Questions raised by the cytokine hypothesis of depression

• Published in: Brain, behavior, and immunity behavior, and immunity, 2002-10, Vol.16 (5), p.610-617
• Main Author: de Beaurepaire, Renaud
• Format: Article
• Language: English
• Subjects: Animals; Antidepressants; Antidepressive Agents - pharmacology; Biogenic Monoamines - metabolism; Cognition; Cytokines - adverse effects; Cytokines - metabolism; Depressive Disorder - immunology; Depressive Disorder - metabolism; Freud; HPA axis; Humans; Sensitization; Serotonin; Sleep; Stress; Stress, Psychological - immunology; Stress, Psychological - metabolism
• ISSN: 0889-1591; 1090-2139
• DOI: 10.1016/S0889-1591(02)00005-3

The cytokine hypothesis of depression raises a certain number of questions. These questions include: the inability of the theory to account for the classical (Freudian) psychodynamics of depression; the role of sensitization in cytokine-induced depression; the compatibility of some of the effects of cytokines (on sleep, on cognition, on the HPA) with the hypothesis; the possibility of occurrence of depression in the absence of an increase in circulating cytokines; the nature of the relationships between cytokines, stress, and depression; the compatibility of the effects of cytokines on brain monoamines with the current monoamine hypothesis of depression; the inability of antidepressants to fully abrogate the brain effects of individual cytokines in animal experiments. Based on these limitations of the theory, it is proposed to define a new clinical entity designated as “the cytokine-associated depressive syndrome.”