The thyroid gland is often described as the master controller of your metabolism. It is responsible for orchestrating the fine balance of energy production in your cells, as well as overseeing many aspects of growth and cognitive development. When the thyroid struggles to meet the demands of the body, many signs and symptoms of dysfunction may follow including: fatigue, unexplained weight gain, hair loss, dry skin, joint pain, menstrual irregularity, and depression.
The medical investigation of thyroid dysfunction will typically initially involve testing one thyroid marker: thyroid stimulating hormone (TSH). This hormone is released from the pituitary gland in the brain, and is responsible for stimulating the thyroid gland itself and initiating the release of thyroid hormone (T4). There are two problems with this approach to investigation. Firstly, the range that is given on pathology results for TSH is significantly wider than it should be, allowing a TSH of up to 4.5 before being considered in an unhealthy range. The vast majority of medical research indicates that a TSH above 2.5 shows a thyroid gland that is struggling to produce adequate thyroid hormone (remember that TSH is effectively telling the thyroid to produce hormone – the higher the TSH, the louder the pituitary is having to shout at the thyroid to get it to respond).
The second issue is that TSH may be within the optimal range (1 – 2.5) however other thyroid markers could still be out of balance. I have consistently seen TSH in range but T4 (released from the thyroid gland) or the active thyroid hormone T3 (converted from T4 in tissues such as the liver and kidneys) below the optimal range. This is because these hormones rely on a complex interplay of physiology to be produced in adequate amounts. For example liver and kidney dysfunction can impact the T4 to T3 conversion, significantly reducing the levels of circulating active thyroid hormone. This will eventually impact the production of TSH but often not until pathology has progressed to a degree where it is much more difficult to treat.
Another issue with adequate thyroid function may occur at the cell itself, where the active T3 hormone must bind to cell surface receptors and initiate a response. Inflammation can effect the expression of cellular receptors for thyroid hormone, as can adrenal dysfunction and subsequent cortisol excess or deficiency.
Another hormone released in the body called reverse T3 will typically slow thyroid activity at a cellular level by blocking the thyroid receptor without stimulating it, stopping the active T3 from binding. An over-production of reverse T3 can cause symptoms of hypothyroidism in the presence of a seemingly ‘normal’ conventional thyroid test panel. This condition is termed ‘Wilson’s Syndrome’ (not to be confused with Wilson’s Disease, in which copper builds up excessively in the body) and testing for reverse T3 along with conventional thyroid markers can give a good indication as to whether this is present.
For many with diagnosed hypothyroidism, the conventional treatment involves medication with thyroxine, a synthetic version of T4 normally produced from the thyroid gland. This may be beneficial, however as mentioned above the T4 hormone must be converted to T3 to be effective in stimulating a thyroid response and for many this conversion process is not efficient (hence the need to monitor TSH, T4 and T3 when using this therapy). For those with Wilson’s Syndrome, the use of thyroxine may exacerbate thyroid dysfunction as the body will show a preference for converting T4 to reverse T3 in these patients. Hence reverse T3 spirals upward, T3 drops, and symptoms worsen. A better solution for medication is typically a compounded T3 and T4 combination, or sometimes purely T3 on its own. Of course my preference is to uncover the cause of the elevated reverse T3, which is often either adrenal dysfunction, systemic inflammation, or chronic infection. Treating the root cause will typically resolve the elevated reverse T3 and restore adequate thyroid function.
In wellness,
James
