Why Is TSH Suppressed When Taking Natural Dessicated Thyroid?

[OllieMurph]

After searching and Googling, can't find an answer: What mechanism causes the TSH to be 'suppressed' (near zero) while taking NDT? Does this always happen? And how to explain this phenomenon to doctor who thinks I'm hyper on NDT even though my FT3 is in the normal range and do not feel hyper?

Also, what mechanism causes the FT4 to drop after starting NDT and what to do if it will not rise even after increasing dosage (cortisol, iron, vitamins etcetera are all good)?

Thank you for help with this!

[gimel]

I reported the problem with the link and they are working on it.

[OllieMurph]

Thanks so much for those notes. Was on synthetic T4 or T4/T3 for years where my TSH was not allowed to go much below 1.0 and my FT3 and FT4 never got above the bottom of their ranges. Never relieved of hypo symptoms - apparently always under-medicated. Not going to let that happen again.

Don't know how this is going to go with the NDT. Hope to persuade doctor with the notes. Still not able to access the link - will keep trying...:-)

Thanks again for your help!

[gimel]

When the link is active you can find the links to the studies I mentioned.  I also think you will find the following info taken from an old post of mine to be of interest.

gimel
Continuation of above.


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).”


The whole point is to medicate a hypothyroid patient adequate to relieve hypo symptoms without creating any hyperthyroid symptoms.  That condition is called euthyroidism.  

The thyroid status is a direct function of tissue thyroid hormone levels and effects.  There are lots of variables that affect tissue thyroid effects, as can be seen in Fig. 1 in the paper.  To think that a TSH test is adequate to determine thyroid status is ridiculous.  

[OllieMurph]

Finally found a copy of the article cached on the web. It appears to refer to L-T4 treated central or primary hypothyroid patients (not Hashimoto's) and does not seem to mention NDT treatment in regards to suppressed TSH.

Not sure if this will fly with doctor, but will give it a shot... :-)

Would love to find specific NDT/Hashi's/Suppressed TSH scholarly-scientific article to better make my case.

Thanks for the offer for doctor recommendations - may need that!

[gimel]

You can make good use of the link above by giving a copy to your doctor and ask him to read it and consider increasing your thyroid medication as needed to relieve those hypo symptoms, and ignoring the resultant TSH.  There is more than adequate scientific evidence in the paper that supports all that.  If the doctor is unwilling to do so, then you need to find a good thyroid doctor.   If you find that you need that, let us know and perhaps we can suggest a doctor in your general area that has been recommended by other thyroid patients.

[OllieMurph]

After reading so many online patient accounts of suppressed TSH with no hyper symptoms while on NDT, it is puzzling why my doctor does not seem to have experience with this.

Hypo symptoms that linger are mainly extreme exhaustion resulting in less exercise and persistent weight gain, puffy face. Seem to fluctuate between hot and cold easily.

Sometimes there is a pounding heartbeat in my head and whooshing noise - maybe hypo related. May be under-medicated, but need to convince doctor... :-)

Sure would be nice to get stabilized for as long as you have!

[gimel]

Not sure why the link is not currently available.  I expect it will be back soon.

You might be interested to know that due to the dosage of thyroid med I take, my TSH has been suppressed below range for so long I am not really sure of the time, but at least 25 years, with never any hyper symptoms.  And I am not the only member with a similar history.  

Those Free T4 and Free T3 results are far from optimal for many people.  Do you still have symptoms of hypothyroidism?

[OllieMurph]

Thanks so much for your reply! Unfortunately the link ( http://www.thyroiduk.org.uk/tuk/TUK_PDFs/diagnosis_and_treatment_of_hypothyroidism_issue_1.pdf )  seems to be unavailable at this time... error 404.

My treatment is for Hashimoto's, and after failing to improve on T4-only (and did not do well with adding in synthetic T3) was switched to NDT. Felt better on NDT, and lost some long-standing hypo symptoms. But after increasing the dosage over several months as required, the TSH bottomed out at 0.04 (0.45-4.50 range).

FT3 2.40 (2.0-4.4)
FT4 0.79 (.82-1.77)

Have been on NDT 7 months. Currently at 113.75mcg. (1 3/4 grains).

I will try the link again later and hope to read the studies. Thanks again... :-)

[gimel]

Our bodies evolved with the expectation of a continuous low flow of thyroid hormone from the thyroid gland.  When we take a large dose of thyroid med all at once, it suppresses the pituitary output of TSH for an extended period.  Scientific studies have shown that patients with central hypothyroidism typically have a suppressed TSH when taking adequate thyroid med.  Also, a study has shown that the majority of patients with primary hypothyroidism also will have a suppressed TSH when taking adequate thyroid med.  That is nothing to be concerned about since it does not mean you are hyper, unless you have accompanying hyper symptoms due to excessive levels of Free T4 and Free T3.  You can read about this in the following link.

http://www.thyroiduk.org.uk/tuk/TUK_PDFs/diagnosis_and_treatment_of_hypothyroidism_issue_1.pdf

I highly recommend reading at least the first two pages, and more if you want to get into the discussion and scientific evidence supporting everything that is recommended.  Note that Recommendation no. 10 talks about TSH being frequently suppressed when taking adequate thyroid med.  There are also references to the scientific studies I mentioned.  Giving a copy to your doctor might change his mind.

Regarding your question about serum levels not rising when starting on thyroid med, when starting on thyroid med, the hypothalamus/pituitary system responds by reducing the output of TSH, and thus the production of natural thyroid hormone.  Serum thyroid levels are the sum of both natural thyroid hormone and thyroid med.  So, from the same recommendation mentioned above, "only when TSH is suppressed enough to no longer stimulate natural thyroid hormone production will serum thyroid levels reflect further increases in thyroid medication."

[grant33]

Does taking one dose of desiccated thryoid at 65mg suppress TSH? How fast does that occur?