TSH is not a reliable marker to measure Thyroid Function

When your doctor tests thyroid function, TSH is the marker they will use to decide whether you are hypothyroid. They will sometimes also test free T4, the inactive thyroid hormone, but rarely free T3, the active thyroid hormone whose level is the most important in diagnosing thyroid function. Or they will test T3 and T4, neither of which are helpful to reach a diagnosis, as in this case, thyroxine (T4) and Triiodothyronine (T3) are bound to carrier proteins and do not enter your cells. Only the free thyroid hormone is available for cellular uptake.However, the standard testing method is TSH and T4. Unfortunately, this paradigm was stuck in the 1950s when they discovered the pituitary-thyroid feedback loop. Scientists figured the feedback loop was linear—from TSH secreted by the pituitary to the thyroid and back again, when decades of thyroidologists had carefully analyzed their patient's clinical symptoms to diagnose hypothyroidism. This TSH-T4 feedback loop was as simple as playing telephone with tin cans. Decades of research since then have demonstrated that this paradigm is simplistic and unreliable. Doctors seldom test free T3, so unseen means unknown. Any results that negate the assumption of the standard are ignored, despite innumerable evidence that hypothyroid patients are not being diagnosed due to this standard. Those who are diagnosed are getting sicker because they are prescribed Levothyroxine and not natural desiccated thyroid made from porcine powder. This FDA-approved medication has been around since the early 1900s. Levothyroxine contains only a synthetic form of T4. Natural desiccated thyroid contains the five hormones the human thyroid makes, including T3. It is important to note that one should not take bovine natural desiccated thyroid, as it contains very high levels of T4, and miniscule amounts of T3, making it as ineffectual as Levothyroxine in treating hypothyroidism.

TSH measures the hypothalamic-pituitary response to thyroid hormones. It does not test free thyroid hormone levels nor the effects of thyroid hormone throughout the body. In cases, as with individuals who have very low TSH, I use it as a possible indicator of thyroid inflammation and the possibility of thyroid nodules. If TSH is very high, it can diagnose hypothyroidism. Still, so many people who are hypothyroid, even if they have what doctors deem is a normal TSH level, make it a flawed means of diagnosing hypothyroidism.

TSH indicates the response of only one organ to circulating thyroid hormones: the hypothalamicpituitary system. All organs and tissues respond differently to the thyroid hormones in circulation. The adrenals, which regulate all immune and autonomic nervous system responses, are always connected to the hypothalamic-pituitary axis. The HPA axis is a very complex system that receives signals from various parts of the brain and the sympathetic nervous system. As such, there is constant crosstalk between the thyroid and adrenal systems.

There are many problems with using TSH as the sole diagnostic tool for thyroid function. TSH levels are individual. Studies have demonstrated that TSH is not a sensitive enough measure to conclude thyroid function, which is made out of many different connections and elements that are part of a person's endocrine system to adapt and maintain homeostasis. Laboratory parameters for TSH reflect a higher intraindividual variation than most. A normal TSH value for one person could indicate thyroid illness in another.

Stress that affects thyroid hormone levels in the body, such as environmental toxins, fasting, or numerous medications, such as benzodiazepines, will lower thyroid hormone uptake into cells. Still, the TSH level will not reflect this, which makes TSH an insufficient indicator for cellular thyroid in any tissue other than the pituitary gland.

The enzymes regulate the level of T4 and T3 hormones deiodinase 1, 2, and 3. Deiodinase 2 communicates with the pituitary and causes the secretion of TSH, which is supposed to trigger more thyroid hormone production. This argument does not work, because deiodonase 2 receptors are only found in certain tissues. Deidonase 1 enzymes do not trigger TSH secretion. Deidonase 2 is more prevalent in brain tissue than deidonase 1. D1 is found in liver, kidney, thyroid, and pituitary tissue. D2 is abundant in skeletal muscle, the nervous system, the pituitary, the thyroid, the heart, and brown fat tissue. Deiodinase 3 converts the primary active thyroid hormone T3 to reverse T3 in a fasting state of acute illness and blunts thyroid hormone production. Irrespective of this, studies demonstrated brain, liver, kidney, and skeletal muscle tissues had low concentrations of thyroid hormones in the presence of normal TSH levels.

The quantity of T3 in tissues is controlled by many factors, but not by TSH levels. It is locally controlled, without pituitary involvement, by all three types of deiodinases. Hence, doctors won't discover low T3 levels if only TSH is measured. People taking Levothyroxine to treat hypothyroidism will never reach adequate T3 levels. Levothyroxine will only normalize TSH levels, leading physicians to conclude the person is euthyroid.

People with normal TSH levels can have hypothyroid symptoms. This fact should mean that TSH should not be used to diagnose hypothyroidism. I have more patients coming to me with normal TSH levels, who on further testing, returned with extremely low, often below range, free T3 levels. Indeed, the TSH parameters are too wide.

Endocrinologists in the early 2000s attempted to bring the upper limit of TSH from 4 and 4.5 mIU/ L to 2 and 2.5 mIU/L, mainly because studies indicated hypothyroid symptoms were evident at 2 mIU/L. Additionally, the American Thyroid Association recommended the upper TSH limit for pregnant women be 2.5 mIU/L because higher levels were associated with risks of miscarriage, stillbirths, lower IQ, nonverbal brain morphology, and autism. Thousands of endocrinologists begged for the ATA to lower the upper limit of TSH for everyone in the 1980s, but the ATA refused.

The conclusion is that TSH is an unreliable measure to diagnose hypothyroidism. Many people can be hypothyroid with TSH levels in normal ranges. The upper limit is too high, and most people, even with a range of 1 mIU/L, can have severely low free T3 and free T4 levels.

Another issue for patients is that once taking natural desiccated thyroid, their TSH levels, if previously high, will not go into wide range dictated by laboratories. For their free T3 and free T4 to rise to an adequate level, TSH has to plummet below zero. The low TSH result will freak out the doctors who unwillingly prescribe the natural desiccated thyroid because they weren't taught about dosing natural desiccated thyroid in medical school. Seeing a low TSH number on the patient's test, they will again rely on TSH, which I have explained is irrelevant as a measure. The doctors will proclaim the patient hyperthyroid and refuse to prescribe natural desiccated thyroid. They will immediately put the patient on Levothyroxine, making them hypothyroid once again. Only free T3 and free T4 measure thyroid levels. If those are too high, then yes, the patient needs to reduce the dose.

The caveat to this is that I have seen patients who are hypothyroid unable to metabolize the T3 in natural desiccated thyroid because of low cortisol levels. Cortisol pulls thyroid hormone into cells. Without it, the T3 can spin around in the bloodstream, making the person not only feel hypothyroid but also make the levels in the bloodstream seem high. For this reason, I always have my patients test their salivary cortisol levels.

The most reliable serological tests of thyroid sufficiency are free T4 and free T3, but their wide laboratory reference intervals mean many patients will not be diagnosed due to variations in individual needs. Pregnancy is an example of this. Pregnant women need much higher levels of free T3 to achieve a healthy pregnancy. Ultimately, both the diagnosis and treatment of hypothyroidism must be clinical.