Thought I answered this previously. Guess I didn't push the right key. Anyway, as far as I have read, suppressed just means that it is below the reference range. As we both are aware, many doctors erroneously believe that a suppressed TSH automatically means you are hyper. In fact you are hyper only if having hyper symptoms due to excessive levels of the Free T3 and Free T4 thyroid hormones. There are also studies showing that TSH is totally unreliable after starting thyroid meds. Again, many doctors don't recognize this, thus their misplaced fear about TSH suppression.
Of course, Free T3 and Free T4 are the biologically active thyroid hormones. Many years ago, after the advent of TSH testing, and before there was acceptable tests for Free T3 and Free T4, TSH became the single test that was supposed to reveal all that was worth knowing about thyroid status. So, TSH is supposed to accurately reflect levels of Free T3 and Free T4, but in reality it cannot be shown to correlate well with either, much less with symptoms, which are the most important concern. So, I find it very amusing that many doctors ignore actual thyroid hormone levels that are well within range, and get overly excited about suppressed levels of TSH. Now that we have sufficiently accurate tests for Free T3 and Free T4, why not just pay attention to the actual thyroid hormones rather than a surrogate test (TSH)? I don't get it.
Have you read or have any information when TSH suppression becomes more common with T4 medication.
All I have is anecdotal and by memory with reading the posts by people here. And it seems to me like with T4 only medication suppression is more common when the dosage gets to be about 175 mcg or above.
Granted I understand that it can happen virtually at any point given the amount of thyroid a persons thyroid gland may be putting out. While it seems pretty common to get TSH suppression with only small amounts of any T3 in it at all.
My wife is going to see her Endo again in early Nov. And we're trying to compile and compose a letter to send to him prior to that appointment.
After the 1st endo visit the End based from the only thing I can determine, that she is over-medicated due to her TSH being .201 to 0.5. So at or below the bottom of the TSH reference range. This despite her FT3 & FT4 being only about 25% to 27% of the range. AND her clinical response of feeling better and less symptomatic as her dosage has been increased of T4 (Currently 137 mcg/day). He seems to want to cut her back to where she was about a year ago. When we left the last Dr because they would not listen to her needing more T4 dosage. Why in the heck would it makes sense to go BACK to a point where you felt worse that you do now? That is TOTALLY ludicrous to me!
The endo did "offer" a clinical trial, as he called it of adding T3 medication. We want to take him up on his offer! However my wife also seems to have responded fairly well to T4 medication and with both FT3 & FT4 being lower in their ranges, I wonder if it would not make sense to do another dosage increase of T4 first? But I'm fearful if no discernible improvement results, he will then conclude that she is in fact over medicated.
I'm a little torn. Because we can I think "cut to the chase" by adding T3. And if she starts to feel well with the T3 medication,which I fully believe she will, but who really knows until you try.
And I'm sure should she start taking T3 medication, that her TSH will go to or near zero. Which may cause him to freak out.
Yes I hear on the Endo wanting to cut back on the T4 dosage. I also have a supressed TSH (It is all the doctors run) of 0.17 @ 200mcg Synthroid.
However since my Endo is on maternity leave until end of Nov. neither my PCP, GYNO, or back up Endo will mess with my dosage upon my request to leave alone until I see my regular Endo. They all agreed that as long as I had no hyper symptoms I was fine to wait until I see her at the end of Nov.
I know she is going to freak out & will cut my dosage, however, I am praying my TSH is not still supressed when I get lab work done again on Nov. 20. All I can do is politely tell her I feel better than ever...on this dosage.
This info should take care of your doctors' concerns.
"Fraser et al investigated the correlation between tissue thyroid activity and serum blood tests (TSH, free T4 and T3) and published their results in the British Medical Journal. The study authors concluded that “The serum concentration of thyroid stimulation hormone is unsatisfactory as the thyrotrophs in the anterior pituitary are more sensitive to changes in the concentration of thyroxin in the circulation than other tissues, which rely more on triiodothyronine (T3).” They found a suppressed or undetectable TSH was not an indication or a reliable marker of over replacement or hyperthyroidism. They state,
“It is clear that serum thyroid hormone and thyroid stimulating hormone concentrations cannot be used with any degree of confidence to classify patients as receiving satisfactory, insufficient, or excessive amounts of thyroxine replacement…The poor diagnostic sensitivity and high false positive rates associated with such measurements render them virtually useless in clinical practice…Further adjustments to the dose should be made according to the patient’s clinical response.” (121)
The positive predictive value of the TSH, which is the likelihood that as suppressed TSH indicates over replacement or hyperthyroidism, was determined to be 16%. In other words, a suppressed TSH is not associated with hyperthyroidism or over-replacement 84% of the time, making it an inaccurate and inappropriate marker to determine appropriate replacement dosing. Additionally, the TSH becomes an even worse indicator the optimal replacement dose in the following situations: if a person has insulin resistance or obesity (68,69,70,71,106); is a chronic dieter (4,51,66,72,112,113,114,115,116,117,118); has diabetes (69,73,74,75,76); has depression (73,77,78,79); has bipolar depression (73,77,81,82); has a neurodegenerative diseases (73,83,84,85,86,87); is of older age (73,74,88-100); has chronic fatigue syndrome (73,101,102); has fibromyalgia (73,103,104); migraines (73); has a chronic infections (MT63)(73); is stressed or anxious (73,79,80); has heart failure or cardiovascular disease (73,99,104,105,108); suffers from migraines (73); has inflammation or a chronic illness (73,109,110,111); or has high cholesterol or triglyceride levels (57,58,60,72,106,107,114).
In a study published in the British Medical Journal, Meir et al also investigated the correlation of TSH and tissue thyroid effect. It was shown that the TSH level had no correlation with tissue thyroid levels and could not be used to determine a proper or optimal thyroid replacement dose. The authors concluded that “TSH is a poor measure for estimating the clinical and metabolic severity of primary overt thyroid failure. … We found no correlations between the different parameters of target tissues and serum TSH.” They stated that signs and symptoms of thyroid effect and not the TSH should be used to determine the proper replacement dose (122).
Alevizaki et al also studied the accuracy of using the TSH to determine the proper thyroid replacement dose in T4 treated individuals. The study found that such a practice of using the TSH, although common, results in the majority of tissues being hypothyroid, except for the pituitary. They conclude, “TSH levels used to monitor substitution, mostly regulated by intracellular T3 in the pituitary, may not be such a good indicator of adequate thyroid hormone action in all tissues (123).”
In a study published in the Journal of Clinical Endocrinology and Metabolism, Zulewski et al also investigated the accuracy of TSH to determine proper thyroid replacement. The study found that the TSH was not a useful measure of optimal or proper thyroid replacement, as there was no correlation between the TSH and tissue thyroid levels. Serum T4 and T3 levels had some correlation, with T3 being a better indictor than T4. In contrast, a clinical score that involved a thorough assessment of signs and symptoms of hypothyroidism was shown to be the most accurate method to determine proper replacement dosing. The authors also agreed that it is improper to use the TSH as the major determinant of the proper or optimal doses of thyroid replacement, stating “The ultimate test of whether a patient is experiencing the effects of too much or too little thyroid hormone is not the measurement of hormone concentration in the blood but the effect of thyroid hormones on the peripheral tissues [symptoms] (124).”
If you want to go further, this is the link where you can see the references to the scientific studies supporting all the above info. Don't let your doctors dismiss all this very conclusive information and decide to reduce meds.
My TSH (55+ at dx) sunk to the basement on 25 mcg synthroid. Thank goodness the doctor had told me to take that dose for 2 weeks, then up to 50, for 2 weeks, then up to 75 and retest 2 weeks later.... that puts us at week 6 after dx. My TSH was then < 0.001; at one point it went all the way up to 0.013. Hey it got better.
Even with TSH of < 0.001, my FT4 was below range...... doctor refused to test FT3 and cut my dosage; had me back to 25 mcg, nearly dead. Fortunately, circumstances were in my favor and I got referred to an ENT, who ultimately referred me to an endo...I took me 4 years to get well. It's only been in the past year that my FT3/FT4 levels have come up to something I can live with, but TSH still lives at < 0.01
gimel has given you the scientific data; doctors aren't going to read a lot, that doesn't agree with their thinking, so you might want to take out a few key points, but make sure the links are provided, in case he cares enough to research.
One of the most frequent questions I receive is from patients regarding their thyroid tests. The thyroid gland produces mainly two different hormones: T3 and T4.
Most doctors do not test for these, but instead check for TSH (thyroid stimulating hormone) which is NOT a thyroid hormone at all. It is produced by the pituitary gland and is an INDIRECT measurement of thyroid function. If the thyroid is doing its job (producing optimal amounts of T3 and T4), then TSH will be low. If TSH is elevated, then the thyroid is likely sluggish. The range of TSH reported by the lab as normal is between 0.4 - 4.5- more than a 10 fold difference! For most healthy people, the TSH should be below 2, but more importantly one should measure the free T3 and free T4- the ACTUAL thyroid hormones. And of course listen to the patient's symptoms.
When you are being treated with thyroid hormone, the TSH should be very low as long as the T3 and T4 are not too high. More often than not, doctors will lower a patient's thyroid medication based on the TSH being "too low" without measuring the actual levels of the hormones directly. This goes back to our training when we are taught that a low TSH is a sign of an overactive thyroid gland; this is true but NOT IN A PATEINT TAKING THYROID MEDICATIONS. A low TSH should be the goal of treatment, not a sign of overtreatment as long as there are no signs or symptoms of overtreatment.
I'm torn. I understand that the Dr may not read the entire article. But I want to refer to it and have the article highlighted for his easy reference.
I'm torn to keep this relatively simple so he will read what I provide in both letter and attachments. We also feel like this is our one and maybe last shot to get proper treatment. At least for another year. You see it is time for my work to choose the HMO for the next year. And by the time we have the appointment, it will be past the date to change HMO's. So we'd be "stuck" with this Dr for another year.
That national academy of hypothyroidism article is 6 pages long but has 12 pages of footnoted references. That is AMAZINGLY sound credible documentation that seems almost unimpeachable.
If you have time before the appointment, I think I would put all your questions in a letter, referencing attached information, and the included extensive references to supporting scientific data supporting your requests. Maybe even put a little pressure on the doctor by saying you need to understand his plans for further treatment for your wife, before the date at which you have to make a decision about your health insurance.
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