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what is the difference between a supressed tsh and a low tsh
so full of questions today does anyone know what is the difference between a suppressed tsh and a low tsh- was reading the new research and can t find the difference
COMMUNITY LEADER
I agree 100% with Deb -- I did some research (gimel, you sent me some good info a while back) into the theory that suppressed TSH causes osteoporosis because this is what my doctor was telling me and he wanted to keep lowering my med to bring my TSH up, but my FT's were just barely in range, so I was being kept hypo.
I'll have to look for it again, but this is a controversial subject right now and most of the data points to it not being the lack of TSH that causes the problems, it's excess T3.
As in my case, with my FT's now being good and only a very few, mild symptoms, I would fight tooth and nail to keep from having my meds dropped at this point, regardless of the fact that my TSH is basically nonexistent. Fortunately, my endo agrees with me, even though he also realizes that this is controversial yet, so I no longer have to beg to keep my med at the level needed.
I'll have to look for it again, but this is a controversial subject right now and most of the data points to it not being the lack of TSH that causes the problems, it's excess T3.
As in my case, with my FT's now being good and only a very few, mild symptoms, I would fight tooth and nail to keep from having my meds dropped at this point, regardless of the fact that my TSH is basically nonexistent. Fortunately, my endo agrees with me, even though he also realizes that this is controversial yet, so I no longer have to beg to keep my med at the level needed.
Sorry..posting was supposed to read...HAD thyroid cancer. Now clear of it with permanant treatment in 2008.
This is just my personal opinion.......
There are studies that "claim this and claim that" and they are just that....Studies.
With Graves disease and hyperthyroid the TSH is commonly low (before any permanant treatment) and it is NOT the TSH that causes the risk of Thyroid Storm (Atrial fibrillation)...it is the HIGH FT3 and FT4. Im hyperthyroidism, the TSH is brought UP to bring the FT3/4 DOWN.
So in actual fact,,,it is the thyroid hormones that cause the more risk than the TSH itself.
There has also been a lot of studies done in regards to Hashi's and Graves.....
With Graves...a risk of heart damage and osteoarthritis.
This is due to a HIGH FT3/FT4 once again and also the heart working overtime to compensation for the high hormone levels.
With Hashi...there is a risk of Myexedema Coma but this isnt because of just the TSH being high...it is because the rest of the organs in the body are not getting enough FT3/FT4 to allow them to function.
So my attitude is.......regardless of WHERE your TSH is....if your FT3 and FT4 levels are within a range comfortable to you, not causing any organ problems then suppressing the TSH has no real danger in itself.
You can have someone with a TSH of 10.0 that is functioning great, FT3/4 levels great and no other problems...but in another case, you can have someone with a TSH of 0.50 and the same scenario of FT3/4 being ideal levels and they do great.
I tend to think that a lot of Doctors associate TSH with the thyroid and although this is correct as the TSH is a Pituitory Hormone and NOT a thyroid hormone (message from Pit. Gland to tell you that thyroid needs more/less hormones)....Docs tend to go by TSH alone which is actual fact is wrong.
In my particular case, I have a heart murmur, prolapse of Mitral & Tricuspid valves (heart) and Tachycardia and also thyroid cancer.
So in reality, I should have my TSH suppressed (med induced) because of the thyroid cancer (RAI and TT done 2008) down to 0.50 but would end up with a heart attack ( Myocardial infarction) as the heart is working faster and too much stress on the heart.
I had a heart attack in 1994 and it was never picked up that my thyroid and Graves disease may have been the reason why.As we all know...untreated hyperthyroidism causes the FT3/4 to soar way past the normal levels.
My first diagnosis showed my FT3 to be at 22.3 and the ranges are : 3.5 -5.0.
So in my personal opinion, it is NOT the TSH that is the important hormone for wellness...that hormone should come secondary.
As in a couple of months ago...my FT3/4 was great and my TSH kept rising.
It wasnt the Pit. Gland telling me that I needed more thyroid hormone, it was the Pit. Gland going into 'overdrive' because of a Pit. tumour.
My attitude to it all is ....Each to their own.
Not one of us has the same DNA, molecular biochemisty and each case should be treated individually.
But...if you told a Doctor this , his mouth would drop to the floor ......with him thinking...:What the He//????"
As I said....my personal opinion on this.
There are studies that "claim this and claim that" and they are just that....Studies.
With Graves disease and hyperthyroid the TSH is commonly low (before any permanant treatment) and it is NOT the TSH that causes the risk of Thyroid Storm (Atrial fibrillation)...it is the HIGH FT3 and FT4. Im hyperthyroidism, the TSH is brought UP to bring the FT3/4 DOWN.
So in actual fact,,,it is the thyroid hormones that cause the more risk than the TSH itself.
There has also been a lot of studies done in regards to Hashi's and Graves.....
With Graves...a risk of heart damage and osteoarthritis.
This is due to a HIGH FT3/FT4 once again and also the heart working overtime to compensation for the high hormone levels.
With Hashi...there is a risk of Myexedema Coma but this isnt because of just the TSH being high...it is because the rest of the organs in the body are not getting enough FT3/FT4 to allow them to function.
So my attitude is.......regardless of WHERE your TSH is....if your FT3 and FT4 levels are within a range comfortable to you, not causing any organ problems then suppressing the TSH has no real danger in itself.
You can have someone with a TSH of 10.0 that is functioning great, FT3/4 levels great and no other problems...but in another case, you can have someone with a TSH of 0.50 and the same scenario of FT3/4 being ideal levels and they do great.
I tend to think that a lot of Doctors associate TSH with the thyroid and although this is correct as the TSH is a Pituitory Hormone and NOT a thyroid hormone (message from Pit. Gland to tell you that thyroid needs more/less hormones)....Docs tend to go by TSH alone which is actual fact is wrong.
In my particular case, I have a heart murmur, prolapse of Mitral & Tricuspid valves (heart) and Tachycardia and also thyroid cancer.
So in reality, I should have my TSH suppressed (med induced) because of the thyroid cancer (RAI and TT done 2008) down to 0.50 but would end up with a heart attack ( Myocardial infarction) as the heart is working faster and too much stress on the heart.
I had a heart attack in 1994 and it was never picked up that my thyroid and Graves disease may have been the reason why.As we all know...untreated hyperthyroidism causes the FT3/4 to soar way past the normal levels.
My first diagnosis showed my FT3 to be at 22.3 and the ranges are : 3.5 -5.0.
So in my personal opinion, it is NOT the TSH that is the important hormone for wellness...that hormone should come secondary.
As in a couple of months ago...my FT3/4 was great and my TSH kept rising.
It wasnt the Pit. Gland telling me that I needed more thyroid hormone, it was the Pit. Gland going into 'overdrive' because of a Pit. tumour.
My attitude to it all is ....Each to their own.
Not one of us has the same DNA, molecular biochemisty and each case should be treated individually.
But...if you told a Doctor this , his mouth would drop to the floor ......with him thinking...:What the He//????"
As I said....my personal opinion on this.
have searched everywhere and can t find it- i re read all of dr lowe again and then went back to the endocrine today blog thought it was there. i thought it was before the discussion of ali and fraiser and the thyrolar but just can t locate it. in essence he was saying that he is a strong advocate of t3 but not but not to the extent that it will cause over suppression of tsh and thereby effect medical complications. well i linked that with the new aace study and started getting nervous because i am on t3. oh well will keep looking---
Yes, please send me the link and save me the time searching for it. I have read a lot of Dr. Lowe's info and find him to be very helpful. Don't remember anything about suppressed TSH right now.
I really believe the concern for osteoporosis and heart issues related to suppressed TSH is overstated. As far as osteo, I have seen several studies that showed no effect on pre or post menopausal women (the most susceptible group), unless they already had conditions for osteo. In that case thyroid meds at any dosage that speeds up metabolism, would speed up the bone loss process. But the way to avoid that problem is to eliminate the cause for bone loss in the first place, not withhold thyroid meds.
In either case, since TSH correlates so poorly, I would much rather be guided by symptoms and the levels of the Frees, than by TSH level. After all, it's not the absence of a pituitary hormone (TSH) that has any detrimental effect on body functions. TSH is just a mediocre indicator of the levels of the active thyroid hormones (FT3 and FT4) that largely regulate metabolism and many other body functions. So why not rely more heavily on symptoms and blood tests for the Frees?
Here is a quote from a lot of thyroid related material from Dr. Lindner.
Toft advocated “TSH normalization” in the past but has changed his tune (BMJ edit. 2003) “The other difficulty in interpreting serum TSH concentrations is to decide what value should be aimed for in patients taking thyroxine replacement. It is not sufficient to satisfy the recommendations of the American Thyroid Association by simply restoring both serum T4 and TSH concentrations to normal, as in our experience most patients feel well only with a dose resulting in a high normal free T4 and low normal TSH concentration, and those patients with continuing symptoms despite “adequate” doses of thyroxine may be slightly underreplaced. Some patients achieve a sense of wellbeing only if free T4 is slightly elevated and TSH low or undetectable. The evidence that this exogenous form of subclinical hyperthyroidism is harmful is lacking in comparison to the endogenous variety associated with nodular goitre, and it is not unreasonable to allow these patients to take a higher dose if T3 is unequivocally normal.” BMJ
And here is another quote from a study.
CONCLUSIONS: This study suggests that at slightly suppressing TSH doses, LT4 therapy has no adverse effects on BMD in both pre- and postmenopausal women, while having an efficacy on nodule size comparable with that reported using an LT4 schedule able to maintain TSH near or below the assay sensitivity limit (.005).
I really believe the concern for osteoporosis and heart issues related to suppressed TSH is overstated. As far as osteo, I have seen several studies that showed no effect on pre or post menopausal women (the most susceptible group), unless they already had conditions for osteo. In that case thyroid meds at any dosage that speeds up metabolism, would speed up the bone loss process. But the way to avoid that problem is to eliminate the cause for bone loss in the first place, not withhold thyroid meds.
In either case, since TSH correlates so poorly, I would much rather be guided by symptoms and the levels of the Frees, than by TSH level. After all, it's not the absence of a pituitary hormone (TSH) that has any detrimental effect on body functions. TSH is just a mediocre indicator of the levels of the active thyroid hormones (FT3 and FT4) that largely regulate metabolism and many other body functions. So why not rely more heavily on symptoms and blood tests for the Frees?
Here is a quote from a lot of thyroid related material from Dr. Lindner.
Toft advocated “TSH normalization” in the past but has changed his tune (BMJ edit. 2003) “The other difficulty in interpreting serum TSH concentrations is to decide what value should be aimed for in patients taking thyroxine replacement. It is not sufficient to satisfy the recommendations of the American Thyroid Association by simply restoring both serum T4 and TSH concentrations to normal, as in our experience most patients feel well only with a dose resulting in a high normal free T4 and low normal TSH concentration, and those patients with continuing symptoms despite “adequate” doses of thyroxine may be slightly underreplaced. Some patients achieve a sense of wellbeing only if free T4 is slightly elevated and TSH low or undetectable. The evidence that this exogenous form of subclinical hyperthyroidism is harmful is lacking in comparison to the endogenous variety associated with nodular goitre, and it is not unreasonable to allow these patients to take a higher dose if T3 is unequivocally normal.” BMJ
And here is another quote from a study.
CONCLUSIONS: This study suggests that at slightly suppressing TSH doses, LT4 therapy has no adverse effects on BMD in both pre- and postmenopausal women, while having an efficacy on nodule size comparable with that reported using an LT4 schedule able to maintain TSH near or below the assay sensitivity limit (.005).
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