Hashimoto's thyroiditis: a primer
Updated: May 19
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Hashimoto's thyroiditis (HT), also known as chronic lymphocytic thyroiditis, or simply Hashimotos, is an autoimmune disorder along the spectrum of autoimmune thyroid diseases (AITDs). HT affects the thyroid gland in specific ways and culminates as a condition of chronically low functioning (hypo) thyroid (hypothyroidism). This state of low functioning thyroid results in a cascade of downstream, typically non-specific (i.e. ascribable to other disorders) symptomatology, ranging from fatigue and slowed movement, to memory loss, or constipation, dry skin, weight gain, cold intolerance, puffy or swollen face, decreased sweating, mild deafness, nerve damage in the extremities, joint and muscle pain, throat swelling and goiter, voice hoarseness, hair loss, irregular menstruation, sleep disturbance, depression, dementia, and a range of other psychiatric disturbances [1-10].
Antecedents, Mediators, Triggers (ATMs)
ATMs are factors or agents that are component or integral in the development and continued state of autoimmune disorders. Functioning as initiating or triggering events, ATM's also exacerbate a state of disease via setting the right conditions to mediate, perpetuate, and sustain a state of body dysfunction. ATMs, therefore describe the pathogenesis of a disease; the manner in which disease develops and the factors that sustain it.
The thyroid is a butterfly shaped, hormone-producing endocrine gland found in the lower front-facing position of the neck. By virtue of producing and secreting thyroid-specific hormones (triiodothyronine [T3], thyroxine [T4], and calcitonin), this gland functions within a vital, homeostatic (balancing) capacity, triggering critical physiologic functions such as metabolism, digestion, heart rate, body temperature, menstruation, wound healing, and body weight.
HT appears to be a multiplex of converging factors (ATMs) manifesting as chronic inflammation of the thyroid, leading hormonal dysregulation, culminating as a constellation of the aforementioned signs and symptoms (S/S), and resulting in chronic hypothyroidism. In short, the pathogenesis of the disease. So what are these factors? What causes thyroid inflammation and low functioning thyroid in the first place? In HT, the initiating or mediating factors appear to be a combination of ATMs ranging from genetic susceptibility, to other antecedent or triggering autoimmune conditions, along with environmental, dietary, and lifestyle factors. For example, preexisting autoimmune diseases, viral infections, medications, ionizing radiation, chronic stress, excess or insufficient iodine consumption, or large amounts of animal protein (potential sources of arsenic and mercury) may all be contributing factors. Moreover, HT itself may function as a triggering condition leading to, or mediating the onset and progression of other autoimmune diseases (comorbidities).
Regardless the multitude of potential ATMs, a common factor in all forms of autoimmune dysfunction is the presence of autoantibodies and their role in the development and progression within the state of disease. So what are autoantibodies? The immune system (IS) has a very specific job, to respond to the presence of ATMs deeming them harmful or "friendly", and thereby acting accordingly. Part of this immune response to ATMs is made possible via antibodies. Thus when the IS identifies an ATM as harmful it will respond via the release of chemical agents called antibodies which function as "markers", tagging potentially unfriendly agents and allowing other components of the IS (white blood cells [WBCs]) to act accordingly, effectively destroying what has been deemed harmful. However, in the case of autoimmunity the IS can overreact, erroneously tagging friendly agents as "foe" and leading to an attack upon self-tissues. In the case of HT, genetic susceptibility appears to play a major role in the development of a specific subset or type of autoantibodies called ant-thyroid antibodies (ATA): anti-thyroid peroxidase (anti-TPO) and anti-thyroglobulin (anti-Tg) antibodies. ATAs therefore, are antibodies produced by the IS itself, leading to an IS-mounted attack upon the thyroid gland (self-tissue), and progressing to thyroid tissue inflammation, tissue destruction, and chronic hypothyroidism [1-10].
Diagnosis and Laboratory Testing
As mentioned previously, the thyroid makes three main hormones: T3, T4, and calcitonin; collectively known as thyroid hormones (THs); T3, the bioactive form colloquially referred to as (the) thyroid hormone (TH). Integral to achieving homeostatic balance, THs are very tightly regulated. This regulation of the thyroid is achieved via feedback from the hypothalamus and pituitary gland; overseeing how much and how often the thyroid releases THs. Refer to graphic, Thyroid Hormones_Schnur, M. (2018).
Thyroid Hormones_Schnur, M. (2018)
Given the multitude of potential ATMs, non-specific S/S attributable to HT, and compounded by the complexity of the thyroid gland itself, diagnostic criteria must assess many interrelated physiologic data points to attain an accurate and true depiction of probable chronic autoimmune disease; in contrast to a sub-clinical, or potentially transient or acute thyroid issue.
Diagnostic and differential criteria must account for factors that "fit" the picture of HT and rule out those that do not. Therefore, assessing thyroid function to discern the presence, progression, and state of HT should fit a combination of the following clinical features: (i) patient medical history (antecedent/ family history/ genetic susceptibility), (ii) any combination of the aforementioned S/S, (iii) blood, or serology testing of (a) complete blood count (CBC); assess for presence of anemia (common in HT), (b) Thyroid and Pituitary hormone levels (TSH, T3, T4, rT3, rT4); low or high levels outside the reference range will inform disease diagnosis (c) the presence of thyroid antibodies (anti-TPO, anti-Tg), (iv) inflammatory markers (CRP, Prolactin; often found elevated in HT), (e) metabolic function indicators (GFR; assess kidney function), (v) ultrasonogram to assess size and presence of thyroid nodules, and (vi) histology, fine-needle aspiration to exam thyroid cells for the presence and extent of tissue damage [1-10].
Given the over-reactive immune activity and inflammatory component of HT, a strategy that aims to address these aspects should be the focal point of any dietary therapy. Moreover, key nutrients such as iodide/ iodine, iron, selenium, vitamin D, and B vitamins that appear to be vital in optimal thyroid function, should also be incorporated into any dietary approach.
Before proceeding to the dietary strategy discussion, consider the following few points of interest regarding nutritional supplement support for thyroid function. The literature has shown mixed results with regard to Selenium (Se) or Iodine/ Iodide (I). For instance, systematic reviews of the available literature suggest significant improvement in TPO antibodies [11, 12]. Notwithstanding, other studies show little to no effect [13, 14], while others have suggested an association between Se intake and normalization in TSH levels . When considering Iodide/iodine and thyroid function, the literature is also largely heterogeneous. For instance, although iodine deficiency is typically associated with hypothyroid and goiter development, hyper nutrient intake has also been associated with thyroid dysfunction [16-21]. What’s the takeaway here? First, it would be ill-advised to self-administer high dose nutritional supplementation for thyroid dysfunction without first consulting your physician. Second, a safe strategy to address any potential nutritional deficiencies is to adopt a dietary pattern that promotes high intakes of nutrient dense foods such as the Autoimmune Protocol (AIP).
In a prospective cohort study, 17 female subjects with HT participated in a 10-week co-therapeutic health-coaching and Autoimmune Protocol (AIP) dietary intervention. Metrics and measures included, pre/post Medical Symptoms Questionnaire (MSQ), health-related quality of life (HRQL), serology testing of (a) complete blood cell count (CBC), (b) complete metabolic profile (CMP), (c) Thyroid function panel, and (d) high-sensitivity C-reactive protein (hs-CRP). Post intervention, a significant improvement in HRQL (p<0.001), as well as significant decrease in inflammation (CRP; p=0.037) and mean reduction in overall immune activity (WBC; p=0.1396). Notwithstanding, no improvement in thyroid markers were observed. From these data, Abbott, et al. (2019) suggest these AIP and health-coaching can significantly improve HRQL as well as decrease systemic inflammation and lower immune activity .
In a single case-study, a 49-year old obese woman with HT was recommended a modified AIP of 1200kcal/day, for 6 months as a dietary strategy in the management of her disease. Al-Bayyari, (2020) noted significant reduction of BMI, and dyslipidemia (p<0.05) along with improvement in HDL and fasting insulin. Moreover, there was a marked improvement in thyroid TSH and TPO markers .
Finally, to posit concluding assertions to be taken into account regarding the therapeutic utility of any dietary intervention, the following should be strongly considered. First, and most importantly, participants within the discussed studies were all on physician prescribed thyroid medication. Therefore, it would be unwise to assume that maintenance or any noted improvement in thyroid markers could be solely, if at all attributable to dietary modalities. Clearly more studies are needed in this area. Second, and pursuant to the first point, it should be understood that a dietary intervention such as AIP is not a replacement for correcting, or "fixing" thyroid dysfunction (i.e. thyroid disease, hormone dysregulation, tissue destruction) but rather it should be used as a co-therapy, or adjunct to help ameliorate or assuage S/S of HT by virtue of attenuation of systemic inflammation and improvement of overall metabolic function. Therefore, with the objective of decreasing inflammation and autoreactive immune activity, adherence to a dietary intervention like AIP should be leveraged as a co-therapy, or a singular but foundational component within a multi-layered strategy toward the long-term management of HT.
- Dan Hansen Mission Healing Engage © 2021
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