Low Thyroid Function Due to Adrenal Fatigue
Hypothyroidism can be primary or secondary. Primary hypothyroidism can easily be cured with administration of thyroid replacement therapy. If hypothyroid symptoms such as low body temperature, fatigue, dry skin and weight gain persist despite thyroid replacement therapy regardless of laboratory values, one must look elsewhere for the cause of the low thyroid function.
Secondary hypothyroidism is low thyroid function caused by malfunction of another organ system. One of the most frequently overlooked causes is adrenal fatigue. Adrenal fatigue is perhaps the most common cause of secondary low thyroid function, both clinically and sub-clinically. Low adrenal function often leads to low thyroid function, classically evidenced by high levels of thyroid binding globulin (TBG), low free T4, low free T3, high TSH, slow ankle reflex and low body temperature. Few physicians are trained to detect this connection. Fortunately, secondary hypothyroidism can be reversed when the underlying root problem (such as adrenal fatigue) is resolved.
When the adrenals are exhausted, the ability of the adrenals to handle the stress associated with normal bodily functions and energy requirements is often compromised. To enhance survival, the adrenals force a down-regulation of energy production. In other words, the body is being metabolic down-regulated to slow down in order to conserve energy as the body needs to rest. Lower energy output reduces the workload of the body. In times of stress, this is exactly what the body wants. As the thyroid down-regulates, production of thyroid hormones T4 and T3 is reduced. The down-regulation also leads to an increase in thyroid binding globulin (TBG) level. As a result of increased TBG, more thyroid hormones are bounded on a relative basis and less is released to the body cells where they work. This leads to reduced free T4 and free T3 levels in the blood if measured (while total T3 and T4 levels may be normal). In this well orchestrated systemic down-regulation to enhance survival, the body also shunts some of the available T4 towards the production of the inactive reverse T3 (rT3) which acts as a braking system and opposes the function of T3. This reduction in T3 combined with an increase in rT3 may persist even after the stress has passed and cortisol levels have returned to normal. Furthermore, rT3 itself may also inhibit the conversion of T4 to T3 and may perpetuate the production of the inactive rT3. If the proportion of rT3 dominates, then it will antagonize T3 and possibly leading to a state called rT3 dominance. This results in hypothyroid symptoms despite sufficient circulating levels of T4 and T3. The body therefore has multiple pathways to down-regulate energy production to enhance survival under the direction of the adrenal glands....