Most traditional physicians view the TSH (thyroid-stimulating hormone) as a as a key indicator of a patient’s need for more or less thyroid hormone.  The TSH level, however, is often a poor gauge of whether or not a particular patient is benefiting from the thyroid hormone she is taking.  

My approach to patient care is to gather as many medical clues as possible.  I listen to patients who have a normal TSH level and yet struggle with low-thyroid symptoms.  There are many possible reasons for these symptoms, and thorough diagnostic testing will reveal them.

With patients throughout the U.S., I offer a free, 15-minute phone consultation to anyone troubled by low-thyroid symptoms.  Scheduling is easy on the Contact Us page or by calling (704) 853-8000.

Understanding How the TSH Works

There is a protective barrier between the bloodstream and the brain.  This blood-brain barrier is particularly thin in a part of the brain called the hypothalamus, so the hypothalamus is able to detect how much thyroid hormone is in the blood.

If there is too little thyroid hormone, the hypothalamus produces TRH (thytropin-releasing hormone), which signals the pituitary gland, at the base of the brain, to release its own signal: TSH (Thyroid-Stimulating Hormone).  TSH causes a healthy thyroid gland to release both T4 (thyroxine) and a small amount of T3 (the active form of thyroid hormone) into the bloodstream.  

If there is enough thyroid hormone (T4 only) in the blood consistently, a patient’s TSH will be in normal range on a blood test.  If too much thyroid hormone is detected (as is the case in Graves’ Disease, for instance), the hypothalamus does not prompt the pituitary to do anything, and  a patient’s blood test will show a very low TSH level.  (See our Graves’ Disease page, under Low-Thyroid Symptoms, in the Menu.)  

Transporting Thyroid Hormone

When T4 and T3 are released into the bloodstream from the thyroid gland, “binding proteins” act as handy transportation.  These proteins attach and carry thyroid hormones to the liver ad to other cells. While attached to these proteins, thyroid hormone is called bound.  After reaching their destination, however, the transport proteins detach and set the hormone “free” again (unbound).  Free T4 and free T3 an be measured on a blood test.  To be useful to cells, thyroid hormone must be free.

Though measuring TSH is helpful, it has limited usefulness, because transporting thyroid hormone to cells is different from getting that hormone into cells.

A Larger Picture of Thyroid Health

The hypothalamus prompts the pituitary to act (to produce more TSH) when T4 (both bound and free) levels are too low in the bloodstream.  The hypothalamus, however, cannot measure how much thyroid hormone actually gets into a cell’s thyroid-hormone-receptor sites.  It also does not measure how much T3 (the active form of thyroid hormone) is available, either outside or inside cells.

Amazingly, there are site receptors for thyroid hormone on every cell in the body, including brain cells. Having enough useful thyroid hormone, therefore, is crucial for a healthy life.  That process involves a larger picture, however: the proper secretion of hormones from the thyroid gland; the proper transportation to cells; the proper release of binding proteins; the proper amount of thyroid hormone entering receptor sites inside cells; and the proper conversion of the inactive to the active form of hormone.

The TSH level on a blood test is a small part of that larger picture that doctors often ignore when treating hypothyroidism.  Every day, a healthy thyroid gland secretes hormone that is about 93% T4 and about 7% T3. To be useful, thyroid hormone must be free (unbound by transporting proteins), and it must get into cells, in order to convert some of that 93% inactive T4 into helpful active T3.

Blocking Thyroid Hormone: Cortisol

Free (unbound) thyroid hormone must get into thyroid-hormone-receptor sites.  These sites are inside cells, on the membrane surrounding the nucleus.  One impediment to thyroid hormone getting into these receptor sites is cortisol.  Cortisol, in fact, actually damages these sites.  The adrenal glands produce cortisol to help regulate metabolism and to aid the body in coping with stress.

If a patient is under stress (chemical, physical, and emotional), there will be increased cortisol production, and this cortisol might be blocking thyroid medication from doing its job.  In this situation, increasing the dosage wouldn’t alleviate symptoms, and it also wouldn’t matter whether that hormone was natural or synthetic.

Physical stressors that raise cortisol production include extreme temperatures; overtraining; overworking; and a lack of sufficient rest. Chemical stressors that raise cortisol production can be an overwhelming list: a poor diet high in refined carbohydrates; artificial sweeteners; hormone replacement therapy (HRT); birth control pills; hormone-laden foods (buy hormone-free meats); heavy-metal toxicity (such as arsenic, mercury and lead); food allergies and sensitivities; parasites; bacteria; viruses; household chemicals; pesticides and herbicides; smoking; air pollution; and alcohol.

Avoiding all of these sources of stress may not be possible, but it’s important to understand that stress increases cortisol production, which affects receptor sites and can lead to low-thyroid symptoms—regardless of a normal TSH level on a blood test.  Cortisol, however, is only one factor contributing to low-thyroid symptoms.  Other problems will be considered in Parts II and III.

Blocking Thyroid Hormone: Reverse T3

Another problem with stress is that it causes the body to produce more of the compound Reverse T3 (rT3).  Reverse T3 has two jobs in the body: to clear out excess T4 from the bloodstream and to prevent too much T3 from getting into cells.  For someone with a high rT3 level, it would be a mistake just to take more thyroid hormone (T4).  Doing so would simply increase the level of Reverse T3 in the blood.

In my practice, I advocate identifying and removing sources of chronic chemical, physical, and emotional stress to the body.  This often requires diet and lifestyle changes and nutritional supplement support.  

Reverse T3 is also increased by the long-term use of beta-blockers, such as propranolol and metoprolol; by Lyme Disease and other infections; and by chronic inflammation in the body.

Unfortunately, traditional Western physicians rarely consider the impact of Reverse T3.  By contrast, at Carolinas Thyroid Institute, we test for rT3 and treat a high level naturally, by identifying and removing sources of chronic chemical, physical and emotional stress; by suggesting that patients increase selenium intake; take nutrients that support adrenals; support the liver with milk thistle or artichoke extract; and reduce/eliminate alcohol, smoking, refined sugar, and gluten products.

Thyroid-hormone-receptor sites are influenced by other factors, also.  These problems will be discussed in Parts II and III, as well as binding and conversion issues.

There is no need to suffer with hypothyroid symptoms.  For anyone in the U.S. who is taking thyroid medication, has a TSH level in normal range, and is still dealing with low-thyroid symptoms, I offer a free, 15-minute phone consultation.  See our Contact Us page for scheduling or call (704) 853-8000.