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The biology of depression is the attempt to identify a biochemical origin of depression, as opposed to theories that emphasize psychological or situational causes. Scientific studies have found that different brain areas show altered activity in humans with major depressive disorder (MDD) . [ 1 ]
Psychomotor agitation is a symptom in various disorders and health conditions. It is characterized by unintentional and purposeless motions and restlessness, often but not always accompanied by emotional distress and is always an indicative for admission.
[15] [16] A family history of depression increases the chance of being diagnosed. [17] There are usually a combination of biological, psychological, and social factors that play into a person's depression. [2] [18] A major depressive episode can often follow acute stress in someone's life, such as the death of a loved one or being fired from a ...
However, the hypothesis is incomplete, as several lines of evidence suggests that depression is more than just a monoamine imbalance. For example, antidepressants usually take several weeks to reduce a patient's depressive symptoms, which is inconsistent with the finding that monoamine levels are affected within hours of using antidepressants. [5]
Epigenetics of depression is the study of how epigenetics (heritable characteristics that do not involve changes in DNA sequence) contribute to depression. Major depressive disorder is heavily influenced by environmental and genetic factors.
Watson and Clark (1991) proposed the Tripartite Model of Anxiety and Depression to help explain the comorbidity between anxious and depressive symptoms and disorders. [1] This model divides the symptoms of anxiety and depression into three groups: negative affect, positive affect and physiological hyperarousal.
Stress appears to play a role in hypertension, and may further predispose people to other conditions associated with hypertension. [48] Stress may precipitate abuse of drugs and/or alcohol. [5] Stress may also contribute to aging and chronic diseases in aging, such as depression and metabolic disorders. [49]
A hypothesized gene–environment interaction between the short/short allele of the 5-HTTLPR and life stress as predictor for major depression has suffered a similar fate: after an influential [34] initial report in 2003 [35] there were mixed results in replication in 2008, [36] and a 2009 meta-analysis was negative. [37] See 5-HTTLPR for more ...