Did you know?
Exophthalmos, or the abnormal protrusion of the eyes, occurs in about 25-30% of individuals with Graves’ disease, which disproportionately affects women.

Graves Disease

Researched by:

Karen Pendergrass ID

Karen Pendergrass

Karen Pendergrass is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease—four years before the first published case study.

May 17, 2025

Graves’ Disease (D) affects approximately 0.5% of the population, predominantly women. First-line treatment options—antithyroid medications, radioactive iodine, and surgery— often result in significant side effects, incomplete remissions, and frequent relapses. Further, current first-line treatment options focus on symptoms management, and reflect an inadequate understanding of the etiology of the condition. However, recent research reveals a […]

Research feed

Karen Pendergrass

Karen Pendergrass is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease—four years before the first published case study.

Researched by:

Karen Pendergrass ID

Karen Pendergrass

Karen Pendergrass is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease—four years before the first published case study.

Last Updated: May 17, 2025

Overview

Graves’ Disease (GD) affects approximately 0.5% of the population, predominantly women. First-line treatment options—antithyroid medications, radioactive iodine, and surgery— often result in significant side effects, incomplete remissions, and frequent relapses. Further, current first-line treatment options focus on symptoms management, and reflect an inadequate understanding of the etiology of the condition. However, recent research reveals a strong causal relationship between GD and the gut microbiome.^[1] Thus, a microbiome-targeted strategy aimed at addressing the root causes of GD moves beyond mere symptom suppression and marks a significant advancement in medical history.

Symptoms

Graves’ disease often presents with a range of symptoms that vary in severity. Common early signs include increased heart rate, weight loss despite normal or increased appetite, anxiety, irritability, hand tremors, sweating, diarrhea, fatigue, muscle weakness, and insomnia. Thyroid enlargement (goiter) may be visible as swelling at the base of the neck. Graves’ ophthalmopathy (GO) can cause bulging eyes, a gritty sensation, eye pain or pressure, puffy or retracted eyelids, and, in severe cases, double vision or vision loss. In rare cases, thick red skin on the shins or feet (pretibial myxedema) may also occur.

Causes

Graves’ disease results from a complex interplay of genetic predisposition, environmental triggers, and immunological dysfunction. Recent microbiome research highlights the causal role of gut microbial dysbiosis in contributing to the disease’s onset and progression.^[2]

Diagnosis

Associated Conditions

Overall, Graves’ disease, as an autoimmune disorder, tends to cluster with other autoimmune conditions. It also causes significant systemic effects due to prolonged hyperthyroidism, necessitating comprehensive management and monitoring.

What conditions are associated with Grave’s Disease?

Complication	Description
Graves’ Ophthalmopathy (GO)	Symptoms include eye bulging (exophthalmos), irritation, dryness, swelling, and in severe cases, vision loss.
Graves’ Dermopathy	Rare skin condition often characterized by thick, red skin on the shins or tops of the feet (pretibial myxedema).
Thyroid Storm	A rare, life-threatening condition characterized by an extreme increase in thyroid hormone levels, leading to fever, rapid heart rate, and potentially, heart failure.
Hashimoto’s Thyroiditis	Some patients may initially have Graves’ disease and later develop Hashimoto’s thyroiditis, leading to hypothyroidism.
Type 1 Diabetes Mellitus	Both are autoimmune diseases, and patients with Graves’ disease are at increased risk of developing type 1 diabetes.
Rheumatoid Arthritis	An autoimmune disorder that causes chronic inflammation of the joints.
Systemic Lupus Erythematosus (SLE)	An autoimmune disease affecting the skin, joints, kidneys, brain, and other organs.
Pernicious Anemia	Anemia caused by an autoimmune response against the cells that produce intrinsic factor, essential for vitamin B12 absorption.
Cardiovascular Conditions	Atrial fibrillation, increased risk of stroke, and congestive heart failure due to prolonged untreated hyperthyroidism.
Osteoporosis	Hyperthyroidism can lead to increased bone resorption leading to weakened bones and higher fracture risk.
Muscle Weakness and Wasting	Hyperthyroidism can lead to muscle weakness, particularly in the upper arms and thighs.
Menstrual Irregularities and Fertility Issues	Women with Graves’ disease may experience irregular menstrual cycles and have struggle with infertility.

Primer

Understanding metal homeostasis and mineral homeostasis is essential for fully elucidating Graves’ Disease, and helps us grasp the broader implications of the condition’s unique microbiome signature.

Metal Homeostasis

Data reveals that elevated levels of cadmium (Cd), lead (Pb), and chromium (Cr) are associated with an increased risk of hyperthyroidism, as these metals can disrupt endocrine functions and cause oxidative damage to the thyroid gland. These toxic elements pose significant health risks due to their cumulative nature. Conversely, higher cobalt (Co) levels are associated with a decreased risk of hyperthyroidism, highlighting its complex role in thyroid metabolism. Additionally, deficiencies in copper (Cu) and zinc (Zn), essential for thyroid hormone synthesis, are also associated with hyperthyroidism and GD. ^[3] While these findings certainly aid in understanding occupational risk factors for GD, further research provides alarming new insight on metal toxicity and carcinogenicity occurring in thyroid cells when chronically exposed to metal concentrations that are slightly increased, even within what is considered the “normal” range. ^[4]

What occupations are risk factors associated with Grave’s Disease due to exposure?

Occupation	Findings
Electroplating Workers	A study on electroplating workers found that occupational cadmium exposure significantly increased levels of thyroid hormones, anti-TPO antibodies, IL-6, MDA, and TNF-α, indicating a link between cadmium exposure and elevated inflammatory and oxidative stress markers. ^[5]
Battery Manufacturing	Lead, cadmium, and arsenic exposure in battery manufacturing workers was significantly higher than controls, with lead levels being the most prominent. This exposure correlates with altered thyroid function and increased oxidative stress, highlighting occupational hazards and potential implications for thyroid diseases like Grave’s disease. ^[6]
Paint Workers	Paint workers exposed to lead (Pb) and solvents are at risk for hyperthyroidism. Studies have shown that T3 (triiodothyronine) and T4 (thyroxine) levels are significantly higher in these workers compared to controls. This suggests that occupational exposure to lead and solvents can disrupt thyroid function, leading to increased thyroid hormone production and the potential development of hyperthyroidism. ^[7]

Mineral Homeostasis

Extensive research shows the thyroid-gut axis (TGA) significantly influences thyroid function. Gut health regulates thyroid roles and pathologies through nutrient intake and microbiota. Essential minerals like iodine and selenium are critical for thyroid hormone synthesis and overall health. The gut-immune interaction affects autoimmune diseases, including Graves’ disease and thyroid cancer.

What minerals are involved in Grave’s Disease and what are their functions?

Mineral	Details
Iodine	Iodine is essential for the synthesis of thyroid hormones (thyroxine [T4] and triiodothyronine [T3]). The thyroid gland absorbs iodine from the bloodstream and incorporates it into these hormones. In Graves’ disease, the thyroid is overstimulated by autoantibodies that mimic thyroid-stimulating hormone (TSH), leading to excessive production of thyroid hormones. Adequate iodine levels are necessary to sustain this increased hormone production, but excessive iodine can exacerbate hyperthyroidism in susceptible individuals. (Frontiers)
Selenium	The thyroid gland has the highest concentration of selenium in the human body, highlighting the element’s significance in thyroid health. This high concentration underscores the potential impact of selenium levels on thyroid-related disorders like Graves’ disease. [x] Selenium is a component of selenoproteins, including glutathione peroxidase and thioredoxin reductase, which protect the thyroid gland from oxidative damage during hormone synthesis. It is also involved in the conversion of T4 to the more active T3. Selenium deficiency has been linked to autoimmune thyroid diseases, including GD.
Zinc and Copper	These trace minerals are important for various enzymatic processes in the body, including those related to thyroid hormone metabolism and immune function. Deficiencies in copper (Cu) and zinc (Zn), essential for thyroid hormone synthesis, are also associated with hyperthyroidism and GD.

Interventions

Researchers involved in the microbiota analyses of GD predict that microbiota-targeted therapeutics will emerge as the new strategy for managing GD/GO in the coming years. ^[8] The section covers interventions for Grave’s Disease, such as pharmacological treatments, drug repurposing, and dietary supplements. It explores ASAPs, utilizing emerging science to find new treatments, and STOPs, which suggest reassessing standard practices. Here we suggest other microbiome-targeted interventions (MBTIs) for the management of GD.

Pharmacological

The therapeutic approach to Graves’ disease (GD) comprises thionamides, radioiodine ablation, or surgery as first-line therapy, and cholestyramine and oral iodine as second-line therapies.

First-Line Pharmacological Treatments for Grave’s Disease

Methimazole: Methimazole up-regulates the levels of Bifidobacterium and Collinsella which are decreased in GD, and down-regulates the levels of Prevotella and Dialister, which are increased in GD. ^[x]

Serum from patients with untreated Graves’ disease had a significantly higher concentration of Cu, Zn-SOD and higher SOD-like activity than those from normal subjects. This is likely due to the presence of Haemophilus parainfluenzae, which is significantly increased in Grave’s Disease, that has a rare Copper-zinc superoxide dismutase ([Cu, Zn]-SOD) encoding. [9]^[x]

It is noteworthy that methimazole treatment produced no significant change in SOD-like activity and Cu, Zn-SOD concentration in patients with Graves’ disease.^[10] Thus, it is likely that a patient not responding to Methimazole treatment has an increased level of H. parainfluenzae.

What are the risks associated with first-line therapies for GD?

Treatment	Associated Condition
Methimazole, Propylthiouracil (PTU)	Methimazole is associated with Antithyroid drug (ATD)-induced severe hepatotoxicity. ^[11]
Methimazole, Propylthiouracil (PTU)	Agranulocytosis
Propylthiouracil (PTU)	Vasculitis
Propylthiouracil (PTU)	Liver Failure
Methimazole	Teratogenic Effects
Methimazole, Propylthiouracil (PTU)	Skin Rash/Allergic Reactions
Methimazole, Propylthiouracil (PTU)	Arthralgia
Methimazole, Propylthiouracil (PTU)	Gastrointestinal Disturbances
Radioactive Iodine Therapy	Thyroiditis
Radioactive Iodine Therapy, Surgery	Hypothyroidism
Radioactive Iodine Therapy	Radiation Thyroiditis
Thyroid Surgery	Permanent Hypoparathyroidism
Thyroid Surgery	Recurrent Laryngeal Nerve Damage

Nonthionamide antithyroid drugs (NTADs)

Although thionamide antithyroid drugs are the cornerstone of hyperthyroidism treatment, some patients cannot tolerate this drug class because of its serious side effects including agranulocytosis, hepatotoxicity, and vasculitis. Therefore, non-thionamide antithyroid drugs (NTADs) play an important role in controlling hyperthyroidism in clinical practice.

What NTADs have been investigated for Grave’s Disease and hyperthyroidism?

NTAD	Findings
Cholestyramine	Cholestyramine enhances the enterohepatic excretion of thyroxine, and has been suggested as a monotherapy in case studies and subsequent reviews due to notable symptom improvements and “complete normalization” within one week of starting the intervention when first-line approaches were contraindicated. ^[12][13]
Lithium carbonate	The role of lithium (Li) as a primary or adjunctive therapy remains contentious. Nonetheless, recent studies suggest that a low therapeutic level of lithium (Li), combined with oral iodine, can effectively suppress thyroid overactivity without any adverse effects. Low-dose lithium carbonate is a safe and effective adjunctive antithyroid medication, particularly when primary therapies for hyperthyroidism are unavailable. ^[14] Use of low doses of carbonate lithium (900 mg/ per day) renders a significant decrease or normalization of thyroid hormones concentration within 7–14 days. ^[15] Lithium carbonate has also been used successfully as a monotherapy for GD. ^[15]
Perchlorate
Glucocorticoids

Drug Repurposing

Metformin: Metformin has shown promising benefits for treating Graves’ ophthalmopathy (GO) by activating the AMPK/mTOR pathway, which reduces inflammation and fibrosis in orbital tissues. ^[15] This suggests metformin could improve symptoms and reduce reliance on antithyroid drugs and other treatments with serious potential side effects. Additionally, metformin increases the abundance of Akkermansia muciniphila— ^[16] a beneficial bacterium that is decreased in GD— and reduced orbital pathology in GO patients has been positively correlated with higher levels of Akkermansia. ^[17]

Rituximab: Research suggests that roughly 70% of GD patients have evidence of Graves’ orbitopathy (GO). ^[18]

Antibiotics

The oral administration of the antibiotic vancomycin reduced the severity of GD/GO in mouse models. ^[19]

Supplements

Vitamin D: Research has increasingly highlighted the significant role of vitamin D in the pathogenesis and management of Graves’ Disease (GD). Numerous studies have observed that patients with GD often exhibit lower levels of vitamin D compared to healthy individuals. Vitamin D is known to modulate the activity of immune cells, such as T and B lymphocytes, dendritic cells, and monocytes, which are crucial in the autoimmune response seen in GD. By regulating these cells, vitamin D can help reduce the production of proinflammatory cytokines and enhance anti-inflammatory cytokines, thereby possibly mitigating the autoimmune attack on the thyroid. [20]^[x] Clinical trials and meta-analyses also suggest that vitamin D supplementation reduces the relapse rate of GD after antithyroid drug (ATD) treatment. ^[21]

Inositol: Research findings indicate that a significant proportion of Anaerostipes species, which are decreased in the Mircobiome Signature of Grave’s Disease, can convert inositol into propionate. [22] Another study highlighted that Myo-inositol and selenium (Myo-Ins-Se) supplementation effectively normalized thyroid-stimulating hormone (TSH) levels and improved overall thyroid function in hyperthyroid and hypothyroid patients. This combined therapy showed promise in restoring euthyroidism, potentially offering a new, effective treatment for Graves’ Disease and other forms of hyperthyroidism and hypothyroidism. ^[23]

Selenium: Selenium deficiency has been linked to autoimmune thyroid diseases, including GD. Adequate selenium levels help mitigate the oxidative stress associated with thyroid hormone production and can support overall thyroid health. Supplementation of selenium has been shown to improve thyroid function and reduce symptoms in patients with GD. ^[24] For patients with Graves’ disease, especially those with mild thyroid eye disease, selenium supplementation may lead to faster remission of hyperthyroidism, improved quality of life, and better eye involvement outcomes.^[x]

Glutathione: Exposure to lead, a redox inactive metal, depletes the cell’s major antioxidant reserves of glutathione.

Berberine: Methimazole combined with berberine achieves a better effect on GD than methimazole alone, and the changes in the gut microbiome include changes in levels of Lactococcus lactis, Enterobacter hormaechei, and Chryseobacterium indologenes. ^[26]

B-12: Vitamin B-12 (B-12) has the largest and most chemically complex structure of all of the vitamins. Also called cobalamin, B-12 is the only active substance in the body containing an atom of cobalt. ^[27] As mentioned previously, higher cobalt (Co) levels are associated with a decreased risk of hyperthyroidism, and may have protective effects.

STOPs

While probiotics often hold potential in managing GD/GO, careful selection and optimization of microbial strains are crucial. Probiotic formulas should exclude strains such as Lactobacillus, Prevotella, and Veillonella, which are often found in increased abundance in GD patients.

Microbiome Signature: Graves Disease

Research Feed

August 19, 2020

•

What was studied?
The study assessed thyroid function and oxidative stress in foundry workers occupationally exposed to lead (Pb) dust and fumes. It investigated the correlation between blood lead levels (BLL) and thyroid hormones, as well as markers of oxidative stress.

Who was studied?
The study involved 59 adult male foundry workers exposed to lead and a control group of 28 male subjects with no history of lead exposure or thyroid abnormalities.

What were the most important findings?

Foundry workers had significantly higher blood lead levels (16.5±1.74 µg/dl) compared to the control group (12.8±1.16 µg/dl).

The exposed group exhibited significantly increased levels of free triiodothyronine (FT3) and free thyroxine (FT4), and decreased levels of thyroid stimulating hormone (TSH).

Markers of oxidative stress showed a significant increase in malondialdehyde (MDA) and a significant decrease in glutathione (GSH) among exposed workers.

A significant positive correlation was found between BLL and duration of employment, while a negative correlation existed between BLL and both TSH and GSH levels.

Elevated thyroid hormones were observed in 32.76% of the occupationally exposed workers.

There was a significant positive relationship between GSH and TSH, and between MDA and FT3 and FT4 among exposed workers.

What are the greatest implications of this study?
The study suggests that occupational exposure to lead dust and fumes can stimulate thyroid function, resulting in increased thyroid hormone levels, which may contribute to an oxidative-antioxidant imbalance. This imbalance, indicated by increased MDA and decreased GSH levels, underscores the potential health risks associated with prolonged exposure to lead, highlighting the need for improved protective measures and monitoring in industrial settings.

September 7, 2018

•

What was studied?
The study investigated the gut microbial composition in patients with Graves’ disease (GD) compared to healthy controls.

Who was studied?
The study involved 27 GD patients and 11 healthy controls, with fecal samples collected for analysis.

What were the most important findings?

The association between gut microbiota and host homeostasis is pivotal for understanding various diseases, including autoimmune disorders like Graves’ disease (GD), characterized by hyperthyroidism and ophthalmopathy. This study hypothesized that gut bacteria play a significant role in GD pathogenicity. To investigate this, the intestinal bacterial composition of 27 GD patients and 11 healthy controls was analyzed using PCR-DGGE of the 16S rRNA gene targeting the V3 region and Real-time PCR for specific bacterial groups. High-throughput sequencing of the 16S rRNA gene (V3+V4 regions) was performed on randomly selected samples using the Hiseq2500 platform.

The results revealed a lower diversity of intestinal bacteria in GD patients compared to controls. Statistical analyses indicated significant alterations in bacterial phyla, with a higher relative abundance of Prevotellaceae and Pasteurellaceae, and a lower abundance of Enterobacteriaceae, Veillonellaceae, and Rikenellaceae in GD patients. At the genus level, Prevotella_9 and Haemophilus were significantly increased, whereas Alistipes and Faecalibacterium were decreased in GD patients. Notably, the species Haemophilus parainfluenza was more abundant in GD patients.

What are the greatest implications of this study?
The findings support the hypothesis of gut microbial dysbiosis in GD, suggesting that changes in the gut microbiota may contribute to the disease’s pathogenesis. These insights could pave the way for novel therapeutic approaches targeting gut microbiota in GD treatment.

February 14, 2023

•

What was studied?

This study investigated the bidirectional causal relationship between Graves’ Disease (GD) and the gut microbiome. Utilizing Mendelian randomization (MR), it examined how alterations in the gut microbiome might influence GD and vice versa, supporting the thyroid–gut axis (TGA) concept. Genome-wide association study (GWAS) summary datasets, which analyze millions of genetic variants across diverse populations to identify associations between genetic markers and specific traits, were sourced from international consortiums to evaluate these interactions.

Who was studied?

The study involved two large datasets. Gut microbiome data included 18,340 samples spanning diverse ethnic groups (European, Middle Eastern, East Asian, Hispanic/Latin American, and African American), while GD data included 212,453 samples of Asian ethnicity, sourced from Biobank Japan. These comprehensive datasets were analyzed to identify instrumental variables linking genetic variants to gut microbiome composition and GD susceptibility.

What were the most important findings?

The study established a bidirectional causal relationship between Graves’ disease (GD) and the gut microbiome, identifying key microbial associations that act as either risk or protective factors. Risk factors for GD included the classes Deltaproteobacteria (odds ratio [OR] = 3.603) and Mollicutes, as well as the genera Ruminococcus torques group, Oxalobacter, and Ruminococcaceae UCG 011. Protective associations were observed for the family Peptococcaceae and the genus Anaerostipes (OR = 0.489). Furthermore, GD was found to alter gut microbiome composition, increasing the abundance of genera like Anaerofilum (OR = 1.584) and reducing taxa such as the Clostridium innocuum group (OR = 0.918) and Sutterella (OR = 0.953). These findings highlight the regulatory activity of the thyroid–gut axis (TGA) and provide strong evidence for its involvement in GD pathogenesis.

What are the greatest implications of this study?

The findings underscore the critical role of the gut microbiome in GD pathogenesis and its reciprocal interaction with thyroid health. Identifying specific microbial taxa as risk or protective factors offers actionable insights for microbiome-targeted interventions (MBTIs), such as probiotics or dietary modifications, tailored to mitigate GD risk or progression. The bidirectional relationship between GD and the gut microbiome highlights the need for integrated approaches addressing both thyroid and gut health. These results could guide the development of precision medicine strategies, leveraging the gut microbiome to modulate immune responses and improve clinical outcomes for patients with GD. This research also establishes a foundational understanding of major microbial associations (MMAs) within the TGA, paving the way for future therapeutic innovations. Further, this study establishes a methodological precedent for using Mendelian Randomization to discern causal effects in microbiome-related research.

References

A cause–effect relationship between Graves’ disease and the gut microbiome contributes to the thyroid–gut axis: A bidirectional two-sample Mendelian randomization study. Cao J, Wang N, Luo Y, et al.. (Front. Immunol. (February 14, 2023))
A cause-effect relationship between Graves’ disease and the gut microbiome contributes to the thyroid–gut axis: A bidirectional two-sample Mendelian randomization study.. Cao J, Wang N, Luo Y, Ma C, Chen Z, Chenzhao C, Zhang F, Qi X and Xiong W.. (Front. Immunol. (February 14, 2023))
Thyroid dysfunction: how concentration of toxic and essential elements contribute to risk of hypothyroidism, hyperthyroidism, and thyroid cancer.. Rezaei M, Javadmoosavi SY, Mansouri B, Azadi NA, Mehrpour O, Nakhaee S.. (Environ Sci Pollut Res Int. (Nov. 8, 2019))
Heavy Metals in the Environment and Thyroid Cancer.. Gianì F, Masto R, Trovato MA, et al.. (Cancers. (Basel) (Aug. 12, 2021))
Effect of occupational cadmium exposure on the thyroid gland and associated inflammatory markers among workers of the electroplating industry. . Ramadan MA, Saif Eldin AS.. (Toxicol Ind Health. (March 20, 2022))
Assessment Of Occupational Exposure To Lead, Cadmium And Arsenic In A Lead-Acid Battery Manufacturing And Recycling Plant In Algeria.. Faiza, Bouchala & Benboudiaf, Sabah & Boos, Anne & Hamadouche, Mohamed & Ronot, Pascal & Masoudi, Islah & Azzouz, Mohamed.. (Pharmacy and Drug Development. (March 3, 2024))
Thyroid functions in paints production workers and the mechanism of oxidative-antioxidants status.. Saad-Hussein A, Hamdy H, Aziz HM, Mahdy- Abdallah H. (Toxicol Ind Health. (2011))
The Role of the Microbiota in Graves’ Disease and Graves’ Orbitopathy. Hou J, Tang Y, Chen Y, Chen D.. (Front. Cell. Infect. Microbiol. (December 22, 2021))
Copper-zinc superoxide dismutase of Haemophilus influenzae and H. parainfluenzae.. Kroll JS, Langford PR, Loynds BM.. (J Bacteriol. (December, 1991))
Serum superoxide dismutase in patients with Graves' disease. Hara H, Ban Y, Sato R.. (Endocrine. (Feb 20, 1993))
Analysis of 90 cases of antithyroid drug-induced severe hepatotoxicity over 13 years in China. . Yang J, Li LF, Xu Q, et al.. (Thyroid. (Mar. 25, 2015))
Cholestyramine as monotherapy for Graves' hyperthyroidism. . Er C, Sule AA.. (Singapore Med J. (Nov. 5, 2016))
Cholestyramine for thyrotoxicosis?. Lin D, Suwantarat N, Bornemann M.. (J Fam Pract. (April 6, 2013))
Use of Lithium in Hyperthyroidism Secondary to Graves' Disease: A Case Report.. Sharma PP.. (Am J Case Rep. (April 28, 2022))
Metformin Attenuates Inflammation and Fibrosis in Thyroid-Associated Ophthalmopathy.. Xu Z, Ye H, Xiao W, Sun A, Yang S, Zhang T, Sha X, Yang H.. (International Journal of Molecular Sciences. (December 7, 2022))
Metformin Exerts Anti-inflammatory and Mucus Barrier Protective Effects by Enriching Akkermansia muciniphila in Mice With Ulcerative Colitis.. Ke H, Li F, Deng W, et al.. (Front Pharmacol. (2021 Sep 30. 2021))
Modulating Gut Microbiota in a Mouse Model of Graves' Orbitopathy and its Impact on Induced Disease.. Moshkelgosha, S., Verhasselt, H. L., Masetti, G., Covelli, D., Biscarini, F., Horstmann, M., et al.. (Microbiome. (2021))
Graves’ ophthalmopathy: epidemiology and natural history. . Hiromatsu Y, Eguchi H, Tani J, Kasaoka M, Teshima Y. . (Internal Medicine (2014))
The Role of the Microbiota in Graves’ Disease and Graves’ Orbitopathy. Hou J, Tang Y, Chen Y, Chen D.. (Front. Cell. Infect. Microbiol. (December 22, 2021))
Vitamin D and the Thyroid: A Critical Review of the Current Evidence.. Babić Leko M, Jureško I, Rozić I, Pleić N, Gunjača I, Zemunik T.. (International Journal of Molecular Sciences. (Feb 10. 2023))
Effect of Vitamin D Supplementation on Graves' Disease: The DAGMAR Trial.. Grove-Laugesen D, Ebbehoj E, Watt T, et al.. (https://doi.org/10.1089/thy.2023.0111)
Conversion of dietary inositol into propionate and acetate by commensal Anaerostipes associates with host health.. Bui TPN, Mannerås-Holm L, Puschmann R, et al.. ( Nat Commun. (Aug 10, 2021))
Treatment with Myo-Inositol and Selenium Ensures Euthyroidism in Patients with Autoimmune Thyroiditis.. Nordio M, Basciani S.. (Int J Endocrinol. (Feb. 15, 2017))
Selenium in the Treatment of Graves' Hyperthyroidism and Eye Disease. . Lanzolla G, Marinò M, Marcocci C.. (https://doi.org/10.3389/fendo.2020.608428)
Selenium in thyroid disorders — essential knowledge for clinicians.. Winther, K.H., Rayman, M.P., Bonnema, S.J. et al.. (Nat Rev Endocrinol. (Jan. 30, 2020))
The potential prebiotic berberine combined with methimazole improved the therapeutic effect of graves' disease patients through regulating the intestinal microbiome.. Han Z, Cen C, Ou Q, Pan Y, Zhang J, Huo D, et al.. (https://doi.org/10.3389%2Ffimmu.2021.826067)
Vitamin B12.. Truswell, Arthur.. (Nutrition & Dietetics. (2007).)

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First-Line Pharmacological Treatments for Grave’s Disease

Nonthionamide antithyroid drugs (NTADs)

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Microbiome Signature: Graves Disease

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What was studied?

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What are the greatest implications of this study?

References

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Graves Disease

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Overview

Symptoms

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Associated Conditions

Primer

Metal Homeostasis

Mineral Homeostasis

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Pharmacological

First-Line Pharmacological Treatments for Grave’s Disease

Nonthionamide antithyroid drugs (NTADs)

Drug Repurposing

Antibiotics

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Microbiome Signature: Graves Disease

Research Feed

What was studied?

Who was studied?

What were the most important findings?

What are the greatest implications of this study?

References

What's on your mind?