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Depression - Biological factors

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Biological causesEdit

Endocrinology in depressionEdit

Main article: Depression - Hormones
  • Hormonal factorsThe levels of hormones, the chemical messengers in the body that help regulate metabolism, have been linked to depression

Genetic factors in depressionEdit


Synapse
Brain chemicals called neurotransmitters allow electrical signals to move from the axon of one nerve cell to the neuron of another. A shortage of neurotransmitters impairs brain communication.
LifeartistAdded by Lifeartist

Neuroanatomy of depressionEdit

  • Neuroanatomy Recent research has suggested that there may be a link between depression and neurogenesis of the hippocampus.

Neurochemistry of depressionEdit

  • Neurochemical There may be changes or imbalances in chemicals that transmit information in the brain, called neurotransmitters. Many modern antidepressant drugs attempt to increase levels of certain neurotransmitters, such as serotonin and norepinephrine. Although the causal relationship is unclear, it is known that antidepressant medications can relieve certain symptoms of depression, although critics point out that the relationship between serotonin, SSRIs, and depression usually is typically greatly oversimplified when presented to the public (see here).


Most antidepressants increase synaptic levels of serotonin, one of a group of neurotransmitters known as monoamines. Serotonin is thought to help regulate other neurotransmitter systems, and decreased serotonin activity may allow these systems to act in unusual and erratic ways.[1] According to this "permissive hypothesis," depression can arise when low serotonin levels promote low levels of norepinephrine, another monoamine neurotransmitter.[2] Some antidepressants also enhance the levels of norepinephrine directly, whereas others raise the levels of dopamine, a third monoamine neurotransmitter. These observations gave rise to the monoamine theory of depression. In its contemporary formulation, the monoamine theory postulates that a deficiency of certain neurotransmitters is responsible for the corresponding features of depression: "Norepinephrine may be related to alertness and energy as well as anxiety, attention, and interest in life; [lack of] serotonin to anxiety, obsessions, and compulsions; and dopamine to attention, motivation, pleasure, and reward, as well as interest in life."[3] The proponents of this theory recommend choosing the antidepressant with the mechanism of action impacting the most prominent symptoms. Anxious and irritable patients should be treated with SSRIs or norepinephrine reuptake inhibitors, and those experiencing a loss of energy and enjoyment of life with norepinephrine and dopamine enhancing drugs.[3]


In the past two decades, research has uncovered multiple limitations of the monoamine theory, and its inadequacy has been criticized within the psychiatric community.[4] Intensive investigation has failed to find convincing evidence of a primary dysfunction of a specific monoamine system in patients with major depressive disorders. The medications tianeptine and opipramol have long been known to have antidepressant properties despite not acting through the monoamine system. Experiments with pharmacological agents that cause depletion of monoamines have shown that this depletion does not cause depression in healthy people nor does it worsen symptoms in depressed patients.[5] According to an essay published by the Public Library of Science, the monoamine theory, already limited, has been further oversimplified when presented to the general public.[6]


See alsoEdit

References & BibliographyEdit

  1. Barlow 2005, p. 226
  2. Shah N, Eisner T, Farrell M, Raeder C (1999). An overview of SSRIs for the treatment of depression. (PDF) Journal of the Pharmacy Society of Wisconsin. URL accessed on 2008-11-10.
  3. 3.0 3.1 Nutt DJ (2008). Relationship of neurotransmitters to the symptoms of major depressive disorder. Journal of Clinical Psychiatry 69 Suppl E1: 4–7.
  4. Hirschfeld RM (2000). History and evolution of the monoamine hypothesis of depression. Journal of Clinical Psychiatry 61 Suppl 6: 4–6.
  5. Delgado PL (2000). Depression: The case for a monoamine deficiency. Journal of Clinical Psychiatry 61 Suppl 6: 7–11.
  6. Lacasse J, Leo J (2005). Serotonin and depression: A disconnect between the advertisements and the scientific literature. PLoS Med 2 (12): e392.

Key textsEdit

BooksEdit

PapersEdit

Additional materialEdit

BooksEdit

PapersEdit

  • [2]] Google Scholar]

External linksEdit

Physical sex differencesEdit

Main article: Physical sex differences and depression

Medical conditions and depressionEdit

  • Medical conditions – Certain illnesses, including cardiovascular disease[1], hepatitis, mononucleosis, hypothyroidism, and organic brain damage caused by degenerative conditions such as Parkinson disease or by traumatic blunt force injury may contribute to depression, as may certain prescription drugs such as birth control pills and steroids. Gender dysphoria can also cause depression.


Main article: Depression and physical illness

Physiological functioning and depressionEdit

The activity of various physiological processes are also associated with depression:

Nutrition and depressionEdit

Main article: Nutrition and depression

Drug abuse and depressionEdit

  • Alcohol and other drugs – Alcohol can have a negative effect on mood, and misuse of alcohol, benzodiazepine-based tranquilizers, sleeping medications and recreational drugs can all play a major role in the length and severity of depression.
Main article: Drug abuse and depression

See alsoEdit

BibliographyEdit

Key texts – BooksEdit

Additional material – BooksEdit

Key texts – PapersEdit

  1. Manev, R, Manev H (2004). 5-Lipoxygenase as a putative link between cardiovascular and psychiatric disorders. Critical Reviews in Neurobiology 16 (1�2): 181�6.

Additional material - PapersEdit

External linksEdit

Depression
Types of depression
Depressed mood | Clinical depression | Bipolar disorder |Cyclothymia | |Dysthymia |Postpartum depression | |Reactive | Endogenous |
Aspects of depression
The social context of depression | Risk factors | Suicide and depression | [[]] | Depression in men | Depression in women | Depression in children |Depression in adolescence |
Research on depression
Epidemiology | Biological factors  |Genetic factors | Causes | [[]] | [[]] | Suicide and depression |
Biological factors in depression
Endocrinology | Genetics | Neuroanatomy | Neurochemistry | [[]] | [[]] | [[]] |
Depression theory
[[]] | Cognitive | Evolution | Memory-prediction framework | [[]] |[[]] | [[]] |
Depression in clinical settings
Comorbidity | Depression and motivation | Depression and memory | Depression and self-esteem |
Assessing depression
Depression measures | BDI | HDRS | BHS |CES-D |Zung |[[]] |
Approaches to treating depression
CAT | CBT |Human givens |Psychoanalysis | Psychotherapy |REBT |
Prominant workers in depression|-
Beck | Seligman | [[]] | [[]] |
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