Dear BLOG readers, dear PEAK customers,

Today I’d like to revisit the topic of thyroid hormones.

In Part 1 on the thyroid gland and thyroid hormones, I provided general information about the thyroid gland. I also tried to explain the connection between the thyroid gland, iodine, and the development of an iodine-deficiency goiter.

Today, I’d like to focus on the classic thyroid disorders and provide information on their causes, diagnosis, symptoms, and treatment. With practical applications in mind, I will then explain the connection between thyroid function and the development of obesity. I will also discuss how to approach exercise when dealing with an existing thyroid disorder. Finally, I’ll conclude with some additional information on the topic of thyroid hormones in relation to doping.

I hope all readers enjoy my discussion.

 

Thyroid Disorders

 

Hyperthyroidism

When the thyroid gland produces too many of its hormones, the body becomes flooded with them, leading to the development of hyperthyroidism.

 

Causes

95% of hyperthyroidism cases are caused by autonomous nodules or what is known as Graves’ disease.

 

Autonomy (hot nodules)

Autonomy refers to thyroid cells that escape natural regulation and produce hormones unchecked. In Part 1, these cells were already referred to as hot nodules. They usually develop as a result of goiter formation. Autonomous activity can manifest as a single nodule (autonomous adenoma), multiple nodules (multilocular autonomous activity), or scattered clusters of cells (disseminated autonomous activity).

 

 

Graves’ Disease (Morbus Basedow)

In this autoimmune disorder, the body produces antibodies against its own thyroid gland. The antibodies bind to the thyroid’s TSH receptors, stimulating them and thereby prompting increased hormone production. The result is hyperthyroidism. In addition to the thyroid gland, the tissue of the eye socket (endocrine orbitopathy) and the skin of the lower leg (pretibial myxedema) are usually affected as well.

 

Rare Causes of Hyperthyroidism

Thyroiditis can also temporarily cause hyperthyroidism by destroying thyroid follicles. This leads to the release of stored thyroid hormone.

During early pregnancy (in the placenta) or due to tumors, there may be an overproduction of hCG. This, too, is a possible trigger for hyperthyroidism. “Endocrine orbitopathy” is very rare; in this condition, increased production of TSH in the pituitary gland leads to an excess of thyroid hormone.

 

 

Iodine and Hyperthyroidism

High doses of iodine can worsen untreated hyperthyroidism or, in cases of latent conditions (most commonly autonomic disorders), trigger hyperthyroidism in the first place.

 

 

Symptoms and Findings

Common symptoms of hyperthyroidism include restlessness, increased irritability, difficulty concentrating, decreased performance, muscle weakness and pain, and myopathy (a feeling of muscle tension). Other symptoms include sleep disturbances, weight loss (accompanied by increased appetite), sweating, heat intolerance, hair loss, and palpitations.

The pulse is rapid, palpable throughout the body, and irregular. Blood pressure is slightly elevated. Sometimes eye problems occur. Mild swelling of the ankles or lower legs (edema) is possible. Diarrhea and frequent bowel movements may occur. Libido and sexual function are reduced. Very rarely, men may develop gynecomastia due to an excess of estrogen.

Enlargement of the thyroid gland can lead to the development of a goiter, which is rarely associated with other symptoms. In isolated cases, difficulty swallowing or shortness of breath may occur.

 

 

Symptoms affecting the eyes occur only in Graves’ disease and are a manifestation of the autoimmune process. These include tearing, sensitivity to light, redness of the conjunctiva, protrusion of the eyes, or visual disturbances.

 

Hyperthyroidism and Advanced Age

In older adults, it can be difficult to diagnose hyperthyroidism because the symptoms often overlap with typical symptoms of “aging.”

 

Thyrotoxic crisis

This term refers to a severe exacerbation of hyperthyroidism symptoms, amounting to thyroid hormone intoxication. In extreme cases, this can even lead to loss of consciousness (thyrotoxic coma).

 

Diagnosis

Blood Tests

Thyroid function is assessed through blood tests to measure hormone levels. The basis for diagnosing hyperthyroidism is the measurement of the TSH level. If the TSH level is normal, hyperthyroidism can be virtually ruled out (there are only very rare exceptions). In cases of hyperthyroidism, TSH levels are too low.

Reason:

The brain receives a signal indicating overproduction or an excess of thyroid hormones and ceases the production and release of TSH.

However, since low TSH levels can also have other causes, a diagnosis of hyperthyroidism requires an additional increase in thyroxine (T4) and/or triiodothyronine (T3).

 

Treatment

Since Graves’ disease is an autoimmune disorder, it tends to resolve on its own (remission). Medication (long-term thyreostatic therapy) may be used as a supportive treatment. The chances of a cure are about 50%. Relapses are common.

 

Drug Therapy

Medications used include thiamazole (synonym: methimazole), carbimazole (which is rapidly converted to thiamazole), and propylthiouracil (PTU). These are all classified as thyrostatic agents and inhibit thyroid hormone production in a dose-dependent manner.

Medications such as perchlorate inhibit iodine uptake and thus indirectly inhibit the production of thyroid hormones.

Beta-blockers or mild sedatives can help relieve symptoms.

 

Radioiodine therapy

Radioactive iodine is preferentially taken up by thyroid cells with increased hormonal metabolism. In Graves’ disease, all cells are affected; in autonomous thyroid function, the treatment specifically targets the diseased parts of the thyroid gland. This procedure gently eliminates hyperthyroidism and reduces the size of a goiter. The therapy is often administered in combination with a thyreostatic agent.

 

Pregnancy

During pregnancy and while breastfeeding, treatment of hyperthyroidism with thyroid-suppressing medications may be continued. However, the increased need for thyroid hormone must be taken into account when prescribing medication, and the dose may need to be adjusted accordingly.

 

Hypothyroidism

In hypothyroidism, the thyroid gland produces too few thyroid hormones. This results in an insufficient supply to the body. In rare cases, sufficient hormone production may occur, but the body’s cells may become resistant to it (peripheral hormone resistance).

 

Causes

Congenital Hypothyroidism

Developmental abnormalities of the bones and nervous system in newborns are signs of congenital hypothyroidism. In most cases, the thyroid gland is not fully developed; rarely, it is completely absent, or hormone production is impaired due to improper iodine utilization (dyshormogenesis) or severe iodine deficiency.

 

 

Inflammation of the Thyroid Gland

Chronic lymphocytic thyroiditis, Hashimoto’s thyroiditis

These conditions are the most common causes of hypothyroidism in adults. The cause of their development is unknown. There is ongoing debate regarding whether they are caused by viral infections or a weakened immune system. Here, too, the underlying mechanism is an autoimmune process involving the production of antibodies (immunothyroiditis) against thyroglobulin (TR antibodies) and against thyroid peroxidase (TPO antibodies).

TR antibodies are antibodies directed against the TSH receptor. Their levels in the blood are elevated in cases of autoimmune thyroid disease.

TPO antibodies are antibodies directed against thyroid peroxidase, an important enzyme involved in the production of thyroid hormone. These antibodies are elevated in the blood in cases of autoimmune thyroid disease.

In the atrophic form of the disease, thyroid tissue is gradually destroyed.

In the hypertrophic form, the thyroid gland enlarges (goiter). The classic condition associated with this is called Hashimoto’s thyroiditis.

 

 

Temporary Hyperthyroidism

If Hashimoto’s thyroiditis develops suddenly, it can temporarily lead to an overactive thyroid. There is a sudden release of stored thyroid hormone. Since the hormones bind to the body’s own proteins, the hormone concentration remains elevated for 4–6 weeks.

 

 

Long-term overdose of medication (thyreostatics)

Long-term use of medications that inhibit hormone production can also lead to hypothyroidism.

 

 

Differentiation

The causes listed above relate to disorders originating in the thyroid gland. The condition is therefore also referred to as primary hypothyroidism.

In rare cases, secondary hypothyroidism may also occur. In these cases, higher-level or regulatory areas such as the pituitary gland or the diencephalon are affected.

insufficient TSH is produced, which normally stimulates the thyroid gland to produce T4 and T3.

 

 

Interactions

Selenium

Recent studies suggest that selenium has a beneficial effect in reducing autoimmune processes targeting the thyroid gland. A lasting improvement has not yet been confirmed, but it is possible.

 

Free Radical Scavengers

There is currently no scientific evidence to support a beneficial effect from free radical scavengers such as zinc.

Iodine

Large amounts of iodine (from supplements) can exacerbate the condition; however, iodine generally does not need to be avoided. The iodine found in a normal daily diet—in fish, meat, or iodized table salt—does not pose a problem. Consuming seaweed or eating sushi frequently could potentially lead to worryingly high levels of iodine.

 

Other Medications

In general, there are no interactions with other medications, including contraceptives (the birth control pill).

 

Pregnancy

It is especially important to continue taking the medication during pregnancy, as the body’s need for it increases. In most cases, a higher dose is recommended.

 

Symptoms and Findings

Weight gain occurs. Those affected tend to feel cold. Blood lipid levels rise. Psychologically, increased apathy, fatigue, lack of motivation, and memory impairment are to be expected. Depressive moods are possible.

Muscle strength is reduced, and muscles tend to stiffen and become painful. The skin appears pale, slightly flaky, and dry. Blood circulation in the skin is poor. Hair growth slows down. Hair loss occurs. The cardiovascular system operates at a reduced rate. This results in a slow pulse, low blood pressure, and calcified coronary arteries. Digestion tends toward constipation. Libido and sexual function are also affected and impaired.

 

Diagnosis

As with hyperthyroidism, a particular challenge—especially in older individuals—is recognizing hypothyroidism, since the symptoms can easily be mistaken for the normal symptoms of “aging.”

Blood tests to measure hormone levels are also performed in cases of hypothyroidism. Primary hypothyroidism is characterized by low T4 and T3 levels accompanied by elevated levels of the pituitary hormone TSH. In latent (hidden) hypothyroidism, T3 and T4 levels are normal, but the TSH level is elevated.

In the rare cases of secondary or tertiary hypothyroidism, both T4 and T3 levels as well as TSH are low.

Another diagnostic approach involves testing for antibodies against thyroid tissue in the blood (TG antibodies, TPO antibodies). These are typically significantly elevated in cases of chronic thyroid inflammation.

Below is a list of options for thyroid diagnostics:

Overview of Thyroid Diagnostic Options

 

Treatment—Hormone Replacement Therapy

The goal of treatment is to replace missing thyroid hormones by taking medication (exogenously, from an external source). In most cases, medication must be taken continuously for life. It is crucial that the patient takes the medication consistently over the long term and that the doctor regularly monitors that the correct dosage is being taken.

The need for thyroid hormones varies from person to person.

 

T4 and T3

A large portion (80–90%) of thyroid hormone is present in the blood as levothyroxine/T4 (a molecule with four iodine atoms). This is the storage form of the thyroid hormone. Our body’s cells draw exactly the amount of T4 needed at any given time from this supply in the blood.

Inside the thyroid cell, T4 is converted into the actually active form, T3. This conversion can occur in all body cells. The remaining amount of thyroid hormone (10–20%) is released directly by the thyroid gland as active triiodothyronine/T3 (a molecule with three iodine atoms).

Since the conversion of T4 to T3 occurs as needed, administering T4 alone is generally sufficient and STILL represents the standard therapy.

However, recent studies show that some patients do experience benefits from a combined regimen of T4 and T3. These individuals feel better and are more refreshed in the morning. Combination therapy may also be beneficial if persistent difficulties with concentration, fatigue, low mood, and excessive weight gain occur during treatment with T4 alone.  Possible reasons include changes in the rhythm of hormone release or shifts in the body’s hormone balance when T4 is administered exclusively.

 

Dosage and Administration

Hormone requirements vary widely. The correct dosage depends not only on thyroid levels in the blood but also on the patient’s well-being. It is entirely possible for patients to feel unwell despite having normal blood test results. Finding the right dosage and combination may therefore take some time.

The standard daily dose ranges from 100 to 200 μg of L-thyroxine (T4) or 2 μg of T4 per kilogram of body weight. In younger patients, the full dose can be administered within a short period of time. In older individuals, treatment should begin with 25–50 μg of T4 and be gradually increased at 4-week intervals until the maintenance dose is reached.

As a general rule, T4—which is identical to the body’s own T4—is taken half an hour before breakfast to ensure complete absorption in the intestines. It should also not be taken together with other medications. There must be at least 1 hour between taking T4 and calcium.

For combination therapy, there are specific medications that are taken in the same manner.

 

 

Possible Comorbidities

Although rare, it is possible for additional autoimmune diseases to develop in the context of Hashimoto’s thyroiditis. The most common of these is vitiligo. In this condition, pigment-producing skin cells are lost, increasing the risk of sunburn.

An autoimmune disease can lead to painless inflammation of the stomach lining, which may cause a vitamin B12 deficiency, which in turn can lead to anemia.

It is very rare for celiac disease (gluten intolerance), Addison’s disease (adrenal insufficiency), or type 1 diabetes to develop.

 

Thyroid Hormones and Obesity

Thyroid hormones regulate metabolism and control many of our body’s systems, including

• thermogenesis (heat production),
• lipogenesis (the formation of fatty acids, primarily from carbohydrates)
• and lipolysis (the release of fatty acids from fat stores).

 

To do this, they influence the expression and activity of a wide variety of enzymes involved in these metabolic pathways.

Illustration: Thyroid Gland and Metabolism

 

 

Hyperthyroidism

In cases of hyperthyroidism, there is an increase in thermogenesis and a corresponding rise in caloric requirements. Additionally, more hunger signals are sent, which increases food intake. To meet the increased caloric needs, lipolysis is stimulated. The increased food intake is intended to promote increased synthesis of adipose tissue (lipogenesis). The body’s goal is to maintain a constant body weight.

Illustration of Hyperthyroidism

 

Hypothyroidism

Here, due to a deficiency of thyroid hormones, thermogenesis and basal metabolic rate both decrease, resulting in weight gain even with a constant caloric intake.

In a hypothyroid state, the activity of an enzyme responsible for converting inactive T4 into T3 is also reduced, resulting in a decrease in serum T3 levels. This stimulates the pituitary gland to release TSH.

 

Overview of Hypothyroidism

 

Elevated TSH Levels

Evidently, elevated TSH levels in hypothyroidism also contribute to weight gain by affecting the satiety hormone leptin.

 

 

 

Thyroid Hormones and Exercise

In cases of hypothyroidism or hyperthyroidism requiring treatment, competitive sports can quickly overburden the cardiovascular system. An autoimmune disease—one of the causes of thyroid disease—combined with exercise places immense stress on the body.

Competitive sports in conjunction with Hashimoto’s thyroiditis should therefore be practiced under medical supervision.

 

Endurance Sports

In general, it is important to respect your own physical limits. People with thyroid disease often have to accept a decline in performance, although the course of the disease varies greatly from person to person. Some individuals become largely symptom-free through thyroid hormone therapy, while others repeatedly struggle with drops in performance.

In any case, it is advisable to monitor your physical condition throughout the day and adjust accordingly. Workouts can then be scheduled during periods of peak energy

During anaerobic exercise involving an oxygen debt, energy is primarily supplied through the breakdown of glucose. It’s important to note that carbohydrate metabolism is impaired in patients with Hashimoto’s thyroiditis. The key here is to determine the appropriate macronutrient balance. In most cases, a balanced, varied diet has proven effective.

 

It is also important to note that individuals who must meet their entire thyroid hormone requirement through exogenous sources may need to take higher doses during regular physical activity, as their needs increase. Conversely, the dosage may need to be reduced during long periods of inactivity to rule out symptoms of hyperthyroidism.

 

Thyroid patients should also be aware of their increased sensitivity to weather changes. Thyroid function is partly influenced by temperature fluctuations. Whenever possible, it is advisable to exercise within a temperature range of 5°C to 25°C.

It is also interesting to note that exercise can have different effects on well-being depending on the type and severity of the thyroid dysfunction. For individuals who are on the verge of hypothyroidism (low T3 and T4 levels), a feeling of malaise often sets in after exercise, as physical activity generally increases the consumption of thyroid hormones (especially T3).

Patients with Hashimoto’s thyroiditis have relatively high T4 levels and, in comparison, low T3 levels. They often feel well after exercise, as physical activity stimulates the conversion of T4 to T3.

If patients with Hashimoto’s thyroiditis experience weakness in their leg, respiratory, or abdominal muscles, or experience increased muscle soreness, their blood iron levels should be checked. More than 70% of all affected individuals suffer from iron deficiency.

 

Exogenous Thyroid Hormones in Bodybuilding

 

 

These three properties of T3 make it a popular performance-enhancing substance, not only in bodybuilding but also in many other sports.

 

T3 and Competition Diets

In bodybuilding, liothyronine (T3) is primarily used as part of a competition diet. Of particular interest is its stimulating effect on fat burning. When T3 is used, all macronutrients (including protein and carbohydrates) are utilized more intensively for energy production (ATP).