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What is the etiology of depression (Major Depressive Disorder)? Show more Show less
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Depression is a mental disorder characterized by a lack of pleasure in familiar activities, a sad mood, and cognitive/somatic changes that limit functioning. Psychologists use three different approaches while explaining the etiology (origin) of depression: biological, cognitive, and sociocultural.

Depression has a biological etiology Show more Show less

Recent developments, including the sequencing of the human genome and the advancement of brain imaging technologies, allowed psychologists to explain depression from a biological perspective. This school of thought argues that biological factors such as genetics and hormone/neurotransmitter levels cause depression.
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High cortisol hormone levels cause depression

The cortisol hypothesis states that depression results from the cessation of neuron birth in the hippocampus and other neural networks related to serotonin, dopamine, and norepinephrine. Cortisol appears to be the reason for this lack of neurogenesis.

The Argument

The cortisol hypothesis of depression argues that depression is the result of the cessation of neuron birth in the hippocampus as well as in other neural networks related to serotonin, dopamine, and norepinephrine. Cortisol appears to be the reason for this lack of neurogenesis. Cortisol is a hormone produced by the adrenal glands and secreted by the body in response to stress. It is involved in the fight or flight response.[1] MDD patients display a symptom called HPA-Axis hyperactivity. Over secretion of cortisol leads to reduced serotonin, dopamine, and noradrenaline in the brain. As a result, MDD patients have smaller hippocampi.[2] Empirical evidence also revealed that cortisol dysfunction is proportionate to MDD severity.[3] The study of Maberg et al. (2000) supports this hypothesis. Researchers concluded that neurogenesis supports the effect of antidepressants in a rat model for depression.[4] The meta-analysis of Videbech and Ravnkilde (2004) also found up to a 10% reduction of the hippocampus in the brains of depressed patients. The shrinking of the hippocampus was significantly correlated to the number of depressive episodes.[5] Overall, the cortisol hypothesis explains depression in terms of neuroplasticity and hormonal imbalance.

Counter arguments

The cortisol hypothesis fails to establish a causal relationship. Supporting empirical evidence only demonstrates a correlation between elevated cortisol levels and depression. There is an ambiguity concerning whether high cortisol levels cause depression or if depression increases cortisol levels. Additionally, the increased incidence of MDD in females is associated with greater cortisol response variability rather than higher baseline levels of cortisol.[3] The association between cortisol and MDD in humans is complex. It appears dependent on the stage of illness, severity, and type of challenge employed. Cortisol dysregulation, specifically in response to stress, is associated with severe and acute presentations of MDD. However, chronic and less severe subtypes of MDD do not exhibit this association. Personality and social factors may be major drivers of these subtypes instead of cortisol levels. This fact weakens the cortisol hypothesis.[3]



Rejecting the premises


This page was last edited on Tuesday, 1 Dec 2020 at 22:36 UTC

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