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Hashimoto’s Autoimmune Thyroiditis

Hashimoto’s Autoimmune Thyroiditis

By Virginia Blake

Incidence

Hashimoto’s autoimmune thyroiditis accounts for around 90% of underactive thyroid diagnoses in the developed world. It can be diagnosed quite late into the disease. This is because thyroid function may appear normal on test results despite the patient feeling that there is something wrong and having symptoms, often over a period of many years. (Aijan & Weetman, 2015).

The incidence of the condition is estimated at 0.8 in 1000 men and 3.5 in 1000 women (Pyzik et al., 2015).

Standard thyroid function tests in primary care do not assess autoimmune reactivity as a matter of course. Testing for antibodies is not a first line recommendation in the NHS and monitoring of antibodies is not recommended (NICE, 2021).

 

Pathophysiology

Recent work has shown that development of the condition is dependent on three factors:

  • an immune defect (e.g. a lower number of Tregs cells and altered protein and receptor expression on these Tregs)
  • genetic susceptibility
  • and an environmental trigger. (Hu et al., 2019)

As with all autoimmune illness, there are 3 stages in the disease process:

 

Stage 1

Silent Autoimmunity - Elevated thyroid peroxidase antibodies (TPOAb) and/or thyroglobulin antibodies (TgAb) with no symptoms or loss of tissue

 

Stage 2

Autoimmune Reactivity - Elevated TPOAb and or TgAB with symptoms and normal TSH levels

 

Stage 3

Autoimmune disease - Elevated antibodies with symptoms, measurable tissue destruction, and elevated TSH 

Thyroid peroxidase is the enzyme in the thyroid that facilitates the production of thyroid hormone. Thyroglobulin is the base protein from which thyroid hormones are made (Boron & Boulpaep, 2003) 

For diagnosis of Hashimoto’s thyroiditis, TPOAb are more relevant than TgAb. TgAb are found in approximately 10% of women. TgAb are also found in many other conditions – present in 50% of Grave’s disease, 20% of thyroid cancer and non-toxic goiter. They can also be found in autoimmune diseases not related to thyroid, such as coeliac disease, type 1 diabetes, Sjogren’s and myasthenia gravis. (Soh & Aw, 2019). Clinically, increased levels of TgAb with in range TPOAb should still be addressed.

Along side the damage to thyroid tissue, the inflammation results in down regulation of 5’deiodinase, and reduced conversion of T4 to T3. Inflammatory cytokines, free radicals and dysregulated hormones such as super oxide anion, hydroxyl radical, hydrogen peroxide and peroxynitrite, increasing production of leptin, TNF-alpha IL1, IL6, interferon gamma, and free fatty acids all work to reduce conversion of T4 to T3 (Mancini et al., 2016).

Inflammatory cytokines also disrupt docking of T3 hormone to target cell. This can explain normal lab results but presence of hypothyroid symptoms. Circulating hormones are in range, but are not attaching to their target cell (Boelen et al., 2011)

 

Symptoms

Symptoms of Hashimoto’s are many and varied as thyroid hormone has system wide effects, but the most commonly reported with normal thyroid function tests in clinic are:

  • General Fatigue – poor work out ability, work out recovery
  • Depression and poor brain function
  • Insomnia
  • Anxiety
  • Chronic constipation – IBS
  • Symptoms dismissed or not believed when reported in primary care setting.

The following symptoms may also be present with normal thyroid function tests and also once the antibodies have triggered damage that registers with raised TSH levels:

Dry hair, puffy face, constipation, depression, eyebrow thinning, enlarged thyroid, slow heart rate, cold intolerance, dry skin, fatigue, forgetfulness, menstrual disorders, infertility, muscle aches, weight gain, brittle nails, cracked heels. (Amino 1988).

In clinic, when assessing fatigue, infertility or mental health disorders, thyroid autoimmunity should be ruled out. Consider thyroid dysfunction in common digestive disorders seen in the NT clinic.

 

Review of triggers and mediators (bacterial, viral, environmental, food etc.)

Once autoimmune thyroid is found, a key area for the Nutritional Therapist to focus on is finding underlying triggers for the condition and factors that contribute to on-going inflammation (mediators).

A full case history and then deciding on the appropriate test, targets the anti-inflammatory strategy. This should increase T4 to T3 conversion and increase T3 docking to receptors in target cells, thus exerting the desired effect of this master hormone.

Below is a table which summarises currently understood triggers and mediators.

Triggers / Mediators for AITD

Dietary Proteins

Lifestyle Factors

Chemicals

Pathogens

Gluten (Virili et al., 2012)

Insomnia (Radomski et al., 2021)

Bisphenol A (Somogyi et al., 2016)

Pesticides (Leeman et al. 2019)

Air pollution

Fire retardants

Benzene

PCBs PBDE Perchlorate

(Benvenga et al., 2015)

H pylori (Figura et al. 1999; Figura et al. 2019)

Sodium (Wen et al., 2016)

Sedentary lifestyle (Radomski et al., 2021)

Mercury (Rezaei et al., 2019)

Toxoplasma Gondii (Tozzoli et al. 2008)

Iodine (Zaletel & Gaberscek, 2011)

Overtraining (Radomski et al., 2021)

Yersinia Enterocolitica (Chatzipanagiotou et al., 2001)

Lectins (Vojdani et al., 2020)

Smoking? (Sawicka-Gutaj et al., 2014) (may be a trigger in Grave’s, protective in Hashimoto’s)

Candida albicans (Vodjani et al. 1996)

Decreased dietary diversity (Ishaq et al., 2017)

Alcohol (Dong & Fu, 2014)

Epstein-Barr virus

Cytomegalovirus

Herpes-virus -6

Parvovirus B-19

Hepatitis C (Mori & Yoshida, 2010)

Dietary protein cross-reactivity  Pro-inflammatory diet Grains Casein Albumin

(Kharrazian et al., 2017)

Drug use

Lack of rest (Radomski et al., 2021) Stress (Markomanolaki et al., 2021)

Clostridium Botulinum (Gregoric et al., 2010)

Borrelia Burgdorferi (Benvenga et al., 2004)

Sars-Cov2 (Vojdani & Kharrazian, 2020)

 

Deciding which tests to run

Intake forms and detailed case history will help to decide which test(s) to run. Our support team can also advise on appropriate tests. Book a call to discuss the case and decide next steps.

Thyroid Assessment

Thyroid Monitor and Home Vitamin Test – Finger prick test that assesses thyroid function, antibodies, inflammatory markers and key micronutrients for thyroid function 

Full range of thyroid tests can be found here.

Pathogens

Stool Testing (for pathogens and for digestive function):

Consider if there are digestive symptoms and/or increasing weight.

GI360 – provides pathogen, parasite, virus, commensal PCR, expanded parasitology, microscopy, bacterial and fungal cultures and sensitivities, digestive markers, inflammatory markers and microbiome  and gut health markers. 

Comprehensive Stool Analysis – as above but without PCR 

H.Pylori add on

Full range of stool tests can be found here.

Cyrex Array 12 – Pathogen Associated Immune Reactivity Screen 

 

Chemicals

Toxic  Metals

Mercury Tri test, looks at mercury in hair, blood and urine, giving excretion rates and likely levels of storage/ exposure.  

Toxic metals – hair, urine (27 different metals), faecal, blood. Book a support call to decide the best medium to measure, e.g. aluminium is better measured in urine, faecal metal may be more useful for recent exposures.

Environmental Pollutants

Great Plains - Urine assessment of environmental exposure including plastics, PBDEs, petrochemicals and mould. 

Cyrex Array 11 Chemical Immune Reactivity Screen

Food Sensitivity testing

Precision Allergy 88 Food Sensitivity Testing – Precision Diagnostics. Unique on the UK market, combines IgE, IgG4, IgG and complement assessment to 88 foods. Serum sample requiring blood draw. 

Precision Dietary – IgA antibodies to 88 foods measured in saliva 

Cyrex Array 3x – Wheat Proteome Reactivity and Autoimmunity

Cyrex Array 4 – Gluten Associated Cross Reactive Foods and Food Sensitivity

Cyrex Array 10 – Multiple Food Immune Reactivity Screen

 

References

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Amino, N. (1988). 4 Autoimmunity and hypothyroidism. Baillière's Clinical Endocrinology And Metabolism, 2(3), 591-617. https://doi.org/10.1016/s0950-351x(88)80055-7
Boelen, A., Kwakkel, J., & Fliers, E. (2011). Beyond Low Plasma T3: Local Thyroid Hormone Metabolism during Inflammation and Infection. Endocrine Reviews, 32(5), 670-693. https://doi.org/10.1210/er.2011-0007
Benvenga, S., Antonelli, A., & Vita, R. (2015). Thyroid nodules and thyroid autoimmunity in the context of environmental pollution. Reviews In Endocrine And Metabolic Disorders, 16(4), 319-340. https://doi.org/10.1007/s11154-016-9327-6
Benvenga, S., Guarneri, F., Vaccaro, M., Santarpia, L., & Trimarchi, F. (2004). Homologies Between Proteins of Borrelia burgdorferi and Thyroid Autoantigens. Thyroid, 14(11), 964-966. https://doi.org/10.1089/thy.2004.14.964
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