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Hashimoto’s: What Causes It?

Firstly, you may like to read my article on autoimmune disease, found here, alongside this article on the autoimmune thyroid condition, Hashimoto’s.

While research has looked in to the genetic link, there are clearly environmental factors triggering/involved in thyroid autoimmunity:

  1. Nutrients
    1. Iodine
    2. Selenium
    3. Iron
    4. Zinc
    5. Vitamin B12
    6. Vitamin D
  2. Pollutants
    1. Organochlorines
    2. Pesticides
    3. Metals
  3. Irradiation
  4. Drugs
    1. Interferon- and TNF-
  5. Pregnancy
  6. Infections
    1. Yersinia enterocolitica
    2. Coxsackie B virus
    3. Hepatitis C virus
    4. Retroviruses
    5. Helicobacter pylori
  7. Stress
  8. Lifestyle
  9. Smoking
  10. Obesity

Sex hormones appear to be the most important according to Jansen et al. (2004), this is largely down to the fact that, compared with men, women have a five- to ten fold higher prevalence of autoimmune thyroid disease. Others have shown a strong correlation with Yersinia and Hepatitis C. As always this demonstrates the importance of testing and personalising treatment accordingly.

It is known that patients with TPO and TG autoantibodies are likely to develop thyroid dysfunction later in life.


The diagnosis of Hashimoto thyroiditis is currently established by a combination of clinical features, presence of serum antibodies against thyroid antigens (mainly to thyroperoxidase and thyroglobulin), and
appearance on thyroid sonogram.

Circulating antibodies to thyroperoxidase are now considered the best serological marker to establish a diagnosis of HT. They are found in about 95% of HT patients but are rare in healthy controls (Caturegli et al., 2014).


Mechanism(s) linking deterioration of cellular antioxidant defense to the pathogenesis of autoimmune thyroiditis is not fully clear.

  1. One theory is around oxidative stress and how overproduction of reactive oxygen species (ROS) is the main event leading to apoptosis and cell necrosis (cell death) and eventually thyroid dysfunction. Elevated ROS beyond that needed for the activation of normal biochemical processes would deplete cellular antioxidants including glutathione.
  2. Another theory involves inflammation as a result of the adipokines, especially leptin, TNF-α, and IL-6, and receptors, called Toll-like receptors (TLR)  present on thyrocytes (thyroid cells). There are able to recognize pathogen-associated molecular patterns (PAMP’s) and damage-associated molecular patterns (DAMP’s). The adipokines are produced by adipose tissue, but have hormone-like and immune modulating properties. As the levels of leptin are significantly higher in females, an explanation for the sex difference in thyroid autoimmunity emerges (Merrel & Mu, 2015).

Two main theories have been proposed for the induction of autoimmunity by infectious agents:

  1. The molecular mimicry theory suggests that sequence similarities between viral proteins and self proteins can induce a cross-over immune response to self antigens
  2. The bystander activation theory proposes that viral infection of a certain tissue can induce local inflammation (e.g. by cytokine release), resulting in activation of autoreactive T-cells that were dormant or suppressed by peripheral regulatory mechanisms. While evidence for molecular mimicry between Yersinia proteins and thyroid antigens exists, these data have not been confirmed. Recent data favor the bystander activation as the predominant mechanism viral agents trigger autoimmunity in autoimmune thyroiditis.

Recently, we have shown that the HCV virus can activate cytokine secretion by thyroid cells (Tober & Humer, 2009)

Things To Be Mindful Of:

Vitamin B12

Autoimmune thyroid disease is also associated with the autoimmune disorders pernicious anemia and atrophic gastritis which may lead to malabsorption of vitamin B-12.

Vitamin B-12 screening is recommended upon initial diagnosis with autoimmune thyroid disease and then periodically thereafter (Collins, 2016)

Peripheral Metabolism

Lifestyle factors, such as stress, caloric restriction, and exercise, influence peripheral metabolism of thyroid hormones. Exposure to toxic metals, chemical poisons, and several drugs can also influence the peripheral fate of thyroid hormones (Kelly, 2000)

PCOS & Hashimoto’s

This prospective study demonstrates a threefold higher prevalence of autoimmune thyroid disease in patients with PCOS (Jansen et al., 2004).

It may be speculated that the imbalance of normal to high estrogens and low progesterone levels, the socalled ‘unopposed estrogens’ thought to be responsible for the apparent increase in prevalence of autoimmune thyroid disease during the menopause, also account for the higher prevalence of autoimmune thyroid disease in PCOS.

The Thyroid & Cardiovascular Health

Thyroid hormones increase the expression of LDL receptors on the hepatocytes, and increase the activity of lipid-lowering liver enzymes, resulting in a reduction in low-density lipoprotein levels (Malik & Hodgson, 2002)

Gluathione & Hashimotos

This is the first study to demonstrate a substantial reduction in GSH status in HT subjects (Rostami, 2013)


Some clinical studies have demonstrated that selenium-deficient patients with autoimmune thyroid disease benefit from selenium supplementation, although the data are conflicting and many parameters must still be defined (Schomburg , 2012)


It was identified as a hormone involved in appetite control through the leptin receptor.Leptin, produced in white adipose tissue, affects appetite through a negative feedback loop involving the leptin receptor in the hypothalamus. It is now known that leptin is one of a number of hormones, the adipokines, which have many functions – most having some impact on the thyroid (Cinar and Gurlek, 2013).

One effect is both to alter thyroid function through disruption of the feed back loop of the HPT axis by altering TRH (Duntas and Biondi,2013).

A second effect is through inflammation and inflammatory molecules (Merrel & Mu, 2015)


When including all blood metals, mercury was associated with decreases in T3 and T4, while cadmium
was associated with decreased TSH. Urinary cadmium was associated with increases in both T3 and T4
(models including all metals measured in urine). Urinary thallium and barium were associated with
decreased T4 (both) and T3 (barium). For TSH, cesium was associated with decreased, and tungsten with
increased levels. Given the high prevalence of exposure to metals, associations of the size reported here
could indicate an appreciable contribution of metals exposure to the prevalence of thyroid disorders (Christensen, 2013).

Clinical Features (Caturegli et al., 2014)

Gastrointestinal systemConstipation is the most common complaint reported by hypothyroid patients. Peristalsis is markedly decreased and can lead to occasional pseudo-obstruction or ileus. Gallbladder hypotonia and alterations in bile composition may result in increased bile duct stone formation.

Skin and appendages: The skin of hypothyroid patients is typically dry, cold, yellowish, and thickened. These changes are sustained by accumulation of hydrophilic mucoproteins (such as hyaluronic acid) in the derma with consequent myxedema, as well as by the atrophy of sweat glands. The hairs are coarse and fall off. The nails are thin and frail.

Cardiovascular system: Bradycardia and decreased amplitude of cardiac waves on the electrocardiogram are classic signs of hypothyroidism. Bradycardia, decreased ventricular contractility, and increased peripheral resistance contribute to an overall reduced cardiac output. Cardiomegaly may be present and accompanied by pericardial effusion. Coronary artery disease is common in patientswith hypothyroidism, likely due to the effect of thyroid hormones on lipid metabolism. Hypothyroidism, in fact, decreases cholesterol and LDL cholesterol levels, well-known atherogenic factors.

Skeletal muscles: Muscles appear falsely hypertrophic due to the myxedematous infiltration of the connective tissue. Their contraction and relaxation times are delayed, and can be a source of pain and cramps.

Pulmonary system: Common respiratory abnormalities are bradypnea and hypoxia. They originate from obstruction of the upper airways by the enlarged soft tissues, respiratory muscle weakness, decreased chest wall and lung compliance, increased capillary permeability, and pleural effusion. Respiratory failure can occur in patients with myxedematous coma.

Hematopoietic system: Anemia is common in hypothyroidism. It can be normocytic (due to a reduction in the renal secretion of erythropoietin), hypo chromic and microcytic (due to a defect in iron absorption), or megaloblastic (due to gastric atrophy with B12 vitamin malabsorption).

Reproductive system: Oligomenorrhea and/or menometrorrhagia are frequent. Menstrual cycles are often anovulatory due to impaired conversion of estrogen precursors. When hypothyroidism is present during pregnancy it has been associated with an increased rate of miscarriage.

Urinary system: Liquid retention from decreased glomerular filtration is described.