Thyroid Q and A or Running Hot and Cold


My Thoughts on TSH testing in Hypothyroidism (Read 613 times)

    My Thoughts on TSH Testing in Hypothyroidism TSH testing evolved because doctors were looking for a better way to test thyroid supplementation in their patients. Prior to TSH tests, doctors primarily relied on their clinical assessment of their patients and treated to relieve symptoms. TSH testing has only been around for 20 years. TSH is thyroid stimulating hormone and is released by the anterior pituitary gland in response to signals received from the hypothalamus (TRH or thyroid releasing hormone). TRH acts on the pituitary, which in turn sends TSH to the thyroid gland to tell it to step up or slow down production of T4 and T3. This means that when you look at TSH, you are looking at the function of the HPT axis = hypothalamus, pituitary, and thyroid glands. When a doctor looks at the TSH, he is using that value to determine if your levels of thyroid hormone are too high or too low. Most current normal values are in the range of 0.4 – 4.5. What does a normal value mean? It means that when the study was performed that determined the range, *most* people were without symptoms when their labs fell between those 2 numbers. Does that mean that *normal* or euthyroid people’s values fluctuated between those 2 values? The answer is NO. People have an individual normal range that is really quite narrow. For example, one person may range between 1-1.5; another might be 2.5 – 3.0. Yet a doctor may tell you that you do not have a problem even when you fall outside your normal range – even if you have symptoms. It seems that men tend to have slightly higher values, and women seem to feel best when they are closer to 1. If your personal values have been 1 – 1.5 and you suddenly start getting readings in the 3+ range – that is a sign that something is not functioning right. Unfortunately, there have been many people who this has happened to with symptoms of hypothyroidism, who have been told that their symptoms are from something else because their TSH is “normal”. There have been questions raised by doctors that the original test group may have included people who were actually subclinically hypothyroid. In fact – the original “normal” values went up to 10, and have only recently been lowered to 4.5-5.0 as the upper limit of normal. Even now there is discussion among doctors as to the further lowering of the normal range to 0.3 – 3.0. If you are euthyroid – your pituitary basically releases TSH in spurts about every 2 hours. That says to me that your thyroid is releasing it’s hormone a little at a time throughout the day. I think of it as keeping your foot on the gas pedal to maintain a steady speed. Thyroid hormone is what drives the activity of every working system in your body. It is that critical. The thyroid gland releases T4, T3, T2, T1 and calcitonin. At this point, medical science is unsure of the role of T2 and T1. Calcitonin is involved with bone metabolism, but the parathyroids also handle that function. The majority of hormone that is released is in the form of T4. This is the storage form of thyroid hormone and it needs to be converted to T3 in order to be used by the cells. Conversion of T4 to T3 seems to take place primarily in the liver, but also at the cellular level. Small amounts of the more potent T3 are also released. What we presently know is that conversion is under the control of three enzymes; type 1 (D1), type 2 (D2) and type 3 (D3) iodothyronine deiodinases. What medical science does not know, is what is going on at the cellular level –current tests just measure what is circulating in the blood. What does this mean as far as your lab tests? Total T4 = both the bound and unbound (free) levels of T4 – only the free portion is available for use by the cells. 99.97% of T4 is bound by carrier proteins. That means that only 0.03% is free for use, and it is that 0.03% that is being measured in your Free T4 labs. Total T3 = both the bound and unbound (free) levels of T3 – only the free portion is available for use by the cells. 99.7% is bound by carrier proteins. That means that only 0.3% is free for use, and it is that 0.3% that is being measured in your Free T3 labs. Question: why would our thyroids release so much hormone only to have the vast majority of it bound and not usable at the cellular level? Is there a reason/purpose for so much being bound and kept in circulation? We won’t know the answer to that until we can see what is going on within the cell. It seems there are different categories – hypothyroid from genetic abnormalities, autoimmune disorders, treatment for hyperthyroidism, and those that have had their thyroids removed. Why are all these categories judged against the same standard TSH values for the purpose of medication doses? I agree that TSH can be an important tool in determining doses, but it should be a tool and not the only standard. Clinical observation, levels of Free T4 and Free T3, and patient symptoms should be equally important. Particularly in the case of total thyroidectomy – your body is basically slammed with a once a day total replacement dose instead of a slow consistent release throughout the day. You have also lost your source of ready made FT3, and all of that must now come through conversion. Studies have shown that people can achieve normal FT3 levels just through dosing with T4 – BUT, it takes a much higher level of circulating T4 to achieve those results. Wouldn’t the single dosing and higher than your previous normal levels of T4 result in a low TSH, but not reflect a hyperthyroid state? If your T4 levels are always high (higher than they were before surgery), and your dose is providing you with all the T4 you need, where is the incentive for the pituitary to send out the TSH signal, when that signal means – give me more T4/T3? Question: People absorb their oral thyroid replacements as different rates. How does the differing rate of absorption affect TSH? Is it possible that a barely detectable TSH in a person post total thyroidectomy actually means that they are being optimally replaced? Particularly if their FT4 and FT3 were within normal range, and there was no clinical signs of being hyperthyroid? (under normal circumstances, low TSH would mean hyperthyroid). Why do some people have hypothyroid symptoms with relatively little change in their TSH levels and others seem hardly bothered by big changes? Could it have something to do with the function of D1, D2, D3? Or is something else going on at the cellular level that we currently don’t know about yet. There seems to be a general reluctance to even test FT3 levels, supposedly because they are thought to be erratic. From what I have been able to find out, part of this “erratic” pattern was found because labs were being done at different times during the day. It appears that to have total reliance on TSH as a “gold standard” test, is to assume normal function of the HPT axis, and normal function of conversion of T4 to T3 at both the liver and cellular level. It seems to me that there is room for a lot of potential problems to arise in areas that science is not yet easily/able to test. I worry that we now have a generation of doctors with an over reliance on the “gold standard” TSH test; a generation of doctors who no longer have the clinical experience to guide them when it comes to the significance of symptoms of hypothyroidism, symptoms that may be disregarded as coming from hypothyroidism because of an over emphasis on the value of the TSH as a stand alone test. People who in the past would have been treated, or treated more aggressively are being told “it’s not your thyroid” because of a TSH value in a certain range. If you read this and do not currently have a thyroid problem, I would advise you to have free T3, and free T4 levels done with your TSH screening so you would be aware of what your normal range is. You should have all your testing done under the same circumstances – first thing in the morning. Keep copies of your own lab work.

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    Go With The Flow
    Thyroid Support Group

      Thank you for putting this all down. Very interesting info.

      Go as long as you can, and then take another step.

        Cheryl, I just got through reading the entire thing but I am glad you put it all down. Your way of explaining the thyroid-pituitary axis made more sense to me than anything else I have read. Thanks!

        Driver, Runner, Bestie

          Thank you for this explanation. I will have to read again. This thyroid stuff is brand new to me; I've been treated since only this summer. It is so complicated.