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There is evidence that thyroid hormone T3 increases serotonergic neurotransmission. Therefore, T3 addition to antidepressants may improve treatment response in major depression. In nonrefractory depression, T3 addition to tricyclic antidepressants indeed accelerates treatment response. Current therapeutic practice favors selective serotonin reuptake inhibitors. This is the first study to investigate the efficacy of T3 addition to paroxetine in major depression. One hundred thirteen patients with major depressive disorder were randomly assigned to 8 wk of double-blind outpatient treatment with low-dose T3 (25 microg), high-dose T3 (25 microg twice daily), or placebo in addition to paroxetine 30 mg daily. A total of 106 patients started treatment and were included in the outcome analysis. Response rate after 8 wk (reduction of Hamilton Rating Scale for Depression score > or = 50%) was 46% in all three treatment arms (P = 0.99). T3 addition did not accelerate clinical response to paroxetine, nor was an effect of T3 found when only women were analyzed. Patients on T3 addition reported more adverse events than patients on placebo comedication. In conclusion, these results do not support a role for T3 addition to selective serotonin reuptake inhibitors in the treatment of nonrefractory major depressive disorder. On the contrary, more adverse reactions occurred in T3-treated patients.

Objective: Major depressive disorder has been associated with changes in the hypothalamus -pituitary -thyroid (HPT) axis and with hypercortisolism. However, the changes reported have been at variance, probably related to in-or outpatient status, the use of antidepressant medication and the heterogeneity of depression. We therefore conducted a controlled study in unipolar depressed outpatients who had been free of antidepressants for at least 3 months. Design: We assessed endocrine parameters in 113 depressed outpatients and in 113 sex-and agematched controls. Methods: Patients were included if they had a major depression according to a Structural Clinical Interview for the Diagnostic and Statistical Manual of Mental Disorders (DSM), fourth edition (SCID-IV) and if they had a 17-item Hamilton rating scale for depression (HRSD) score of $ 16. Endocrine parameters contained serum concentrations of TSH, (free) thyroxine, tri-iodothyronine, cortisol, thyroid peroxidase (TPO) antibody titre and 24-h urinary excretion of cortisol. Results: The serum concentration of TSH was slightly higher in depressed patients as compared with controls (P , 0.001), independent of the presence of subclinical hypothyroidism and/or TPO antibodies (n ¼ 28). All other HPT axis parameters were similar in both groups. The 24-h urinary cortisol excretion was similar in patients and controls. In atypical depression, serum cortisol was lower than in non-atypical depression (P ¼ 0.01). Patients with neither melancholic depression nor severe depression (HRSD $ 23) had altered endocrine parameters. Finally, serum TSH values could not be related to cortisol values. Conclusion: When compared with matched control subjects, outpatients with major depression had slightly higher serum TSH, while urinary cortisol levels were similar. Furthermore, we observed lower serum cortisol in atypical depression than in non-atypical depression.