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Optimizing Thyroid Function by Terry Wingo, RPh

Our optimum health depends on optimum functioning of all endocrine hormones at the cellular, biochemical level.  Many patients experience poor health or impaired well-being due to inefficiencies in endocrine systems, especially related to insulin, adrenal hormones, and thyroid hormones.  In this article, we will examine the role thyroid hormones play in maintaining proper metabolic function and look at some of the common problems associated with recognizing the thyroid role in our impaired health.  So if you are concerned about weight gain, dry skin, hair loss, depression, low libido, fibromyalgia, or other symptoms associated with impaired thyroid function, read on…

Thyroid hormones regulate intracellular metabolic rate, the speed or efficiency of biochemical activity, which controls efficiency of organs and systems (immune response, tissue repair, detoxification, energy processes, neurotransmitter production, etc.).  The thyroid gland uses the mineral iodine and l-tyrosine, an amino acid, to produce l-thyroxine (T4), which is subsequently converted to tri-iodo-l-thyronine (T3) and its isomer reverse T3 (rT3).  T3 is the primary active hormone within the cells.  Some T4 is converted to T3 in the thyroid gland to provide an immediate supply in circulation, but the majority of this conversion occurs in target tissue (the cells themselves) as needed.  The production of T4 in the thyroid gland is regulated by thyroid stimulating hormone (TSH) produced by the pituitary gland.   Within the pituitary T4 is converted to T3 and the result evaluated; TSH is then sent back as the messenger to increase or decrease T4 production.  Higher levels of TSH (the work harder! message) mean T4 is too low based on the pituitary evaluation; very low TSH might indicate excessive T4 production.

Problems associated with the thyroid gland are production problems (hypothyroidism for low production, hyperthyroidism for excessive production) and are considered primary problems; these may be related to genetic predisposition, development of autoimmune responses, or thyroid tumors.  Generally, primary hypo- or hyperthyroid issues are identified by basic serum testing for TSH and T4.  The greatest concern in this discussion, however, are the issues associated with secondary hypothyroid responses, or those leading to low thyroid symptoms even though the production of thyroid hormone appears to be normal.  These are essentially utilization issues which may or may not be related to production.

If we want to evaluate the utilization of thyroid hormones at the cellular level we must consider four factors: production efficiency, degree of protein binding, conversion efficiency, and receptor response.  As mentioned earlier, TSH levels are considered the standard for evaluating production.   The newest national standards define normal range for TSH as 0.3 to 3.5, however, local labs still use old standards which identify much higher TSH values as normal.  Further, functional practitioners generally try to maintain TSH values less than or equal to 2.  Common factors (other than disease processes) that might affect production include inadequate protein intake or impaired protein digestion (less l-tyrosine available) and drinking tap water (both chlorine and fluoride can displace iodine binding).

The majority of thyroid hormones in circulation are bound to a storage protein, thyroid binding globulin; only the unbound or free hormone is available for activity.  The most common factor reported that affects binding globulin is relative level of estrogens.  It has been documented that any oral estrogen supplementation increases thyroid binding globulin and generally recognized that relative estrogen dominance has this same effect.  Remember, increases in binding globulin mean less free thyroid hormone, thus lower cellular activity, although the usual T4 lab would not change since it measures both bound and free hormone.

Appropriate conversion of T4 to T3 is a delicately balanced process, primarily regulated by adrenal activity.  Free T4 is converted to free T3 and reverse T3; the free T3 is active (increases metabolic rate) but the rT3 isomer merely blocks receptors, reducing activity.  Adequate cortisol is required for proper conversion and the 7-keto metabolite of DHEA has also been demonstrated to increase free T3 levels.  Additionally, proper tissue levels of selenium, iodine, zinc, and copper are necessary for effective conversion.  For example, the enzyme involved in peripheral (cellular) conversion of T4 to T3 requires selenium as a cofactor, although the pituitary conversion process does not, leading to a scenario where TSH is normal but cellular activity is sub-normal.  Similarly, iodine is required for production of T4, involved in conversion of T4 to T3, and necessary for metabolic breakdown of estrogens (and higher estrogens lower thyroid hormone availability).   

Alterations in cellular receptor response to T3 lead to a functional impairment that might be considered thyroid resistance.  Factors known to decrease or impair response include high insulin levels, elevated cortisol levels (stress response), and elevated mercury levels, as well as other heavy metals and some environmental toxins.

Two questions remain- how can we tell if a secondary hypothyroid problem may be present and what can we do about it?  The first step is a functional measurement of the effect of T3 in the cellular biochemistry, accomplished with an oral thermometer.  Some authorities suggest basal temperature as a guide but we suggest average daytime oral temperature, measured for several consecutive days, as an appropriate marker.  Our biochemistry is such that optimum function occurs when our temperature averages 98.6 degrees; an average temperature less than 98.2 degrees would be considered significant (our biochemical engine is idling too slowly).  A significantly suppressed average oral daytime temperature indicates impairment in thyroid utilization but doesn’t tell us why, so the next step may be seeking broader thyroid serum values.  There are several possible lab measurements that could be done (TSH, T4, T3, freeT4, freeT3, rT3, T3 uptake, TPO, etc.) but a good assessment can usually be made using TSH, freeT4, and freeT3.  These values must be interpreted in relation to each other (not just to the normal ranges) in order to assess production and conversion efficiency.  Intervention may be as simple as supplementation with selenium or iodine, as involved as chelating excess mercury, or may require prescription intervention.  

What’s the next step?  Check your temperature, yes, then educate yourself about the process and available options.  There are several good books related to functional thyroid impairment (ex. Hypothyroidism: The Unsuspected Illness, Broda Barnes M.D.) as well as useful web information (ex.www.drrind.com).  Recognize that secondary hypothyroid issues are just that, and the primary reason for impaired response must be identified and addressed to fully correct your concerns.  Remember that symptom list we started with?  The best thing about correcting secondary hypothyroid responses is how good it feels when all those symptoms fade away…