Complete Iodine Thryoid with Elements
The Complete Iodine Thyroid Profile with Elements combines a urine test and bloodspot to evaluate not only the availability of iodine, but also its capacity to be utilized for thyroid hormone synthesis as well as measuring eviromental exposure to brominbe, arsenic, selenium, mercury and cadmium all consider influential in thyroid health.
Thyroid dysfunction is a health issue often caused by iodine deficiency as well as iodine excess. Although iodine is an essential component of the thyroid hormones thyroxine (T4) and triiodothyronine (T3), very little clinical emphasis is placed on iodine’s availability for synthesis of thyroid hormones or its role in conditions of thyroid dysfunction (hypothyroidism or hyperthyroidism).
The Adrenal Stress test measures cortisol and DHEA levels in order to quantify adrenal function and detect general stress levels.
Cortisol is a steroid hormone that increases blood sugar and is released in response to stress. Cortisol levels are sampled 4 times throughout the day, offering a diurnal collection that reflects the circadian rhythm of cortisol. These readings are helpful for assessing intermittent fatigue or sleep irregularities. Multiple cortisol readings throughout one day are considered more helpful than a single morning collection when evaluating cortisol and adrenal status.
DHEA is an important endogenous steroid hormone that plays a role in stress response and immune function. The measured DHEA-S is a product of DHEA metabolism. DHEA-S production initiates at adrenarche (early sexual maturation) just prior to puberty, peaks at adolescence, and declines with age. Lower levels may signal adrenal dysfunction from those who experience chronic stress.
Stress, adrenal function, cortisol and DHEA-S levels.
Symptoms and conditions:
Complete Iodine Thyroid
Iodine levels and thyroid function
Symptoms and conditions:
Dried Urine – Iodine
Iodine is an essential component of the thyroid hormones T4 and T31. About 90% of iodine consumed from any source (e.g., diet, supplements, medication) is eliminated in urine within 24-48 hours; therefore urine is an excellent source to determine an individual’s iodine status. When urine iodine levels are outside optimal ranges (too low or high), thyroid hormone synthesis can be abnormal. Therefore information about urinary iodine status could provide clues to thyroid dysfunction and the means to correct it (i.e., increase or lower iodine levels).
Dried Bloodspot – Thyroglobulin
Thyroid hormone synthesis begins when iodine is transported into the thyroid gland by a trans-membrane protein called the sodium iodide symporter (NIS)21. In the thyroid follicular cell, iodide (I-) interacts with hydrogen peroxide (H202) and thyroid peroxidase (TPO) to form iodine (I2) which chemically reacts with the tyrosine residues of the protein thyroglobulin, a tyrosine rich protein synthesized only in the follicular cells of the thyroid gland. Iodine reacts with tyrosine residues to form monoiodotyrosine (MIT) and diiodotyrosine (DIT) conjugates, which then couple to form the precursors of T4 (DIT + DIT) and T3 (DIT + MIT). Iodine-enriched thyroglobulin is stored in the colloidal lumen for future thyroid hormone (T3/T4) synthesis. Through a thyroid-stimulating hormone (TSH)-activated response, the iodinated thyroglobulin is then translocated back into the follicular cell where it is hydrolyzed by lysosomal enzymes to release T4 and T3, which then passively diffuse from the follicular cell into the bloodstream.
Although a very high thyroglobulin level in blood is conventionally used as a marker for thyroid carcinoma, a moderately elevated thyroglobulin in the absence of thyroid cancer is a good marker of an individual’s average exposure to iodine over a period of weeks. In this sense, thyroglobulin is considered a better marker of iodine exposure than urinary iodine, which can fluctuate from day to day depending on the consumption of iodine-containing salt, foods, or supplements. Finger stick DBS have been shown to be a convenient and patient-friendly way to test for thyroglobulin as well as other thyroid hormones.
Thyroglobulin synthesis is initiated in the thyroid follicular cell by TSH. TSH is released from the pituitary as the hypothalamus senses low thyroid (T4/T3) hormone levels in the bloodstream.
When the iodine level in the thyroid follicle is low, due to chronic iodine deficiency, inhibitors of iodine uptake or organification (goitrogenic effects), thyroglobulin is poorly iodinated and is more likely to “leak” into the bloodstream instead of being stored in the colloidal lumen for future thyroid hormone synthesis. This wasting effect results in low iodinated-thyroglobulin reserves, which is more likely to compromise thyroid hormone synthesis when iodine levels are low. When the thyroid gland is destroyed by autoimmune thyroiditis (Hashimoto’s), there is also excessive release of thyroglobulin along with thyroid hormones into the bloodstream, causing a wasting effect.
Thus, excluding thyroid carcinoma, moderate elevations in blood thyroglobulin are usually an indication that the average iodine levels over the previous weeks have been insufficient for normal thyroid hormone synthesis. Iodine prophylaxis usually results in return of blood thyroglobulin levels to normal (< 10 ng/ml), indicating adequate iodine supply to the thyroid gland.
Dried Blood Spot – Total T4, Free T4, Free T3
The blood level of total T4 provides information about the thyroid’s capacity to synthesize, process and release T4 into the bloodstream. If total T4 is low, or low normal, and thyroglobulin and TSH are elevated, this would suggest that hypothyroidism is likely caused by low iodine, or goitrogen inhibition of iodine uptake or iodinization of thyroglobulin.
In contrast to total T4, free T4 and free T3 provide information on the peripheral bioavailabilty of the active thyroid hormones to tissues. Knowing the level of these hormones in the bloodstream, however, does not predict response of target cells to them, which can be altered by many other nutritional (e.g., zinc and selenium deficiencies) and hormonal (e.g., low or high cortisol, high estrogens, low progesterone) states. Normal levels of T3, T4, and TSH, but persistent symptoms of thyroid deficiency would suggest poor cellular response to T3 and a need to investigate deeper into the underlying etiology.
Although free T4 and free T3 provide useful information on the availability of these hormones to tissues, they have not been shown to be a good surrogate marker of iodine status1. When iodine levels are very low, compensatory mechanisms come into play to assure that adequate levels of T4 and T3 are available, resulting in less fluctuation in these hormone levels with iodine deficiency. The colloidal lumen of the follicular thyroid cells normally contains a large reservoir of iodinated thyroglobulin (see above) for thyroid hormone synthesis; however, this reservoir can be drained by prolonged iodine deficiency.