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It is every bit as real as a physical condition.

In 2014, 6.7% of adults in the United States suffered one or more depressive crises. That number in the adolescent population was 11.4%.

Unipolar depression is mood disorder wherein a depressed mood is present. About one in two people originally thought to have unipolar depression, are now thought to suffer from bipolar depression. Documenting a patient’s family history and the impressions of a close friend or family member, can help to properly diagnose.

It used to be thought that about 86% of mood disorders were those with major depressive disorder, 2% bipolar I, 2% bipolar II, and 10% unspecified. The more recent view hold that approximately 50% of those with significant disturbance in mood have major depressive disorder, 2% have bipolar I, 15% suffer from bipolar II, and the last 33% have some illness in the bipolar spectrum.

Mayo Clinic states that clinical depression, also known as major depression, is not the same as suffering a loss, or having a difficult physical medical condition.

Major depression is the most common mood disorder. It is diagnosed after one episode of major depression, but moat experience more than one episode.

Melancholia is a type of major depression. It causes an unrealistic amount of sadness. It tends to cause people to feel hopeless when confronted with problems. Possible for all types of depression, but more common in melancholia, is the loss of interest in hobbies that were once fun and fulfilling. Melancholia can cause, or worsen, anxiety, irritability, and problems thinking.

Dysthymia is not as painful as major depression, but it lasts more than two years, and is known for being more persistent.

Double depression is when one experiences a major depressive episode while suffering from dysthymia. It usually leads to significant problems in completing daily activities, and/or in socially connecting with others.

Postpartum depression is pretty self-explanatory.

Atypical depression usually involves an extreme appetite, and significant gain of weight. People with atypical depression also tend to be overly tired a lot, which leads to excessive sleeping. They are more sensitive than other people to social rejection.

Seasonal Affective Disorder (SAD) is depression that’s caused by change in season. It might more specifically be a reaction to change in daily light. Generally, there  are two types of SDA, the winter time, and the summer time. Most of these symptoms are also seen in other depression types.

  1. Winter
    1. Weight gain
    2. Reduction in sexual interest
    3. Fatigue
    4. Being irritable
    5. Lack of social interest
  2. Summer
    1. Agitation
    2. Weight loss
    3. Lack of appetite
    4. Trouble sleeping
    5. Restlessness

People of all ages and backgrounds can become clinically depressed. That said, certain peoples present with depression at a higher rate, and the ultimate danger of depression: suicide. Here we have an infographic, centered around the UK, but still informative.

The Diagnostic Statistical Manual, a handbook for diagnosing mental illness, lists criteria for clinical depression. Five are more of the traits listed below must be present almost ever day, and for the majority of the day, over a period of two weeks. One of the symptoms has to be a loss in pleasure or a significantly low mood.

  • Depressed mood (in children and teens, depressed mood can appear as constant irritability)
  • Significantly reduced pleasure in all or most activities
  • Significant weight loss when not dieting, weight gain, or change in appetite (in children, failure to gain weight as expected)
  • Insomnia or increased desire to sleep
  • Observable restlessness or slowed behavior
  • Fatigue
  • Excessive feelings of worthlessness or inappropriate guilt
  • Significant cognitive trouble (thinking)
  • Recurrent thoughts of death or suicide

After the first episode of depression, treatment must go on for 6 months to a year. After the second time, two years, as the risk o relapse is 70%. If it happens a third time, the chance of relapse is over 90% if one stops their medication, so treatment is recommended indefinitely.

People who are significantly depressed tend to have under-activity in the hippocampus and cortical regions of the brain.

Some suggest that depression is largely caused by an impaired cortex, which doesn’t have the power to regulate the amygdala and other limbic regions as well.

  • The old hypothesis of depression, termed the monoamine hypothesis, simply stated that depression is caused by a lack of activity of the monoamine chemicals (dopamine, norepinphrine, serotonin, epinephrine), mainly serotonin.
  • Currently, depression is thought to be caused largely by a lack of neuroplasticity (physical change in pathways and structure) and neurotrophic activity (the formation of new neurons).

Some terms:

  • Neurotrophins
    • Peptides that increase the connections and health of neurons, even leading to the creation of new neurons
  • Reuptake inhibitor
    • A substance that blocks a neurotransmitter from being recaptured by the cell that released it
    • Recaptured, they will be broken down or primed for re-release
  • Serotonin
    • The main neurotransmitter associated with depression
  • Neurogenesis
    • New neurons being created
  • HPA axis
    • The hypothalamic-pituitary-axis
    • This network is heavily involved in stress chemicals, and isn’t healthy for neurons
  • Epigenetics
    • This is a new term
    • It’s the study of changing how genes are expressed
    • Not actually changing DNA, but in effect doing so, as different genetic material is made active

This how SSRI therapy might mainly work to decrease depression:

  1. First, there is an inhibition of reuptake, inhibition of metabolism, activation of a receptor, blocking activation of a receptor, or action on intracellular activity.
  2. Initially, serotonin is prevented from binding to the reuptake pump and being transported back in the presynaptic neuron, so more of it exists in the synapse
  3. The body, attempting to maintain balance, then decreases the amount of those chemicals that it produces.
  4. This leads to neurotrophic activity.
  5. Finally, after a period of weeks or months, there is increased plasticity, reduced cell death, neurogenesis, greater survival of existing neurons, and greater protection against neurotoxicity.
  6. Inflammation decreases, the HPA axis becomes less dominant, and epigenetic changes begin to manifest.

Epigenetics doesn’t only happen after taking antidepressants. In fact, new as the study is, it holds true that one’s gene expressions can change in a myriad of circumstances

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This is a view of how antidepressants would work:

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This image is somewhat complicated, but is well explained in the section and subsections of A Scientific Overview

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There are various non-psychiatric conditions that may cause depression.

  • collagen disorders
  • cardiovascular disease
  • disorders of the endocrine system
  • various types of infections
  • metabolic disorders
  • ingesting an improper amount of minerals and/or vitamins
  • neurological disorders

Additionally, some drugs and medications can cause depression.

  • steroids
  • reserpine
  • opiates
  • oral contraceptives
  • anti-parkinsonian medications
  • alcohol
  • amantadine
  • beta-blockers
  • hydralazine
  • guaneithidine
  • clonidine
  • central nervous system depressants (such as sleep or anxiety medications)

Finally, the process merits therapy to entirely work!

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Sources: Condensed Psychopharmacology 2013: A Pocket Reference for Psychiatry and Psychotropic Medication, Abnormal Psychology: An Integrative Approach, Endocannabinoid Regulation of Monoamines in Psychiatric and Neurological Disorders, Stahl’s Essential Psychopharmacology,,,,,…494861.496764..496911…0.0..0.86.1142.15……1….1..gws-wiz-img.Mo7HuUwO-Mo#imgrc=WuToqJhMhDuvOM:,