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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The objective of this study was to examine the relationship between autoimmune thyroid disease and depression in perimenopausal women. Thyroid function [TSH, free T4, and thyroid peroxidase antibodies (TPO-Ab)] and depression (using the Edinburgh Depression Scale) were assessed cross-sectionally together with other determinants of depression. The subjects were 583 randomly selected perimenopausal women (aged 47-54 yr) from a community cohort of 6846 women. The main outcome measures were the occurrence of thyroid dysfunction (abnormal free T4 and/or TSH or elevated levels of TPO-Ab) and the concomitant presence of depression according to the Edinburgh Depression Scale. Neither biochemical thyroid dysfunction nor menopausal status was related to depression. Apart from several psycho-social determinants (the occurrence of a major life event, a previous episode of depression, or financial problems), an elevated level of TPO-Ab (> or = 100 U/mL) was significantly associated with depression (odds ratio, 3.0, 95% confidence interval, 1.3-6.8). We conclude that women with elevated TPO-Ab levels are especially vulnerable to depression, whereas postmenopausal status does not increase the risk of depression.
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PMID:Are autoimmune thyroid dysfunction and depression related? 974 25

A study was undertaken to test whether the elimination of metabolic pathways strongly involved in growth and fatness, comprising thyroid hormones (TH) and growth hormone (GH), is responsible for a substantial part of the genetic change produced by selection. Lines used in this study have been selected for about 50 generations for high (PH) and low (PL) body weight at 10 weeks and for high (F) and low fat content (L) at 14 weeks, producing a 3-fold difference in body weights and a 5-fold difference in fat content. Thyroid ablation was achieved by repeated backcrossing into the four selection lines of a transgene comprising the HSV1-tk gene coupled to the promoter of the thyroglobulin gene. Hemizygous pregnant dams were treated with ganciclovir leading to thyroid-ablated dams and offspring and therefore to a lack of TH and subsequently of GH. In the absence of TH and GH, lines still differ in body weight over the period studied (10 d to about 100 d; e.g. at the end PH = 32.1 g vs PL = 10.2 g) and in fat content (F = 16.2% vs L = 3.8%); the corresponding values for the wild-type controls were PH = 49.9 g vs PL = 17.4 g and F = 27.5% vs L = 4.8%. The effect of the transgene depended on the genetic background for body weights at most ages and for relative gonadal fat pad weights, but less for fat content. The L line showed the lowest growth depression. The lit gene, which causes GH but not TH deficiency, was also transferred by repeated backcrosses into three of these lines (PH, PL, F). The combined deficiency of TH and GH had bigger effects on body weights at earlier ages than did GH deprivation. The data show that changes in the TH- and GH-systems are not the only cause of line differences in growth and fatness resulting from long-term selection, but both are involved to a significant extent. The interactions between the effects of the transgene and of the lit gene and the genetic background were, nevertheless, relatively small and therefore these results support a polygenic model of selection response.
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PMID:Effects of thyroid hormone deficiency on mice selected for increased and decreased body weight and fatness. 980 60

Lithium is used in the prophylaxis of bipolar depressive disorder in augmentation treatment of depression and in the therapy of some cases of unipolar depression. Lithium affects cell function via its inhibitory action on adenosine triphosphatase (ATPase) activity, cyclic adenosine monophosphate (cAMP), and intracellular enzymes. The inhibitory effect of lithium on inositol phospholipid metabolism affects signal transduction and may account for part of the action of the cation in manic depression. Lithium also alters the in vitro response of cultured cells to thyrotropin-releasing hormone (TRH) and can stimulate DNA synthesis. Lithium is concentrated by the thyroid and inhibits thyroidal iodine uptake. It also inhibits iodotyrosine coupling, alters thyroglobulin structure, and inhibits thyroid hormone secretion. The latter effect is critical to the development of hypothyroidism and goiter. Effects on brain deiodinase enzymes and alterations in thyroid hormone receptor concentration in the hypothalamus are under investigation in relation to the therapeutic effect of lithium. The ion affects many aspects of cellular and humoral immunity in vitro and in vivo. This accounts for a rise in antithyroid antibody titer in patients having these antibodies before lithium administration whereas there is no induction of thyroid antibody synthesis de novo. Goiter, due to increased thyrotropin (TSH) after inhibition of thyroid hormone release, occurs at various reported incidence rates from 0%-60% and is smooth and nontender. Subclinical and clinical hypothyroidism due to lithium is usually associated with circulating anti-thyroid peroxidase (TPO) antibodies but may occur in their absence. Iodine exposure, dietary goitrogens, and immunogenetic background may all contribute to the occurrence of goiter and hypothyroidism during long-term lithium therapy. It is currently unclear whether the reported association of lithium therapy and hyperthyroidism are causal, although there is suggestive epidemiological evidence. Finally, lithium therapy is associated with exaggerated response of both TSH and prolactin to TRH in 50%-100% of patients, although basal levels are not usually high. It is probable that the hypothalamic pituitary axis adjusts to a new setting in patients receiving lithium.
Thyroid 1998 Oct
PMID:The effects of lithium therapy on thyroid and thyrotropin-releasing hormone. 982 58

Hypothyroidism may give rise to frank depression that usually responds to thyroxine therapy. Depressed subjects with subclinical hypothyroidism and/or autoimmune thyroiditis should probably also be treated similarly. Most patients with depression, although generally viewed as chemically euthyroid, have alterations in their thyroid function including slight elevation of the serum thyroxine (T4), blunted thyrotropin (TSH) response to thyrotropin-releasing hormone (TRH) stimulation, and loss of the nocturnal TSH rise. These changes are generally reversed following alleviation of the depression. The role of adjuvant triiodothyronine (T3) treatment in resistant depression has not been established, but the data suggest that it will be beneficial in about 25% of cases. However, controlled trials to establish this approach are needed. The underlying mechanism leading to the beneficial response from T3 is unknown, but may reflect brain hypothyroidism in the context of systemic euthyroidism. The hypothalamus in culture, which is analogous to a deafferentated hypothalamus in vivo, shows a paradoxic increase in TRH production after glucocorticoid stimulation. It is known that in human depression there is a functional disconnection of the hypothalamus with impairment of the inhibitory glucocorticoid feedback pathway from the hippocampus to the hypothalamus that results in the typical elevated cortisol levels and impaired dexamethasone suppression. It is postulated that a similar situation prevails with regards to the thyroid axis and that the increased T4 in depression, as well as the blunted TSH response to exogenous TRH, reflects glucocorticoid activation of the TRH neuron leading to increased TRH secretion with resultant down regulation of the TRH receptor on the thyrotrope. Normalization of thyroid function after treatment may result in part from an inhibitory response of the TRH neuron to antidepressant medication, although other effects may also be responsible.
Thyroid 1998 Oct
PMID:The thyroid axis and depression. 982 65

Recent clinical reports have shown that intrathecal administration of thyrotropin-releasing hormone (TRH) can induce 2 to 3 day remissions of major depression more reliably than i.v. administration. Although clinically impractical, these remissions are rapid, occur within hours, and they survive at least one night's sleep. TRH and related peptides have regulatory effects in the limbic forebrain. Electroconvulsive shock (ECS) in rats induces synthesis of TRH in multiple subcortical limbic and frontal cortical regions, which are known in humans to be involved in both depression and in sleep. The increases in TRH and related peptides are regionally specific. The quantitative TRH increases in individual limbic regions have been correlated with the amount of forced-swimming done by the individual animal after ECS. Intraperitoneal TRH also gives a positive response in this test, as do all effective antidepressants. This article provides a heuristic framework for interdisciplinary neuroscientific study of the interrelated fields of depression and sleep, with a focus on TRH. Preclinical data suggest that glutamatergic, subcortical limbic circuits contain TRH and related peptides as inhibitory cotransmitters that may normally restrain glutamatergic hyperactivity. It is suggested that, in depression, pathologically overdriven glutamatergic circuits escape inhibitory regulation by TRH. This escape is especially pronounced during rapid eye movement (REM) sleep, and these phenomena may explain the prolonged latency of antidepressant treatment.
Thyroid 1998 Oct
PMID:A heuristic model of mental depression derived from basic and applied research on thyrotropin-releasing hormone. 982 66

Natural killer (NK) cell activity of peripheral blood lymphocytes (PBL) against k562 human tumor cell targets was studied in patients with Graves' disease and Hashimoto's thyroiditis. NK activity was measured in a standard 4-hour 51chromium (Cr) release assay. Cytotoxicity was expressed as lytic units (LU)/10(6) PBL. Significantly decreased NK cell activity was demonstrated in both groups of patients, with mean (+/- SE) lytic units of 10.3 (+/- 9.1) and 13.3 (+/- 10.3) for patients with Graves' disease and Hashimoto's thyroiditis, respectively, compared with 36.0 (+/- 26.3) for age- and sex-matched normal subjects. When patients with Graves' disease were analyzed according to their thyroid status; NK activity was significantly depressed in (1) hyperthyroid patients before treatment; (2) hyperthyroid patients receiving antithyroid therapy; and (3) euthyroid patients receiving antithyroid therapy, compared with normal subjects. Graves' disease patients who were hypothyroid after radioactive iodine therapy or thyroidectomy had normal NK activity. No significant differences between hyperthyroid and euthyroid patients or between hypothyroid patients and normal subjects were demonstrated. NK activity in patients with Graves' disease did not correlate with serum levels of thyroxine, the presence or severity of ophthalmopathy, or titers of serum thyroid antibodies. In patients with Hashimoto's thyroiditis there was no correlation between NK activity and goiter size, titers of antithyroid antibodies, or thyroid status. These findings suggest that depression of NK activity in both disorders is secondary to abnormalities of thyroid hormone secretion, although an effect of the underlying autoimmune reactions has not been excluded.
Thyroid 1998 Nov
PMID:Natural killer cell activity in patients with Graves' disease and Hashimoto's thyroiditis. 984 16

Thyroid hormones affect the functions of several organs including the heart and kidney. Using isolated left papillary muscles we have investigated the action of thyroid hormones on the mechanical and electrical properties of the heart. We found that pure hypothyroidism causes a depression in contractile and electrical parameters, but we noticed that superimposed hypoparathyroidism accounts for the marked prolongation in contractile kinetics and action potential duration. At kidney level we have shown that thyroid hormones affect proximal tubular sodium transport and this effect is only partially mediated by the action of thyroid hormones on Na-K-ATPase activity. Using the micropuncture technique, we hypothesized that the early effect of thyroid hormone action is on the potassium permeability of proximal tubular cell membrane. This latter effect would explain the increase in isotonic fluid reabsorption through an increase in the driving force for sodium. Finally, hypothyroid patients have a decrease in glomerular filtration rate and renal plasma flow that are completely reversed by thyroxine administration. On the other hand, hyperthyroid subjects exhibit a significant increase in both parameters.
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PMID:Effects of thyroid hormones on heart and kidney functions. 1020 61

It has long been known that primary thyroid disorder is associated with mood disorder and vice versa so that the features of major depression can occur in individuals with hypothyroidism. Also, primary depression is often associated with disturbance of the hypothalamic-pituitary-thyroid axis. Roberton's historic description of the relatively common occurrence of postpartum hyperthyroidism eventually led to the discovery that thyroid antibody-positive women are prone to hypothyroidism, which is often preceded by transient hyperthyroidism after delivery. Various aspects of depression and the association with thyroid antibody status are described and the importance of treatment and management of the condition emphasized, particularly in view of the risk of later permanent hypothyroidism in mothers. The effects of associated mood disorder on attachment to the baby, the family, and later development of the child are also described.
Thyroid 1999 Jul
PMID:Postpartum depression and thyroid antibody status. 1044 17

The involvement of the central nervous system either in hypothyroidism or in hyperthyroidim has previously been shown on the basis of visual, auditory, somatosensory, and central motor evoked potential studies by some investigators. In to our previous study, we found that abnormal electrodermal activity in nonmedicated hyperthyroid patients was not associated with psychiatric symptoms. In this study, our purpose was to investigate whether hypothyroidism results in electrodermal abnormalities in the absence of measurable psychiatric symptoms. Electrodermal activity was recorded with a skin conductance unit connected to a personal computer. Basal levels of electrodermal activity and responsiveness to repeated acoustic stimulation were studied in 14 nonmedicated hypothyroid patients and 14 healthy controls. Psychiatric rating scores indicated that patients and healthy controls had normal levels of anxiety and depression. Hypothyroid patients had lower skin conductance levels, lower fluctation rates and prolonged onset latencies compared with controls. None of the hypothyroid patients had amplitude changes. In conclusion, hypothyroid patients may have abnormal electrodermal activity that is related to the change of hypothalamic-pituitary-thyroid axis function, without associated psychiatric symptoms.
Thyroid 1999 Aug
PMID:Electrodermal activity in hypothyroid patients and healthy subjects. 1048 71

This review tries to give the state of the art of the therapeutic use of thyroid hormones in psychiatric disorders, mainly in depression. Four hypotheses suggest an effect in these ailments: 1) a local relative T4 excess present (or better postulated to be present) in the brain of depressed patients is lowered by triiodothyronine (T3), by lowering serum levels of thyroxine (T4), 2) the effect of a depression-mediated cerebral lack of catecholamines is compensated by the T3/T4 induced activation of beta-receptors, 3) a postulated depression-induced local cerebral hypothyroidism can be counteracted by T3 and T4. 4) thyroid hormones increase the cerebral content of serotonin. This may be beneficial in depression, where shortage of serotonin in the brain is accused to be etiologically important. Thyroid hormones have been used so far in the following ways: 1) as T3 monotherapy in depression; 2) initial additive T3 for acceleration of the response to treatment with tricyclic antidepressants (TCA); 3) additive T3 for augmentation of the response to TCA in therapy-resistant patients with depression, 4) as high-dose (250-500 micrograms/die) T4-treatment of "rapid cycling bipolar disorder". Low dose (5-50 mg/die) T3 "augmentation therapy" is the best documented form of treatment with thyroid hormones in depression. The results suggest a convincing benefit for a varying percentage of non responders to therapy with TCA. For the other forms of treatment placebo-controlled double blind studies are not yet available or give conflicting results.
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PMID:[Administration of thyroid hormones in therapy of psychiatric illnesses]. 1052 31


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