What exactly is Hashimoto’s thyroiditis?

Hashimoto’s thyroiditis is a chronic inflammation of the thyroid gland, which, due to a misguided immune system, inevitably leads to hypothyroidism with many symptoms.

This disease is triggered by the body’s own immune system, in which 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 the destroyed tissue, the thyroid is no longer able to produce and provide the body with sufficient thyroid hormones.

This autoimmune disease often causes severe symptoms of hypothyroidism , but the autoimmune disease itself also comes with a whole range of symptoms.

Unfortunately, these are often not taken into account and are often left out when  treating the patient .

The course of Hashimoto’s disease differs enormously from patient to patient, so that some of those affected cope very well with the disease and have hardly any problems, while others are severely restricted by the disease and have severe symptoms.

Hashimoto’s thyroiditis progresses in phases

Hashimoto’s thyroiditis often occurs in flares, so that it is quite difficult to catch at the beginning, since the symptoms of the disease change again and again and therefore often no absolutely clear clinical picture can be diagnosed.

During a flare-up, the released antibodies attack and break down the remaining thyroid tissue. As a result, suddenly and not controlled by the pituitary gland, more thyroid hormones than required enter the bloodstream and cause a strong but temporary overactive function. This, in turn, leads to a large number of unpleasant symptoms.

The functions of a healthy thyroid

The thyroid gland, in technical jargon called glandula thyreoidea or simply thyroidea, is a small organ with a not inconsiderable effect. Especially when the thyroid is no longer able to produce the hormones T3 and T4 on its own.

Thyroid hormones have a major impact on the body’s metabolism. They ensure that the body runs either at full speed or on the back burner.

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 the physical and mental development of  children .

But the cardiovascular system, the gastrointestinal tract as well as the nerves and muscles are also strongly influenced by the  thyroid hormones  . Last but not least, thyroid hormones also regulate mental well-being, sexual desire and fertility of both sexes.

What exactly happens in Hashimoto’s thyroiditis?

The thyroid is able to produce the thyroid hormones T1, T2, T3, T4 and calcitonin, which are vital for humans. The hormone calcitonin is produced in the C-cells in the thyroid tissue and is responsible for lowering the level of calcium in the blood.

But the two most well-known thyroid hormones are undoubtedly T3 and T4. The thyroid produces about 100 µg T4 and up to 50 µg T3 daily. Both hormones have an iodine content.

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With the longer-lived and less metabolically active T4, an iodine atom is split off, resulting in the metabolically active T3.

The majority of both hormones are in the blood, bound 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 are available as free and unbound hormones.

We are talking about free T3 ( fT3 ) and free T4 ( fT4 ). Only in the free and unbound form do the thyroid hormones have an impact on our metabolism.

The timing of release into the blood and the amount of hormones stored in the thyroid are coordinated by the brain. The hypothalamus (part of the diencephalon) and the pituitary gland (pituitary gland) are responsible for this.

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 uses the TRH to signal that the pituitary gland should release more TSH. The increased TSH in turn tells the thyroid to release more T1, T2, T3 and T4 into the blood.

This sophisticated feedback mechanism ensures that the healthy thyroid gland is able to keep the concentration of the required thyroid hormones at a constant level at all times

In the case of Hashimoto’s thyroiditis, this system no longer works according to the principle mentioned and the entire control loop gets out of joint. Because Hashimoto’s thyroiditis is an autoimmune disease, the body mistakenly produces antibodies against its own thyroid gland, confusing it with viruses, bacteria, and other invaders.

Over time, this causes the thyroid to decompose or become smaller and smaller. Due to the shrinking thyroid tissue, the production of hormones in the thyroid also decreases, which inevitably leads to hypofunction ( hypothyroidism ).

The body then tries to stimulate the thyroid gland to produce the required hormones by increasing TRH and TSH.

However, since there is not enough healthy, hormone-producing thyroid tissue, the thyroid gland is simply no longer able to produce the appropriate amounts and hormone replacement tablets initially become unavoidable.

Facts and frequency of Hashimoto’s thyroiditis

Hashimoto’s thyroiditis is now one of the most common autoimmune diseases of mankind, but is still often underestimated by most doctors and usually not treated properly.

Contrary to the exotic name, Hashimoto’s is the most common cause of chronic inflammation and primary hypothyroidism.

In the largest, population-based study on Hashimoto’s disease, the Wickham study, the following data could be determined:

  • Elevated levels of autoantibodies in the blood can be found in 10% of the general population. These are a sure sign of Hashimoto’s thyroiditis.
  • In 7.5% of English women and 2.8% of men, the basal TSH value is also increased with normal thyroid hormone values.
  • 1.9% of the population have a manifest hypofunction of the thyroid gland, ie the TSH is elevated and the thyroid hormones fT3 and fT4 are reduced

What is alarming is the fact that approximately  75%  of all people suffering from Hashimoto’s thyroiditis do not know that they have a thyroid disorder.

And  90%  of all cases of hypothyroidism are actually undetected Hashimoto’s thyroiditis.

These numbers quickly make it clear that both doctors and patients are clearly not informed enough about this widespread disease, although there is now enough  literature on the subject of Hashimoto  to better understand and treat this disease.

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Who is affected by this disease?

Hashimoto’s syndrome particularly affects women in their third to sixth decade of life, including 8% of all women before and 16% of all women after menopause. Overall, women suffer from Hashimoto’s thyroiditis 10 times more often than men.

A possible explanation for this may be that women   are exposed to strong hormone fluctuations due to the monthly cycle and often due to pregnancy .

But men with a weak immune system, chronic inflammation in the body, who eat poorly and are under a lot of stress are also ideal candidates for Hashimoto’s thyroiditis.

There is also a familial predisposition to this disease. Children of parents with Hashimoto’s have a 25% chance of also developing thyroiditis.

Female offspring in particular should have their thyroid and antibody levels checked from primary school onwards in order to identify Hashimoto’s early on.

According to the current state of knowledge, experts now assume that every second person in Germany suffers from a disease of the thyroid gland. Unfortunately,   family doctors and endocrinologists are still unable to make a proper diagnosis .

Possible causes and triggers of Hashimoto’s thyroiditis

The following factors are known in medicine to date, which can lead to the development or outbreak of Hashimoto’s thyroiditis:

  • Intestinal complaints and intolerances (gluten sensitivity, histamine intolerance,  candida ,  leaky gut , general irritation of the mucous membranes in the intestine, etc.)
  • Genetic predisposition – In about half of all Hashimoto’s cases there is a genetic disposition which, in combination with the possible causes mentioned here, leads to the onset of the disease
  • Excessive intake of iodine : diet containing iodine, medicines containing iodine
  • Hormonal special situation usually with high estrogen but low progesterone levels: puberty, pregnancy, often after childbirth, breastfeeding, less often while taking the pill, more often after stopping the pill, premenopause, hormone substitution in menopause
  • chronic infections
  • Heavy metal exposure (chronic poisoning with environmental toxins such as lead, arsenic, mercury, cadmium or other heavy metals)
  • Viral infections and bacterial infections such as mononucleosis, shingles, EBV (Epstein-Barr virus), Yersinia enterocolitica, herpes viruses, Lyme disease, Helicobacter pylori, hepatitis C, Coxsackie B viruses, mumps, rubella and others
  • Lack of vital substances due to permanently poor nutrition (fast food)  – The thyroid gland requires certain amounts of selenium,  zinc , magnesium, vitamin D and iron. A lack of trace elements can quickly affect the thyroid gland
  • Stress (relationship, family, work, finances, etc.)
  • personal crises
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Most often, the cause of the disease lies in a combination of the above points. Detailed information on the possible  causes and triggers of Hashimoto’s thyroiditis  can be read separately.

The naming of Hashimoto’s thyroiditis

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

His grandfather Gen’i Hashimoto was already a respected surgeon in the Edo era. He studied at a Dutch medical school and introduced western surgical techniques to Japan.

Also Hakaru’s father Dr. Kennosuke Hashimoto was a medical graduate and headed a rural medical clinic.

When he died, Hakaru Hashimoto began studying at the medical school in Fukuoka, where he also passed his exams in 1907.

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

At that time, there was a striking number of goiter patients at the Kyushu University Hospital, who usually had their thyroid gland partially or completely removed. Hakaru Hashimoto noticed that four of his patients had accumulations of the body’s own defense cells in the form of lymphocytes (lymphocytic infiltrates) in the thyroid tissue.

He described his discovery under the name ” Struma lymphomatosa ” and in 1912, at the age of 30, published this discovery in his dissertation ” On the knowledge of the lymphomatous changes in the thyroid gland (Struma lymphomatosa) ” in the Berlin “Archive for Clinical Surgery”.

However, it was clear that a piece of the puzzle that caused the accumulation of defense cells ( lymphocytes ) in the thyroid tissue had to be missing.

At the time of the First World War, however, his discovery was lost, so that it was not until the 1930s that American and English studies confirmed that thyroiditis (goiter lymphomatosa) was an independent disease.

From now on, the term ” Hashimoto’s thyroiditis ” was established in the medical literature to describe this type of goiter.

In 1956, however, the big sensation came : Coincidentally, two research teams discovered the missing piece of the puzzle at almost the same time. They were able to demonstrate that autoantibodies against thyroid proteins were present in the serum of Hashimoto’s patients. So Hashimoto’s discovery was an autoimmune disease.

However, Hakaru Hashimoto could not live to see this achievement. After the death of his mother, he emigrated to Göttingen and researched tuberculosis there. Because of the war he returned to Japan in 1915 and worked there as a country doctor. Unknown but valued.

During a home visit, the doctor contracted typhus and died in 1934 at the age of only 52 as an unknown country doctor who actually deserved a Nobel Prize.

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