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Low Minerals And Vitamins And The Thyroid Connection

We recommend that all those suffering symptoms of hypothyroidism should ask their GP or endocrinologist to test the following to see whether any of the results are returned low within the reference range. This is because if low, thyroid hormone (either your own, or through thyroid hormone replacement) is unable to be fully utilised at the cellular level.

Should your GP or endocrinologist tell you that there is no connection between these minerals or vitamin levels and low thyroid, please print the following to show him/her

Low iron/ferritin: Biologically, insufficient iron levels may be affecting the first two of three steps of thyroid hormone synthesis by reducing the activity of the enzyme thyroid peroxidase, which is dependent on iron. Iron deficiency, in turn, may also alter thyroid metabolism and reduce the conversion of the inactive T4 to the active T3, besides modifying the binding of T3. Additionally, low iron levels can increase circulating concentrations of Thyroid Stimulating Hormone (TSH)

That severe iron-deficiency leads to anaemia as manifested by low haemoglobin and haematocrit on a CBC blood test is well known. However, mild iron-deficiency leads to low ferritin in blood tests BEFORE a drop in haemoglobin and haematocrit occurs.

An article published in the May 2003 British Medical Journal showed that patients with low ferritin, but normal haemoglobin and haematocrit, have fatigue, that is reversed by iron treatment.

Iron deficiency is shown to significantly reduce T4 to T3 conversion, increase reverse T3 levels, and block the thermogenic (metabolism boosting) properties of thyroid hormone (1-4). Thus, iron deficiency, as indicated by an iron saturation below 25 or a ferritin below 70, will result in diminished intracellular T3 levels. Additionally, T4 should not be considered adequate thyroid replacement if iron deficiency is present (1-4)). See also Iron supplementation for unexplained fatigue in non-anaemic women: double blind randomised placebo controlled trial (5)

  • Dillman E, Gale C, Green W, et al. Hypothermia in iron deficiency due to altered triiodithyroidine metabolism. Regulatory, Integrative and Comparative Physiology 1980;239(5):377-R381.
  • Smith SM, Johnson PE, Lukaski HC. In vitro hepatic thyroid hormone deiodination in iron-deficient rats: effect of dietary fat. Life Sci 1993;53(8):603-9.
  • Zimmermann MB, Khrle J. The Impact of Iron and Selenium Deficiencies on Iodine and Thyroid Metabolism: Biochemistry and Relevance to Public Health. Thyroid 2002;12(10): 867-78.
  • Beard J, tobin B, Green W. Evidence for Thyroid Hormone Deficiency in Iron-Deficient Anemic Rats. J. Nutr. 1989;119:772-778.
  • BMJ 2003;326:1124

Vitamin B12: Vitamin B-12 is the cobalt-containing vitamin and levels can be judged by cobalt levels in the hair analysis. B-12 is critical for iron metabolism and a deficiency of B-12 will lead to anaemia and probable hypothyroidism.

If you are hypo and supplementation with iron causes a problem, then suspect either a B-12 deficiency or a copper deficiency. If you are hyper and B-12 causes an increase in hyper symptoms, then suspect a copper deficiency (because B-12 will push iron metabolism and thereby suppress copper).

B-12 deficiency is very likely in persons with hypothyroidism and persons who have been taking copper and iron to recover from hyperthyroidism. Supplementation with high amounts of the other B vitamins, iron, and possibly manganese may use up B-12 creating a deficiency. This may be detected by experiencing adverse reactions to copper, iron, manganese, B vitamins, and many foods.

  • Vitamin B12: (5) Jabbar A, Yawar A, Waseem S, Islam N, Ul Haque N, Zuberi L, Khan A, Akhter J. Vitamin B12 deficiency common in primary hypothyroidism. Department of Medicine, Aga Khan University, Karachi, Pakistan. 2008 May;58(5):258-61. Clinical Chemistry September 2001 vol. 47 no. 9 1738-1741
  • Jabbar A, Yawar A, Waseem S, Islam N, Ul Haque N, Zuberi L, Khan A, Akhter J. Vitamin B12 deficiency common in primary hypothyroidism. Department of Medicine, Aga Khan University, Karachi, Pakistan. 2008 May;58(5):258-61.

Vitamin D and D3: Vitamin D is an important vitamin that not only regulates calcium, but also has many other beneficial actions. Not many endocrinologists realize this, but several articles published over 20 years ago showed that patients with hypothyroidism have low levels of vitamin D. This may lead to some of the bone problems related to hypothyroidism. It was thought that one of two mechanisms may explain the low levels of vitamin D in patients with hypothyroidism

  1. the low levels of vitamin D may be due to poor absorption of vitamin D from the intestine or
  2. the body may not activate vitamin D properly. Other articles have demonstrated that patients with Gravess disease also have low levels of Vitamin D.
  3. Importantly, both vitamin D and thyroid hormone bind to similar receptors called steroid hormone receptors. A different gene in the Vitamin D receptor was shown to predispose people to autoimmune thyroid disease including Graves disease and Hashimotos thyroiditis. For these reasons, it is important for patients with thyroid problems to understand how the vitamin D system works.

    Folate: Three different kinds of anaemia are seen in hypothyroidism: (1) normocytic, normochromic anaemia; (2) microcytic, hypochromic anaemia; (3) macrocytic normochromic anaemia. The latter is either a true pernicious anaemia, which occurs fairly frequently in Hashimoto’s thyroiditis, or maturation disorder of erythropoiesis as a result of folic acid deficiency. In three patients with primary hypothyroidism and macrocytic anaemia there were decreased levels of serum folic acid. After short-term administration of folic acid and 1-year of thyroxine the blood picture became normal in two of the patients.

    • B. CATARGI, F. PARROT-ROULAUD, C. COCHET, D. DUCASSOU, P. ROGER, and A. TABARIN. Thyroid. December 1999, 9(12): 1163-1166. doi:10.1089/thy.1999.9.1163. Published in Volume: 9 Issue 12: January 30, 2009
    • Bjrn G. Nedreb, Ottar Nygrd, Per M. Ueland, and Ernst A. Lien; Plasma Total Homocysteine in Hyper- and Hypothyroid Patients before and during 12 Months of Treatment. Clinical Chemistry September 2001 vol. 47 no. 9 1738-1741

    Magnesium: Because of the competing nature of calcium and magnesium, excessive calcium intake from foods or supplements can lead to a magnesium deficiency. The symptoms of magnesium deficiency are identical with many of the symptoms of thyroid disease, especially hyperthyroidism. People of Asian descent who get hyperthyroidism often become completely rigid and may be found lying in the streets this way. The condition is called hypokalemic periodic paralysis and is highly associated with hyperthyroidism. It’s possible that the origin of the disease is not from low potassium (hypokalemia) but from low magnesium, which we know is a factor in hyperthyroidism.

    Functions: The principal function of magnesium that is critical in thyroid disease is that it enables muscles to relax. With inadequate magnesium, the muscles cramp. When this happens to the heart muscles the heart does not go through a complete relaxation phase, and the next calcium-driven contraction begins before the relaxation is complete. This results in rapid heart beat and irregular heart rate known as arrhythmia.

    In one study of children who exhibited symptoms of hypothyroidism, a deficiency of selenium was recognized. After Selenium supplementation, hormone levels returned to normal and symptoms disappeared. [1] Another study found that a low T3/T4 ratio in healthy elderly subjects could be corrected by supplementation with selenium. [2]

    Copper and Zinc: Your body is an amazing machine, in which everything works in harmony and synchrony. The vitamins copper and zinc work in synchrony, while seeing to it that the thyroid gland is healthy, up and doing what it is suppose to. Zinc and copper, the two vitamin supplements also protect the thyroid gland from infections and other such problems.

    Both have completely different and distinct roles to play while maintain your thyroid gland. But both at the same time are proportionate with each other, in the sense if one’s found in excess, the others found to be deficient. A proper proportion is required and is supposed to be maintained so that these supplements can prevent thyroid diseases and regulate the release of hormones, from the thyroid gland throughout the whole body. Copper and zinc have grave overdose risks; if the intake of these metals is usually high, they may cause a severe malfunction of the thyroid gland. Excretion of copper is very slow; it takes about seventy two hours to excrete 10% of the total copper consumption of the day.

    Copper and Zinc like Bonnie and Clyde, soap and water, shoes and socks; although work in conjunction, complementing each other perfectly, they both play, completely distinct roles while preventing thyroid crisis, thus maintaining the gland.

    Thyroid’s hormone fabrication, assimilation thyroid metabolism are regulated by copper. Copper controls the body’s calcium levels, thus preventing over assimilation of T4 (thyroxine) by the blood cells, while it stimulates the fabrication of the thyroxine hormone. Copper also plays a very vital part during the amalgamation of phospholipids, which are a type of fats found in the nerves; these fats are responsible for protecting the nerves. The stimulation of the Thyroid Stimulating Hormone or TSH is dependent on these Phospholipids. Precise levels of these fats are required to protect nerves and to prevent any thyroid issues; these are also used for treatment of thyroid illness.

    • Lawrence Wilson, MD .COPPER TOXICITY SYNDROME Revised, July 2011, The Center For Development.
    • Vivek R Joshi, Ayaz K Mallick, Manjunatha Goud B K, Ravindra Maradi, Maheshwar G Reddy, Raghavendra Tey, Gaurav Shorey. Effect of serum copper concentration and ceruloplasmin on lipid parameters leading to increased propensity to cardiovascular risk. Department of Biochemistry, Melaka Manipal Medical College, Manipal University. ISSN: 0975-8585

    Zinc: Zinc increases thyroid function and is usually high in hypers and low in hypos. Studies show that hypers usually have low zinc in the blood and this information seems to be the source of the very common nutritional advice that hypers need zinc. I have found that this is exactly the wrong thing to do in most cases. Some hypers are deficient in both copper and zinc, but usually even these persons should start supplementing with copper first, before zinc supplementation is begun. Generally for hyperthyroidism, copper should be supplemented first, then iron, and then zinc only if necessary. For hypothyroidism, zinc should be supplemented first (along with selenium). When night-time rapid heart beat begins, then iron and copper should be added

    • Iham Amir Al-Juboori , Rafi Al-Rawi, Hussein Kadhem A-Hakeim. . Estimation of Serum Copper, Manganese, Selenium
    • Zinc in Hypothyroidism Patients. IUFS Journal of Biology Short Communication 121 IUFS J Biol 2009, 68(2): 121-126


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Previous comments

Hi, I have a few questions. Please could you put the reference ranges after the levels that are normal for Iron saturation and Ferritin, as the reference ranges vary so much in different countries. Please could you advise what the optimum levels (with reference ranges please) should be for the other minerals and vitamins? And am I wrong in thinking that Zinc and copper are minerals, not vitamins? Also, it would be so helpful if you would be able to recommend supplements for all these minerals and vitamins, please could you let us know which ones do you think are the best? Thanks very much :)