Hashimoto’s is a lymphoproliferative autoimmune disease, where the body produces antibodies that attack the thyroid gland. But these antibodies can exist in the body for many, many years before causing damage to the thyroid or altering the levels of thyroid hormones in the body. So patients tend to come to medical attentiona long after the onset of the disease, often having suffered from unexplained symptoms and medical problems for many years. But this does not mean the autoantibodies are inactive in the body: they can affect many of the body’s systems, and cause problems with cholesterol levels, infertility, and miscarriage, among others.
Autoimmune thyroiditis (AITD) accounts for over 90% of hypothyroidism in iodine-sufficient countries. Women are 5–10 times more likely to be affected, typically at 50–60 years of age – whether this reflects the onset of Hashimoto’s, or merely the start of the end game is not reflected in the research data. We do know that autoimmune hypothyroidism runs at around 1–2% amongst the world’s white population, whereas the thyroid antibodies (indicative of Hashimoto’s) can be found in up to 20% of these women. (2)
Scientists have also found that AITD can be initiated in individuals who are genetically predisposed to it by non-genetic (environmental) triggers, such as dietary iodine, infection, pregnancy, or cytokine therapy. (6)
How the Thryoid Suffers Under Hashimoto’s Attack
In Hashimoto’s the thyroid becomes increasingly under attack. Sometimes many years after the detection of thyroid antibodies, it starts to undergo a “dense infiltration” – an intrusive invasion – of lymphocytes, plasma cells, and macrophages, and germinal centre formation. Thyroid follicles are progressively destroyed, all the while changing during this destructive process: the cells undergo hyperplasia and oxyphil metaplasia. There is a variable degree of fibrosis, and by the end stage – myxedema – the normal lobular architecture of the thyroid is destroyed and there is extensive fibrosis.
The Many Types of Antibodies Involved in Hashimoto's
High numbers of circulating autoantibodies against Thyroglobulin (TG) and thyroid peroxidase (TPO) are found in people with Hashimoto’s. Less well known is that around 20% of patients also demonstrate TSH-receptor blocking antibodies; and 15–35% of Hashimoto’s patients even have autoantibodies against T4 and T3. (3) Autoantibodies against other thyroid-specific antigens such as thyrotropin receptor and sodium iodide symporter were also found in serum of Hashimoto’s patients (5), though these occured at low frequency. Hashimoto’s patients may also develop antibodies against pituitary antigens.(4)
Associated Diseases
Hashimoto’s often coexists with other autoimmune diseases and conditions, including: Sjogren syndrome, rheumatoid arthritis, SLE, type 1 diabetes (T1D), celiac disease, rheumatoid arthritis, multiple sclerosis (MS), vitiligo, ataxia (memory loss), encephalopathy (stroke-like episodes, myoclonus, and cognitive impairment), and it confers an increased risk of lymphoma.
This means that if you have Hashimoto's, you have a greater risk of developing one of these conditions.
Hashimoto’s can also be expressed as part of an autoimmune polyendocrine syndrome (type 2/APS-2) – i.e. a syndrome defined by the occurrence of two or more of the following: Addison's disease (always present), AITD and/or type 1 diabetes in the same patient.
Autoimmune thyroiditis also commonly sits alongside antiphospholipid syndrome (also known as Hughes’ Syndrome), causing recurrent miscarriage and premature birth through a blood-clotting mechanism. High levels of thyroid peroxidase autoantibodies (as found in Hashimoto’s) during pregnancy has also been shown to dramatically increase the occurrence of postpartum thyroiditis.
Doesn’t Hashimoto’s Affect Cholesterol Levels, Too?
People with Hashimoto’s have been found to contain many immune complexes (ICs – combinations of protein antigens and specific antibodies) in their thyroid gland and blood. These natural antigen formulations circulate in the blood, and can cause dramatic disease such as vasculitis, and contribute to atherosclerosis. This is because the ICs found in Hashimito’s can trigger cholesterol ester accumulation in macrophages (white blood cells), causing activation of these cells, inflamation, and plaque formation(1).
Finding a Cure
As autoimmune specialists Noel Rose and Ian MacKay note, very little is really understood about the cause and development of autoimmune thyroiditis: “Despite two decades of research, the role of T-cell mediated, thyroid-specific immunoregulation in man is still unclear.” (7) Find out more about possible cures and potentially damaging vitamins.
NOTES
- “The autoimmune diseases”, Noel R Rose, Ian R MacKay, 4th Edition; Academic Press, 2006.
- Ibid, p.467
- Ibid, p.469
- Ibid, p.551
- “Immunogenetics of Hashimoto's thyroiditis”; Dimitry A Chistiakov; Journal of Autoimmune Diseases, 2005; 2:1.
- Christiakov, Ibid.
- Rose and MacKay, op cit, p.474
