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      Hypothyroidism and Depression

      a , * , b

      European Thyroid Journal

      S. Karger AG

      Thyroid, Hypothyroidism, Depression, Thyroxine

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          Abstract

          Background: A relationship between hypothyroidism and depression has been assumed for many years; however, the true nature of this association has been difficult to define with many conflicting studies. In recent years, our knowledge in this area has increased significantly with large cohort studies and genetically driven studies being published. Objectives: We reviewed the literature on thyroid function and depression to determine if this relationship has been clarified. Methods: We performed a search on the Pubmed database using the terms ‘thyroid
 ’ and ‘mental health
 ’, ‘depression
 ’ and ‘well-being
 ’. Results: Large epidemiological studies generally suggest no association between thyroid function and depression in subjects without thyroid disease. Subjects on thyroxine have poorer psychological well-being than subjects with no thyroid disease even if biochemically euthyroid, they also show an association between thyroid function and well-being. Whilst there is some early evidence that genetic factors can influence well-being on thyroxine and response to combination therapy, there is also evidence to suggest that much morbidity on thyroxine may be due to initial misdiagnosis and mis-attribution of symptoms. Conclusion: Despite the large number of studies, the relationship between thyroid function and depression remains poorly defined. Clarification of the proportion of subjects on thyroxine incorrectly may assist the large (perhaps genetically driven) studies needed to move forward in this area, as it is expected that they cloud the results.

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          Most cited references 90

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          The Colorado thyroid disease prevalence study.

          The prevalence of abnormal thyroid function in the United States and the significance of thyroid dysfunction remain controversial. Systemic effects of abnormal thyroid function have not been fully delineated, particularly in cases of mild thyroid failure. Also, the relationship between traditional hypothyroid symptoms and biochemical thyroid function is unclear. To determine the prevalence of abnormal thyroid function and the relationship between (1) abnormal thyroid function and lipid levels and (2) abnormal thyroid function and symptoms using modern and sensitive thyroid tests. Cross-sectional study. Participants in a statewide health fair in Colorado, 1995 (N = 25 862). Serum thyrotropin (thyroid-stimulating hormone [TSH]) and total thyroxine (T4) concentrations, serum lipid levels, and responses to a hypothyroid symptoms questionnaire. The prevalence of elevated TSH levels (normal range, 0.3-5.1 mIU/L) in this population was 9.5%, and the prevalence of decreased TSH levels was 2.2%. Forty percent of patients taking thyroid medications had abnormal TSH levels. Lipid levels increased in a graded fashion as thyroid function declined. Also, the mean total cholesterol and low-density lipoprotein cholesterol levels of subjects with TSH values between 5.1 and 10 mIU/L were significantly greater than the corresponding mean lipid levels in euthyroid subjects. Symptoms were reported more often in hypothyroid vs euthyroid individuals, but individual symptom sensitivities were low. The prevalence of abnormal biochemical thyroid function reported here is substantial and confirms previous reports in smaller populations. Among patients taking thyroid medication, only 60% were within the normal range of TSH. Modest elevations of TSH corresponded to changes in lipid levels that may affect cardiovascular health. Individual symptoms were not very sensitive, but patients who report multiple thyroid symptoms warrant serum thyroid testing. These results confirm that thyroid dysfunction is common, may often go undetected, and may be associated with adverse health outcomes that can be avoided by serum TSH measurement.
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            Thyroid status, disability and cognitive function, and survival in old age.

            Despite the equivocal outcomes of randomized controlled trials, general clinical opinion favors screening and treatment of elderly individuals with subclinical thyroid disorders. To determine whether subclinical thyroid dysfunction should be treated in old age and the long-term impact of thyroid dysfunction on performance and survival in old age. A prospective, observational, population-based follow-up study within the Leiden 85-Plus Study of 87% of a 2-year birth cohort (1912-1914) in the municipality of Leiden, the Netherlands. A total of 599 participants were followed up from age 85 years through age 89 years (mean [SD] follow-up, 3.7 [1.4] years). Complete thyroid status at baseline; disability in daily life, depressive symptoms, cognitive function, and mortality from age 85 years through 89 years. Plasma levels of thyrotropin and free thyroxine were not associated with disability in daily life, depressive symptoms, and cognitive impairment at baseline or during follow-up. Increasing levels of thyrotropin were associated with a lower mortality rate that remained after adjustments were made for baseline disability and health status. The hazard ratio (HR) for mortality per SD increase of 2.71 mIU/L of thyrotropin was 0.77 (95% confidence interval [CI], 0.63-0.94; P = .009). The HR for mortality per SD increase of 0.21 ng/dL (2.67 pmol/L) of free thyroxine increased 1.16-fold (95% CI, 1.04-1.30; P = .009). In the general population of the oldest old, elderly individuals with abnormally high levels of thyrotropin do not experience adverse effects and may have a prolonged life span. However, evidence for not treating elderly individuals can only come from a well-designed, randomized placebo-controlled clinical trial.
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              Association between mutations in a thyroid hormone transporter and severe X-linked psychomotor retardation.

              Monocarboxylate transporter 8 (MCT8) is a thyroid hormone transporter, the gene of which is located on the X chromosome. We tested whether mutations in MCT8 cause severe psychomotor retardation and high serum triiodothyronine (T3) concentrations in five unrelated young boys. The coding sequence of MCT8 was analysed by PCR and direct sequencing of its six exons. In two patients, gene deletions of 2.4 kb and 24 kb were recorded and in three patients missense mutations Ala150Val, Arg171 stop, and Leu397Pro were identified. We suggest that this novel syndrome of X-linked psychomotor retardation is due to a defect in T3 entry into neurons through MCT8, resulting in impaired T3 action and metabolism.
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                Author and article information

                Journal
                Eur Thyroid J
                Eur Thyroid J
                ETJ
                European Thyroid Journal
                S. Karger AG (Allschwilerstrasse 10, P.O. Box · Postfach · Case postale, CH–4009, Basel, Switzerland · Schweiz · Suisse, Phone: +41 61 306 11 11, Fax: +41 61 306 12 34, karger@karger.ch )
                2235-0640
                2235-0802
                September 2013
                27 August 2013
                1 March 2014
                : 2
                : 3
                : 168-179
                Affiliations
                aCardiff University School of Medicine, Heath Park, Cardiff, UK
                bDepartment of Endocrinology, Sir Charles Gairdner Hospital, Nedlands, W.A., Australia
                Author notes
                *Colin M. Dayan, MA, FRCP, PhD, Cardiff University School of Medicine, Heath Park, Cardiff CF14 4XN (UK), E-Mail DayanCM@ 123456cardiff.ac.uk
                Article
                etj-0002-0168
                10.1159/000353777
                4017747
                Copyright © 2013 European Thyroid Association Published by S. Karger AG, Basel
                Page count
                Figures: 4, Tables: 2, References: 80, Pages: 12
                Categories
                Clinical Thyroidology / Review

                thyroid, hypothyroidism, depression, thyroxine

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