How does Hashimoto's Disease Start?

Oct 28, 2010
Sarah Tomley

Hashimoto's disease has a genetic factor - Petros Perros

The onset and development of Hashimoto's disease, the autoimmune form of thyroiditis, is a curious mixture of genes and environment.

Thyroid autoimmune diseases are polygenic – this means that they occur as part of a multiple gene inheritance, which is why autoimmune disease tends to run in families. Autoimmune diseases such as Hashimoto's are thought to occur when a particular group of genes exist together and then start to interact with each other and their environment. This means that genetic and environmental abnormalities have to actually converge before a full-blown autoimmune disease can develop, but unfortunately this seems to happen far too often.

The Four Stages of Hashimoto's Disease

In Hashimoto's, or autoimmune thyroid disease, the disease goes through four stages:

Stage 1: This may be induced by an environmental trigger such as dietary iodine, viral infection or toxins. The triggering factor causes insult to the thyrocytes (the hormone-producing cells of the thyroid), and the release of thyroid-specific proteins, which in turn serve as self-antigenic peptides that sit on the cell surface of the Antigen-presenting cells [APCs].
Stage 2: Now loaded with autoantigens, the APCs travel from the thyroid to the draining lymph nodes, and begin to interact with autoreactive T-cells, and B-cells; this interaction results in the production of thyroid autoantibodies (the TPOs tested for diagnosis of Hashimoto's disease).
Stage 3: Antigen-producing B-cells, macrophages, and cytotoxic T-cells infiltrate the thyroid gland, and accumulate there (this process is mediated by cytokines – signalling molecules).
Stage 4: In this stage large numbers of autoreactive T cells, B cells, and antibodies cause massive depletion of thyrocytes – the cells in the thyroid gland that produce and secrete thyroxine (T4) and triiodothyronine (T3). This ultimately results in the autoimmune destruction of the thyroid. (1)

At each stage, numerous factors – from both inside and outside the body – can cause the abnormalities that are characteristic of that stage. And each stage is one step towards the development of thyroid autoimmune disease.

Signalling Immunity and Autoimmune Thyroiditis

The body's signalling devices are also thought to play a huge part: during the initial attack of stage 1, the body is thought to activate TLR3s – toll-like receptors that recognize double-stranded RNA and signal an increase in cytokines, setting off a chain of immune reactions; an overexpression of TLR3s seems to be implicated in autoimmune disease. The blocking of the signalling and overexpression of TLR3 by the introduction of MMI or C10 is one route now being considered as one potential means to slow or disrupt the process of Hashimoto's disease (autoimmune thyroiditis)(2), although TLR signalling is complex and is not yet entirely understood. Interestingly, one study found TLR3 protein in the thyrocytes of 100% of the patients tested with Hashimoto's thyroiditis, but not in thyrocytes of healthy people, not those suffering from Graves' disease. (2)

The Role of Iodine in Hashimoto's Disease

Iodine is an important external factor in thyroid autoimmune disease, acting as a modulator at every stage of the disease process. Weirdly, although iodine deficiency is a common cause of hypothyroidism, in the case of Hashimoto's disease – autoimmune thyroid disease – iodine excess actually accelerates the process (1); while iodine deficiency slows down disease progression. The message is clear: iodine consumption should therefore be limited in anyone with Hashimoto's disease, and iodine-rich foods, such as seaweeds, should be avoided.

How Does Iodine Worsen Hashimoto's Disease?

It seems that iodine interferes at several stages during the autoimmune process, particularly in the first (afferent) and last (efferent) stages. At these points, iodine is thought to cause alterations in the metabolism of the thyrocyte cells – the cells in the thyroid gland that make and secrete the thyroid hormones (T4, T3) – and may even cause necrosis (cell death).

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References:

"Iodine and Thyroid Autoimmune Disease in Animal Models "; C. Ruwhof, H.A. Drexhage; Thyroid. May 2001, 11(5): 427-436.
"Thyrocytes Express a Functional Toll-Like Receptor 3: Overexpression Can Be Induced by Viral Infection and Reversed by Phenylmethimazole and Is Associated with Hashimoto’s Autoimmune Thyroiditis"; Norikazu Harii, Christopher J. Lewis, Vasilly Vasko, Kelly McCall, Uruguaysito Benavides-Peralta, Xiaolu Sun, Matthew D. Ringel, Motoyasu Saji, Cesidio Giuliani, Giorgio Napolitano, Douglas J. Goetz and Leonard D. Kohn; Molecular Endocrinology 19 (5): 1231-1250