nightingale-56

I had Graves from 1973, which was not treated well until I finally had a sub-total thyroidectomy in 1978. All that time I did not suffer aches and pains from bones, like I have since the operation. After operation was not treated for hypothyroidism until 1997. All that time I ached badly along with other symptoms,until I was finally given Norton Levo and after that went off the market Goldshield Eltroxin. All was well until this changed to Mercury Pharma generic Levo in 2010 and I have ached and been in pain ever since. 10 years ago a DEXA Scan was good, but don't know what is would be like now. My son was good for a DEXA Scan ten years ago too, but last year showed as Osteopenia.

Musicmonkey

Very good questions! Unfortunately I don't have any answers. However, my TSH is 'supressed' at 0.01 and even if there is a risk to my bones, I have to consider that potential future risk against feeling rubbish now if I don't continue on combination therapy. Also I would need to weigh up all the other risk factors of not being optimally treated.

jimh111

Fig 2 academic.oup.com/jcem/artic... gives a nice picture of relative risks. A high TSH is more harmful than a low one. Bones have TSH receptors and TSH stimulates deiodinase in bone turnover, so having some TSH is beneficial. Can't go into more detail because I have little knowledge of bones.

Hidden in reply to jimh111

Interesting. It only talks of patients taking T4 only though, so it would be interesting to see any differences with patients taking T3 as well. Suppressed TSH seemed to indicated problems, but not "low". Thanks for the link.

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Baobabs

There have been a number of posts recently asking similar questions. From my perspective there seems to be inconclusive and scant evidence regarding the affects of varying levels of TSH on bone health. Medics don't appear to address the association unless we present as having a suppressed TSH due to hormone treatment associated with thyroid disease. I for one would welcome some objective, credible research into this whole issue.

Nanaedake

Yes, I agree, I really would like clarity on the issue of keeping the skeleton healthy in people with hypothyroidism. Especially in women who have to go through menopause. I am of the opinion that even if people have only partial thyroidectomy they could be at higher risk for osteoporosis. Also, what is the connection with losing some, but not all parathyroid glands?

At the moment if you have at least one parathyroid there is no follow up monitoring of bone health. We know calcium deficiency doesn't always show in blood tests. So why isn't the NHS monitoring people who've list part of their thyroid along with parathyroid glands??

Baobabs in reply to Nanaedake

Probably because many believe the NHS is in crisis.

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SlowDragonAdministrator in reply to Nanaedake

Almost certainly no ongoing testing is due to costs

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holyshedballs

The article linked by jimh111 give some evidence that there is a higher risk of osteoporosis (OP) when TSH is high compared to when TSH is low. What I find amazing is that there is no direct evidence liking the action of TSH on bones.

in other words, so far, i have not seen any proof that TSH actively acts on non thyroid tissues. I see a correlation which is not the same as causation. From what I have read so far, it is an excess or deficiency of T3 that causes AF or OP.

if that is the case, then it is not logical to measure TSH, except as an indicator. i can see that in the 1970's when there were no assays for T4 and T3, measuring TSH was carried out. However, these days T4 and T3 CAN be measured, so I don't see a need to measure TSH. Unless TSH has non thyroidal action. if anybody knows different please let me and the community know.

If this is so, then measuring TSH is not logical. The Bolitho case says that a doctors actions must be logical. if I am correct, then measuring TSH is not logical, and this would then have implications for the treatment of thousands of patients (which would turn classical endocrinology on its head).

It is particularly important for the reason that GPs give to reduce doses of medication - There is a risk of AF and OP because of low TSH.

I believe this is not true and not logical.

Even if it were, the ACTUAL risk is very low and the GMC guidance on consent says that a patient must be able to weigh up the risks and benefits of options and make a decision (with the doctor).

My own view is that the risk is so small, and Graham Leese's paper says that there is no risk if TSH is not totally suppressed but low that I would prefer to run the risk of possible AF or OP and maintain my wellbeing NOW.

I have a small device to monitor my heart rate that alerts to AF (~£100). I can also see my T wave which is an indicator of AF

pmsinstruments.co.uk/acatal...

My blood pressure monitor has a warning for AF. The cheapest Omron (£40) has an irregular heartbeat detector, also helping to monitor for AF.

I mitigate my very low risk of OP by supplementing with Vit D3 and K2 and exercising.

This to me is logical and should with stand scrutiny.

holyshedballs

Minimal Cardiac Effects in Asymptomatic Athyreotic

Patients Chronically Treated with Thyrotropin-

Suppressive Doses of L-Thyroxine*

L. E. SHAPIRO, R. SIEVERT, L. ONG, E. L. OCAMPO, R. A. CHANCE, M. LEE,

M. NANNA, K. FERRICK, AND M. I. SURKS

(J Clin Endocrinol Metab 82: 2592–2595, 1997)

Concluded re. AF - "patients were minimally

affected by TSH-suppressive doses of T4. They had few symptoms and no increase in extrasystoles or basal heart rate. Based on current

knowledge, the increase in LVMi observed in patients without associated

significant systolic or diastolic abnormalities does not have

clinical or prognostic importance. Therefore, in the absence of symptoms of thyrotoxicosis, patients treated with TSH-suppressive doses

of L-T4 may be followed clinically without specific cardiac laboratory

studies".

This was in 1997 though.

holyshedballs

Long-term treatment with supraphysiological doses of thyroid hormone in

affective disorders — effects on bone mineral density

Roland Ricken, Felix Bermpohl, Peter Schlattmann, Tom Bschor, Mazda Adli,

Norbert Mönter, Michael Bauer

R. Ricken et al. / Journal of Affective Disorders 136 (2012) e89–e94

Background: To investigate the long-term effects of supraphysiological, TSH suppressive doses

of levothyroxine (TSDL) on bone mineral density (BMD) in patients with affective disorders during an average treatment duration of 69 months.

Methods: In 22 patients, BMD of the spine (lumbar vertebrae L1–4) and femur (femoral neck)

was measured by dual energy X-ray absorptiometry (DXA). Forty (40) measurements from the

prior study and 48 new follow-up measurements were included. BMD was expressed as Zscores

as a population standard reference. We used a linear mixed model to investigate the duration of TSDL as an explanatory factor for change in BMD compared to an age and gender

matched reference population.

Results: We found no significant differences in bone loss between the study and the reference

population. The estimated non-significant decrease in Z-score compared to the reference population found was: a) lumbar spine (L1–4): −0.00069/month (p=0.9759) b) neck region of femur: −0.01405/month (p=0.4436). We did not find the factors age, thyroxine-dose or postmenopausal state as predictors for a decline in BMD.

Limitations: Small sample size, no bone density assessment prior to treatment with TSDL, no

patient control group with mood disorders who did not receive TSDL, variable bone density

follow-up intervals.

Conclusion: This study did not demonstrate evidence that long-term treatment of affectively ill

patients with TSDL accelerates loss of BMD compared to an age- and gender-matched reference

population.

jimh111

There is evidence linking TSH and bones, like some other tissues bones have TSH receptors and respond to TSH (as well as T3). This study frontiersin.org/articles/10... addresses the issue. I don't like to quote studies I haven't read thoroughly, I've only skimmed this one (I was only interested in the effect of TSH on deiodinase). I don't know much about bones and don't have time to read up and learn such a complex subject.

In summary, T3 has effects on bones but so does TSH in promoting local deiodinase and direct effects on bone metabolism. Ideally we will have nice TSH of 1 or 2 and normal fT3, fT4 levels. Many patients need a low TSH to survive in which case I'd recommend not worrying but keeping up vit D levels and doing sensible exercise.

holyshedballs in reply to jimh111

Really interesting but needs a few read throughs though for me.

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helvellaAdministrator in reply to holyshedballs

I have also purposely ignored that fact that TSH exists in several differently glycosylated forms. That is, dfferent bits of sugars tacked on to the basic TSH molecule.

There has been depressingly little research into how these slightly different forms affect us at the cellular level.

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holyshedballs in reply to helvella

Plus, there is another form of TSH that affect the hypothalamus and the seasonal circadian rhythms.

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TSH110

How can it possibly be good for anything including bones to have a TSH of 10 or more or even 2.5?

Baobabs in reply to TSH110

I'm with you on that and have asked the same question so many times.

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TSH110 in reply to Baobabs

Yes quite - it is not normal it is abnormal. Why on earth do the people who believe this sort of nonsense think we were given a thyroid gland that in the majority of cases pumps out enough thyroxine to keep TSH below 2.5? It is so blindingly obvious that anything above that is unlikely to make any human being feel human it beggars belief that anyone might even question it. As if the laws of nature can be dismissed for pseudo science masquerading as good medicine

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Baobabs in reply to TSH110

I absolutely agree. Sometimes non scientific commoner garden common sense needs to prevail. Four folk I know without thyroid problems have a TSH between 1 and 2. Surely a TSH of 3 could be causing damage to someone's body and be contributing to osteoporosis. To wait until a TSH is ten just blows my mind and I would think this reasoning is purely based on financial coffers of a health service.

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