Stress and Thyroid Autoimmunity

Department of Clinical and Biomedical Sciences: Barwon Health, The Geelong Hospital, Geelong, Victoria, Australia.
Thyroid (Impact Factor: 4.49). 01/2005; 14(12):1047-55. DOI: 10.1089/thy.2004.14.1047
Source: PubMed


While many studies have shown a connection between stress and autoimmune disease, most of the evidence for stress contributing to the onset and course of autoimmune disease is circumstantial and the mechanisms by which stress affects autoimmune disease are not fully understood. The best circumstantial evidence for an effect of stress on autoimmune thyroid disease is the well-known relationship between the onset of Graves' hyperthyroidism and major stress but even this is debated. However, most of the recent case-control studies have supported stress as a factor that affects the onset and clinical course of Graves' disease. On the other hand, there have been few reports concerning the possible relationship between stress and Hashimoto's thyroiditis. Because the onset and course of Hashimoto's thyroiditis is generally insidious, the effect of stress on Hashimoto's thyroiditis might be overlooked. Numerous human and animal studies have demonstrated that psychological and physiologic stressors induce various immunologic changes. Stress affects the immune system either directly or indirectly through the nervous and endocrine systems. These immune modulations may contribute to the development of autoimmunity as well as the susceptibility to autoimmune disease in genetically predisposed individuals. Stress can be one of the environmental factors for thyroid autoimmunity.

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Available from: Audrey Li, Jun 18, 2014
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    • "Some criticisms of case-control studies were proposed (Chiovato & Pinchera, 1996; Mizokami, et al, 2004 ). There are some general methodological problems and limitations in studies dealing stress, especially preceding retrospective studies based on the assessment of life events preceding thyrotoxicosis or the diagnosis of GD. "
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    ABSTRACT: This chapter reviwed the role of psychosocial factors including personality traits as well as stresses on the onset and clinical course of Graves' disease including our reports. Because there are some studies about the relationships between stress and other thyroid diseases including Hashimoto' s thyroiditis, Plummer' disease and benign thyroid nodule, we also introduced these reports.
    Full-text · Chapter · Jan 2014
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    • "These results suggest that depressive personality, even when euthyroid during treatment, in GD is related to the aggravation of hyperthyroidism. Because depressive patients experience more daily hassles and fewer daily uplifts than non-depressive patients, emotional stresses may aggravate hyperthyroidism by the neuro- immuno-endocrine system [24] in depressive patients. Although in this study remission was judged by normal serum free T4 and TSH concentrations for more than 12 months after ATD withdrawal, a time interval of 12 months may be too short to prove stable remission. "
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    ABSTRACT: We previously reported that depressive personality (the scores of hypochondriasis, depression and psychasthenia determined by the Minnesota Multiphasic Personality Inventory (MMPI)) and daily hassles of Graves' disease (GD) patients treated long trem with antithyroid drug (ATD) were significantly higher in a relapsed group than in a remitted group, even in the euthyroid state. The present study aims to examine the relationship among depressive personality, emotional stresses, thyroid function and the prognosis of hyperthyroidism in newly diagnosed GD patients. Sixty-four untreated GD patients responded to the MMPI for personality traits, the Natsume's Stress Inventory for major life events, and the Hayashi's Daily Life Stress Inventory for daily life stresses before and during ATD treatment. In the untreated thyrotoxic state, depressive personality (T-scores of hypochondriasis, depression or psychasthenia greater than 60 points in MMPI) were found for 44 patients (69%). For 15 (23%) of these patients, the scores decreased to the normal range after treatment. However, depressive personality persisted after treatment in the remaining 29 patients (46%). Normal scores before treatment were found for 20 patients (31%), and the scores were persistently normal for 15 patients (23%). The remaining 5 patients (8%) had higher depressive personality after treatment. Such depressive personality was not associated with the severity of hyperthyroidism. Serum TSH receptor antibody activity at three years after treatment was significantly (p = 0.0351) greater in the depression group than in the non- depression group. The remission rate at four years after treatment was significantly (p = 0.0305) lower in the depression group than in the non- depression group (22% vs 52%). The data indicate that in GD patients treated with ATD, depressive personality during treatment reflects the effect of emotional stress more than that of thyrotoxicosis and that it aggravates hyperthyroidism. Psychosomatic therapeutic approaches including antipsychiatric drugs and/or psychotherapy appears to be useful for improving the prognosis of hyperthyroidism.
    Full-text · Article · Aug 2011 · BioPsychoSocial Medicine
    • "Genetic factors such as HLA (Human leukocyte antigen) and CTLA-4 (Cytotoxic T lymphocyte antigen – 4) determine the susceptibility to GD.[22] Stress may lead to immunologic perturbations and may affect the immune response to TSH receptor through modulation of hormones, neurotransmitters and cytokines. A defect of antigen-specific suppressor T-lymphocytes has been proposed to be partially responsible for the initiation of GD.[23] Stress may result in a defect in the immunologic surveillance leading to production of TSH receptor antibodies.[24] In genetically susceptible individuals stress favors the development of GD by shifting the Th1-Th2 immune balance away from Th1 towards Th2.[25] "
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    ABSTRACT: In the modern environment one is exposed to various stressful conditions. Stress can lead to changes in the serum level of many hormones including glucocorticoids, catecholamines, growth hormone and prolactin. Some of these changes are necessary for the fight or flight response to protect oneself. Some of these stressful responses can lead to endocrine disorders like Graves' disease, gonadal dysfunction, psychosexual dwarfism and obesity. Stress can also alter the clinical status of many preexisting endocrine disorders such as precipitation of adrenal crisis and thyroid storm.
    No preview · Article · Mar 2011
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