What is a normal thyroid hormone level?
The pituitary gland produces a hormone called thyroid stimulating hormone (TSH). The pituitary gland regulates the production of TSH, something we’ll look at in more detail in a minute.
TSH is designed to stimulate the thyroid into producing T4, also known as thyroxine. Different people produce different amounts of TSH, and depending on where in the world you live, you may be defined as hypothyroid in one country and euthyroid (normal thyroid) in another country, based on the arbitrary “normal” reference range.
When the thyroid does not produce enough T4, your TSH level rises to try to stimulate your thyroid into making up the short fall. This means that a high TSH value is indicative of primary hypothyroidism. If the thyroid is not making enough T4 in response to TSH, this means with certainty that the thyroid itself is damaged in some way.
In the UK, the “normal” range for TSH is considered to be between 0.5 and 5. In the US, this was the case, however, doctors revised the normal range down to be 0.3-3. Unfortunately there has been much dithering over this in the US, and many labs are still using the old reference range, resulting in a treatment lottery.
TSH levels vary throughout the day by as much as 2-3 points. They are roughly the same at 6AM and 6PM, lowest at noon, and rise in the evening to be highest at midnight. Google books reference (pdf). Sleep inhibits TSH production, so your TSH levels fall throughout the night. Sleep deprivation prevents this inhibition and leaves TSH levels high.
I’m not able to find a decent page explaining whether the menstrual cycle affects TSH output in humans, most say there is very little difference. In rats, TSH is high at the start of the menstrual cycle and falls low towards the end. There are slight hints of a similar, very small variation in human women, but nothing substantial.
The controversy over TSH is that doctors have a tendency to regard it as the gold-standard for thyroid testing and may not even test actual T4 and T3 levels. There is also the assumption that if TSH falls within the normal range, that the thyroid function is normal. This is not true. Many patients with primary hypothyroidism complain of continuing hypothyroid symptoms when their TSH has reached the normal range, and may not recover fully until TSH levels have fallen relatively low. There seems to be little treatment standard regarding this, though I have found in several places recommendations that doctors who are tailoring their patient’s thyroxine dosage should shoot for a TSH of around 1, and many patient advocacy groups say that hypothyroid patients feel best when their TSH is below 1. There are also many instances of patients with TSH in the normal range having significant hypothyroid symptoms that resolve with thyroxine treatment.
Welcome to the murky world of the clinical presentation versus the laboratory test. Thyroid Australia have a number of quotes and links regarding this.
Individuals appear to have their own unique “set point” requirement for T4 levels. One can test in the “normal” range, but actually have a clinical presentation of hypothyroidism because one is below one’s own particular set point. My own T4 levels are scraping the bottom of the “normal” range. Technically I am regarded as having “subclinical hypothyroidism” because my T4 is still “normal”, but I have a clinical presentation of carpal tunnel syndrome, eczema, weight gain problems, massive food intolerances, mood disturbance, and a basal body temperature of 35.5°C. Obviously my own “set point” for T4 should be a lot higher than it is.
High individuality causes laboratory reference ranges to be insensitive to changes in test results that are significant for the individual. Narrow Individual Variations in Serum T4 and T3 in Normal Subjects: A Clue to the Understanding of Subclinical Thyroid Disease.
Usually, but not always, when a person’s own unique “set point” is breached, TSH rises. But it doesn’t always.
Back to the pituitary gland. Sometimes the pituitary gland gets damaged. When this happens, it may not produce enough TSH to stimulate the thyroid into making enough T4. Though many endocrinologists regard this as relatively less common compared to primary hypothyroidism, in recent years a number of specialists have made a connection with fibromyalgia and chronic fatigue syndrome.
Because the pituitary gland is not making enough TSH, the TSH levels may appear “normal” or low. The T4 levels may also appear to be “normal” or low. Whatever the case, the person’s own unique “set point” for thyroid hormone production has been breached, and as a result they are experiencing the clinical symptoms of hypothyroidism.
As you can see secondary subclinical hypothyroidism can, under some circumstances, be impossible to spot with a laboratory test. All one has to rely on is the clinical presentation of the patient. Hence, patients may be written off as having “fibromyalgia”, “ME”, or “Chronic Fatigue Syndrome”, when in fact they have secondary subclinical hypothyroidism.
There are a number of private specialists in the UK and around the rest of the world who are willing to treat patients based on their symptoms of hypothyroidism rather than a laboratory test. As a result, they have faced strict sanctions and in some cases have been suspended or struck off. However, the patient advocacy forums I have found are buzzing with people who were formerly diagnosed as having fibromyalgia, who have now recovered after being prescribed thyroxine. This is actually quite a shocking situation.
The pituitary gland is the organ that regulates metabolism during a diet. Apparently in animals, there is a very strong TSH level fluctuation during fasting, however, in humans, this metabolic variation is quite small. Nonetheless, the pituitary gland will lower TSH output in response to a strenuous, long-term diet or fast, thereby reducing metabolism by reducing T4 levels. This usually corrects again once a normal amount of calories is eaten.
The probable reason that this metabolic response is limited in humans, is that the brain requires thyroid hormone. Though most of the tissues in the body are able to adapt to lower thyroid hormone levels, the brain cannot, and responds by stimulating the pituitary gland to make more TSH. Humans have particularly large brains with a high energy consumption. Twenty percent of our caloric intake is burned by the brain. It makes sense, therefore, that people with subclinical hypothyroidism experience mental symptoms long before they experience physical ones: the body can adapt to some extent, but the brain cannot. Hence, brain fog, attention deficit disorder, memory problems and mood swings are the early warning signs of hypothyroidism, but are rarely ever diagnosed as such because they may be caused by relatively mild thyroid hormone deficiencies.
What makes the pituitary gland release TSH? Another hormone, secreted by the hypothalamus, called thyrotropin-releasing hormone, or TRH.
Tertiary hypothyroidism is relatively rare. If the hypothalamus is damaged, it will not release enough TRH, thereby failing to stimulate the pituitary gland to produce enough TSH, thereby failing to stimulate the thyroid into producing enough T4.
It may actually be possible to measure secondary subclinical hypothyroidism with a TRH challenge test. By giving TRH, one should get a relatively predictable response from the pituitary gland, which should release a “normal range” of TSH. If the patient’s output of TSH is blunted, this is indicative of secondary subclinical hypothyroidism.
Thyroid Hormone Resistance and T4 to T3 Conversion
These are controversial topics. Doctors say that resistance to thyroid hormone is quite rare, however, on a subtle level it is not. There are many genetic polymorphisms to thyroid hormone receptors. There is some limited evidence that people with red hair (MC1R and POMC) may have slightly different behaviour of the hypothalamic-pituitary-thyroid axis than other genotypes due to crossovers between this system and the melanocortin system. This however, should be seen as part of a bigger picture of genetic diversity, all of which contributes to an individual’s unique “set point” for thyroid hormones.
There is also a lot of anecdotal evidence from patients who do not respond well to synthetic T4 treatment that they may also require supplementary T3. Most of the conversion of T4 to T3 occurs in the liver, kidneys, and in peripheral tissues all over the body, however the thyroid gland does put out about 20% of T3 itself, which it would not be able to if it is damaged or impaired. There may also be genetic reasons that this conversion is impaired in some people, who do better on Armour thyroid or other natural thyroid extracts that contain T3 than they do on synthetic T4 preparations like levothyroxine. This is thought to be particularly true in cases of long-standing hypothyroidism.
Where do you go from here?
If you have hypothyroid symptoms but your doctor tells you that your test results are normal, ask for a copy of your test results yourself. If they appear borderline to you, you may wish to pursue the thyroid theory. You may also wish to monitor your basal body temperature in the morning and ensure that it is in range, bearing in mind that it fluctuates with your menstrual cycle. This is not necessarily indicative: my basal body temperature has been at the low end of the normal range for years. Monitor your weight too. Calculate the right number of calories for your metabolism. If you are prone to easy weight gain and bloat despite caloric control, you should consider hypothyroidism.
If you can’t get your doctor to treat you based on your clinical symptoms, Mary Shoman has a very good list of recommended doctors from around the world who are willing to listen to patients first and foremost above the results of laboratory tests.