To the Editor: Several studies of peripheral thyroid economy in seasonal affective disorder have shown inconsistent results (1). However, measurements of the peripheral thyroid state may not provide a reliable index of the central thyroid state (2).

In contrast to the peripheral tissues, where most of the nuclear-bound triiodothyronine (T₃) is imported from the plasma pool, in the brain the supply of T₃ depends mostly on the cellular uptake and intracellular deiodination of thyroxin by type II 5′-iodothyronine deiodinase (3). The existence of a separate pathway in the brain for thyroxin deiodination suggests that the adult central nervous system has the ability to autoregulate thyroid status (4).

A short photoperiod and low ambient temperature are direct stimuli that could affect type II 5′-iodothyronine deiodinase activity (5). Other effects of temperature and photoperiod (e.g., decreased pituitary and gonadal hormones) could be indirect factors that stimulate type II 5′-iodothyronine deiodinase activity. Thus, seasonal changes in light andtemperature may affect the metabolism of brain thyroid hormones.

T₃ may itself be a neurotransmitter, and it may have an antidepressant effect (6). It enhances the effects of norepinephrine (7), serotonin (8), and γ-aminobutyric acid (9). Small alterations of brain thyroid economy, independent of peripheral changes in thyroid status, may produce significant behavioral effects. Therefore, it is reasonable to suggest that brain thyroid hormones might be involved in the mechanisms of seasonal changes in mood and behavior.