Feasibility of reducing L-thyroxine dose in patients with a suppressed serum TSH.
Leese GP1, Jung RT, Browning MC.
Author information
Abstract
A total of 748 patients on L-thyroxine with a suppressed serum TSH were requested to reduce their dose and this was achieved in 601 patients. Thyroxine dosage was reduced by 25 or 50 micrograms of L-thyroxine and patients were reviewed six months later. Of all 601 patients, 54.4% remained with a suppressed serum TSH despite dose reduction and in 5.8% an elevated serum TSH resulted. 25 micrograms reductions and 50 micrograms reductions were equally likely to result in an detectable but non-elevated serum TSH (42.8% vs 34.1% ns) but 25 micrograms reductions were less likely to result in an elevated serum TSH (3.8% vs 10.0% p < 0.01). Only 7/601 patients in the study (1.2%) appeared to require a dose of over 150 micrograms. If dose reduction is thought to be necessary for patients with a suppressed serum TSH, we would recommend 50 micrograms reductions if the original dose is 200 micrograms or more, and 25 micrograms reductions if the original dose is 175 micrograms or less.
Six months later- under half of the subjects had no TSH recovery after a thyroxine reduction of 25 or 50 g!! And they had suffered, I presume, on a lowered dose all that time. Despite the pitiful results, the experimenters still suggest lowering the dosage on patients.
My question is: Why don't they inject people with TSH to see if the thyroid gland would actually respond to TSH at all? Mine certainly never did when I had three months of sky high TSH when breast feeding my child, and I stopped taking my thyroxine! The logic would be: if the thyroid gland doesn't respond to TSH at all, then lowering the dosage will ONLY make a person hypo. This has been my experience.
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katyabat1
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PS not entirely clear, but it looks to me that all they achieved was less than 0,01?? That's truly not worth the bother to the patient, I would have thought!
They have to try and confirm their idea that suppressed TSH will cause more problems, when in fact it may even assist patients feeling much better. That's why they make statements like - osteoporosis or heart problems which may most likely be due to under-dosing or undiagnosed hypo.
No doubt they do consider this too old, but it's rather a large study compared to the other ones. 600 people is a lot. That means for at least 300 of them reducing the Thyroxine didn't work at all.
I still think that reduced TSH seems to create osteo problems, having read lots of articles that links this, independent of T3 and T4 levels.
I just think that the endo doctors are so unimaginative, in every respect, in that they can't begin to understand the problems low thyroid has on a person's mental and physical wellbeing, nor can they think of new ways to tackle the problem. No body is thinking laterally at all. My endocrinologist just says: These are the medicines at our disposal [take it or leave it].
It seems a huge amount of people and a large sample so that surely not all had pituitary problems necessarily. Maybe that's my problem too, cos I can't reduce my thyroxine at all.
Musicmonkey: no I mean low TSH, or suppressed TSH. It's what all the doctors care about. Rather than looking to help us feel ok- they want a 'normal' reading for the TSH. Suppressed Tsh apparently statisticallly leads to more likelihood of osteoporosis or osteopenia.
But it doesn't. That's just a myth. And l don't know if they really believe it or if they're just trying to scare us out of wanting things like T3 and NDT.
Hi Greygoose- I've seen lots of scholarly articles on this- there are more showing the correlation of repressed TSH and osteopenia/porosis -than the other way round. That's the problem: that's why every endocrinologist and even my GP even in Italy- has decided that we have to reduce our thyroxine to 'get well' and raise TSH at the expense of the patient's wellbeing. It's a problem for me too because I've got osteopenia, but I want to understand the potential risk.
Well, just look at the lack of response your last link to this subject roused. People weren't saying 'omg I'd better reduce my levo now!!!' they were just yawning and saying 'oh, that old chestnut again...'
We just do not believe it's true. And if you search the subject on here - using the search box at the top of the page, you will find many articles saying it isn't true. In fact, if you search or member Diogenes, who is a researcher - and hypo - himself - I'm pretty sure he has recent research saying that it isn't true.
Well, I hope you're right, but I'm still reading! Where can I access actual articles on Health Unlocked, as opposed to posts? Are the links to be found in individual threads?
The effects of subclinical hyperthyroidism on bone mineral density (BMD) induced by suppressive thyroxine therapy in patients with well-differentiated thyroid cancer (WDTC) remains unclear. An overview of the current literature was undertaken to evaluate studies to date.
Methods
A systematic medline search yielded a total of 11 studies appropriate for review which included premenopausal women, postmenopausal women, and men on suppressive thyroxine post thyroidectomy for WDTC. Main outcome measures were bone mineral density and bone turnover markers.
But they're still only talking about the TSH and they're not taking FT3 levels into consideration. So their conclusions are useless. It's the T3 that is important, not the TSH.
And they found no conclusive proof that suppressed TSH affects bone loss. Well, that's good enough for me. There are so many other things in life to worry about, that slight risk is way down on my list of priorities.
I'm 71, I've had a suppressed TSH for around 10 years. As far as I know I have no problems with my bones. I'm far more concerned about living what's left of my life to the full, without fatigue, without pain. And I think you'll find most people on here feel the same, whatever their age.
There are so many other factors that could account for bone loss - like diet - that they Don't seem to have taken into account. They just concentrate on the TSH because that's what they're all obsessed about. Because that's what Big Pharma wants them to be obsessed about! If I were you, I'd just forget it, and concentrate on getting well.
Sorry, but that's my opinion. And if I come across as a bit pushy, it's because it really annoys me that they worry people with these scare stories when there are so many studies saying TSH doesn't have any effect on bone. But, if you want to focus in on the ones that do, then that's your priviledge.
Katyabat, this abstract you've quoted implies this :
9 Studies: Show no evidence of bone thinning in anyone
1 Study: Shows evidence of bone thinning in postmenopausal women, but none in any other groups.
1 Study: Shows no evidence of bond thinning, or maybe even improvement in postmenopausal women, and no change in any other groups.
This is the absolute definition of the study finding no evidence of bone thinning. They will have been looking at probabilities, And the thing with probabilities is you will always find 1 in 20 or so studies with anomalous results, but they looked at TEN STUDIES suggested there was no effect on the bones at all.
One study found some effect, but in the description the studies are not very good anyway. So this may have been a single person (or some other very small number) who developed bone problems, and its just a coincidence that they also happened to have a suppressed TSH.
I don't know if I'm clear, but because of the way statistics and probability are done, you are always trying to work out whether things you see are just a coincidence or whether they are because of some effect (like having a suppressed TSH causing thin bones).
If you take a sample of post menopausal women, some will have depleted bones. So the question researcher needs to answer is, does that person just happen to have depleted bones, because that is what was going to happen anyway, or is it because of the effect they're looking for.
There is no way to really tell by looking at one woman with thin bones if it's a coincidence or not. All we can do is making a guess by using probability and statistics on the whole group of people. And this will just tell us how unusual this outcome is (whether the number of women we've found with depleted bones is any different from the general population). So it is always up to our judgement if we think something is unusual enough to have happened just by chance, or if we want to say it's being caused by something from outside, in this case the effect of a suppressed TSH on bone density.
So one of these studies found something that would be unusual, and they concluded that meant a suppressed TSH was causing it. But the other 10 studies didn't see anything that unusual.
When you look at all 11 studies together, you can probably conclude that the one study did happen to find some unusual women, and it might just be a coincidence. Like if you take eleven dips into a pond of tadpoles or stand outside your local supermarket and count eleven groups of people. You wouldn't be surprised if one out of those 11 groups had something unlikely about it, because you've looked at 10 other groups and they've all been run of the mill. Finding this one study that disagrees with the other 10 studies is like that.
This is the kind of thinking you have to do when looking at journal articles. It's not every tiny thing that means something, only the whole body of articles as a whole. Because a lot of things do just happen by chance.
thanks also for your responses Greygoose. Still believe there is something in this correlation, having read so much about it in different contexts, but I agree entirely with you that you have to live your life now, and feel well.
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Only if it's a "natural" suppression, ie if the suppressed TSH is due to hyper/Graves - that's what studies show. And that means it might not be the TSH level that's the problem but sky high Ft4 and Ft3.
Hi Angel of the North! I see what you're saying, but that's not the case in the articles I've been reading. Osteoporosis/penia is happening in patients with normal levels of T4 and T3 who have suppressed TSH. I wish what you were saying is what I've been finding! Could you direct me to the articles you know?
There's a difference between people with suppressed TSH who were hyper (TSH rising lags behind falling T4 and T3) and those with suppressed TSH from being medicated for hypo. See thyroidscience.com/hypothes... for a discussion of differences. Lots of people get osteoporosis without ever being on thyroid meds.
Get a DEXA scan if you are worried. No article I've ever seen distinguishes between people who were previously hyper and those who were hypo. I've also not seen any that say categorically that suppressed TSH cause osteoporosis in those who would not have been expected to get it anyway (eg elderly, inactive, vitD deficient).
Even this one: Although the HRs for subclinical hyperthyroidism and all outcomes are significantly positive, the absolute excess number of fractures is still relatively small (i.e., 1 excess hip fracture for every 1000 person-years).
Subclinical Hyperthyroidism Is Associated with Increased Risks of Hip Fractures, Fractures at Any Site, Nonspine Fractures, and Clinical Spine Fractures in the Largest Meta-analysis to Date
To cite this article:
Leung Angela M.. Clinical Thyroidology. July 2015, 27(7): 174-176. doi:10.1089/ct.2015;27.174-176.
No study seems to have evaluated vit D and exercise, and FT3 over a period of time as well as TSH. And if someone had cancer of anything, it isn't just a problem with that organ, but one with the whole system, so why would you expect the rest of the body to be healthy?
So decide whether it is more important not to increase one possible factor for osteoporosis among many and feel well, or possibly to increase a factor for heart disease, have brain fog and low mood etc, and feel ill.
Btw, I have had a dexa scan- that's the only reason I'm so worried about this! Especially since the concensus among doctors seems so strong about this correlation- I live in Italy and they're exactly the same as the GPs/endos in the UK!!
Is it safe for patients taking thyroxine to have a low but not suppressed serum TSH concentration? .
There were a total of 16 426 patients on thyroxine replacement (86% female, mean age 60 years) with a total follow-up of 74 586 years. Cardiovascular disease, dysrhythmias and fractures were increased in patients with a high TSH (adjusted hazards ratio 1.95 (1.73–2.21), 1.80 (1.33–2.44) and 1.83 (1.41–2.37) respectively), and patients with a suppressed TSH (1.37 (1.17–1.6), 1.6 (1.1–2.33) and 2.02 (1.55–2.62) respectively), when compared to patients with a TSH in the laboratory reference range. Patients with a low TSH did not have an increased risk of any of these outcomes (HR: 1.1 (0.99–1.123), 1.13 (0.88–1.47) and 1.13 (0.92–1.39) respectively.
People on long-term thyroxine with a high or suppressed TSH are at increased risk of cardiovascular disease, dysrhythmias and fractures. People with a low but not suppressed TSH did not have an increased risk of these outcomes in this study. It may be safe for patients treated with thyroxine to have a low but not suppressed serum TSH concentration.
This is excellent news of course for those who are low but not suppressed: I am 0.01. What is the risk factor here? This is a huge study! (more than 16 thousand people)
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