In order to understand what causes hypothyroidism and which micronutrients and hormones can be used to treat it, let's first take a closer look at how the thyroid gland works.

The protein thyroglobulin is stored in the thyroid cells. When iodine is delivered through the blood, it binds as iodide to the tyrosine amino acids in the thyroglobulin and, with the help of the enzyme TPO (thyroid peroxidase) and iron as a cofactor, the thyroid hormones T4 (thyroxine, also known as tetraiodothyronine) and T3 (triiodothyronine) are produced. The significantly larger part (93%) is converted into T4 and only 7% into T3.

This means that iron deficiency reduces TPO activity and thus limits the synthesis of T3 and T4!

T3 and T4 are then stored in the thyroid until the hormone TSH (thyroid stimulating hormone), which comes from the pituitary gland, gives the signal to release T3 and T4 into the blood. TSH enters the thyroid via the blood and binds to so-called TSH receptors. After the receptors have been bound, the thyroid releases T3 and T4 into the blood.

Free T4 in particular inhibits the release of TSH, so that the amount of thyroid hormones in the blood normally regulates itself and a balance is established.

The production and release of TSH depends on the TRH level (thyrotropin releasing hormone). TRH is produced by the hypothalamus, which sets the target value of the thyroid hormones in the blood and constantly measures their actual value.

TRH release is promoted by stress or cold, for example, and inhibited by cortisol or T3. TSH release is also inhibited by cortisol; it is promoted, as explained, by TRH, but also by dopamine.

T3 is the active hormone, T4 is the "storage hormone" and is slowly converted into T3 in the blood. The conversion of T4 into T3 takes place by deiodination by the so-called deiodinases. These are selenoenzymes (ie they require selenium as a cofactor) that activate T3 by removing an iodine atom. This means that a selenium deficiency reduces deiodinase activity and thus the conversion of T4 into more effective T3 in the liver and kidneys.

Since 60% of T4 is converted to T3 in the liver, normal thyroid function depends on a functioning liver. Therefore, we would like to point out the CLEAN preparation from QIDOSHA, which contains many ingredients to strengthen the liver, such as choline.

Among the deiodinases, a distinction is made between 5' and 5 deiodinase. The iodine atoms in T4 are located in the 5th position on the outer and inner ring. The iodine atoms in the 5th position on the outer ring are referred to as 5' and those on the inner ring as 5. Only the 5' deiodinase leads to the conversion into T3. The 5 deiodinase leads to rT3; this is biologically inactive and has no mitochondrial effect, ie it does not contribute to cellular energy production. This undesirable 5 deiodinase leads to functional hypothyroidism, also known as "low T3 syndrome".

The unwanted 5-deiodinase can be triggered by stress, fasting, illness or cortisol.

The cofactors required for the desired 5' deiodinase are selenium, zinc and iron (for TPO / see above).

hypothyroidism

Hypothyroidism (underactive thyroid) is rarely congenital, but usually acquired.Triggers for hypothyroidism can include:

• iodine deficiency
• liver dysfunction
• Deficiency of the cofactors selenium, zinc and iron
• autoimmune diseases (Hashimoto)
• Hormonal imbalance in the sex hormone area, especially progesterone (progesterone is a sex hormone that regulates processes such as the menstrual cycle, pregnancy, etc., especially in women)
• Long-term stress

Typical symptoms that can indicate hypothyroidism include:

• sensitivity to cold
• lethargy
• swelling of the eyes and face
• Thick Tongue
• weight gain
• hoarseness
• muscle weakness
• hair loss
• loss of appetite
• Brittle nails

Consequences of hypothyroidism can be:

• Slowed metabolism
• Irregular cycle
• infertility
• decrease in progesterone sensitivity

In the following, negative factors influencing the thyroid gland along the activation chain will be presented in order to clarify possible starting points for micronutrients and hormones:

1. Hypothalamus --> serotonin, dopamine deficiency, increased prolactin --> progesterone deficiency
2. pituitary gland --> increased cortisol
3. Thyroid --> Iodine deficiency, Hashimoto
4. T4/T3 synthesis --> selenium, zinc, iron deficiency, increased cortisol, progesterone deficiency
5. T4/T3 transport --> estrogen dominance, low TBG
6. SD receptor --> increased cortisol, progesterone deficiency

Ad 2/6: One of the most common causes of hypothyroidism is lack of sleep: after just one night of insufficient sleep, the cortisol level does not drop sufficiently in the evenings in the following days, which leads to a mild, permanent stress situation.

In summary, the following hormones and micronutrients are helpful in supporting thyroid function (source and quantity guidelines: Dr. Robert Berger):

• iron and vitamin B12 (ferritin >100)
• Selenium (50-200 mcg)
• Bioidentical progesterone (25-200 mg)
• zinc (10-30 mg)
• Vitamin B6 (20 mg)
• iodine (500 mcg)
• Magnesium (400-1000 mg)
• Vitamin D (2000 IU)
• Melatonin (physiological melatonin substitution from middle age onwards counteracts the age-related disruption of T3 formation) (0.5-1 mg)
• Vitamin C (500 mg)

If hypothyroidism is suspected, the basal TSH should first be determined, the reference range of which is 0.4-2.5 mU/l. If the value is elevated, the free T4 should then be determined: if this is low despite a high TSH, then there is manifest hypothyroidism. If the free T4 is (still) normal, this is called latent hypothyroidism.

If, on the other hand, the TSH value is too low and T3 and T4 are increased at the same time, this is referred to as overactive thyroid, so-called hyperthyroidism.

EXCURSUS JOD

What does iodine have to do with the healthiest people in the world?

The Japanese are considered to be the healthiest people in the world, with the highest life expectancy and the lowest infant mortality rate. It is noteworthy in this context that the Japanese consume an average of 13.9-45 mg of iodine per day through their diet, which is 13900 mcg - 45.000 mcg! For comparison: the DGE recommends a daily iodine intake of just 200 mcg for healthy, non-pregnant adults!

Germany is now considered an iodine-deficient area, which is due to the lack of iodine in soil and groundwater, as well as in animal and plant foods. But an increased need, such as due to pregnancy or growth, can also be the cause of an iodine deficiency. Only about 9% of the population has an adequate iodine intake; about 15% of adults have a real iodine deficiency.

Official intake recommendations from DGE and BfR:

• infants                     50-80 mcg iodine/day
• Children                       100-140 mcg iodine/day
• teenagers & adults      180-200 mcg iodine/day
• Pregnant & breastfeeding women        200-300 mcg iodine/day

The upper recommended limit in the USA, however, is 1.1 mg and in Japan it is even 3 mg (ie 3000 mcg!) per day!

However, in order to reach the officially valid intake of 200 mcg of iodine in Germany, for example, 1 kg of spinach, 154 g of mussels, 340 g of oysters or 104 g of plaice would have to be eaten daily. It should be noted that iodine is a volatile element that evaporates even at low temperatures. This means that the iodized salt used by many households supplies the cooker hood with sufficient iodine, but not necessarily the body.

About 70-80% of all iodine in the body is found in the thyroid gland. The rest is distributed between the muscles, gall, pituitary gland, salivary and mammary glands, eyes, spleen and adrenal glands as well as exposed mucous membranes. In addition to its involvement in the formation of thyroid hormones, it has other important functions such as acting as an antioxidant (protects cell membranes, fats, proteins and THEN from radicals  iodolipids), has antiviral and antibacterial effects, lowers cholesterol, is necessary for protein formation and induces antiproliferative and apoptotic effects via iodolactones and thiol depletion.

Inorganic iodide (the main form in food) is absorbed by the small intestine to 90-100%, whereas iodine bound to proteins is only absorbed to 40-70%. Obstacles to iodine absorption are mainly large amounts of chlorine, fluorine, lithium and bromine, which can be contained in pesticides or even food.

Up to 70% of the iodine absorbed reaches the thyroid on day 1 of intake. Absorption there is inhibited primarily by cabbage, beets (oxazolidin-2-thiones), rapeseed and soy (goitrogens).

EXCURSUS SELENIUM

Why can't the thyroid gland do without selenium?

Selenium is a trace element and can be found in both organic (food proteins) and inorganic form (e.g.in drinking water or through supplements):

Organic

Plant-based: Seleno-Methionine - is nonspecifically incorporated into all proteins

Animal: Seleno-Cysteine - is specifically incorporated into selenoproteins

Inorganic

Selenite (SeO3) / Redox status: +4 - is specifically incorporated into selenoproteins / Attention: do not take vitamin C at the same time, as selenite (mostly sodium selenite in supplements) would then be reduced to elemental and inactive selenium; recommendation: 1 hour interval when taking vitamin C and sodium selenite

Selenate (SeO4) / Redox status: +6 - is specifically incorporated into selenoproteins

Selenium is absorbed in the upper small intestine to about 80-90%. The absorption of organic selenium is better, but slower, than that of inorganic selenium. Within the group of organic selenium, the availability of seleno-cysteine ​​is faster than that of seleno-methionine.

After absorption, the selenium enters the erythrocytes and is bound to plasma proteins. Selenium also reaches the organs and binds to metal chelates, among other things; selenium therefore also plays an important role in detoxification (see below).

The most important selenoproteins (contain selenium as selenocysteine) include:

• Iodothyronine deiodinases: deiodination of T4 to active T3 and vice versa
• Glutathione peroxidases: degradation of peroxides
• Thioredoxin reductases: control of the intracellular redox status (essential for cell division and differentiation) and regulation of transcription factors (e.g. NFkB)

Effects of selenium:

• Thyroid hormone metabolism (iodothyronine deiodinases / see above)
• Detoxification: Detoxification of heavy metals (e.g. mercury, cadmium, lead, arsenic) by forming inactive selenium compounds, which can then be excreted in the urine. Example: Hg2+ + Se --> HgSe
• Immunocompetent: Selenium improves/increases apoptosis in tumors, interferon-gamma (marks antigen-presenting cells), the activity of T cells, NK cells, cytotoxic cells and macrophages
• Anticarcinogenic (inactivation of oncogenic gene segments): Selenium protects healthy cells, but not cancer cells (since selenium only forms selenium disulfide in tumor cells with high glutathione concentration, which reduces the antioxidant protection of the tumor cell) from radicals. Selenium is also involved in the DNA repair of damaged "normal" cells and acts as a trigger for apoptosis and growth arrest of cancer cells (e.g. via transcription factor p53)
• cell proliferation and cell differentiation (thioredoxin reductases)
• Antioxidant (cofactor of glutathione peroxidases) in erythrocytes, fatty acids, cell organelles, phospholipid membranes; selenite binds organic oxyl and hydroxyl radicals
• Anti-inflammatory by inhibiting redox-sensitive transcription factors NFkB (thioredoxin reductases), which promote inflammation

How can I increase selenium levels naturally?

The recommended selenium intake is 20-100 mcg/day - depending on the initial situation. However, the actual intake for men in Germany is only 47 mcg/day, and for women it is only 38 mcg/day.

About 85% of the selenium intake in adults comes from meat.A notable exception are Brazil nuts, which contain a lot of selenium.

Selenium sources in mcg/100 g:

• Brazil nuts: up to 2550 (= up to 90 mcg selenium per nut)
• offal: 60
• Seafood: 30-70
• Egg yolk: 30
• Mushrooms: 12-25
• Meat: 12-22
• Potatoes, vegetables, fruit: 0.5-1

Causes of selenium deficiency:

• Selenium-poor soils
• vegan diet
• absorption disorders (especially in the small intestine)
• Increased selenium requirement depending on life situation

Consequences of selenium deficiency can be:

• hypothyroidism
• Changes in skin, hair, nails
• Muscular diseases with muscle weakness
• Low HDL cholesterol
• heart muscle diseases and hypertension
• weakening of the immune system
• joint pain
• infertility in men
• growth delays in children
• Cancer

HASHIMOTO

Hashimoto's thyroiditis is primarily a female disease, as it affects about 9 times as many women as men. Typical symptoms are sweating, lack of motivation and tiredness - in other words, the typical menopausal symptoms. What is remarkable in this context is the occurrence of Hashimoto's thyroiditis with hormonal changes such as menopause and childbirth as well as particularly stressful situations.

Hashimoto is a autoimmun caused by thyroid disease, in which the body forms antibodies against its own thyroid, which leads to inflammation. After initial symptoms of hyperfunction (due to immunological destruction of hormone-storing thyroid tissue, i.e. cell destruction triggers passive hormone release), the transition to chronic hypofunction follows and in the long term the inflammation leads to the destruction of the organ. Particularly in the early phase of the disease, courses with fluctuating hormone levels are occasionally possible. During this "rollercoaster ride" between hyperfunction and hyperfunction, depending on the time of the blood sample, normal values ​​can also arise that conceal deviations in hypofunction and hyperfunction.

Presumably, with a corresponding genetic predisposition, the immune system becomes unbalanced due to stress/adrenal cortex dysfunction, infections or other factors such as excessive iodine intake and immune cells directed against the thyroid gland become out of control. Free radicals and oxidative processes fuel the immune process in the thyroid gland.

This chronic inflammation of the thyroid gland cannot be cured, but there are a number of things that can be done to improve the condition. In this context, adaptogens from phytotherapy, which has a immunomodulatory effect This means that in the case of an excessive immune response, as in the above-mentioned case, they contribute to a “down-regulation” of the system. Adaptogens in Ayurveda are Ashwaganda, Shatavari and Brahmi. In TCM, Reishi, Agaricus blazei (almond mushroom) and Hericium particularly strong adaptogens.

To reduce the effects of free radicals, we have an enzymatic antioxidant system that, in the event of an overload of antioxidants, which are supplied through food. Particularly strong antioxidants include Quercetin and OPC grape seed extractA combination of various, particularly strong antioxidants, some of which act synergistically in that some substances reduce other antioxidants, can also be found in the ANTI-OX preparation from QIDOSHA.

Hashimoto is diagnosed using the following parameters:

• Microsomal antibodies (TPO-AK) increased in about 90%
• Antibodies against thyroglobulin (Tg-AK) increased in about 70%
• TSH receptor antibodies (TRAK) not increased
• Inhomogeneous, hypoechoic ultrasound image

The primary therapy for Hashimoto is the administration of thyroid hormones, e.g. 50-100 mcg L-thyroxine. As a complementary therapy, an additional administration of progesterone is often recommended to replace the thyroid hormones, which reduces anti-TPO (30-50% within 2-6 months). Sleep, mood and physical and mental resilience also often improve as a result. It is also important to compensate for a frequently existing selenium, zinc, iron and vitamin D deficiency (source: Schulte-Uebbing 2012). As explained, selenium, zinc and iron are important cofactors; with vitamin D, it is primarily about its immunomodulatory and anti-inflammatory effect.