In order to understand what causes an underactive thyroid gland (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 supplied by the blood, it binds as iodide to the tyrosine amino acids in 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 ). With 93%, the significantly larger part is converted into T4 and only 7% into T3.

I.e. iron deficiency lowers TPO activity and thus limits the synthesis of T3 and T4!

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

V.a. the 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 distribution of TSH in turn depends on the TRH level (thyrotropin releasing hormone). The TRH is produced by the hypothalamus, which specifies 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, for example. TSH release is also inhibited by cortisol; As explained, it is promoted by the TRH, but also by dopamine.

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

Since 60% of the T4 is converted into T3 in the liver, normal thyroid activity depends on a functional liver. Therefore, reference should be made to the CLEAN preparation from QIDOSHA at this point, which contains many Contains ingredients to strengthen the liver, such as choline.

With the deiodases, a distinction is made between the 5' and the 5 deiodase. In T4, the iodine atoms are 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' deiodase converts to T3. The 5 deiodase leads to rT3; this is biologically inactive and has no mitochondrial action, i.e. does not contribute to cellular energy production. This undesirable 5 deiodase leads to functional hypothyroidism, also known as "low T3 syndrome".

The unwanted 5 deiodase can be triggered, for example, by stress, fasting, illness or cortisol.

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

Underactive thyroid

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

• Iodine deficiency
• Malfunction of the liver
• Deficiency in the cofactors selenium, zinc and iron
• Autoimmune diseases (Hashimoto)
• Hormone imbalance in the area of ​​sex hormones, here primarily progesterone (progesterone is a sex hormone that primarily affects women, such as the menstrual cycle, pregnancy, etc.regulated)
• Prolonged stress

Typical symptoms that can be used to identify hypothyroidism include:

• Sensitivity to cold
• Lethargy
• Eye and face swelling
• Thick tongue
• weight gain
• Hoarseness
• Muscle weakness
• Hair loss
• Loss of appetite
• brittle nails

Consequences of hypothyroidism can be:

• Slow metabolism
• Irregular cycle
• Infertility
• Reduction in progesterone sensitivity

In the following, negative influencing factors on the thyroid gland along the activation chain are presented in order to clarify possible points of contact for micronutrients and hormones:

1. Hypothalamus --> serotonin, dopamine deficiency, increased prolactin --> progesterone deficiency
2. pituitary --> 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 with too little sleep, the cortisol level in the evening does not drop sufficiently in the following days, which leads to a slight permanent stress situation

In summary, the following hormones and micronutrients are helpful to support 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 counteracts the age-related disturbance 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, one speaks of 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 called hyperthyroidism.

EXCURSION JOD

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

The Japanese are considered the healthiest people in the world, with the longest life expectancy and the lowest infant mortality rate. In this context, it is worth noting that the Japanese consume an average of 13.9-45 mg of iodine per day through food, that is 13,900 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 deficiency area, which is due to the low levels of iodine in the soil and groundwater, as well as in animal and vegetable 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 intake of iodine; around 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
• Adolescents & adults 180-200 mcg iodine/day
• Pregnant & lactating women 200-300 mcg iodine/day

The upper recommendation limit in the USA, on the other hand, is 1.1 mg and in Japan even 3 mg (i.e. 3000 mcg!) per day!

In order to only achieve the officially valid intake of 200 mcg 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 at low temperatures. This means that the iodine salt used by many households supplies the extractor 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 among the muscles, bile, pituitary, salivary and mammary glands, eyes, spleen and adrenal glands, as well as exposed mucous membranes. However, in addition to its participation in the formation of thyroid hormones, it has other important functions such as an antioxidant (protects cell membranes, fats, proteins and THEN against radicals  iodolipids), has an antiviral and antibacterial effect, reduces cholesterol, is necessary for protein formation and induces via iodolactones and thiol depletion antiproliferative and apoptotic effects.

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

Up to 70% of ingested iodine reaches the thyroid on day 1 of ingestion. The absorption is inhibited there primarily by cabbage, beets (oxazolidine-2-thione), rapeseed and soya (goitrogens).

EXCURSION SELEN

Why can't the thyroid do without selenium?

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

Organic

vegetable: seleno-methionine - is incorporated unspecifically into all proteins

Animal: seleno-cysteine - is specifically incorporated into selenoproteins

Inorganic

selenite (SeO3) / redox status: +4 - is specifically built into selenoproteins / caution: no simultaneous intake of vitamin C, since selenite (usually sodium selenite in supplements) would then be reduced to elemental and inactive selenium; Recommendation: 1 hour interval when taking vitamin C and Na-selenite

selenate (SeO4) / redox status: +6 - is specifically incorporated into selenoproteins

Selenium is absorbed to about 80-90% in the upper small intestine. The absorption of organic selenium is better but slower than that of inorganic selenium. Within the organic selenium group, 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 there. Selenium also reaches the organs and binds to metal chelates, among other things; therefore selenium also plays a major role in detoxification (see below).

The most important seleno proteins (contain selenium as seleno-cysteine) include:

• Iodothyronine deiodases: deiodination of T4 to active T3 and vice versa
• Glutathione peroxidases: Breakdown 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 deiodases / see above)
• Detoxification: Detoxification of heavy metals (e.g. mercury, cadmium, lead, arsenic) through the formation of 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 (labels 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 a high glutathione concentration, which reduces the antioxidant protection of the tumor cell) from radicals. In addition, selenium is 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 the 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. The actual intake for men in Germany is only 47 mcg/day, for women even only 38 mcg/day.

About 85% of adult selenium intake comes from meat. A notable exception are the 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)
• Innards: 60
• Seafood: 30-70
• yolk: 30
• fungi: 12-25
• meat: 12-22
• Potatoes, vegetables, fruit: 0.5-1

Causes of selenium deficiency:

• Soil poor in selenium
• Vegan diet
• Absorption disorders (especially in the small intestine)
• Increased selenium requirement depending on life situation

Consequences of selenium deficiency can be:

• Underactive thyroid
• Changes to skin, hair, nails
• Disorders of the muscles with muscle weakness
• Low HDL cholesterol
• Cardiac muscle disorders and hypertension
• Weakening of the immune system
• Joint problems
• Male infertility
• Growth delays in children
• cancer

HASHIMOTO

Hashimoto's thyroiditis is predominantly a female disease, as about 9 times as many women as men are affected. Typical symptoms are sweating, lack of drive and tiredness – i.e. the typical menopausal symptoms. In this context, it is worth noting the occurrence of Hashimoto's thyroiditis with hormonal changes such as menopause and childbirth as well as special stressful situations.

Hashimoto is an autoimmune thyroid disease in which the body produces antibodies against its own thyroid gland, causing it to become inflamed After initial symptoms of hyperfunction (due to immunological destruction of hormone-storing thyroid tissue, i.e. the Cell destruction triggers passive hormone release) followed by the transition to chronic hypofunction and in the long term the inflammation leads to the destruction of the organ. Courses with fluctuating hormone values ​​are occasionally possible, especially in the early phase of the disease. During this "roller coaster ride" between hyperfunction and hypofunction, depending on the point in time at which the blood was taken, normal values ​​can also arise that conceal deviations in hypofunction and hyperfunction.

Presumably, with a corresponding genetic disposition, the immune system gets out of balance due to stress/adrenal dysfunction, infections or other factors such as excessive iodine intake and immune cells directed against the own thyroid get out of control. Free radicals and oxidative processes fuel the immune process in the thyroid.

There is no cure for this chronic inflammation of the thyroid gland, but there are a number of things that can be done to improve the condition. In this context, reference is made to adaptogens from phytotherapy, which have an immune-modulating effect . In other words, if the immune response overshoots, as in the above case, they contribute to a "down regulation" of the system. Ashwaganda, Shatavari and Brahmi are considered adaptogens in Ayurveda. In TCM, Reishi, Agaricus blazei (almond mushroom) and Hericium are particularly strong adaptogens.

To reduce the effects of free radicals, we have an enzymatic antioxidant system that should be supplemented in the event of an antioxidant intake from the diet. Particularly strong antioxidants include Quercetin and OPC grape seed extract. A combination of a wide variety of particularly strong antioxidants, some of which have a synergistic effect in that some substances reduce other antioxidants again, can also be found in the ANTI-OX preparation from QIDOSHA.

Hashimoto is verified using the following parameters:

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

The primary therapy for Hashimoto is the administration of thyroid hormones, e.g. 50-100 mcg L-thyroxine. As an additional therapy, an additional administration of progesterone to replace the thyroid hormones is often recommended, whereby anti-TPO decreases (30-50% within 2-6 months). Sleep, mood and physical and mental resilience 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; vitamin D is primarily about its immune-modulating and anti-inflammatory effect.

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