Cortisol levels are more closely associated with depressiveness and other psychopathologies than catecholamine levels

Czech version

Authors: Z. Hess ¹; J. Podlipný ²; H. Rosolová ¹; O. Topolčan ³; B. Petrlová ¹
Authors‘ workplace: II. interní klinika Lékařské fakulty UK a FN Plzeň, přednosta doc. MUDr. Jan Filipovský, CSc. ¹; Psychiatrická klinika Lékařské fakulty UK a Plzeň, přednosta doc. MUDr. Jiří Beran, CSc. ²; Oddělení imunoanalýzy Lékařské fakulty UK a FN Plzeň, přednosta prof. MUDr. Ondřej Topolčan, CSc. ³
Published in: Vnitř Lék 2007; 53(10): 1040-1046
Category: Original Contributions

Overview

Objective:
Quantification of changes in the levels of the above hormones, i.e. cortisol, adrenalin, noradrenalin and dopamine depending on the presence of depressive symptoms and other psychopathological symptoms. Sample: 259 randomly selected individuals from the population of the city of Pilsen.

Method:
Zung self-assessment scale and SCL-90 questionnaire were used to assess depressiveness and other psychopathologies. Serum cortisol levels were measured, as well as the levels of cortisol and catecholamine (adrenalin, noradrenalin and dopamine) in a 24-hour urine sample. The studied sample was divided, by an arbitrarily defined limit, into a group with a higher and a group with a lower excretion of the monitored hormones.

Results:
The group with cortisol excretion higher than 300 nmol/24 h had a significantly higher score in terms of the SCL-90 questionnaire interpersonal sensitiveness, depression, anxiety, phobia, paranoidism and psychoticism as compared with the group with cortisol excretion below 300 nmol/24 h (p < 0.05). The group with cortisol excretion above 300 nmol/24 h had also a significantly higher score on Zung’s self-assessment depression scale as compared with the group with cortisol excretion below 300 nmol/24 h (p < 0.05). Division of the sample according to the score on Zung’s self-assessment depression scale (SDS index ł 50) has shown that women with a record of depressive symptoms had a statistically significant higher of urinary cortisol excretion in 24 hours (average 219.40 as compared with 191.64 nmol/24 h, respectively, p = 0.02). The group of men with depressive symptoms according to the score obtained on Zung self-assessment scale only showed a trend towards higher urinary noradrenalin excretion in 24 hours (average of 69.77 as compared with 63.84 μg/24 h, p = 0.17).

Conclusion:
As shown by the above results, there is a link between 24-hour urinary cortisol excretion levels and the monitored parameters of psychic condition.

Keywords:
depression – cortisol – catecholamines

Sources

1. Diagnostic and Statistical Manual of Mental Disorders: DSM-IV. 4th ed. Washington (DC): American Psychiatric Association 1994.

2. Delay J, Lainé B, Buisson JF. Note concernant l’action de l’isonicotinylhydrazide dans le traitement des etats dépressifs. Ann Med Psychol (Paris) 1952; 110: 689-692.

3. Yamada M, Yasuhara H. Clinical pharmacology of MAO inhibitors: safety and future. Neurotoxicology 2004; 25: 215-221.

4. Saura JM, Kettler R, Da Prada M et al. Molecular neuroanatomy of MAO-A and MAO-B. J Neural Transm 1990; 32: 49-53.

5. Ehlwuegi AS. Central monoamines and their role in major depression. Prog Neuropsychopharmacol Biol Psychiatry 2004; 28: 435-451.

6. Varghese FP, Brown ES. The hypothalamic-pituitary-adrenal axis in major depressive disorder: a brief primer for primary care physicians. Prim Care Companion J Clin Psychiatry 2001; 3: 151-155.

7. Stokes PE. The potencial role of excessive cortisol induced by HPA hyperfunction in the pathogenesis of depression. Eur Neuropsychopharmacol 1995; 5(Suppl 1): 77-82.

8. Thomas L (ed). Labor und Diagnose. 4. ed. Marburg: Die Medizinische Verlagsgesellschaft 1995.

9. The World Health Organization MONICA Project (monitoring trends and determinants in cardiovascular disease): a major international collaboration. WHO MONICA Project Principal Investigators. J Clin Epidemiol 1988; 41: 105-114.

10. Zung WW. A Self-Rating Depression Scale. Arch Gen Psychiatry 1965; 12: 63-70.

11. Derogatis LR, Lipman RS, Covi L. SCL-90: an outpatient psychiatric rating scale-preliminary report. Psychopharmacol Bull 1973; 9: 13-28.

12. Kessler RC, McGonagle KA, Zhao S et al. Lifetime and 12-month prevalence of DSM-III-R psychiatric disorders in the United States: Results from the National Comorbidity Survey. Arch Gen Psychiatry 1994; 51: 8-19.

13. Harris T. Depression in women and its sequelae. J Psychosom Res 2003; 54: 103-112.

14. Makaremi A. Sex differences in depression of Iranian adolescents. Psychol Rep 1992; 71: 939-943.

15. Young AH, Sahakian BJ, Robbins TW et al. The effects of chronic administration of hydrocortisone on cognitive function in normal male volunteers. Psychopharmacology (Berl) 1999; 145: 260-266.

16. Wolkowitz OM, Reus VI, Chan T et al. Antiglucocorticoid treatment of depression: double blind ketoconazole. Biol Psychiatry 1999; 45: 1070-1074.

17. Schweiger U, Deuschle M, Webber B et al. Testosterone, gonadotropin, and cortisol secretion in male patients with major depression. Psychosom Med 1999; 61: 292-296.

18. Weber B, Lewicka S, Deuschle M et al. Increased diurnal plasma concentrations of cortisone in depressed patients. J Clin Endocrinol Metab 2000; 85: 1133-1136.

19. Gold PW, Wong ML, Goldstein DS et al. Cardiac implications of increased arterial entry and reversible 24-h central and peripheral norepinephrine levels in melancholia. Proc Natl Acad Sci USA 2005; 102: 8303-8308.

20. Rao U, McCracken J, Lutchmansingh P et al. Electroencephalographic sleep and urinary free cortisol in adolescent depression: a preliminary report of changes from episode to recovery. Biol Psychiatry 1997; 41: 369-373.

21. Rao U, Dahl RE, Ryan ND et al. The relationship between longitudinal clinical course and sleep and cortisol changes in adolescent depression. Biol Psychiatry 1996; 40: 474-484.

22. Catalán R, Gallart JM, Castellanos JM et al. Plasma corticotropin-releasing factor in depressive disorders. Biol Psychiatry 1998; 44: 15-20.

23. Hughes JW, Watkins L, Blumenthal JA et al. Depression and anxiety symptoms are related to increased 24-hour urinary norepinephrine excretion among healthy middle-aged women. J Psychosom Res 2004; 57: 353-358.

24. Fujita H, Hata K, Ogata E et al. Spot determinations of urinary cortisol for the screening of Cushing’s syndrome. Endocrinol Jpn 1991; 38: 441-444.

25. Maes M, Calabrese J, Meltzer HY. 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. Prog Neuropsychopharmacol Biol Psychiatry 1994; 18: 503-517.

26. Lupien S, Lecours AR, Schwartz G et al. Longitudinal study of basal cortisol levels in healthy elderly subjects: evidence for subgroups. Neurobiol Aging 1996; 17: 95-105.

27. Otte C, Neylan TC, Pipkin SS et al. Depressive symptoms and 24-hour urinary norepinephrine excretion levels in patients with coronary disease: findings from the Heart and Soul Study. Am J Psychiatry 2005; 162: 2139-2145.

28. Reuben DB, Talvi SL, Rowe JW et al. High urinary catecholamine excretion predicts mortality and functional decline in high-functioning, community-dwelling older persons: MacArthur Studies of Successful Aging. J Gerontol A Biol Sci Med Sci 2000; 55: M618-M624.

29. Cohn JN, Levine TB, Olivari MT et al. Plasma norepinephrine as a guide to prognosis in patients with chronic congestive heart failure. N Engl J Med 1984; 311: 819-823.

30. Christensen NJ, Schultz-Larsen K. Resting venous plasma adrenalin in 70-year-old men correlated positively to survival in a population study: the significance of the physical working capacity. J Intern Med 1994; 235: 229-232.

31. Anand IS, Fisher LD, Chiang YT et al. Changes in brain natriuretic peptide and norepinephrine over time and mortality and morbidity in the Valsartan Heart Failure Trial (Val-HeFT). Circulation 2003; 107: 1278-1283.

32. Mann DL, Kent RL, Parsons B et al. Adrenergic effects on the biology of the adult mammalian cardiocyte. Circulation 1992; 85: 790-804.

33. Meredith IT, Broughton A, Jennings GL et al. Evidence of a selective increase in cardiac sympathetic activity in patients with sustained ventricular arrhythmias. N Engl J Med 1990; 325: 618-624.

34. Podrid PJ, Fuchs T, Candinas R Role of the sympathetic nervous system in the genesis of ventricular arrhythmia. Circulation 1990; 82: I103-I113.

35. Benedict CR Neurohumoral aspects of heart failure. Cardiol Clin 1994; 12: 9-23.

36. Carney RM, Freedland KE, Veith RC et al. Major depression, heart rate, and plasma norepinephrine in patients with coronary heart disease. Biol Psychiatry 1999; 45: 458-463.