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Major Depressive Disorder

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People are casual with the words “depressed” and “depression”. The word gets used interchangeably with “sad”, in thoughts like “I’m so depressed that Kyle and Travis broke up”, “depressed I’m not in Paris right now”, “you need to stop dressing like a depressed hobo”. It’s often stated that such statements trivialize

What is Depression?

According to the American Psychiatric Association in the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), major depressive disorder (MDD) is a psychological disorder that occurs when a person experiences five or more of the following symptoms: (1) feeling sad or hopeless all day, for most of the day, (2) loss of pleasure in almost all daily activities, (3) appetite changes, weight loss or weight gain, (4) sleep changes, insomnia or hypersomnia, (5) motor agitation or retardation, (6) low energy, (7) feelings of worthlessness or guilt, (8) inability to concentrate or make decisions, (9) suicidal ideation. For a diagnosis to occur, these symptoms must be present for at least two weeks, must impair the sufferer’s ability to function socially or occupationally, and none of the symptoms should be attributable to another disease (such as anemia, which might cause low energy or inability to concentrate).

MDD can involve a single episode, or a series of episodes (Kopala-Shipley & Klein, 2017). Three quarters of depression sufferers experience more than one depressive episode, classifying depression as a chronic illness. (Strain & Blumenfield, 2018).

Most patients with depression have psychological comorbidities, such as generalized anxiety disorder or PTSD (Belmaker & Agam, 2008). There are also many common physical comorbidities – for example, there’s a strong correlation between depression and cardiovascular disease. In some patients, the depression predates cardiovascular disease, in others, cardiovascular disease comes first (Belmaker & Agam, 2008). Stroke also has a bidirectional relationship with depression. (Strain & Blumenfield, 2018), as does arthritis, though it has not been studied as extensively (Aguilar-Gaxiola, Loera, Vigo, Talamantes, & Scott, 2017). Depression and other mental disorders have also been linked with hypertension and some cancers (Aguilar-Gaxiola et al., 2017).

The complicated thing about Major Depressive Disorder is that many of these symptoms are experienced a normal, undisordered life – as part of the grieving process, or as part of processing trauma, just having a crappy day. All of the symptoms can occur, at times, in perfectly healthy people (Belmaker & Agam, 2008). Major depressive disorder also has a tendency to run very different courses even in the people who do have it, making it even harder to pin down (Strain & Blumenfield, 2018). and Many of the symptoms show overlap with other psychological disorders, like PTSD, bipolar disorder adjustment disorder, and abnormal grief. In many cases, depression symptoms can show up in a person experiencing a normal grief response (Strain & Blumenfield, 2018). DSM-5 tries to minimize false diagnoses with time-specific criteria, but it can still be difficult to demarcate.

Some hesitate to even call depression a “disease”, since neither its etiology nor mechanisms have been figured out, and it lacks any clear biological indicator (Dantzer et al., 2011). The symptoms are vague – for example, “change in eating” can mean weight loss in one patient and weight gain in another, and similarly “changes in sleep patterns” can mean sleeping all day in one patient and insomnia in another. The lines here are badly drawn. And yet they are the lines we have. And we can measurably show that those who are suffering from depression have to deal with social and economic costs, lower productivity at work, and impaired functioning (Strain & Blumenfield, 2018).

Prevalence of Depression

MDD has become the most prevalent psychological disorder in the United States. About 17% of adults and 12% of adolescents experience it at some point (Strain & Blumenfield, 2018). Over their lifetimes, 12% of men and 20% of women will experience depression (Belmaker & Agam, 2008).

Studies looking at prevalence of depression have repeatedly shown that depression in women is about twice as high as it is in men. Many different hypotheses for the gender difference have been proposed – some suggest it is sociocultural, others suggest it might be hormonal. But no real consensus has been reached about the reason women suffer more (Kopala-Shipley & Klein, 2017).

Depression does occur in children, but it is much more common from in adolescence and adulthood. (Kopala-Shipley & Klein, 2017).

The Developing Understanding of Depression in History

Depression is arguably one of the easier psychological diseases to trace through history. Hippocrates defined depression symptoms not all that dissimilarly from the way it is presently defined all the way back in the 5th century B.C.: despondency, lack of appetite, restlessness, and insomnia (Horowitz, Wakefield, & Lorenzo-Luaces, 2016). Working from within the context of his theory of four humors, he attributed the cause of this “melancholia” to an exorbitance of black bile, or “melancholy”. His working definition was reiterated in many other Greek and Roman texts (Horowitz et al., 2016).

The Hippocratic definition persisted until the 17th century. Following the shift in intellectual and scientific thought spearheaded by figures such as Sir Francis Bacon and Sir Issac Newton, an English physician named Thomas Sydenham proposed the idea that the cause of melancholia might actually be disturbances in the brain, rather than an imbalance of bodily fluids (Horowitz et al., 2016). Rational thinking began to split depression into two different categories – a serious melancholia that was characterized by deep mental anguish and hopelessness, leading to possible suicidal thoughts, and neurotic depression. This was sort of a mix of anxiety and fatigue, but the depressive symptoms were considered part of it (Horowitz et al., 2016). These were not marks on the same ruler – they were considered two very different diseases, and one (melancholia) was treatable only by an “alienist” (a type of psychiatric-ish doctor), and the other (neurotic depression) was treated by your friendly family G.P. – or, you know, the 1689 equivalent of a friendly family G.P. (Horowitz et al., 2016).

While the working definitions were certainly altered in different ways – in the early 20th century, Emil Kraeplin began to separate out a “bipolar” depression that involved periods of mania from a more “unipolar” version of the disease, while Sigmund Freud, in his lone paper on depressive symptoms, focused on distinguishing the disease from normal symptoms of mourning (Horowitz et al., 2016) – this separation between “melancholic depression” (which was a brain dysfunction linked to psychotic behavior) and “neurotic depression” (which was linked to psychosocial triggers, such as losing a loved one) persisted well into the 20th century. The original Diagnostic and Statistical Manual of Psychological Disorders (DSM) and DSM-II, published in the 1950s and 1960s by the American Psychiatric Association, held fast to these ideas (Horowitz et al., 2016).

In 1976, following a period of debate about what depression was, R.E. Kendall published a paper that was the professional paper equivalent of throwing up his hands and saying “none of us know what we’re talking about and we’re all constantly contradicting each other here”. And by that I mean he analyzed twelve wildly different classification symptoms for depression that had been published (Horowitz et al., 2016). But a mere four years after the publication of this article, the 1980 DSM-III managed to come up with a definition of depression that was fairly immediately accepted by all. The new umbrella term of “major depressive disorder” was largely based off two studies – an empirical Walter Cassidy study in 1957 and a classification system called “the Feigner criteria” published in 1972 that was based on the Cassidy study. Both papers finished with large disclaimers that they only preliminary research – and yet they are essentially identical to the operational definition of depression that is still used today (Horowitz et al., 2016).

The real innovation that DSM-III brought was the idea of “major depressive disorder” as an umbrella term for all depressive disorders. “Neurotic depression” and “melancholic depression” were both included as subcategories under the brand new MDD umbrella, but once merged into a larger whole they began to fade away (Horowitz et al., 2016). But the downside, perhaps, of such a widely-accepted definition, is that there have been no real major breakthroughs in depression research in the last thirty-some years.

Why Does Depression Occur?

In truth, there’s not a veil we can pull back on the root cause of MDD. There are many hypotheses about what causes depression and if you ask “but does x really seem to cause depression?” the answer for every single one of them is “Well, yes! I mean, kind of! Maybe!”

Is it an environmental problem? Maybe. Education level, income, social capital, and quality of neighborhood have all been shown to have an impact on depression rates (Cohen, 2017). Stressful life situations, such as abuse, neglect, negative experiences with parents, poor-quality relationships with peers and/or family members can all be linked to depressive symptoms (Kopala-Shipley & Klein, 2017). But environment and stressors cannot explain all cases of depression. While depression is certainly linked to these things, it can and does patients with none of these environmental problems present at all (Belmaker & Agam, 2008).

So then, is it a biological problem? Maybe. Twin studies of depression have shown some correlational heritability is present (37.5%), but this is interestingly much lower than the heritability rate for other common psychological disorders like bipolar disorder (40-70%) and schizophrenia (80%) (Belmaker & Agam, 2008). For the most part, family studies have shown is that there is no one gene that is present in all sufferers, but there are some “of interest” chromosomal areas that have shown up in studies involving multiple families (Belmaker & Agam, 2008). More generic (non-family) genetic studies of 9000 individuals did not reveal any genetic links between them, and neither did a follow-up that studied 17,000 people. But a Nature study of 5000 depressed Chinese women and 5000 controls showed two genetic markers, and found two “of interest” genes that the women shared. (Kopala-Shipley & Klein, 2017). Genetic links are important discoveries because they could potentially flag problem proteins or other issues that might be causing depression on a cellular level. (Kopala-Shipley & Klein, 2017).

In that vein, one of the most investigated genetic links in depression research is the 5-HTTLPR allele, which affects serotonin transporting on a molecular level in the amygdala. (Belmaker & Agam, 2008). This plays directly into one of the most infamous causal theories – that depression is caused by a deficiency of the neurotransmitter serotonin, which is thought to regulate feelings of happiness and well-being. This theory is the instrument behind anti-depressant medication (Kirsch et al., 2008), and since it’s difficult to measure neurotransmitter levels in a living person’s brain, the functionality of anti-depressant medication has always been the largest shred of evidence to support the monoamine-deficiency hypothesis (Rottenberg, 2010). But recent data has actually shown evidence of increased serotonin in some depressed persons and other studies have shown that the idea of a single serotonin “level” is fallacious (Rottenberg, 2010). None of this means that serotonin plays no role at all in depression, just that it’s likely more complicated than simple deficiency of a neurotransmitter.

MDD patients may also struggle to regulate stress biologically. Generally, when stress occurs in the body, cortisol, a stress hormone, is released, and then suppressed once the stressful event has passed. Depressed patients have been shown to have less ability to suppress cortisol in this way. Interestingly, their bodies’ ability to manage this is shown to be much better with anti-depressants, which might explain why anti-depressants do help some sufferers (Belmaker & Agam, 2008).

A new biological theory is that depression might be linked to the immune system, and specifically to the inflammation mechanism. Clinical studies have confirmed this correlation (Dantzer et al., 2011). Patients with MDD had more of pro-inflammatory cytokine TNF-Alpha and less anti-inflammatory cytokines than control subjects do (Greenblatt, 2011). It’s easier to observe in patients who have physical comorbidities (such as heart disease) alongside their depression, rather than patients with only psychological disorders (Dantzer et al., 2011). One study had depressed patients take an antidepressant and aspirin, which is an anti-inflammatory medication. More than 50% of patients responded to this treatment combination, and more than 80% of that 50% that responded ended the study with their depression fully in remission (Greenblatt, 2011).

It’s also been theorized that depression begins in the personality itself, and with more negative cognitive patterns. Children who are reticient and inhibited at 3 were more likely to show depressive symptoms in adolescence, but these personality traits did not predict anxiety or substance abuse (Kopala-Shipley & Klein, 2017). Some believe that the theory that social-environmental stressors cause depression cuts out the middle-man, and that the social-environmental stressors actually cause negative personality traits to develop, which then might cause depression (Kopala-Shipley & Klein, 2017). And getting back to our old friend the 5-HTTLPR allele, it’s theorized that this gene seems to do is predispose carriers not to depression by itself, but to having a more pessimistic personality. Brain imaging has shown that patients with this gene present visibly process emotions differently than control subjects. A 5-HTTLPR carrier who is exposed to stress is more likely to develop depression than a stressed person without the gene, but the gene by itself does not seem to cause the disease (Belmaker & Agam, 2008).

Treating Depression

Psychotherapy, problem-solving therapy, acceptance and commitment therapy, cognitive behavioral therapy, interpersonal therapy, psychodynamic therapy, and mindful-nessbased cognitive behavior therapy (whew) are all used to treat depression (Platkin et al., 2017). Studies have suggested that computerized cognitive behavioral therapy (such as MoodGYM, Beating the Blues, and even gamified CBT for children, such as video game Camp Cope-A-Lot) can be as effective as therapist-led cognitive behavior therapy (Platkin et al., 2017).

Medication is also a common treatment option. SSRIs (selective serotonin reuptake inhibitors) made their debut as a drug to treat depression in the 1970s. Following the serotonin-deficient hypothesis of depression, these drugs block serotonin reuptake by transporter proteins, which typically remove excess neurotransmitters to the neurons that originally release them. This causes serotonin levels in the brain to rise. This mechanism takes about an hour, and yet SSRIs, when effective, don’t tend to improve symptoms until about four weeks after the patient has started taking them. (Kirsch et al., 2008). Animal trials of SSRI anti-depressants have always been fairly effective, but anti-depressants have only ever worked for some human patients (Belmaker & Agam, 2008). One study of new anti-depressants fluoxetine, venlafaxine, nefazodone, and paroxetine showed that none of them produced more results than a placebo (Kirsch et al., 2008).

One of the problems with depression treatment is that many sufferers never even receive treatment. Only a little more than half of adults with depression are treated, and the number is even lower in adolescents. And these numbers are for those who receive any kind of treatment at all – the number of people who are treated well is even lower. Depression treatment originating from general medical care rather is measurably less effective than depression treatment done by psychiatrists. (Strain & Blumenfield, 2018).


Despite MDD’s prevalence and our long-standing historical awareness of it, knowledge of the causes and treatment remains murky at best, and outright contradictory at worst. Stress, personality, psychosocial factors, biologic and our heritage all seem to be play some part, but there’s no clean answer or solution. But the slow turn away from the serotonin-deficient hypothesis seems like it could be an encouraging for future research.

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