Hashimoto’s Thyroiditis | When the Thyroid gland makes sick

What is Hashimoto?

Hashimoto’s thyroiditis is a chronic inflammation of the thyroid gland, which inevitably leads to hypothyroidism with many ailments.

This disease is triggered by the body’s own immune system, while it attacks the thyroid tissue due to a misguided immune process and almost completely destroys it over time. Due to the misguided immune system and destroyed tissue, the thyroid gland is no longer able to produce and deliver enough thyroid hormones to the body.

Thus, in this autoimmune disease often occur severe symptoms of hypothyroidism, but also the autoimmune disease itself, comes with a whole series of complaints. Unfortunately, these are often not taken into account and left out of the patient’s therapy.

The course of Hashimoto’s disease varies enormously from patient to patient, so that some sufferers get along with the disease very well and only have few problems, while others are severely limited by the disease and have a strong symptomatology.

In addition, the Hashimoto thyroiditis occurs in recurrent attacks, so it is quite difficult to recognize at the beginning, since the signs of the disease alternate again and again, and so often can not be diagnosed with an absolutely clear clinical picture.

The tasks of a healthy thyroid gland

The thyroid gland, in technical jargon named Glandula thyreoidea or just Thyreoidea, is a small organ of significant importance. Especially when the thyroid gland is no longer able to produce the hormones T3 and T4. Thyroid hormones have a major impact on the body’s metabolism. They ensure that the body is either running at full speed or on a low flame.

Almost all vital functions and organs depend on a healthy thyroid gland. Such as energy consumption, body heat, mineral and water balance. They also influence children’s physical and mental development. But also the cardiovascular system, the gastrointestinal tract, as well as the nerves and muscles, are strongly influenced by the thyroid hormones. Last but not least, thyroid hormones also regulate the emotional wellbeing, sexual desire and fertility of both sexes.

What exactly happens with Hashimoto’s thyroiditis?

The thyroid gland is able to produce the thyroid hormones T1, T2, T3, T4 and calcitonin that are essential to us humans. The hormone calcitonin is produced in the C cells in the thyroid tissue and is responsible for the reduction of calcium in the blood.

HashimotoThyroiditis Butterfly

But the two best-known thyroid hormones are undoubted T3 and T4. The thyroid gland produces about 100μg T4 daily and up to 50μg T3. Both hormones have an iodine content. At the more durable and less metabolically active T4, an iodine atom is cleaved, to create the metabolically active T3.

The majority of both hormones are bound in the blood to the specific transport protein TBG (thyroxine-binding globulin). This special protein transports the thyroid hormones to the organs, and only a small fraction of the hormones is available as a free and unbound hormone. The free T3 (fT3) and free T4 (fT4). Only in the free and unbound form, the thyroid hormones do influence our metabolism.

The point of delivery to the blood and the amount of hormones stored in the thyroid are coordinated by the brain. For this the hypothalamus (a section of the diencephalon) and the pituitary gland are responsible. The hypothalamus releases a hormone called TRH (Thyrotropin Releasing Hormone), which directs the release of TSH (Thyroid Stimulating Hormone).

If the level of thyroid hormones in the blood is too low, the hypothalamus indicates with the help of TRH that the pituitary gland should release more TSH. The raised TSH, in turn, signals the thyroid gland to deliver more T1, T2, T3, and T4 into the bloodstream. This sophisticated feedback mechanism ensures that the healthy thyroid is always able to keep the concentration of thyroid hormones needed at a constant level.

In Hashimoto’s thyroiditis, this system no longer functions according to the above principle, and the entire control loop gets out of joint. Because Hashimoto’s thyroiditis is an autoimmune disease, the body falsely produces antibodies against its own thyroid gland, making it equivalent to viruses, bacteria, and other invaders. Over time, the thyroid gland is decomposed or getting smaller. Due to the shrinking thyroid tissue also the hormone production in the thyroid gland disappears, which inevitably leads to hypofunction (hypothyroidism).

The body then tries to increase the TRH and TSH to move the thyroid gland to produce the needed hormones. But since too little healthy, hormone-producing thyroid tissue is present, the thyroid gland simply is no longer able to produce the appropriate amounts, and a hormone replacement in tablet form is initially unavoidable.

Facts and Frequency of Hashimoto’s Thyroiditis

Hashimoto’s thyroiditis is now one of the most common autoimmune diseases of humanity, but is still widely underestimated by most physicians and often is not treated properly. Contrary to its exotic name, Hashimoto is the leading cause of chronic inflammation and primary hypofunction of the thyroid gland.

  • In the largest, population-based, progressive study of the Hashimoto disease, the Wickham study, the following data were obtained:
  • In 10% of the total population, increased levels of auto-antibodies are found in the blood. These are a sure indication of Hashimoto’s thyroiditis.
  • In 7.5% of English women and 2.8% of men, the basal TSH is elevated, but with normal thyroid hormone levels.
  • 1.9% of the population have a manifest hyperthyroidism, which means that the TSH is elevated and the thyroid hormones fT3 and fT4 are decreased.

“Alarming is the fact that about 75% of all people with Hashimoto’s disease do not know that they are suffering from a disorder of the thyroid gland. And 90% of all cases of hypothyroidism are in fact an undiscovered Hashimoto’s thyroiditis. “

These figures quickly make it clear that both doctors and patients are clearly under-informed about this common disease, although there is now enough literature on Hashimoto available to better understand and treat this disease.

Who is affected by this disease?

Women affected by Hashimoto’s disease are especially those in the 3rd to 6th decade of life, 8% of all women before and 16% of all women after the menopause. Overall, women suffer 10 times more frequently from Hashimoto’s thyroiditis than men.

One possible explanation for this is that women are exposed to severe hormone fluctuations as a result of the monthly cycle, as well as due to pregnancies.

But even men with a weak immune system, a chronic inflammation in the body, that eat unhealthy and have a lot of stress are the optimal candidates for Hashimoto’s thyroiditis.

In addition, there is also a familial predisposition to this disease. Children of parents with Hashimoto have a 25% chance that they also will develop thyroiditis. Especially the female offspring should have their thyroid and antibody levels checked from time to time, from primary school age on, to recognize the Hashimoto early.

According to current knowledge, experts now assume that in Germany every second person suffers from a disease of the thyroid gland. Unfortunately, it is currently still a problem to get a proper diagnosis from GPs and endocrinologists.

Possible causes and triggers of Hashimoto’s thyroiditis

In medicine, the following factors are known to date that can lead to the onset or outbreak of Hashimoto’s thyroiditis:

  • Bowel problems and intolerances (gluten sensitivity, histamine intolerance, Candida, Leaky Gut, general mucosal irritation in the intestine, etc. )
  • Genetic predisposition – In about half of all Hashimoto cases a genetic predisposition is present, which leads, in combination with the possible causes listed here, to the onset of the disease
  • Excessive iodine intake: iodine-containing diet, iodine-containing drugs
  • Hormonal special situation usually with high estrogen but low progesterone levels: puberty, pregnancy, often after childbirth, lactation, more rarely during pill intake, more often after discontinuation of the pill, premenopause, hormone replacement in menopause
  • Chronic infections
  • Heavy metal contamination (chronic poisoning with environmental toxins such as lead, arsenic, mercury, cadmium or other heavy metals)
  • Viral infections and bacterial infections such as: glandular fever, shingles, EBV (Epstein-Barr virus), Yersinia enterocolitica, herpesviruses, Lyme disease, Helicobacter pylori, hepatitis C, Coxsackie B viruses , Mumps, rubella, etc.
  • Lack of nutrients due to permanent poor diet (fast food) – The thyroid gland needs certain amounts of selenium, zinc, magnesium, vitamin D3 and iron. Lack of trace elements can quickly affect the thyroid gland
  • Stress (relationship, family, work, finances, etc.)
  • Personal Crises

Mostly, the cause of the disease is a combination of the above mentioned. Detailed information on the possible causes and triggers of Hashimoto’s thyroiditis can be found separately.

The naming of Hashimoto’s thyroiditis

Dr. Hakaru Hashimoto

Dr. Hakaru Hashimoto was born on May 5, 1881, in the southeast of Kyoto, Japan, and was the third son of a traditional medical family.

Even his grandfather Gen’i Hashimoto was a respected surgeon in the Edo era. He studied at a Dutch medical school and introduced Western surgical techniques in Japan.

Also Hakaru’s father Kennosuke Hashimoto had medical training and was head of a rural health clinic. When he died, Hakaru Hashimoto began studying at Fukuoka Medical College, where he graduated in 1907.

Later, he worked as a surgical assistant at the same college, which was later renamed Kyushu University Hospital. His local boss, Prof. Hayari Miyake, was a pioneer in neurosurgery and supported Hakaru Hashimoto in his scientific ambitions.

At Kyushu University Hospital at the time, there were a striking number of patients with goiters who usually got removed the thyroid gland partially or completely. In four of his patients Hakaru Hashimoto recognized accumulations of endogenous defense cells in the form of lymphocytes (lymphocytic infiltrates) in the thyroid tissue.

He described his discovery under the name “Struma lymphomatosa” and published it in 1912, at the age of 30, in his dissertation “To the knowledge of the lymphomatous change of the thyroid (Struma lymphomatosa)” in the Berlin “Archive for Clinical Surgery”. But it was clear that there was still a missing piece of the puzzle, that caused the accumulation of immune cells (lymphocytes) in the thyroid tissue.

But at the time of the First World War, his discovery moved into the background, so that only in the 1930s American and English studies confirmed, that the thyroiditis (struma lymphomatosa) was a separate disease. From now on, the medical literature established the name “Hashimoto” to describe this type of goiter.

In English-speaking countries, Hashimoto later became known as “Hashimoto’s Disease” or “Hashimoto’s Thyroiditis”. In German-speaking countries, one usually speaks of “Hashimoto’s thyroiditis”, “autoimmune thyroiditis”, “Hashimoto’s syndrome” or “Hashimoto’s disease”.

But in 1956, the big sensation occured: Coincidentally, two research teams almost simultaneously discovered the missing piece of the puzzle. They were able to show that autoantibodies to thyroid proteins were present in the serum of Hashimoto patients. Hashimoto’s discovery was an autoimmune disease.

But unfortunately Hakaru Hashimoto could not witness this achievement. He had emigrated to Göttingen after the death of his mother, and researched there on tuberculosis. Due to the war, he returned to Japan in 1915 and worked there as a country doctor. Unknown, but highly esteemed. During a home visit, the doctor got infected with typhus and died in 1934 at the age of just 52 as an unknown country doctor, who actually deserved a Nobel Prize.

Image source:

  • hashimoto-thyroiditis-butterfly: © Ghazi-Michael Ayed
  • h.hashimoto-klein: Wikipedia
  • hashimoto-thyroiditis: © serhiibobyk – Fotolia.com