Nutritional Management of Thyroiditis of Hashimoto

Nutritional Management of Thyroiditis of Hashimoto

Abstract: Since the thyroid gland is one of the organs most affected by autoimmune processes, many patients with thyroiditis of Hashimoto seek medical advice on lifestyle variance and dietary modifications to improve and maintain their thyroid function. In this review, we aim to present and discuss some challenges associated with the nutritional management of thyroiditis of Hashimoto, focusing on environmental and dietary deficits, inflammatory and toxic nutrients, cyanotoxins, etc. We discuss the relationships among different diets, chronic inflammation, and microbiota, and their impact on the development and exacerbation of thyroiditis of Hashimoto in detail. We share some novel insights into the role of vitamin D and melatonin for preserving thyroid function during chronic inflammation in autoimmune predisposed subjects. A comprehensive overview is provided on anti-inflammatory nutrients and ecological diets, including foods for cleansing and detoxification, which represent strategies to prevent relapses and achieve overall improvement of life quality. In conclusion, data from biomedical and clinical studies provide evidence that an appropriate dietary and lighting regimen could significantly improve the function of the thyroid gland and reduce the reactivity of autoantibodies in thyroiditis of Hashimoto. Compliance with nutritional guidelines may help thyroiditis of Hashimoto patients to reduce the need for medicines.

One. Introduction

The thyroid gland is the organ most affected by autoimmune processes. Between twenty percent and forty percent of American Caucasians and British citizens show lymphocytic infiltration in post-mortem specimens, while the highest percentage is typical for white females. The intra-thyroidal lymphocytic infiltration induces chronic inflammation and autoimmune conditions, which most often results in autoimmune hypothyroidism or thyroiditis of Hashimoto. Thyroiditis of Hashimoto development leads to scarring and destruction of the thyroid gland and is manifested by a decrease of plasma free triiodothyronine and thyroxine, elevated plasma levels of thyroid-stimulating hormone and by the presence of antibodies to thyroid peroxidase and thyroglobulin. It is generally accepted that the pathogenesis of thyroiditis of Hashimoto, like other autoimmune diseases, represents the combination of environmental (i.e., lighting regimen, pollution, micronutrients,

variety of physical and social factors), existential (lifestyle, hormonal status, diet, gut microbiota), as well as genetic factors that provoke immunological dysfunction and support the autoimmune destruction of the gland.

To treat the condition in the long term, patients with thyroiditis of Hashimoto-associated hypothyroidism often require lifetime hormone replacement therapy with levothyroxine. There is growing evidence of the existence of a thyroid-gut axis that controls many autoimmune disorders, and patients frequently report changes in their quality of life and thyroid function as a result of dietary modifications.

Genetic factors contribute to seventy to eighty percent of autoimmune thyroid diseases. The major histocompatibility complex genes, thyroid-related genes, genes associated with thyroid peroxidase antibody synthesis, and genes regulating immune response are the common genetic factors.

From the environmental factors, a vast variety of nutrients play an important role in the onset and development of thyroiditis of Hashimoto. High iodine intake, deficiencies of selenium and iron, inadequate intake of proteins, unsaturated fatty acids, and dietary fibers could favor thyroiditis of Hashimoto. Proinflammatory foods may induce dysbiosis and oxidative stress that can cause intestinal inflammation and spread it towards different organs, including the thyroid gland. The reduction and replacement of commensal microbiota caused by dietary supplementation significantly change the immune function and epithelial metabolism of the intestinal mucosa and the absorption of nutrients. Drugs such as pembrolizumab, interferon alpha, antiretroviral therapy, and estrogens used for oral contraception or hormone replacement therapy are also crucial for thyroiditis of Hashimoto. Smoking and moderate alcohol consumption protect against thyroiditis of Hashimoto, but quitting smoking may provoke this disease. Immunomodulatory therapies and infections such as rubella, hepatitis C, and Epstein-Barr virus could also be responsible for the development of thyroiditis of Hashimoto.

Cyanotoxins such as cylindrospermopsin and microcystins, in addition to their general toxicity, increase the permeability of epithelial and model pseudo-epithelial layers of human intestines. They even possess the ability to affect the function of the gastrointestinal epithelium and other cell types, and thus induce "leaky gut" syndrome, inflammation, oxidative stress, and apoptosis. Furthermore, microcystins dose-dependently reduce thyroid hormone levels, and influence deiodinase activity and transcription of genes related to thyroid hormones' synthesis and metabolism. Direct harmful effects of acute and chronic exposure to cyanotoxins on the hypothalamic-pituitary-thyroid axis may lead to hypothyroidism.

Individual characteristics such as age, lifestyle, gender, pregnancy, and certain diseases, such as allergic rhinitis, prolactinoma, and subacute thyroiditis, may serve as an important predisposition or triggers for thyroiditis of Hashimoto. Current treatment of thyroiditis of Hashimoto in hypothyroid subjects includes replacement monotherapy with levothyroxine, which greatly reduces relapses of the disease and slows down the progression of thyroid damage. However, a proportion of the patients continue to experience various symptoms and deteriorating overall quality of life. Unfortunately, there are limited data on any effective concomitant treatment other than levothyroxine, which by itself does not target the autoimmune processes related to disease severity. It is already known that the diet and lifestyle of patients with thyroiditis of Hashimoto can play a key role in the management of disease episodes, which necessitates an in-depth study of complex external and internal factors. Intensive research shows that many dietary supplements have the potential to positively affect thyroiditis of Hashimoto symptomatology due to their anti-inflammatory and antidepressant activity, thus improving the overall sense of well-being. Among the most attractive candidates which may be able to influence the severity of clinical symptoms and improve thyroid function are vitamins from the groups A, B, C, and D, fatty acids, antioxidants, phytochemicals, but also the indole-amine melatonin.

The interest in dietary vitamin D and melatonin is based on research findings of their physiological role as regulators of the production of inflammatory cytokines and prostaglandins. The controlled dietary supplementation of vitamin D and melatonin might represent an essential strategy for treating thyroiditis of Hashimoto via their molecular mechanisms on the cellular level. Data suggest that appropriate nutritional protocols may help to decrease the chronic inflammation in the thyroid gland, other tissues, and organs, as well as to suppress or stop the thyroid gland degradation and thus improve patients' quality of life.

In this review, we aim to present and discuss challenges associated with the nutritional management of thyroiditis of Hashimoto, focusing on environmental factors and dietary deficits, inflammatory and toxic nutrients, cyanotoxins, etc. We analyze the relationships between different diets, chronic inflammation, and microbiota, and their impact on the development and exacerbation of thyroiditis of Hashimoto in detail. We share some novel insights into the roles of vitamin D and melatonin for preserving thyroid function during chronic inflammation in autoimmune predisposed individuals.