines for depression provide for a comprehensive assessment of its use.

Although antidepressant therapy is a common technique to treat depression, it remains unclear whether efficacy can be improved. Various experimental therapy tests have been conducted with antidepressant medications or antidepressant combinations, but the idea of these combinations, such as the first-stage therapies, should be considered necessary. One study also highlights the difference between practice patterns and combination therapy evidence (Davidson, 2010). Lithium carbonate is still used as an increase in the second generation's strategy, and antipsychotics have been extensively examined.

Major Depressive Disorder: Conclusion

The paper examined the major depressive disorder in detail and discussed topics such as DSM-5 Criteria, Persistent Depressive Disorder, studies in this field, and treatment advancements. Moreover, it compared Major Depressive Disorder with Persistent Depressive Disorder, analyzes genetic, molecular, and neuroimaging studies, and covers psychotherapy and pharmacotherapy. It is evident throughout the article that Major Depressive Disorder can be treated with the right diagnosis and treatment strategies.


Davidson, J. R. (2010). Major depressive disorder treatment guidelines in America and Europe. The Journal of clinical psychiatry.

Hasin, D. S., Sarvet, A. L., Meyers, J. L., Saha, T. D., Ruan, W. J., Stohl, M., & Grant, B. F. (2018). Epidemiology of adult DSM-5 major depressive disorder and its specifiers in the United States. JAMA psychiatry.

Mill, J., & Petronis, A. (2007). Molecular studies of major depressive disorder: the epigenetic perspective. Molecular psychiatry.

Moussavi, S., Chatterji, S., Verdes, E., Tandon, A., Patel, V., & Ustun, B. (2007). Depression, chronic diseases, and decrements in health: results from the World Health Surveys. The Lancet.

Phillips, M. L., Ladouceur, C. D., & Drevets, W. C. (2008). A neural model of voluntary and automatic emotion regulation: implications for understanding the pathophysiology and neurodevelopment of bipolar disorder. Molecular psychiatry.

Rhebergen, D., & Graham, R. (2014). The re-labelling of dysthymic disorder to persistent depressive disorder in DSM-5: old wine in new bottles?. Current Opinion in Psychiatry.

Uher, R. (2009). The role of genetic variation in the causation of mental illness: an evolution-informed framework. Molecular psychiatry.

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Baris Yalcin
Baris Yalcin
Content Editor at Tamara Research. Movie and music addict. Bachelor's degree in Translation and Interpreting.

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