Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dietary nitrate significantly inhibits the growth of male and female rats. To test the possibility that the growth hormone-releasing factor (GRF) content in hypothalamic tissue is deranged under these conditions, male and female rats were fed a diet containing 3% KNO3 for 6 weeks, compared to a normal diet (4 X 5 animals). The food intake of rats fed nitrate was reduced significantly (23 and 28% resp.). Weight gain was also decreased by 35 and 41% in male and female rats. The mean Sm-C/IGF-I concentration was 1.61 and 1.03 rU/ml in male and female control rats, whereas the concentrations in nitrate-exposed rats were 0.92 and 0.64, respectively (P less than 0.01). The GRF content of hypothalamic tissue also decreased significantly from 407 and 533 ng/g protein in controls to 174 and 229 in treated male and female rats. Nitrate exposure is characterized by hypothyroidism, food intake depression, low Sm-C/IGF-I concentrations in plasma and a decreased hypothalamic GRF content. Independent of the peripheral changes, the content of Sm-C/IGF-I in the brain remains constant. The results of the study demonstrate that thyroid hormone deficiency leads to an inhibition of GH axis already at the hypothalamic level.
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PMID:Nitrate-induced hypothyroidism is associated with a reduced concentration of growth hormone-releasing factor in hypothalamic tissue of rats. 186 11

A depressive man was evaluated for developing chronic fatigue and cold intolerance, in whom laboratory findings showed decreased thyroid hormone levels (T4, 2.7 micrograms dl-1; T3, 0.76 ng ml-1) with normal blood levels of TSH. A single bolus injection of TRH (500 micrograms) significantly stimulated prolactin secretion, but did not cause an increase in blood TSH levels (basal level, 1.2 microU ml-1 vs. 1.3 microU ml-1 30 min after injection). By contrast, TRH-induced TSH stimulation occurred after repeated injection of TRH for 4 consecutive days (basal level, 1.5 microU ml-1 vs. 5.6 microU ml-1 30 min after injection). Blood thyroid hormone concentrations were restored to normal levels after long-term administration of TRH. Other pituitary functions remained unchanged. A diagnosis of central hypothyroidism due to isolated TRH deficiency was made in this case, and the data presented here indicate that partial resistance of pituitary thyrotrophs to TRH may be associated with depression.
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PMID:Central hypothyroidism due to isolated TRH deficiency in a depressive man. 190 Oct 77

Smell and taste disorders are common in the general population, yet little is known about their nature or cause. This article describes a study of 750 patients with complaints of abnormal smell or taste perception from the University of Pennsylvania Smell and Taste Center, Philadelphia. Major findings suggest that: chemosensory dysfunction influences quality of life; complaints of taste loss usually reflect loss of smell function; upper respiratory infection, head trauma, and chronic nasal and paranasal sinus disease are the most common causes of the diminution of the sense of smell, with head trauma having the greatest loss; depression frequently accompanies chemosensory distortion; low body weight accompanies burning mouth syndrome; estrogens protect against loss of the sense of smell in postmenopausal women; zinc therapy may provide no benefit to patients with chemosensory dysfunction; and thyroid hormone function is associated with oral sensory distortion. The findings are discussed in relation to management of patients with chemosensory disturbances.
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PMID:Smell and taste disorders, a study of 750 patients from the University of Pennsylvania Smell and Taste Center. 202 70

When antidepressant therapy fails to ameliorate the cardinal features of depression--e.g., sleep disturbance, appetite disturbance, suicidality--the clinician must seek an alternate treatment strategy. Treatment nonresponse is usually defined as persistence of depression after 6 weeks of adequate doses as shown by plasma concentrations of antidepressant medication. After the clinician has reassessed the patient and, in particular, the diagnosis of major depression, two major options are available: (1) taper the current antidepressant and initiate a trial of an unrelated antidepressant or (2) potentiate the antidepressant effects of the current antidepressant and initiate a trial of an unrelated antidepressant or (2) potentiate the antidepressant effects of the current antidepressant with either thyroid hormone, usually T3, or lithium. This paper describes in detail the usefulness of these two adjuncts in potentiating the effects of antidepressants and in converting antidepressant medication nonresponders to responders. Other augmentation strategies are also briefly described, including the concurrent use of two antidepressants from different drug classes.
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PMID:Augmentation regimens for depression. 203 Jan 1

An analysis was performed to determine the mechanism of depressed maternal weight gain and its effect on perinatal lethality following prenatal exposure to diethylstilbestrol (DES). Pregnant Sprague-Dawley rats were dosed orally by gavage with DES or corn oil (control) during various intervals of gestation. The maternal weight-gain patterns of control and treated dams and the number of live offspring were recorded. The amounts of feed and water intake and feces and urine output in pregnant dams were measured, and metabolic rate and thyroid hormone levels were also determined. DES (at 45 micrograms/kg/day) was embryo- and fetolethal during implantation and parturition, and there was an accompanying decline in maternal weight. Growth of adult males, nonpregnant females, and weanlings of both sexes was also depressed. During pregnancy, the net intake of feed and water was not altered by the drug, but maternal serum thyroxine and metabolic rate were significantly elevated. Reduced metabolic efficiency, then, is the likely mechanism for weight depression. Reduction of maternal weight gain during pregnancy by DES is a diagnostic indicator of fetolethality, but is probably not causally related to it.
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PMID:Diethylstilbestrol-induced perinatal lethality in the rat. I. Relationship to reduced maternal weight gain. 204 30

Several studies have demonstrated that a consistent part of patients with severe depression shows anomalous responses of neuroendocrine axes. In the last years, altered TSH responsiveness to exogenous TRH have been reported also in patients with panic disorders. Because of these suggestions we studied stimulated TSH secretion in 24 untreated hospitalized patients (8 males and 16 females), aged from 21 to 76, in whom the psychiatric examination disclosed mild but inequivocal signs of persistent depression (score range on Rufin and Ferreri Iventory from 20 to 35). The TRH-test (200 mcg i.v.) was started between 9.00 and 9.30 a.m.. The same test was performed also in 14 sex- and age-matched volunteers defined without psychiatric disorders. As comparison parameter, delta-TSH (maximum increase during TRH stimulation) was accounted. All the patients had normal serum thyroid hormone levels. TSH responsiveness of patients with minor depressive disorders was not found statistically different when compared with normal control volunteers, but a reverse significant correlation was found between delta-TSH and percentage score of anxiety in group of patients (with blunted TSH response in 6 (25%) patients), that was not found in normal subjects. A significant correlation between delta-TSH and depression degree was not found. The present data, although preliminary, could indicate the existence of depressed subjects in whom blunted TSH response to TRH seems related to anxiety degree. Additional studies, particularly on the medullo-adrenal function, might clarify the nature of these alterations, that at state is unclear, although the mechanisms suggested also for alterations of pituitary hormone responses in major depression could be taken in account.
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PMID:[Stimulated secretion of TSH in patients with depression of mild nature]. 211 18

Changes in cardiac myosin isozymes and serum thyroid hormone levels were investigated in rats following 10 Gy whole-body gamma irradiation. The percent beta-myosin heavy chain increased from 21.3 +/- 1.8 to 28.1 +/- 6.8 (NS) at 3-day postirradiation, 37.7 +/- 1.9 (P less than .001) at 6-day postirradiation, and 43.8 +/- 3.3 (P less than .001) at 9-day postirradiation. Along with the change in myosin isozymes was a significant 53% decrease (P less than .001) in the serum thyroxine (T4) level by day 3 postirradiation, remaining depressed through day 9 postirradiation. The serum 3,5,3'-triiodothyronine (T3) level, however, was normal until day 9, when significant depression was also observed. In contrast, the thyroid-stimulating hormone (TSH) level was significantly increased by fourfold at day 3, returning to near normal values by day 9 postirradiation. Daily injections of physiological doses of T3 (0.3 microgram/100 g body weight) prevented the change in the myosin isozymes following whole-body irradiation. Daily pharmacological injections of T3 (3.0 micrograms/100 g body weight) to the irradiated rats produced a further decrease in the percent beta-myosin heavy chain (below control values) indicating tissue hyperthyroidism. Thus, this study suggests that the change in myosin isozymes following whole-body irradiation is caused by an alteration in thyroid hormone activity.
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PMID:Alterations in rat cardiac myosin isozymes induced by whole-body irradiation are prevented by 3,5,3'-L-triiodothyronine. 213 61

The development of highly sensitive immunometric assays for thyroid-stimulating hormone (TSH) has provided increased understanding of thyroid hormone regulation but, paradoxically, has contributed to a kaleidoscopic complexity of thyroid function test variability in hospitalized patients with nonthyroidal illness (NTI). In primary hypothyroidism, an elevated TSH is the most sensitive chemical index available, although early cases may show a hyperresponse of TSH to thyrotropin-releasing hormone (TRH) stimulation when the TSH is still within the normal range. The ability of the new TSH assays to discriminate between normal and low levels now allows the diagnosis of thyrotoxicosis to be confirmed by a suppressed TSH in the presence of elevated serum thyroxine (T4) and/or triiodothyronine (T3). The TRH stimulation test is virtually obsolete for the diagnosis of thyrotoxicosis but remains of much interest in the investigation of psychiatric syndromes. Approximately 25% of patients with depression have a blunted TSH response (a rise of less than 5 microU/mL) that differs from thyrotoxicosis, wherein the TSH response is suppressed under 1 microU/mL. The cause of the blunted TSH is uncertain but is not due to hyperthyroidism. In contrast, close to 15% may have a TSH hyperresponse to TRH and/or elevated antithyroid antibodies. Thyroid hormone treatment may benefit the depression in some of these cases. In the sick thyroid state of nonthyroidal illness, a low T3 level is the initial manifestation. In more severe cases, the T4 also falls, the free T4 level in this situation is variable, both normal and low levels being reported from different laboratories. A diagnosis of hypothyroidism requiring treatment with thyroid hormone therapy is unlikely unless there is a concomitant lowfree T4 and elevated TSH in a patient who is not in the process of recovery. In acute psychiatric admissions, there is a high frequency of hyperthyroxinemia. The TSH in these cases is generally either normal or high, suggesting central activation of the hypothalamic-pituitary-thyroid axis. In most instances, the thyroid function tests normalize within 2 weeks, and treatment directed toward the thyroid gland is not indicated. Suppressed TSH levels, usually associated with a normal free T4, has also been described in such patients. Finally, various medications utilized in psychiatric practice have diverse effects on thyroid function and can cause diagnostic difficulty. These include lithium, phenytoin sodium, and carbamazepine, and their effects are reviewed.
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PMID:Review: thyroid function in psychiatric illness. 219 97

Abnormal thyroid status and affective disorders have been associated in the human clinical literature. It has recently been shown that pretreatment with thyroid hormone can prevent escape deficits produced by inescapable shock in an animal analogue of depression. In this report we provide evidence that hypothyroid status can produce an escape deficit in rats. While sham-operated rats improved their performance on a simple escape task over three days of testing, thyroparathyroidectomized rats showed a pronounced decrease in their responses. Markov transition analysis was used to obtain conditional probabilities of escaping given a prior escape or failure to escape for the two groups. This analysis shows that the structure of the data set may be similar for the two groups. These results suggest that if intact rats learn to escape, then hypothyroid rats may learn not to escape.
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PMID:Thyroparathyroidectomy produces a progressive escape deficit in rats. 223 64

There is extensive literature documenting an association between abnormalities of the hypothalamic-pituitary-thyroid axis and disorders of mood. However, the specific abnormality in thyroid functioning associated with primary affective disorder remains poorly understood. Various aspects of the relationship between thyroid functioning and affective illness are reviewed. Particular attention is paid to psychiatric symptoms and clinical thyroid disorders as well as abnormalities of basal thyroid hormone levels in depression and the use of thyroid hormones in the treatment of depressive illness. Current hypotheses regarding the association between altered thyroid functioning and depressive illness are critically reviewed.
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PMID:A perspective on the thyroid and depression. 228 29


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