(Caleb Greer, RN)

The American Thyroid Association estimates that 20 million Americans have some kind of thyroid disease, but due to the ambiguity of many of the symptoms, who knows how many are, undiagnosed or unaware of their ailment. Within the category of thyroid disorders lies Hashimoto’s disease, an autoimmune condition that can result in a wide array of symptoms. Historically, the disease was characterized by an infiltration of white blood cells into the thyroid tissue. Now, with more advanced techniques, diagnosis is dependent on the presence of antibodies to the thyroid tissues.

Hypothyroidism is one of the most frequent metabolic disorders we see in the clinic, and a majority of them have antibodies to their actual thyroid gland, which is definitive for Hashimoto’s disease. In these cases, there are a few components that we really dig into – genetic background, gut health, and pathogen load. While the major contributor to the development of this disease is inflammation, the source of the inflammation can come from many different places and will require different interventions to reach a solution. For antibodies to the thyroid to be made, the cells of the thyroid must first present the specific part, known as the antigen. There are two antigens that the immune system incorrectly recognizes as foreign in Hashimoto’s, thyroid peroxidase (TPO) and thyroglobulin (Tg). Why these proteins are tagged as foreign in the first place is not known; however, the literature suggests multiple different theories that revolve around the three components mentioned earlier.


In the immune system, there are many fail-safes to prevent autoimmunity, and it starts in an organ called the thymus. Without getting too deep into immunology, the thymus is the factory that makes a majority of antigen-presenting immune cells. When these cells are made there is a process by which their ability to recognize self versus foreign body is assessed – those who fail are destroyed and not allowed in circulation. Certain differences in some of the genes that encode antigen responsiveness and sensitivity lead to a greater susceptibility or even predisposition to autoimmune diseases like Hashimoto’s. Other under-functioning genetic variants that play a role in the development of Hashimoto’s are the vitamin D receptor and white blood cell receptors that regulate expansion. The (VDR) is involved pathways that regulate cell survival, pathogenic responses (including promotion of self-tolerance), membranous transport, and epigenetic modifications to DNA. When there is poor VDR function, all downstream signaling takes a hit, which results from problems in the aforementioned pathways – and just supplementing vitamin D won’t help. As for the latter variant, many of the immune cells have receptors that reduce further immune activation and can help control the responses, like a negative feedback loop. Unfortunately, some individuals have a genetic profile that under-expresses these receptors, which leads to an unbridled inflammatory cascade that can increase the likelihood of autoimmunity.

Gut Health

There has been a large buzz around the gut’s influence on the entirety of the body, and this has lead to an increased interest among clinicians and researchers alike. The link between intestinal health and integrity with autoimmunity is well established in the scientific literature and a majority of the conclusions regarding the ‘why’ establish inflammation as the cause. Inflammation in the gut can arise from a large number of things, from the food we eat to the medications we take, but an in-depth review is beyond the scope of this paper. Inflammation leads to intestinal permeability, often called leaky gut, which results in larger-than-normal molecules passing the gut immune system and getting tagged as foreign objects. Our body’s immune system is like the most strict immigration policy imaginable, meaning that any foreign body detected is tagged for removal. Pertaining to Hashimoto’s, many commonly consumed foods have proteins that have very similar sequences to TPO and Tg. So, if said foods or proteins get tagged for removal and antibodies are made for them, tissue cross-reactivity can occur, thus leading to tissue destruction and a perpetuated immune response. Gut issues can also lead to the manifestation of autoimmune-predisposing factors discussed in the previous section.

Pathogen Load

To piggyback on the previous section, all pathogens will, or rather should induce an inflammatory response from the immune system – it’s supposed to happen. Inflammation has been given a bad connotation, but in reality, it is a necessary tool that our body utilizes to maintain homeostasis. That being said, unresolved inflammation is the real enemy. Sustained inflammation has the nasty habit of reducing liver detoxification pathways, damaging the blood-brain and intestinal barriers, and disrupting normal signaling pathways. Everyone is exposed to various bacteria, viruses, molds, parasites, and other agents of infection throughout their lives, and very seldom are they ever truly eliminated. Viruses hang out inside cells, bacteria and mold hide behind biofilms, and other pathogens can even change forms to survive until more favorable host circumstances are had, i.e. stress, sleep deprivation, fatigue, nutrient deficiency, etc. All that being said, these passengers are continually eliciting a low-grade inflammatory signal that can take its toll when other environmental stressors weigh in as well. Aside from their contribution to cellular distress and inflammation, the evidence is being brought against viruses in the case of molecular mimicry – similar to how food derivatives become immunological agents of doom. Viruses have the daunting ability to change the expression of immune cell receptors and thyroid cells alike, which allows for increased susceptibility to destruction by the immune system. Increased tissue destruction results in more intracellular antigens being released into the surrounding areas, leading to a heightened chance for autoantigen binding and processing.


There are many pieces to this clinical puzzle – thyroid markers, viral and bacterial loads, genetic work up, and many more. Having one marker determine your path is as efficient as sailing with a broken compass. Your condition may fit the typical mold and it may not, it may be autoimmune, or it may be unfortunate tissue destruction at the hands of some other inflammatory activity. Hashimoto’s thyroiditis is a complicated disease process with many contributing factors, but the primary takeaway is that it all begins with inflammation. Inflammation from what? That is where your clinician comes in – that is where a journey to understanding your body starts, and that is a road that will lead you to optimal health.