by Al Galves, Ph.D.
In Medscape’s article on Depression and Suicidality, the section entitled “Etiology of Depression and Suicidality” contains statements that are not supported by scientific evidence. This section is based on ideology, not on science. It is based on the ideology of the Biopsychiatric Belief System.
The section places unsupported emphasis on the physiological factors associated with depression and greatly underplays the psychosocial factors associated with depression. It contains this statement: “A decrease in the functional balance of (serotonin and norepinephrine) causes certain types of depression”. This statement is not supported by scientific evidence. There may be evidence that depression is associated with changes in neurochemicals, but that is not evidence that the changing neurochemicals caused depression. This is an important distinction. Correlation is not causation.
Furthermore, if we have a research finding an association between depression and a change in neurotransmitters, proper scientific practice would be to be careful about making a determination of the meaning of such an association. There are at least three possible interpretations. One is that the change in neurotransmitters is causing the depression. A second is that the depression is causing change in neurotransmitters. A third is that the relationship between the neurotransmitter dynamics and the depression is so intertwined that it is virtually impossible to determine which causes which. Proper scientific practice would be to use parsimony in choosing an interpretation. In other words, we would base our interpretation on what is clearly known about other mind-body dynamics.
The most widely and deeply studied of such dynamics is the stress response. The stress response is a profound physiological dynamic that affects the entire body. That physiological dynamic is clearly caused by a psychosocial event – a perception of threat and a cognition that the threat is real and needs to be addressed. Thus, through the use of parsimony, we would choose the interpretation that the depression is causing the neurotransmitter changes.
This section of the Medscape article is also inappropriately certain about the current state of knowledge about neurotransmitter dynamics and depression. Many people with neurotransmitter changes do not experience depression. There is more serotonin in the stomach than in the brain, which throws a large monkey wrench into the relationship between serotonin and depression. There is no evidence of depression ever being reliably diagnosed through measurements of neurotransmitter levels in the brain.
The Medscape article erroneously downplays the association between psychosocial factors and depression. The following is evidence of such association: Persons who derive their sense of self-worth from social relationships are more vulnerable to depression after interpersonal loss than those who obtain self-esteem from other domains (Johnson and Roberts, 1995); women who use a ruminating style of thinking suffer more severely from depression than those who don’t (Lehmicke and Hicks, 1995); people who score low on self-esteem and high on stress are more likely to be depressed (Kreger, 1995); nursing home residents who had a bird in their room were significantly less depressed after being moved to a skilled rehabilitation facility than those who didn’t (Jensen, Cardello and Baun, 1996); persons who score high on a Self-Defeating Personality Scale are more likely to be depressed than others (McCutcheon, 1995); chronic pain sufferers are more likely to be depressed (Banks and Kerns, 1996); persons with more emotional strength and resiliency and a higher level of ego control are less likely to be depressed (Hirschfelt et.al., 1989); recovery from depression is facilitated by events that lessen ongoing difficulty or deprivation (Brown, Lemyre and Bifulco, 1992), and; psychotic depressed patients had significantly poorer pre-morbid functioning - particularly adolescent social functioning - than non-psychotic depressed patients (Sands and Harrow, 1995).
In short, this section of the article is ideology, not science.
Banks, S.R. and Kerns, R.D. (1996). Explaining high rates of depression in chronic pain: A diathesis-stress framework. Psychological Bulletin, 119: 95-110
Brown, G.W., Lemyre, L. and Bifulco, A. (1992). Social factors and recovery from anxiety and depressive disorders: A test of specificity. British Journal of Psychology, 161:44-54
Hirschfeld, R.M.A., Klerman, G.L., Lavori, P. et al. (1989). Pre-morbid personality assessments of first onset of major depression. Archives of General Psychiatry, 46:345-50
Jensen,J., Cardello,F., and Baun,M. (1996). Avian companionship in alleviation of depression, loneliness and low morale in older adults in skilled rehabilitation units. Psychological Reports 78, 339-348
Johnson, S.L. and Roberts, J.E. (1995). Life events and bipolar disorder: Implications from biological theories. Psychological Bulletin, 117(3), 443-449
Kreger, D.W. (1995). Self-esteem, stress and depression among graduate students. Psychological Reports, 76, 345-346
Lehmicke,N. and Hicks,R. (1995). Relationship of Response-set differences in Beck Depression Inventory scores of undergraduate students. Psychology Reports, 76, 15-21
McCutcheon, L.E. (1995). Further validation of the Self-Defeating Personality Scale. Psychological Reports, 76:1135-38
Sand, J.R. and Harrow,M. (1995). Vulnerability to psychosis in unipolar major depression: Is pre-morbid functioning involved? American Journal of Psychiatry, 152, 1009-1015