"An acceleration of antidepressant effect by T3 has been initially shown more than 30 years ago in several reports [63–66]. A meta-analysis of these early double-blind placebo controlled trials concluded that T3 was effective in accelerating the clinical response to tricyclic antidepressants in patients with nonrefractory depression. "
[Show abstract][Hide abstract] ABSTRACT: The relation between thyroid function and depression has long been recognized. Patients with thyroid disorders are more prone to develop depressive symptoms and conversely depression may be accompanied by various subtle thyroid abnormalities. Traditionally, the most commonly documented abnormalities are elevated T4 levels, low T3, elevated rT3, a blunted TSH response to TRH, positive antithyroid antibodies, and elevated CSF TRH concentrations. In addition, thyroid hormone supplements appear to accelerate and enhance the clinical response to antidepressant drugs. However, the mechanisms underlying the interaction between thyroid function and depression remain to be further clarified. Recently, advances in biochemical, genetic, and neuroimaging fields have provided new insights into the thyroid-depression relationship.
Journal of Thyroid Research 01/2012; 2012(1):590648. DOI:10.1155/2012/590648
"In depressed patients activation of the thyroid axis, as indicated by increased secretion of thyroid hormones, is predictive of a rapid response to therapy with a tricyclic antidepressant (TCA) (Whybrow and Prange, 1981). Furthermore, concurrent administration of L-triiodothyronine (T 3) with a TCA has been found to accelerate the antidepressant effect in women (Prange et al., 1969; Wilson et al., 1970; Wheafly, 1972; Coppen et al., 1972) and to produce a therapeutic response in patients of both sexes who previously did not respond to TCA treatment alone (Earle, 1970; Hatotani et al., 1974; Ogura et al., 1974; Goodwin et al., 1982). The notion that thyroid hormones affect brain function is strengthened by evidence that in rats thyroid hormones are taken up into the synaptosomal fraction of brain neurons, and that L-thyroxine (T4) is converted there to its more potent metabolite T "
[Show abstract][Hide abstract] ABSTRACT: The effects of hyperthyroidism or hypothyroidism, alone or in combination with the tricyclic antidepressant desmethylimipramine (DMI), on brain beta-adrenergic and serotonin (5HT2) receptors were studied in adult male Sprague-Dawley rats. Intraperitoneal administration of T3 or T4 for 7 days increased the number of cortical beta-adrenergic and 5HT2 receptors. These increases were significant at levels of 250 μg/kg or above for both hormones. Neither thyroidectomy nor “reverse” T3 (rT3) (500 μg/kg) produced an effect on either receptor type. The down-regulation of beta-adrenergic receptors produced by daily subcutaneous injections of 20 mg/kg of DMI for 7 days was partially offset by concurrent administration of T4, whereas the down-regulation of 5HT2 receptors produced by the drug was not affected by concurrent administration of either T3 or T4. Hypothyroidism (thyroidectomy) did not significantly affect the adaptation of these receptor populations to DMI.As regards brain regions other than cortex, T4 (250 μg/kg) produced the same changes in hippocampus as in cortex, while thyroidectomy decreased beta-adrenergic receptors only in the cerebellum. Thyroxine also elevated 5HT2 receptors in the hippocampus; thyroidectomy caused a significant decrease in 5HT2 receptors in the striatum.
"The only major exception to this is a study by Coppen et al. (1972) in which patients treated with 9 g tryptophan daily showed a similar respons e to those treated with imipramine. However, the rest of the data point to the existence of a therapeutic window in unipolar patients. "
[Show abstract][Hide abstract] ABSTRACT: The reports by Coppen et al. (1963) and by Pare (1963), that tryptophan was capable of potentiating the antidepressant action of monoamine oxidase inhibitors, were followed by the claim of Coppen et al. (1967) that tryptophan, given alone was as effective as electroconvulsive therapy in the treatment of depression. These initial encouraging reports have been followed by more than 20 other papers in the literature, which have reached a wide variety of conclusions on the efficacy of tryptophan as an antidepressant. Even reviews on this subject reveal no consensus (Poitou and Boulu, 1977; Wirz-Justice, 1977; Murphy et al., 1978; Cooper, 1979). The purpose of this paper is to discuss some of the factors that will affect the response of depressed patients to tryptophan, and to suggest how it may be used effectively as an antidepressant.
Advances in Experimental Medicine and Biology 02/1981; 133:727-37. DOI:10.1007/978-1-4684-3860-4_40 · 1.96 Impact Factor
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.