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Cortisol, serotonin and depression: All stressed out?

  • P. J. Cowen (a1)
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Bauer, M. E., Vedhara, K., Perks, P., et al (2000) Chronic stress in caregivers of dementia patients is associated with reduced lymphocyte sensitivity to glucocorticoids. Journal of Neuroimmunology 103, 8492.
Cowen, P. J., Clifford, E. M., Williams, C., et al (1995) Why is dieting so difficult? Nature, 376, 557.
Da Roza Davis, J. M. & Cowen, P.J. (2001) Biochemical stress of caring. Psychological Medicine, 31, 14751478.
Deakin, J. F. (1988) 5-HT2 receptors, depression and anxiety. Pharmacology, Biochemistry and Behavior, 29, 819820.
Dinan, T. G. (1994) Glucocorticoids and the genesis of depressive illness. A psychobiological model. British Journal of Psychiatry, 164, 365371.
Fernstrom, J. D. & Wurtman, R. J. (1971) Brain serotonin content: physiological dependence on plasma tryptophan levels. Science, 173, 149152.
Goodall, E. M., Cowen, P. J., Franklin, M., et al (1993) Ritanserin attenuates anorectic, endocrine and thermic responses to d-fenfluramine in human volunteers. Psychopharmacology, 112, 461466.
Maes, M., Jacobs, M. P., Suy, E., et al (1989) Cortisol, ACTH, prolactin and beta-endorphin responses to fenfluramine administration in major-depressed patients. Neuropsychobiology, 21, 192196.
Maes, M., Calabrese, J. & Meltzer, H. Y. (1994) The relevance of the in-versus outpatient status for studies on HPA-axis in depression: spontaneous hypercortisolism is a feature of major depressed inpatients and not of major depression per se. Progress in Neuropsychopharmacology and Biological Psychiatry, 18, 503517.
McAllister-Williams, R. H., Anderson, R. J. & Young, A. H. (2001) Corticosterone selectively attenuates 8-OH-DPAT-mediated hypothermia in mice. International Journal of Neuropsychopharmacology, 4, 18.
Sargent, P. A., Kjaer, K. H., Bench, C. J., et al (2001) Brain serotoninIA receptor binding measured by positron emission tomography with [11C] WAY-100635: effects of depression and antidepressant treatment. Archives of General Psychiatry, 57, 174180.
Smith, K. A., Fairburn, C. G. & Cowen, P. J. (1997) Relapse of depression after rapid depletion of tryptophan. Lancet, 349, 915919.
Strickland, P. L., Deakin, J. F. W., Percival, C., et al (2002) The bio-social origins of depression in the community. Interactions between social adversity, cortisol and serotonin neurotransmission. British Journal of Psychiatry, 180, 168173.
Van West, D. & Maes, M. (1999) Activation of the inflammatory response system: a new look at the etiopathogenesis of major depression. Neuroendocrinology Letters, 20, 1117.
Walsh, A. E. S., Oldman, A. D., Franklin, M., et al (1995) Dieting decreases plasma tryptophan and increases the prolactin response to d-fenfluramine in women but not men. Journal of Affective Disorders, 33, 8997.
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The British Journal of Psychiatry
  • ISSN: 0007-1250
  • EISSN: 1472-1465
  • URL: /core/journals/the-british-journal-of-psychiatry
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Cortisol, serotonin and depression: All stressed out?

  • P. J. Cowen (a1)
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eLetters

Why mental illness?

Saad F. Ghalib, consultant in old age psychiatry
03 August 2011

The findings reported in the Cowen's editorial, if one thing, do showthat the biopsychosocial model of depression,contrary to the author's conclusion, is not very well integrated . we now know that neither high cortisol levels, nor stressful life events are necessary or sufficient forthe development of depressive disorders. Furthermore,the long held belief,that serotonin levels in people with depression are lower than normal subjects, which is suppose to underpin the theoretical basis of treatment with SSRIs, is not strongly supported by evidence. So, where does that leave depression as a clinical entity?Well, we know that depression does exist, and people who suffer from it can attest to that. Therefore, the concept is not a fictional one.However, one can not help but to notice that the causal foundations of the biopsychosocial model of depression arebeginning to show several cracks when subjected to stringent testing.Curiously, even the likes of schizophrenia and bipolar disorder,that are reliably distinct at a phenomenological levels, do in fact share close ''pathogenetic'' mechanisms (1),when viewed from a biological perspective.

So, where have we gone wrong? well, the dualists(mind-brain dichotomy), will see this as another nail in the coffin of pure biologicalformulations of mental disorders!In reality though,dualist philosophies did not help very much in elucidating the principles of brain functions. An alternative explanation is that; may be, phenomenology is governed bydifferent causal principles to that of biology. Therefore, the results inone field can not be translated into another field, i,e, the two languagesare not interchangeable.Obviously, this argument may bare some truth, but then one has to account for the fact that nature often permits different causal languages to be interchangeable. For example, at the quantum level the word 'position' of an electron(2) has no definite meaning(a position of a single electron can be spread out) . Still, when the experimental setup is defined clearly, the word 'position' will resume it is natural and classical meaning.Even those who hold on to the premise that the mind is aseparate entity to the brain, surely, would have to admit that the mind after all, is part of nature and should be subject to the same causal lawslike everything else.Therefore, the language of phenomenology can, and should be reduced to the language of chemicals and genes as two parts of one coherent whole. This however, has not proved possible yet.

There is another possibility though. One that might explain the findings reported in the Cowen's article, and that is; abnormalities(disease status) only exist at the phenomenological level. Whereas, findings from genetic and biological studies,have so far provideda glimpse of the ''brain's natural'' and inbuilt mechanisms when faced with adversity.That's why, for example, cortisol levels will go up as a result of stress( biologically inbuilt), but may not increase when the person suffers from depression(phenomenological).One is somehow reminded by the work of psychologist Julian Jaynes who suggested(3) that prior to 1200BC (before meta-awareness),for humans, volition came as a voice in thenature of a command. Therefore,it seems that a bit of madness is inherent in all of us.Incidentally,this may explain the relatively higher than previously considered prevalence rates of non-clinical psychotic symptoms in population-based studies(4).This however, should not qualify for ''disease status'', although mistakenly gets labelled as such, by those studying genes and chemicals!

To say that abnormality exists only phenomenologically( signs and symptoms) is however, not the same as declaring that mental illness is a human invention . On the contrary,those conceptual difficulties should actas an incentive towards further understanding as to why it seem somehow easier to capture abnormality at a phenomenological rather than biologicallevel? May be we should re-phrase the question from; why mental illness? to why not mental illness?

declaration of interest; noneReferences;1.Craddock N, Owen MJ. The Kraeplinian dichotomy-going,going ..but still not gone.Br J Psychiatry 2010; 196,92-95.2.Heisenberg W. Physics and Philosophy.Penguin Books,2000.3.Jaynes J. The origin of consciousness in the breakdown of the bicameral mind.1990.4.kelleher I,Jenner JA, Cannon M. Psychotic symptoms in the general population-an evolutionary perspective.Br J Psychiatry 2010; 197, 167-169

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Conflict of interest: None declared

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