Vitamins, Minerals and your Thyroid - what your Doctor may not know - Part Two
The B-vitamins are essential co-enzymes to maintaining mitochondrial ATP production. Compromised mitochondrial function leads to low metabolic (thyroid) activity. Thiamine (VitaminB1), B12, Vitamin D and folic acid are synergistic to copper. Supplementing these nutrients where required helps restore body copper balance. Vitamin D metabolism is enhanced by copper.
The Thyroid Hormones:
It's not my intention to detail or even outline the anatomy and physiology of the thyroid-related endocrine system and the hormones involved. There are many excellent thyroid texts written by better-educated and more qualified folk than me. I simply wish to convey to the lay reader what thyroid hormones they might request tested - and why:
1. Thyroid Stimulating Hormone (TSH): produced by the (anterior) Pituitary Gland - TSH regulates thyroid hormone production from the thyroid gland. TSH has long been regarded as the most reliable and sensitive indicator of thyroid function, however its limitations are these:
a. TSH does not reflect low metabolic activity; cell mitochondrial energy output and the necessary nutrients to furnace the body.
b. TSH does not reflect sufficient and quality conversion of the inactive thyroid hormone Thyroxine (T4) to the active, cell-influencing Triiodothyronine (T3).
c. TSH does not reflect deficiency of any of the numerous nutrients crucial toT4 - T3 synthesis, conversion, and activation.
d. TSH does not reflect T3 interaction with its mitochondrial or DNA receptors within the cell itself. If this interface fails - T3 cannot influence cell activity in any meaningful way.
e. TSH does not reflect elevated Reverse Triiodothyronine (rT3) levels which interfere with T4 - T3 conversion and T3's activation of its intra-cell receptors.
f. TSH does not immediately reflect increasing thyroid antibodies in autoimmune thyroiditis.
Difficulties with any of the above has been termed 'Euthyroid Sick Syndrome' - patient's exhibit symptoms of an under functioning thyroid but their TSH and T4 results are 'normal'.
2. Thyroxine (T4): T4 is secreted by the thyroid gland in response to hypothalamic-pituitary stimulation (TRH/TSH). This secreted T4 then circulates in the blood - bound to a carrier protein - until synthesised (in the liver and kidneys) to T3.
T4possesses no interfacing receptors of its own, but is the inactive precursor of T3.
3. Triiodothyronine (T3): although some T3 is produced by the thyroid gland, greater than 80%results from T4 conversion. T3 is our active thyroid hormone, which profoundly regulates body metabolism.
4. Reverse Triiodothyronine (rT3): rT3 is an adapted non-active form of Triiodothyronine. In times of protracted physiological and emotional stress or illness, T4's normal conversion to T3 is corrupted - and rT3 results. Lee (2005) found forty percent of the synthetic thyroid hormone replacement Thyroxine sodium (Oroxine et al) is altered to rT3.
In healthy, minimally stressed people rT3 is quickly purged from the body. When rT3 levels are allowed to become excessive, it inhibits and distorts T4 - T3 conversion - thus producing further rT3.
Elevated levels of rT3 are commonly detected in Chronic Fatigue and Fibromyalgia sufferers. Arem (1999) proposes these two debilitating illnesses are manifestations of thyroid dysfunction. A characteristic of 'Wilson's Thyroid Syndrome' is patients' exhibit high rT3 levels because T4 is continually corrupted to rT3 at the expense of T3.
rT3 disrupts thyroid homeostasis by inhibiting the production and function of T3. rT3 binds to - but does not activate - T3intra-cell receptors; effectively blocking T3 interface and activation.
Dr. John Lee was the first practitioner to facilitate the testing of rT3 in Australia.
5. Thyroid antibodies: thyroid antibodies are detectable indicators within the circulatory system that our immunity is primed against our thyroid gland. The presence of thyroid antibodies is sometimes discounted by medicos because a percentage of the population shows low levels of antibodies without any discernable thyroid disease.
Elevated levels typically signify autoimmune thyroiditis -'Hashimotos' if the patient exhibits an under active thyroid state, and 'Graves' Disease' if their symptoms/pathology suggest the thyroid is over active.
The usual thyroid antibodies tested in Australia are:
* Thyroid Peroxidase Antibodies (TPOAb) - the more sensitive test.
Researchers suggest a strong association between autoimmune thyroiditis and Coeliac Disease. Patients exhibiting both conditions were able to eliminate thyroid antibodies by adopting a Gluten-free diet (Baratosy: 2005). An Italian study of female nursing home geriatrics with hypothyroidism, found that by eliminating gluten from the diet, the hypothyroid symptoms in these patients greatly diminished or disappeared.
The crucial roles sex and steroid hormones play in thyroid homeostasis - particularly Cortisol, Progesterone, and DHEA -have not been discussed here. Suffice to say the thyroid-adrenal relationship is mutually dependant, and a Saliva Hormone Assay of these and other relevant hormones is an integral part of the complete investigative process.
Toxic heavy metals - principally Lead, Mercury, Cadmium, Aluminum and Arsenic block the function of Vitamins and Minerals necessary for thyroid homeostasis. Where patients relate long-standing illness, toxic heavy metals should be an early assessment priority. Accurate and convenient testing is achieved by HTMA.
The thyroid hormone cascade is incredibly involved and complex. Vitamins, minerals, amino acids, trace elements, essential fatty acids (DHA/EPA), sex and steroid hormones, as well as the immune system must all be adequately available - and harmonious to each other - for T3 to accomplish its task. If any one of these vital components are lacking the process will stall - and optimal body functioning diminished.
In all this - hair is the expendable extravagance; usually the first tissue to suffer a withdrawal of metabolic and nutrient support.
It should now be appreciated that 'gimmicky' single treatments such as laser combs, commercial hair loss programs etc can do nothing to influence nutritional, metabolic or hormonal disturbance. These areas must be individually tested for - but reviewed and treated as part of the total picture.
About the author:
Tony Pearce is a Specialist Trichologist & Registered Nurse. Heis a founding member of the Society for Progressive Trichology &the official lecturer for Analytical Reference Laboratory (ARL)for hair loss & hormone imbalance. He is the Clinical Director for Trichology Hair Solutions of Virginia/DC in the United States. In Australia he can be contacted on 61 2 9542 2700, or through his website at www.hairlossclinic.com.au.