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Is the thyroid still important in major depression?

For more than a century, there have been rich descriptions in the clinical literature of prominent depressive symptoms in patients with thyroid disease, particularly clinical hypothyroidism.1,2 This link between the thyroid and depression1,2 provided optimism that study of the thyroid axis in unipolar depression would unravel the mystery of the etiology of the disorder. An enormous research effort over the last 50 years3 failed to achieve this goal but, nonetheless, produced some important findings. First, the vast majority of patients with major depression are euthyroid.3 Second, basal peripheral thyroid hormone levels are not particularly informative,4 although subjects with depression have higher mean thyroxine (T4) levels compared with when they are remitted and also compared with healthy control subjects.3–7 Moreover, significant decreases in T4 levels occur with response to various treatments, including antidepressant drugs,3–5 electroconvulsive therapy6 and cognitive– behavioural therapy.7 Significant changes in triiodothyronine (T3) levels are inconsistent.3,4 Last, one-quarter to one-third of subjects with depression will have a blunted thyrotropin response to thyrotropin-releasing hormone (TRH).5,6 This finding is consistent with the increased T4 levels observed in depression3,4 and suggests overactivity of the thyroid axis in depressive illness,8 the pathophysiological significance of which remains to be clarified. Despite the consistent observations about the thyroid and depression reported in both the psychiatric and endocrine literature, interest in the thyroid as a major factor in the biology of depression has waned, and the thyroid axis has received little attention in current models of the etiology of depression.9,10 Recent clinical and preclinical studies would suggest that the thyroid should not be overlooked.