Thyroid Supplementation Enhances Antidepressant Response

Paula Moyer, MA

September 21, 2006

September 21, 2006 (Paris) — Supplements of triiodothyronine (T3) enhance the antidepressant effects of selective serotonin reuptake inhibitors (SSRIs), according to a team of Israeli and US investigators who presented their findings here at the 19th congress of the European College of Neuropsychopharmacology.

"Our findings show that T3 is efficacious as an enhancer of antidepressant therapy," said presenting and senior investigator Bernard Lerer, MD, during his presentation. He is a professor of psychiatry at Hadassah-Hebrew University Medical Center in Jerusalem, Israel. Dr. Lerer added that this link had been seen when tricyclic antidepressants were widely used, but this study is the first to consider an association with SSRIs.

Dr. Lerer and coinvestigators conducted a randomized, double-blind, placebo-controlled, proof-of-concept trial to determine whether T3 supplementation had any augmentation effect on SSRIs. The study involved 124 patients with major depressive disorder who were not at risk of suicide; patients with hypothyroidism were excluded. Of the participants, 60 were assigned to receive T3, and 60 received placebo. All of the patients received the SSRI sertraline (Zoloft), which is commonly used in Israel. A total of 103 patients completed the eight-week study, 53 in the T3 group and 50 in the placebo group.

In the T3 group, 37 patients (69.8%) responded to treatment compared with 25 patients (50%) in the placebo group (odds ratio [OR], 2.93; P = .002). The investigators defined response as a 50% decrease in Hamilton Rating Scale for Depression (HAM-D) score. Remission occurred in 31 patients (58.5%) receiving T3 compared with 19 patients (38%) in the placebo group (OR, 2.69). The difference between the 2 groups was also significant in the intent-to-treat analysis, Dr. Lerer said (P = .002).

The 2 groups had similar average baseline levels of T3, total thyroid, and thyroid-stimulating hormone (TSH). However, those in the group receiving T3 supplements had lower levels of T3 and TSH after the study. TSH is typically secreted in excess, compensatory amounts in hypothyroid patients; conversely, supplementation would cause it to drop. There was no relationship between posttreatment levels and response to antidepressant therapy, Dr. Lerer said.

"A proven clinical role for T3 needs to be further developed so that we can identify predictors of response," he said.

"It was good to see a study validating what many of us do in clinical practice," said David Nutt, MD, in an independent comment. He noted that empiric thyroid supplementation is often used in the clinical setting in patients who have not responded to antidepressant treatment. Dr. Nutt is a professor of psychiatry at the University of Bristol in the United Kingdom.

Zoloft is manufactured by Pfizer, but the study was not funded by the company.

ECNP 19th Congress: Presentation S.13.05. Presented September 18, 2006.


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