I'm done.
Good luck to all.

Snippy

Your TSH is the same as my current TSH.

I just started a thread about my doctor who is quite thyroid-savvy.

http://www.dailystrength.org/c/Graves_Disease/forum/13668970-my-doctor-thinks-outside

I've even had unmeasurable TSH ( less than .006) and my doctor hasn't blinked an eye.

On a "good" day, my TSH is .011

(I have Graves' blocking antibodies now - they not only suppress TSH but, make the patient hypo - this happens to about 20% of Graves' patients after remission. It can be temporary but, just like hyperthyroidism, it needs to be treated)

Atc we are not trying to run you off we are just asking to see where you got your info.

Snippy, how horrible about your dog. I could not imagine my dog not being with us, and I feel your pain.

Hey, not to be disruptive and I hope you gals know I have you up with god. But I always researched anything god-like too, so I also tried to see what ACT sees.

This is what I found in 5 seconds:

http://www.ncbi.nlm.nih.gov/pubmed/18083940

I can not find more details but it IS a trusted website. So there is a school of thought out there that can quatify ATC's statement.

BTW, I am not suggesting that Snippy has to up her dose, that seems absolutely counter effective, she would be hypo before you know it, I am sure. But maybe there is a point of thruth in the TSH has effect on boneloss?

ATC, I would be interested in your sources. You know I do not always agree with you or the "tone" of the post, but I also realize often the intention gets lost in someone's writing style. So please, would you like to give your sources, so I can use it to educate my self and others?

Thanks.

okay so now I am followig links:

http://www.ncbi.nlm.nih.gov/pubmed/18925834

"CONCLUSIONS:

Within the normal range of serum TSH, serum TSH was not associated with BMD. The small groups of men and women with serum TSH consistent with hyperthyroidism had lower BMD at the forearm than those with serum TSH in the normal range"

I am just another thyroid brain nutcase but what I have read in this small article is that they excluded patients with thyroid meds AND the BMD loss is with people that have low TSH AND consitent with hyperthyroidism. Now that makes me wonder: Did they mean in a hyperthyroid state or also people that are NOT hyper thyroid anymore under the influence of ATD, thus normal Free T but antibody caused low TSH.

So, still not really have an answer, but now I am on a mission.

I know some of you do not enjoy her input, but I really hope that ATC wants to share her sources, because I am just curious now. Don't shoot me but this is how was the most annoying student in nursingclass and I also ended up in the top 3 graduating. LOL

It is well-documented that suppressed TSH in the absence of highly elevated thyroid hormone levels is not a problem.

I will go digging for the studies - I have SO many links that, even with titles and categories, I have trouble finding them sometimes.

OK.....here's a site that has a large number of links to medical journals

http://www.altsupportthyroid.org/tsh/tshmedrefs5.php#bone

The key to our situation is the fact that our antibodies suppress TSH.

If our thyroid hormone levels are in-range, we're good.

It's the people who have hyperthyroid levels as a result of Graves' or those who are taking too-high doses of thyroid hormone replacement that are at risk.

TSH in and of itself has no physiological implications.

TSH is like FSH (one of the tests to gauge menopause).

Having a certain FSH doesn't mean our health is at risk - it just means whether or not we'll have a menstrual period.

Same concept with TSH - it doesn't mean our health is at risk - it *might* mean we are hyper or hypo but, again, our antibodies can make TSH information unreliable.

nursenat

As you are discovering, it's suppressed TSH *in conjunction with* hyperthyroidism (over-range thyroid hormone levels) that put us at risk.

To everyone

Check out the final sentence of this link

http://www.ncbi.nlm.nih.gov/pubmed/12915350?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_SingleItemSupl.Pubmed_Discovery_RA&linkpos=4&log$=relatedreviews&logdbfrom=pubmed

" TSH determination is diagnostically misleading and only free hormone measurements are reliable for thyroid function assessment."

So, just playing advocate off the devil here, I am not challeging anyone's knowledge or feelings, I hope you girls hear my investigative thoughts and heart.

But when I read this

"We can now provide results that not thyroid hormones but also TSH itself has an equally important role to play in bone remodeling"

I do not read any denial of the fact that TSI surpresses TSH, I totally see that and how that works. But apareantly there has been some research done that makes doctors say this too. Both things can go together, one statement does not denie the other. I got to run and get my toddler ready for preschool but I can still see how atc gets her ideas. Although I am not sure if I agree with it, I can SEE her point based on these summaries.

I wish atc would have posted what she found on this topic...I am sorry she felt she could not. There is so much info out there...some is very out dated. Perhaps this info you posted nursenat are results of hyperthyroidism where antibodies are not present. Just wondering. There are cases of this happening. Big Hugs...Kathy

YEAH, Dairy, I never thought of that! Just common sense, huh?

Well, I just read this thing with links

http://mythyroid.com/osteoporosis.html

My final conclusion based on reading this, is that the labeling of low TSH and being hyperthyroid is being interchanged and for some people mean the same thing. And this article ofcourse is not about Graves but people being treated for hyPO/cancer. But still, after reading back and forward, I also think your very keen observation is right Ms Dairy (-: Also from reading all of the stuff I dived my self into, I do think even if TSH alone could effect BMD (which I suspect is not a huge influence if any) it does not outway the benefits to keep yourself feeling well in general and like the conclusion said: You can always supplement if BMD is an issue.

So my curiosity is satisfied! Thanks for putting up with me! LOL

To all and everyone: Feel good and make sure you get your calcium and Dvits!

The problem with Snippy is that they are ONLY looking at her tsh when her frees are at the BOTTOM of the range or even lower on more meds. She had many symptoms of being overdosed too. This is what docs do with Graves patients all the time. She may have antibodies too for Hashi's and the blocking antibodies are keeping her tsh low. Some people have low tsh for months and months or longer but you don't treat by that, you are supposed to be treated by FT4 and hers was extremely low.She probably didn't have enough FT4 to convert to FT3 either so she really felt crappy.
Snippy,if you stay on 5 and get tested in 6 weeks from when you started, see where you are in your free levels then. This will buy you time to find another doc. Nobody stays on a 20 mg dose after a few months,especially when your numbers fell like they did, you need to gradually taper down not up. Bone loss is NOT caused by low tsh, high thyroid hormone levels are. If you can find documentation about how Graves shouldn't be treated by tsh you could show the doctor. Maybe CD can help you find something. Look on Elaine Moore's site.. type it in the search engine. MM do you have that article somewhere?

I think many here are familiar with a popular thyroid hormone replacement med called "Armour".

Here's a link to the prescribing information for Armour:

http://www.frx.com/pi/armourthyroid_pi.pdf

If you scroll down to page 2-3, you will see the indications and usage section.

Paragraph 2 of this section reads "Armour Thyroid tablets are indicated

2. As pituitary TSH suppressants, in the treatment or prevention
of various types of euthyroid goiters, including thyroid nodules,
subacute or chronic Iymphocytic thyroiditis (Hashimotos),
multinodular goiter, and in the management of thyroid cancer. "

So, if it's safe for people with Hashi's, nodules, and thyroid cancer to have suppressed TSH, I would think no one should have concerns about suppressed TSH as long as thyroid hormone levels (FreeT4 and FreeT3) are in-range.

You folks have already heard me say how happy I am with my current doctor since she has said "we know to ignore TSH in Graves' disease".

Here's Elaine Moore's writing about proper dosing with medical references at the bottom

http://elaine-moore.suite101.com/antithyroid-drugs-in-graves-disease-a125139

I copied and pasted this article from the online thyroid textbook Thyroid Disease Manager. It includes the ground-breaking study about our antibodies affecting TSH.

At the end, it mentions that treatment should be guided by serum T4 & T3 (FreeT4 & FreeT3) and not serum TSH


"Long-term TSH suppression in Graves- hyperthyroidism
Topic: GRAVES- HYPERTHYROIDISM
Title:Continued suppression of serum TSH level may be attributed to TSH receptor antibody activity as well as the severity of thyrotoxicosis and the time to recovery of thyroid hormone in treated euthyroid Graves- patients.
Authors: Chung YJ, Lee BW, Kim J-Y, Jung JH, Min Y-K, Lee M-S, Lee M-K, Kim K-W, Chung JH.
Reference: Thyroid 16: 1251-1257, 2006
SUMMARY
Background:
Serum TSH may remain suppressed for weeks or months despite normalization of serum T4 and T3 concentrations during antithyroid drug treatment in patients with Graves- hyperthyroidism.
Purpose:
To evaluate the relationship between TSH receptor antibodies or other clinical parameters and the continued suppression of serum TSH during antithyroid drug therapy in Graves- disease.
Patients & Methods:
One hundred and sixty seven patients with Graves- disease were studied. They had remained euthyroid for at least 12 months after normalization of serum T3 and T4 during treatment with antithyroid drugs. Initial therapy with 200-450 mg of propylthiouracil (n=137) or 15-45 mg of methimazole (n=30) resulted in normal serum T3 and T4 after 2.8 - 1.6 months in all patients. Antithyroid drugs with dose adjustments were continued for up to 36 months. Recovery of serum TSH was defined as a return of serum TSH to levels >0.30 mU/L. TSH receptor antibodies were measured using a first generation TBII assay: values >15% were considered positive.
Results:
At the time of diagnosis, there were no differences in age, sex ratio, serum T4 and TSH between TBII-positive (N=133) and TBII-negative (N=34) patients, but serum T3 and I-131 uptake were higher in TBII-positive patients. The interval between onset of treatment and recovery of TSH was 8.7 - 5.9 months. This interval was positively correlated to pretreatment serum T3, uptake of I-131, and TBII. The interval until recovery of serum TSH was 9.4 - 6.1 months in TBII-positive and 6.0 - 4.0 months in TBII-negative patients. Recovery of serum TSH at 3, 6, 12, 18, 24, and 30 months, after the normalization of serum T3 and T4 were 39%, 62%, 63%, 74%, 88%, and 86% respectively in TBII-positive patients. The corresponding figures in TBII-negative patients were 74%, 91%, 91%, 91%, 94%, and 90% respectively. There was no difference in serum T3 or T4 between TBII-positive and TBII-negative patients at 3, 6 and 12 months after normalization of serum T3 and T4, but TSH levels at these time-points were lower in the TBII-positive patients. TBII correlated inversely only with serum TSH.
Conclusions:
Continued suppression of serum TSH in patients with Graves- disease during antithyroid drug treatment is related to TBII, pre-treatment severity of hyperthyroidism, and time to normalization of serum T3 and T4.
COMMENTARY
Present study confirms and extends previous reports that TBII may be causally related to continuous TSH suppression in treated patients with Graves- hyperthyroidism, despite normal serum T3 and T4 concentrations. Evidence supporting a causal relationship is provided by the longer time interval between normalization of serum T3/ T4 and normalization of serum TSH in the TBII positive patients, as compared to the TBII-negative patients, and the inverse relation between TBII and TSH, independent of ambient serum T3 and T4 concentrations. The mechanism proposed to explain this observation is the binding of TBII to TSH receptors in the pituitary. TSH receptors have been demonstrated in folliculo-stellate cells of the human pituitary. Binding of TSH to these receptors might down-regulate TSH synthesis and release, thereby providing an ultra-short loop feedback in the regulation of TSH. How the folliculo-stellate cells signal to the thyrotroph cells remains to be elucidated. Binding of TBII to the folliculo-stellate TSH receptors might likewise inhibit pituitary TSH release.
The present study also showed that the time period required for normalization of TSH was determined - besides TBII - by pretreatment T3 levels as well as by the rapidity of normalization of serum T3 and T4. Because pretreatment T3 was higher in TBII-positive patients, it remains plausible that these two other determinants of TSH recovery time were not independent factors. Nevertheless, the clinical relevance of the present study is that as long as serum TSH is suppressed, dose-adjustments of antithyroid drugs should be guided by serum T3 and T3 results and not by serum TSH. Some patients maintain a suppressed TSH for years and, occasionally, one may see patients with clearly decreased FT4 levels because they receive a dose of antithyroid drugs that is too high in the presence of a TSH that is still suppressed.(Summary and commentary prepared by Wilmar Wiersinga)
Present summary and commentary are related to Chapter N- 11 (Section on Antithyroid Drug Therapy) of TDM"