• Jasmine Blake Hollywood, MS, HHP

What is Grave's Disease?

Updated: Sep 7, 2020

What is Graves' Disease?

Graves' disease is an autoimmune condition known as thyrotoxicosis. It is defined as the overstimulation of the thyroid hormones in the thyroid gland. The gland produces too much thyroid hormone. It is an autoimmune disease. Autoimmunity is when the self-tolerance of the immune system fails. Considering the pathways of this disease, treatment options vary but are well maintained in conventional medicine. However, cures are not currently possible.

Nutrition could be a cause for the condition. By using food, diseases like this could be reversed, says some scientists. Likewise, by using both biomedical and alternative medicine in stress reduction, both could be an approach to optimal health. Areas such as alcohol intake, lipid deficiencies, and deficiencies in specific vitamins such as B7 (biotin) giving false positives; could be factors in the occurrence of Graves disease. With the reduction of alcohol and the correction of fats, the condition could show a decrease in numbers on labs.

Areas such as alcohol, intoxicants, lipid deficiencies, an increase in vitamins and minerals, false lab readings, and many others, such as nutrition, are currently being explored. The research of thyroid and the endocrine system, autoimmunity, and nutrition from clinical reports are explored in this article. Furthermore, this article focuses on underlying etiology, pathology, mechanisms of disease, clinical manifestations, diagnosis, systems integration, and nutritional inputs of Graves.

Graves' disease is when self-tolerance fails. When self-tolerance fails, the attack that happens on the human body can be organ-specific or systemic. Meaning wither one particular organ can be affected like the thyroid in thyroid disease, or the whole system can be affected like in Lupus.

There are diverse pathways for Graves Disease to emerge, and these pathways can be either direct or indirect. Clinical manifestations include enlargement of the thyroid organ itself and symptoms, signs, and metabolic events. Viewing blood work from lab assessments can offer assistance in analyzing and diagnosing this disease.

Moreover, Graves Disease might be interconnected to Hashimoto’s Thyroiditis. This has been said to be through a new condition now known as Hashitoxicosis. Lab work can define the difference between these two diseases. Strategies to treat this disease are being studied.

Overview of Prevalence

Graves' disease is considered to be an upcoming condition. It is currently becoming one of the most common autoimmune disorders. In Braun and Anderson (2017), Applied Pathophysiology book in reviewing the prevalence, this disease is estimated to occur in 0.5 out of 1,000, people.[2]. However, other sources such as the National Institute Health, U.S. National Library of Medicine: Genetics Home Reference (2018) claim the prevalence is more like 1 in 200 people.[6].

When it comes to comparing the risk of men and women, Braun et al. (2017) state that women top men, ranging 7-10 times more likely to be diagnosed. [2].The National Institutes of Health (NIH), National Institute of Diabetes and Digestive and Kidney Diseases (2017) writes that Graves' Disease often affects people between the ages of 30 and 50, but can sometimes affect a person beginning at early adulthood. [5].

Just the same, NIH et al (2017) authors also indicate people with other autoimmune diseases are also more likely to develop this condition than those that do not have an autoimmune condition. [5]. One disease in particular, Diabetes Mellitus (DM), has an overall prevalence of over 50% of patients with DM also being diagnosed with Graves Disease. In specific cases of diabetes, Type 1 DM (T1DM) and Type 2 DM (T2DM), both diseases have high prevalence rates of thyroid dysfunction. [9]. In addition, DM is also considered to be a nutritional disease.

Cause and Development

Although there is no specific event that can be directed to the causation of Graves Disease, researchers continue to get closer to a resolution. Initially, autoimmunity is onset. It's accompanied by enlarged goiter, anxiety, hormonal, and metabolism issues. Autoimmunity (i.e., when self-tolerance fails) is the cause of these signs and symptoms. In other words, the body fails to distinguish self from nonself of specific self-antigens. It mistakes its cells for a foreign substance or pathogen, and the body's immune system should recognize its cells.

Eventually, the body orders a response to create antibodies to destroy these antigens. Graves disease presents to the body as an impairment of thyroid cells or tissues in the gland. It makes the body think the functioning of the endocrine system is damaged. The body thinks this because of the production of antibodies constantly being directed at the thyroid gland.

Researchers and scientists have found three possible pathways that can lead to Graves Disease. The pathways one and two can be considered as indirect pathways. Microorganisms cause pathway one. [2].The second pathway is genetic and involves the HLA-DR class II receptors. [3]. The third pathway is considered to be direct. It is caused by anti-thyroid-stimulating hormone (TSH) antibodies cross-reacting with thyroid-stimulating hormone receptor (TSHR). [2].

Effects and Mechanisms of Graves' Disease

Long-standing Grave’s Disease is identified by excess thyroid hormone secretion for an extended period. This excess is regardless of medication being used or attempt to remove diseased sections of the goiter surgically. In the state of hyperthyroidism, the thyroid undergoes hyperplasia (increase in cells or volume of tissue). If the condition continues to excel in a chronic state, it can cause progressive thyroid failure. Hyperplasia is due to the constant stimulation of the gland resulting in either complete failure, hypothyroidism, or death. [2].

Braun et al. (2017) categorize Graves Disease as a type II hypersensitivity of the immune system. [2]. Type II hypersensitivity is when the antibodies are directed against the thyroid gland itself. [2]. Although hypersensitivity reactions are identified as being related to immediate responses to allergens, they can also be related to antibody-mediated responses.

The development of tolerance in type II hypersensitivity is closely connected with the restriction of T cell receptors (TCRs). This development occurs when trying to validate an antigen only when presented by a human leukocyte antigen (HLA) molecule. The action of eliminating or retaining T cells occurs in the thymus. Self-antigens are said to be presented on HLA molecules to the T cells that mature in the thymus. Presenting them suggests that an antigen must be either inside the thymus or inside the circulatory system for tolerance to develop. When major histocompatibility complex (MHC) molecules present foreign antigens, they allow T cells to react and be retained, yet self-antigens are not deleted. [16].

With all areas evaluated, Braun and colleagues (2017) state that there are many reasons for autoimmunity to develop. [2]. Chronic infections such as a virus or bacteria, environmental triggers such as constant exposure to toxins. Robinson, Waller, Parham, DeGroot, Bontrop, Kennedy, and Marsh (2003) emphasized on Graves disease in relation to genetics and the human leukocyte antigen-DR (HLA-DR). [13]. They said that these related receptors and that genetic factors are greatly considered in developmental research.

Other possibilities for Graves disease to develop could be the result of molecular mimicry (close resemblance of foreign and self-antigens in the amino acid sequence) of the immune system. [14]. In any event, the most preeminent proof that the cancellation of T cells in the thymus anticipates autoimmunity comes from another studied disease called Autoimmune Polyglandular Syndrome Type 1 (APS-1). This study suggests this is the consequence of an inactive autosomal transformation within the Autoimmune Regulator (AIRE) gene expressed by the thymus. [16].

Clinical Manifestations

The two primary clinical manifestations that are directly related to Graves disease are the enlargement of the thyroid gland (i.e., goiter) and excessive metabolic rate. Usually, weight loss is accompanied by the excess in metabolism, but weight fluctuation along with weight gain, can be factors as well. Nervousness or irritation and hand tremors are common signs. Heat intolerance, frequent bowel movements or diarrhea, fatigue, muscle weakness, restlessness, or trouble sleeping can be also be experienced. [5]. Anxiety, rapid and irregular heartbeat, increased sweating, increased appetite, and irregular menstrual in women are other symptoms that may be experienced. [6]. Other signs that are noticed in patients with Graves disease and considered by practitioners can be ophthalmopathy (i.e., protrusion of the eyes). [2].

Various autoimmune conditions are associated with Graves' disease. The conditions may cause onset autoimmune thyroid disease or may be explicitly caused by Graves' disease. NIH et al. (2017) state autoimmune conditions in connection with Graves disease are diabetes, lupus, rheumatoid arthritis, pernicious anemia, and Addison's disease. [5]. Weetman et al. (2016) also list autoimmune diseases in connection to Graves disease as alopecia, vitiligo, myasthenia gravis, and Sjögren's syndrome. [16].

In discussing treatment options, nourishment could be the key to unlocking more possibilities. Mostly, treatment options are generally practiced in conventional medicine administering medication, radioactive iodine (I-131), or surgery. Radioactive iodine therapy is usually administered orally as a capsule or liquid. Medicines used to treat Graves disease can be beta-blockers (i.e., reduce symptoms) and antithyroid medication (i.e., methimazole or propylthiouracil). Surgery is the effort to remove a portion or all of the infected thyroid gland; this can also be an option. Prednisone and rituximab can be used to treat ophthalmopathy separately. [5].


Patient history and physical examination are considerable ways to diagnose Graves' disease. [2]. Considering the relationship between Graves' disease and association with other autoimmune disorders, a history of autoimmune disease in the patient or family history of thyroid diseases or other autoimmune diseases will be used in the diagnosis of this condition as well. With this in mind, after a physical examination and patient history, a blood test is utilized to diagnose this disease. A practitioner will view the lab assessment and determine reference ranges for T4, T3, and TSH.

Other reference ranges considered are thyroid peroxidase (TPO) antibodies, thyroglobulin (Tg) antibodies, and newly, immunoglobulin E (IgE) levels. [16]. These antibodies are significantly used to identify any thyroid disease. Since thyroid-stimulating immunoglobulin (TSI) is considered to be a form of immunoglobulin G (IgG), TSI and TSHR autoantibodies can also be used to diagnose the severity of Graves disease. [15]. Furthermore, the reference ranges for radioactive iodine uptake and the measurement of serum-free thyroxine are the two primary ways to identify disease through blood work. [2].

Inputs: Nutritional Areas of Concern

Alcohol was researched by Ballhara and Deb (2013), in relation to the hypothalamus-pituitary thyroid (HPT) axis and was clinically proven to affect this region. [1]. Studies have now been conducted since the early 1980s in researching hormonal changes during alcohol consumption such as dysregulation of the HPT axis, neuroendocrinological implications due to intoxication, and endocrinological issue due to alcoholism. Studies found that alcohol does, in fact, affect all areas of the thyroid gland. The unbalance in the thyroid gland, and the regulation of hormones in the hypothalamus could be reversed with the reduction of alcohol intake. [1].

Similarly, when considering nutrition, researchers have been able to correlate triglyceride levels to autoimmune thyroid disease. Nikkila and Kekky (1972) researched triglyceride transport kinetics in 16 hyperthyroid patients, 12 hypothyroid patients, and euthyroid control subjects. [11].They found that patients with Graves disease had slightly high triglyceride levels circulating in the blood. These levels were compared to levels of those patients who had hypothyroidism. Patients in the hypothyroid state had reduced levels of triglycerides. To conclude, Nikkila et al. (1972) suggested that the results of the studies propose that thyroid hormones could control both the production and elimination of plasma triglycerides. [11].

In a recent study involving nutrition and Graves disease, researchers Elston, Sehgal, Du Toit, Yarndley, and Conaglen (2016) reported that patients that had an excess of Biotin consumed from the diet had abnormal labs for thyroid disease. [4].Biotin can willingly bind to become a hormone or antibody to that hormone. This occurrence is because biotin is a tiny molecule. Biotin markers on these assessments can mimic high reference ranges of thyroid hormones, in particular, Graves disease, proposing a misdiagnosis of patients. With the elimination of biotin, reference ranges go back to normal. [4].

Systems Integration

Kırmızıbekmez, Yeşiltepe Mutlu, Dursun, and Günay (2014) completed a study that indicated there might be a rare condition of autoimmune thyroid disease. [8]. In brief, Hashimoto's Thyroiditis or hypothyroid illness in exceptional cases is systemically related to Graves' disease. Patients in this study had previously experienced either thyroid failure due to surgery or failure due to partial removal of the thyroid gland. The operation and form of treatment had inevitably forced the thyroid into a hypothyroidism state.

Kirmizibekmez and colleagues also mentioned that sometimes an autoimmune state could fluctuate from Graves' disease to Hashimoto's Thyroiditis. [8].This was noticed in cases, and they referred to this rare condition as Hashitoxicosis. Biomarkers that indicate high TSI, high TPO antibodies, as well as, high Tg antibodies are indicators of this rare condition. Researchers are looking more into this scope of the study. [8].

There is a new correlation in the research between thyroid disorders and DM, showing that thyroid dysfunctions are more prevalent in people with diabetes. Hage, Zantout, and Azar (2011) wrote that thyroid dysfunction could ultimately impact DM negatively and impact systemic complications. [7]. Also, those with coexisting DM and Graves disease could increase the risk of vision loss. [9].

DM patients having a higher prevalence of retinopathy and nephropathy was noticed in patients with DM and hypothyroidism. Glycemic control in patients with DM could be impaired by hyperthyroidism. Furthermore, thyroid hormones may alter carbohydrate metabolism even further by interaction with gut hormones, leptin, adiponectin, and ghrelin. [7].


Some ideas that would help cope with Graves' disease would be limiting alcohol. Since research points to drink as a possible contributor, it is probably best to either avoid it or limit it. However, several articles mentioned alcohol as not being a direct contributor, but in combination with other contributors such as stress. [10;17]. Stress, in combination with other triggers, seems to be a serious contributor to autoimmune disease onset. Therefore, it's recommended alternative medicine in practicing a mindfulness lifestyle such as meditation or mindfulness eating in combination with conventional medicine prescribed by an individuals practitioner.


  1. Balhara, Y. P. S., & Deb, K. S. (2013). Impact of alcohol use on thyroid function. Indian Journal of Endocrinology and Metabolism, 17(4), 580–587. Retrieved from http://doi.org/10.4103/2230-8210.113724

  2. Braun, C. A., Anderson, C. M. (2017). Applied physiology: A conceptual approach to the mechanisms of disease (3rd Ed.). PA: Wolters Kluwer

  3. Davies, T. F., Yin, X., & Latif, R. (2010). The genetics of the thyroid stimulating hormone receptor: History and relevance. Thyroid, 20(7), 727–736. Retrieved from http://doi.org/10.1089/thy.2010.1638

  4. Elston, M. S., Sehgal, S., Du Toit, S., Yarndley, T. & Conaglen, J. V. (2016). Factitious graves’ disease due to biotin immunoassay interference—A case and review of the literature. The Journal of Clinical Endocrinology & Metabolism, 101(9), 3251- 3255. Retrieved from https://doi.org/10.1210/jc.2016-1971

  5. Graves' Disease. (2017). National Institutes of Health, National Institutes of Diabetes and Digestive and Kidney Diseases. Retrieved from https://www.niddk.nih.gov/health-information/endocrine-diseases/graves-disease

  6. Graves Disease. (2018). National Institutes of Health, National Library of Medicine: Genetics Home Reference. Retrieved from: https://ghr.nlm.nih.gov/condition/graves-disease#inheritance

  7. Hage, M., Zantout, M. S. & Azar, S. T. (2011). Thyroid disorders and diabetes mellitus. Journal of Thyroid Research, 2011, 439463. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3139205/

  8. Kırmızıbekmez, H., Yeşiltepe Mutlu, R. G., Dursun, F. & Günay, M. (2014). A typical presentation of hashimoto’s disease in an adolescent: Thyroid-associated ophthalmopathy. Journal of Clinical Research in Pediatric Endocrinology, 6(4), 262–265. http://doi.org/10.4274/jcrpe.1450

  9. Lombardo, F., Messina, M. F., Salzano, G., Rabbone, I., Lo Presti, D., Calcaterra, V., Aversa, T., De Luca, F. & Wasniewska, M. (2011). Prevalence, presentation and clinical evolution of graves' disease in children and adolescents with type 1 diabetes mellitus. Hormone Research in Paediatrics, 76(4):221-5. doi: 10.1159/000327587. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/21811047

  10. Matos‐Santos, A. , Nobre, E. L., Costa, J. G., Nogueira, P. J., Macedo, A. , Galvão‐Teles, A. & De Castro, J. J. (2001). Relationship between the number and impact of stressful life events and the onset of graves' disease and toxic nodular goitre. Clinical Endocrinology, 55, 15-19. doi:10.1046/j.1365-2265.2001.01332.

  11. Nikkilä, E. A. & Kekki, M. (1972). Plasma triglyceride metabolism in thyroid disease. The Journal of clinical investigation, 51(8), 2103-14. Retreived from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC292367/

  12. Radosavljević, V. R., Jankovićand, S. M. & Marinković, J. M. (1996). Stressful life events in the pathogenesis of graves' disease. European Journal of Endocrinology, 134(6), 699-701 https://doi.org/10.1530/eje.0.1340699

  13. Robinson, J., Waller, M. J., Parham, P., DeGroot, N., Bontrop, R., Kennedy, L. J., Marsh, S. G. E. (2003). IMGT/HLA and IMGT/MHC: Sequence databases for the study of the major histocompatibility complex. Nucleic Acids Research, 31(1), 311–314. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC165517/

  14. Saladin, K. S.(2015). Anatomy and physiology: The unity of form and ( 7th Ed.). NY: McGraw-Hill Education

  15. Thyroid Stimulating Immunoglobulin (TSI), Serum. (n.d.) Mayo Clinic Laboratories. Retrieved from https://www.mayomedicallaboratories.com/test-catalog/Clinical+and+Interpretive/8634

  16. Weetman, A. & DeGroot, L. J. (2016) Autoimmunity to the thyroid gland. In: De Groot LJ, Chrousos G, Dungan K, et al., editors. Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000-. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK285552/

  17. Winsa, B., Karlsson, A., Bergstrom, R., Adami, H. O., Gamstedt, A., Jansson, R., Adamson, U. & Dahlberg, P. A. (1991). Stressful life events and graves' disease. The Lancet, 338(8781), 1475-1479. https://doi.org/10.1016/0140-6736(91)92298-G


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