When working to identify the root cause, we keep asking questions until we find the answer. So now we know that hyperthyroidism occurs because of thyroid destruction and that thyroid destruction occurs because of self-antibodies, why does the immune system make self-antibodies?
In addition to oxidative damage, immune cells may also be attracted to the thyroid as a result of a viral/bacterial infection that either infects the thyroid cells and needs to be cleared, or look similar to the thyroid cells, causing ‘Molecular Mimicry’.
An antigen is a substance that evokes the production of antibodies. Molecular Mimicry is the theory that bacterial cells or other microbes triggers off a similar appearance to the cells that make up parts of our physiology or self-antigens. When an infection occurs, these infectious cells are recognised as foreign. This is really great for getting rid of infections, sometimes the immune system targets proteins in infectious cells and resemble the proteins in our own cells. This inadvertently causes a cross-reaction with our self-antigens, i.e. our own cells. This case of mistaken identity is thought to trigger the start of autoimmunity.
In our experience, the biggest examples of this are viral infections. Various pathogens have been suggested to play a role in the development of Hashimoto’s ranging from bacteria to viruses to fungi and parasites. Often, it is not merely one type of bacteria or virus that triggers that autoimmune process, but a combination of pathogens present:
Bug X + Bug Y = Disease Z
Which bacterial and viruses have been associated with triggering autoimmune thyroiditis ?
A variety of bacterial infections have been implicated in triggering autoimmune thyroiditis including Helicobacter pylori (the same bacteria that causes ulcers) and Yersinia enterocolitica. Antibodies to Yersinia in people with Hashimoto’s have been found 14 times more often than in people without Hashimoto’s. Additionally, in our experience, the biggest single viral-cause in Hashimoto’s is Epstein Barr virus, regardless whether someone has had glandular fever or not in the past.
In addition to the foregoing and genetic susceptibility and other triggers, there is a third piece of the puzzle that must be present for Hashimoto’s or Graves’ to develop. This common link is present in all autoimmune conditions and gets closer to the root cause of the development of autoimmunity: increased intestinal permeability, aka, leaky gut.
So what does the gut have to do with the immune system and autoimmunity?
Everything! It is the intestinal lining that prevents autoimmunity.
Researchers have found, in addition to digesting and absorbing nutrients and keeping water and electrolyte balance, the intestine is also responsible for helping the immune system recognise foreign invaders from self-antigens, thus facilitating the control of pathogens preventing autoimmune reactions.
What exactly is leaky gut?
Leaky gut is an abnormally increased permeability of the small intestine. In leaky gut, the intestinal junctions become looser, allowing substances that normally would not gain systemic access to get into the circulation.
Once substances like food, bacteria and self-antigens get past the intestinal barrier into the circulation, the immune system recognises them as foreign substances and leads to inflammation of the body and gut, further increasing permeability and autoimmunity.
Testing for intestinal permeability is very simple and can be performed through Cyrex Array 2. This test will show epithelial cell damage, breakdown in the tight junctions or whether bacterial pathogens are breaching the gut lining.
For autoimmune thyroid patients, the incidence of Coeliac Disease is 1 in 20 and if you include lesser levels of gluten intolerance, possibly as many as one half of autoimmune thyroid patients may be gluten-sensitive. In our practice, we get all autoimmune clients off gluten as so many clients derive quick benefits from removing this completely from their diets. Additionally, gluten reactions may be a trigger for thyroid autoimmunity. In fact, in some cases, going gluten free may reverse an existing autoimmune thyroid condition. Secondly, Coeliac Disease may cause irregular absorption of thyroid medication.
Finally, we come back to our friend, Molecular Mimicry again. Because the molecular structure of gluten so closely resembles that of the thyroid gland, the problem may be one of mistaken identity.
Address adrenal connection
Chronic stress depresses thyroid function. High cortisol levels damage the hypothalamus long term, so when your hypothalamus sees chronic high cortisol levels, it sends hormones to the adrenal glands to turn down cortisol release. It also sends messages to your pituitary and thyroid to stop secreting thyroid hormone because it can’t handle anymore stimulation. Additional messages go to your muscles and other organs and they don’t respond as well to thyroid hormone, and also prevents your body from converting T4 to T3 efficiently.
Chronic stress is bad for thyroid function. If you’re prescribed thyroid medication and it makes you feel terrible, because you are stressed and your HPA (hypothalamus – pituitary) axis can’t handle it. You have to decrease stress and calm down the HPA axis before you add the hormone.
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