To understand what triggers 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 thyroglobulin. 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 proportion (93%) is converted into T4, while only 7% is converted into T3.

D.h. 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 originates from the pituitary gland, signals the release of T3 and T4 into the blood. TSH enters the thyroid via the bloodstream and binds to so-called TSH receptors. After binding to the receptors, the thyroid releases T3 and T4 into the blood.

V.aThe free T4 in turn 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, in turn, depends on the level of TRH (thyrotropin-releasing hormone). TRH is produced by the hypothalamus, which sets the target level of thyroid hormones in the blood and constantly measures their actual levels.

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

T3 is the active hormone, while T4 is the "storage hormone," and is slowly converted into T3 in the blood. The conversion of T4 into T3 occurs via deiodination by the so-called deiodinases, which are selenoenzymes (d.h. require selenium as a cofactor), which activates T3 by removing an iodine atom. D.hA 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 into 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.

Deiodinases are divided into 5' and 5' deiodinase. The iodine atoms are located in T4 u.a. at the 5th position on the outer and inner rings. The iodine atoms in the 5th position on the outer ring are designated 5', and those on the inner ring are designated 5'. Only 5' deiodinase leads to conversion to T3. 5' deiodinase leads to rT3; this is biologically inactive and has no mitochondrial activity. d.h. 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, for example, by stress, fasting, illness or cortisol.

The cofactors required for the desired 5' deiodinase are, in addition to selenium, zinc and iron (for TPO/s.o.).

Hypothyroidism

Hypothyroidism (underactive thyroid) is rarely congenital, but i.d.R. 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, here v.a.Progesterone (progesterone is a sex hormone that v.a. in women, it regulates processes such as menstrual cycles, pregnancy, etc.)
• 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 include:

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

In the following, negative factors influencing the thyroid 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, cortisol levels do not drop sufficiently in the evening 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 recommended amounts: 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 production) (0.5-1 mg)
• Vitamin C (500 mg)

If hypothyroidism is suspected, the basal TSH level should first be determined, the reference range of which is 0.4–2.5 mU/L. If the level is elevated, the free T4 level should then be determined. If this level is low despite a high TSH level, this indicates overt hypothyroidism. If the free T4 level is (still) normal, it is referred to as latent hypothyroidism.

If, on the other hand, the TSH value is too low and T3 and T4 are elevated at the same time, this is referred to as hyperthyroidism.

EXCURSUS IODINE

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

The Japanese are considered the healthiest people in the world, with the highest life expectancy and the lowest infant mortality rate. It's noteworthy in this context that the Japanese consume an average of 13.9–45 mg of iodine per day through their diet, or 13,900–45,000 mcg! By comparison, the German Society for Occupational Health (DGE) recommends a daily iodine intake of just 200 mcg for healthy, non-pregnant adults!

Germany is now considered an iodine-deficient area, due to the low iodine content of soils and groundwater, as well as animal and plant foods. However, increased iodine requirements, such as those due to pregnancy or growth, can also be a cause of iodine deficiency.Only about 9% of the population has an adequate iodine intake; about 15% of adults suffer from a genuine 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 even 3 mg (d.h. 3000 mcg!) per day!

However, in order to reach the officially valid intake of 200 mcg of iodine in Germany, one would have to eat 1 kg of spinach, 154 g of mussels, 340 g of oysters or 104 g of plaice every day. It should be noted that iodine is a volatile element that evaporates even at low temperatures. D.h. the iodized salt used by many households provides v.a. the extractor hood sufficiently with iodine, but not necessarily the body..

Approximately 70-80% of the body's total iodine is found in the thyroid gland. The remainder is distributed among the muscles, bile, pituitary gland, salivary and mammary glands, eyes, spleen, and adrenal glands, as well as exposed mucous membranes. In addition to its involvement in the production of thyroid hormones, it has other important functions, such as acting as an antioxidant (protecting cell membranes, fats, proteins, and other lipids from radicals  iodolipids), acting as an antiviral and antibacterial agent, lowering cholesterol, being necessary for protein synthesis, and inducing antiproliferative and apoptotic effects via iodolactone and thiol depletion.

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

Up to 70% of the iodine absorbed reaches the thyroid on day 1 of intake. Absorption there is inhibited v.a. 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 supplied in both organic (food proteins) and inorganic form (e.g. in drinking water or through supplements):

Organic

Plant-based: Seleno-Methionine - is incorporated non-specifically into all proteins

Animal: Seleno-Cysteine - is specifically incorporated into selenoproteins

Inorganic

Selenite (SeO3)/Redox status: +4 - is specifically incorporated into selenoproteins/Caution: no simultaneous intake of vitamin C, as selenite (mostly sodium selenite in supplements) would then be reduced to elemental and inactive selenium; recommendation: 1 hour interval between intake of vitamin C and sodium selenite

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

Selenium is absorbed in the upper small intestine to approximately 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 selenocysteine ​​is faster than that of selenomethionine.

After absorption, selenium enters the erythrocytes and binds to plasma proteins. Selenium also reaches the organs and binds there u.a. to metal chelates; therefore selenium also plays a role in detoxification (s.u.) plays a big role.

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/s.o.)
• Detoxification: Detoxification of heavy metals (z.B. Mercury, cadmium, lead, arsenic) by forming inactive selenium compounds, which can then be excreted in the urine. E.g.: 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 concentrations, which reduces the antioxidant protection of the tumor cells) from radicals. Selenium is also involved in DNA repair of damaged "normal" cells and acts as a trigger for apoptosis and growth arrest in 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 my selenium levels naturally?

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

About 85% of adults' selenium intake comes from meat. A notable exception is Brazil nuts, which contain very high levels 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 (v.a.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 problems
• Infertility in men
• Growth delays in children
• Cancer

HASHIMOTO

Hashimoto's thyroiditis is primarily a female disease, affecting approximately nine times more women than men. Typical symptoms include sweating, lack of motivation, and fatigue – the typical symptoms of menopause. It is noteworthy in this context that Hashimoto's thyroiditis often occurs during hormonal changes such as menopause and childbirth, as well as during particularly stressful situations.

Hashimoto is a autoimmun caused thyroid disease in which the body produces antibodies against its own thyroid, leading to its inflammation. After initial symptoms of hyperactivity (due to immunological destruction of hormone-storing thyroid tissue, d.h. Cell destruction triggers passive hormone release), a transition to chronic hypofunction follows, and in the long term, the inflammation leads to organ destruction. Especially in the early stages of the disease, courses of fluctuating hormone levels are occasionally possible. During this "roller coaster ride" between hyperfunction and hypofunction, depending on the time of the blood draw, normal values ​​can also emerge 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 uncontrollable. Free radicals and oxidative processes fuel the immune process in the thyroid.

This chronic inflammation of the thyroid is not curable, but there are many things that can be done to improve the condition. In this context, u.a. on Adaptogens from phytotherapy, which has a immunomodulatory effect have. D.h. in case of excessive immune response as in o.gIn this case, they contribute to a "down-regulation" of the system. Adaptogens in Ayurveda are Ashwagandha, Shatavari and BrahmiIn 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 are u.a. Quercetin and OPC grape seed extractA combination of various, particularly powerful antioxidants that z.T. synergistic effect, in that some substances reduce other antioxidants, can also be found in the ANTI-OX preparation from QIDOSHA.

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