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.. 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..
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. .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. .
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. . 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. . 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. .The second pathway is genetic and involves the HLA-DR class II receptors. . 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). .
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. .
Braun et al. (2017) categorize Graves Disease as a type II hypersensitivity of the immune system. . Type II hypersensitivity is when the antibodies are directed against the thyroid gland itself. . 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. .
With all areas evaluated, Braun and colleagues (2017) state that there are many reasons for autoimmunity to develop. . 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). . 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. . 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. .
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. . Anxiety, rapid and irregular heartbeat, increased sweating, increased appetite, and irregular menstrual in women are other symptoms that may be experienced. . Other signs that are noticed in patients with Graves disease and considered by practitioners can be ophthalmopathy (i.e., protrusion of the eyes). .
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. . Weetman et al. (2016) also list autoimmune diseases in connection to Graves disease as alopecia, vitiligo, myasthenia gravis, and Sjögren's syndrome. .
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. .
Patient history and physical examination are considerable ways to diagnose Graves' disease. . 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 thyroi