Abstract
Depression is the second leading cause of disability worldwide with prevalence ranging from 2.5 to 20 % of the population dependent on the country. It can present as a single condition, but often it is co-morbid with chronic diseases. Medical professionals commonly treat depression as a neurotransmitter imbalance; yet, many effects ascribed to antidepressant medication, such as selective serotonin reuptake inhibitors, have also been explained by the placebo effect in patients with mild to moderate depression. Largely ignored research indicates that depression is caused by highly complex interactions of neuroendocrine and inflammatory mechanisms. In addition, culture/stigma, access to mental health services, and social instability play significant roles in perpetuating HPA and inflammatory pathways to maintain the disease and treatment resistance. The presented evidence highlights the need to appreciate depression through a multi-disciplinary lens to properly treat it and successfully reduce the debilitating effects on quality of life, co-morbidity and mortality, especially from suicide.
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Notes
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What Do These Findings Mean? These findings suggest that, compared with placebo, the new-generation antidepressants do not produce clinically significant improvements in depression in patients who initially have mild to moderate depression, but show significant effects only in the most severely depressed patients. The findings also show that the effect for these patients seems to be due to decreased responsiveness to placebo, rather than increased responsiveness to medication. Given these results, the researchers conclude that there is little reason to prescribe new-generation antidepressant medications to any but the most severely depressed patients unless alternative treatments have been ineffective. In addition, the finding that extremely depressed patients are less responsive to placebo than less severely depressed patients but have similar responses to antidepressants is a potentially important insight into how patients with depression respond to antidepressants and placebos that should be investigated further (http://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.0050045).
- 2.
Andres Lozano: Parkinson’s, depression and the switch that might turn them off. January 2013 at TEDxCaltech http://www.ted.com/talks/andres_lozano_parkinson_s_depression_and_the_switch_that_might_turn_them_off?language=en.
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History: 50 years ago, clinical depression was either endogenous (melancholic) or reactive (neurotic). Endogenous depression was a categorical biological condition with a low lifetime prevalence (1–2 %). By contrast, reactive depression was exogenous—induced by stressful events affecting a vulnerable personality. (Parker, G. Is depression overdiagnosed. BMJ, 2007;335:328.) DSM-IV criteria:
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Anhedonia (the inability to find pleasure in positive things) and
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Lack of mood reactivity (i.e., mood does not improve in response to positive events) and at least three of the following:
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Depression that is subjectively different from grief or loss
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Severe weight loss or loss of appetite
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Psycho-motor agitation or retardation
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Early morning awakening
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Guilt that is excessive
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Worse mood in the morning
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Bennett, J.M., Sturmberg, J.P. (2016). Depression: Not Just a Top–Down Phenomenon. In: Sturmberg, J. (eds) The Value of Systems and Complexity Sciences for Healthcare. Springer, Cham. https://doi.org/10.1007/978-3-319-26221-5_13
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