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 The etiology of depression, though the most researched mood disorder, is far from understood completely.  Many cases of depression are prompted by stressful life events, however, that is not the case for everyone

Depression Myths & Facts about Depression

 Contributing factors include: • Intensity and Duration • Genetic endowment • Coping Skills • Social Support Network  Depression is one of several mental disorders that is generally described as: the product of a complex interaction between biological & psychosocial factors (1)

Researchers have detected abnormal concentrations of many neurotransmitters and their metabolites in Urine Plasma Cerebrospinal fluid (Thase & Howland, 1995)


Elevated levels of corticotropin-releasing factor (Nemeroff, 1992, 1998; Mitchell, 1998)

Abnormalities in second messenger systems (Drevets, 1998; Rush et al., 1998, Steffens & Krishnan, 1998).

** It is difficult to pin these biological alterations to depression as they could also be a consequence of sleep deprivation or weight loss

Research discovered that reserpine, a medication for hypertension, caused depression. It depleted the brain of: Serotonin Dopamine Norepinephrine Epinephrine


 Such findings led to the “catecholamine hypothesis” which led to the“monoamine hypothesis”  After more than 30 years of research monoamine hypothesis has been found an insufficient explanation. Problems:  Many other neurotransmitter systems are altered in depression, including GABA and acetylcholine  Lifting of symptoms still does not prove cause by defective monoamine neurotransmission.

 Research suggests that depression results from death and dysfunction of particular neurons, especially those found in the hippocampus (Duman et al., 1997)

 Many currently available medications that relieve depression enhance monoamine activity (SSRIs)– therefore, the monoamine theory is still used to aid in treatment.


 Life Changing Events Death Grief  Parental Neglect  Malnourishment  Physical / Sexual Abuse  These factors may help shape your Personality/Temperament


Traits likely to have poor coping ability: Avoidance Dependence Reactivity Impulsivity Interpretation of event Attachment of Personal Meaning  Faulty Thinking  “SHOULDs” Learned Helplessness

 Researchers have provided ample evidence that brain function and anatomic structure can be influenced by stress (Weiss, 1991).

 Many aspects of the acute stress response are exaggerated, persistent, or irregular with depression (Thase & Howland, 1995).

 Much attention has been focused on CRH, which is hypersecreted in depression (Nemeroff, 1992, 1998).


CRH is released by the hypothalamus to activate the pituitary in the acute stress response.

 CRH injections into the brain of laboratory animals produce the signs and symptoms found in depressed patients including:  Decreased appetite  Weight loss  Decreased sexual behavior and sleep (Sullivan et al., 1998).

 CRH is found in higher concentrations in the cerebrospinal fluid of depressed patients

Gender:  In the United States, women are about as twice as likely as men to be diagnosed and treated for major depression. Approximately 20-25% of women and 12% of men will experience a serious depression at least once in their lifetimes

Marital factors:  Higher rate of major depression in Unhappily married, divorced or separated



 While clinical depression usually occurs for the first time when a person is between the ages of 20 and 50, people over the age of 65 are especially vulnerable. Heredity:  People who have relatives who have had clinical depression or bipolar disorder have a greater chance of developing it themselves. (TWIN STUDIES) Previous episode:  Having one episode of depression increases your changes by up to 50% of experiencing it again. (2)

 Patients with combinations of anxiety and depression are the rule rather than the exception  Many of the medications used to treat one are often used to treat the other.



Similarities in antecedents, correlates, and consequences of each condition  Elevated levels of CRH  Smaller volume of hippocampus  Changes in the amygdala & hypothalamus (3) Effecting emotions, sleep, memory & hormone secretion among others “In both conditions, excess glucocorticoid exposure was thought to be the culprit in inducing the atrophy of hippocampus neurons.” (Sheline, 1996)

Drevets, W. C. (1998). Functional neuroimaging studies of depression: The anatomy of melancholia. Annual Review of Medicine, 49, 341–361.

Duman, R. S., Heninger, G. R., & Nestler, E. J. (1997). A molecular and cellular theory of depression. Archives of General Psychiatry, 54, 597–606. Nemeroff, C. B. (1992). New vistas in neuropeptide research in neuropsychiatry: Focus on corticotropin-releasing factor. Neuropsychopharmacology, 6, 69–75. Sheline, Y. I. (1996). Hippocampal atrophy in major depression: A result of depression-induced neurotoxicity? Molecular Psychiatry, 1, 298–299.

Sullivan, G. M., Coplan, J. D., & Gorman, J. M. (1998). Psychoneuroendocrinology of anxiety disorders. Psychiatric Clinics of North America, 21, 397–412. Thase, M. E., & Howland, R. H. (1995). Biological processes in depression: An updated review and integration. In E. E. Beckham & W. R. Leber (Eds.), Handbook of depression (2nd ed., pp. 213–279). New York: Guilford Press. Weiss, J. M. (1991). Stress-induced depression: Critical neurochemical and electrophysiological changes. In J. Madden (Ed.), Neurobiology of learning, emotion, and affect (pp. 123–154). New York: Raven Press.

Etiology of Depression