There are MANY reasons and many medical conditions associated with thyroid disease that stop thyroid hormone from getting into the cells, where it does its work.

The main condition responsible for stopping thyroid hormone from working are:

1. Your thyroid hormone dose is too low.

Often this is the case, and the doctor or consultant wont increase it, since the blood levels appear perfectly okay. Sometimes, though, the dose of thyroxine is quite high 200 mcg 300 mcg but you still dont feel well.

2. Partial response to the single synthetic thyroxine replacement.

Your thyroid produces four other hormones apart from thyroxine, and most of us need them all. Without them our response is limited and synthetic thyroxine may not suit the system as well as the natural thyroid hormones.

3. Adrenal fatigue or exhaustion.

This is very commonly met with indeed. The production of thyroxine (T4), its conversion to triiodothyronine(T3), and the receptor uptake (called binding) requires a normal amount of adrenal hormones, notably, of course, cortisone. (Excess cortisone can shut production down, however).

4. Failure of the 5 de-iodinase enzyme.

This is what happens if the adrenals are not responding properly, and provision of cortisone usually switches it on again. But sometimes it doesnt. If the illness has been going on too long, the enzyme seems to fail. This conversion failure (in explicably denied by many endocrinologists) means the thyroxine builds up, unconverted. So it doesnt work, and T4 toxicosis results. This makes you feel quite unwell, toxic, often with palpitations and chest pain. (I refer to this further on.) If provision of adrenal support doesnt remedy the situation, the final solution is the use of the thyroid hormone, already converted, T3.

5. Receptor resistance.

Being hypothyroid for some considerable time may mean the biochemical mechanisms which permit the binding of T3 to the receptors is downgraded; the T3 just wont go in. With slow build up of T3, with full adrenal support and adequate vitamins and minerals, the receptors do actually come on line again. But this can be quite a slow process, and care has to be taken to build the dose up gradually.

6. Food allergies.

The most common food allergy is allergy to gluten, the protein fraction of wheat. The antibody generated by the body, by a process of molecular mimicry, cross reacts with the thyroperoxidase enzyme, (which makes thyroxine) and shuts it down. So allergy to bread can make you hypothyroid.

There may be other food allergies with this kind of effect, but information on these is scanty. Certainly allergic response to certain foods can affect adrenal function and imperil thyroid production and uptake.

7. Presence of systemic candidiasis.

This is where candida albicans, a yeast, which causes skin infections almost anywhere in the body, invades the lining of the lower part of the small intestine and the large intestine. Here, the candida sets up residence in the warmth and the dark, and demands to be fed. Loving sugars and starches, candida can make you suffer frightful sweet cravings. (I wouldnt be surprised if it can synthesize a neurotransmitter, which causes such craving that you have to have chocolate, on pain of death.) Candida can produce toxins which can cause very many symptoms of exhaustion, headache, general illness, and which interfere with the uptake of thyroid and adrenal treatment. Sometimes the levels which we usually test for can be very high indeed, and make successful treatment difficult to achieve until adequately treated. (More of this further on.)

8. Hormone imbalances.

The whole of the endocrine system is linked; each part of it needs the other parts to be operating normally to work properly. An example of this we have seen already, with cortisone. But another example is the operation of sex hormones. The imbalance that occurs at the menopause with progesterone running down, and a relative dominance of oestrogen is a further case in point oestrogen dominance downgrades production, transportation and uptake of thyroid hormones. This is why hypothyroidism may first appear at the menopause; the symptoms ascribed to this alone, which is then treated often with extra oestrogen, making the whole thing worse. Deficiency in progesterone most especially needs to be dealt with, since it reverses oestrogen dominance, improves many menopausal symptoms like sweats and mood swings, and reverses osteoporosis. Happily natural progesterone cream is easily obtained: when used it has the added benefit of helping to stabilise adrenal function.

9. Mercury Poisoning:

There are numerous heavy metals which can be toxic to one’s health. Some of the more common ones include aluminium, lead, cadmium, arsenic and then there’s mercury. A lot of people with thyroid and autoimmune thyroid conditions have high levels of mercury in their tissues. And this heavy metal can potentially lead to the development of these conditions. In other cases mercury isn’t a direct cause of a thyroid or autoimmune thyroid disorder, but still is something that eventually needs to be addressed.

10. Low Levels of Specific Nutrients

Thyroid hormone cannot be fully utilised if levels of specific nutrients are too low in the reference range. These are iron, transferrin saturation%, ferritin, vitamin B12, vitasmin D3, magnesium, folate, copper and zinc. Ask your doctor to test these for you and get the results, together with the reference range for each of these tests and post them here on the forum so we can help with their interpretation. In fact, always post the reference range of whatever tests you have had done. Doctors are not really taught very well how to interpret blood test results, and quite often, if they appear ANYWHERE within the range, they will tell you that your results are normal. It matters whether they are at the bottom, the middle or the top of the range.

LOW MINERALS AND VITAMINS AND THE THYROID CONNECTION

We recommend that all members should ask their GP or endocrinologist 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 hypothyroidism, please copy the following references to show him/her.

Good luck!

Low iron/ferritin:
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)

1. 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.
2. 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.
3. 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.
4. Beard J, tobin B, Green W. Evidence for Thyroid Hormone Deficiency in Iron-Deficient Anemic Rats. J. Nutr. 1989; 119:772-778.
5. BMJ 2003;326:1124

Vitamin B12:
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(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 D3:Julia Brsony, P. Lakatos, J. Fldes and T. Fehr. Effect of vitamin D3 loading and thyroid hormone replacement therapy on the decreased serum 25-hydroxyvitamin D level in patients with hypothyroidism. Acta Endocrinol November 1, 1986, 113, 329-334

Folate:
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:
Jones, John E., Desper, Paul C., Shane, Stanley R., and Flink, Edmund B. Magnesium Metabolism in Hyperthyroidism and Hypothyroidism: Journal of Clinical Investigation. Vol. 45, No. 6, 1966

Copper:
Lawrence Wilson, MD. Copper Toxicity Syndrome (revised July 2011). The Center For Development. http://www.drlwilson.com/articles/copper_toxicity_syndrome.htm
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:
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