Depression continues with, or develops secondary to, a stress or, as in animal models, learned helplessness. Stress increases the secretion of norepinephrine (NE) in the brain and, secondary to this, the down regulation in the .13 adrenergic receptors. The increase of NE secretion secondary to stress causes a depletion of NE with time. When the action potential reaches the synaptic cleft, it causes an increase in the entrance of calcium ions into the cell, thus fuses the PLA2 mediated synaptic vesicsles to the presynaptic membrane and causes the secretion of neurotransmitters (NE, 5-HT etc.) into the synaptic cleft. In this study, it was hypothesized that excessive PLA2 activity could deplete 5-HT and NE stores and cause depression in predisposed people (thorough genetic penetrance?). In this study 72 inpatients who were diagnosed as having depression (major depression or dysthymia) according to DSM-III-R criteria and HDRS, and who didn't use medicaments were investigated. Blood PLA2, cortisol, IgA, IgM, estradiole, progesterone, HDL/LDL cholesterol and 5-HIAA levels in 24-hours urine were determined before and after treatment. During the treatment, that continued for 6 weeks, the depression levels of the patients were investigated every week with HDRS.