Thyroid UK
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Risk of Atrial Fibrillation and Osteoporosis

i am reading a few posts about doctors reducing the dose of thyroid medication because of the risk of Atrial Fibrillation and Osteoporosis.

Doctors shouldn't simply say that there is "a risk". They should say

"there is an increase in the risk of Atrial Fibrillation of x% and an increase in the risk of osteoporosis of y% if you are taking more thyroid hormone than actually (clinically) need."

I have read research that says that the actual increase in the risk is small, but does anybody know the actual increase in risk for those patients who are slightly hyper?

I am hoping diogenes may have some information on that, but anybody else with some real statistics can help.

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HI holyshedballs this study might help with that answer.

academic.oup.com/jcem/artic...

Here is just a snippet from the abstract but you can find the full study in the link above :-)

"The aim of the study was to determine the safety of patients having a low but not suppressed serum TSH when receiving long-term T4 replacement."

"Patients were categorized as having a suppressed TSH (≤0.03 mU/liter), low TSH (0.04–0.4 mU/liter), normal TSH (0.4–4.0 mU/liter), or raised TSH (>4.0 mU/liter)"

"Conclusions: Patients with a high or suppressed TSH had an increased risk of cardiovascular disease, dysrhythmias, and fractures, but patients with a low but unsuppressed TSH did not. It may be safe for patients treated with T4 to have a low but not suppressed serum TSH concentration."

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This is perhaps the best study I have seen on the subject academic.oup.com/jcem/artic... . This answers your question in terms of hazard ratios, how more or less likely are you to are to develop these conditions if you are treated with levothyroxine with TSH in a certain range.

In reality it's not as simple as this. The study shows 'relative risk', how more likely you are to develop a disorder, not 'absolute risk' which is your chances of having the disorder. For example if I go out in the rain I have a much greater (relative) risk of being struck by lightning but it's not something I should worry about. AF and osteoporosis are quite common so the absolute risk is relevant and if I have an incresed relative risk it makes sense that I should try to reduce the risk by e.g. exercising.

The other issue is that the risk is determined by looking at TSH which is the best they can do with a retrospective analysis. TSH is far from ideal since some patients might have a TSH that is low for other reasons such as insufficient stimulus from the pituitary.

In practicle terms I think the best your can do is look at your TSH, if it is low and fT3 or fT4 or more importantly both, are getting high then you are probably at increased risk. If your pulse is increasing or you have a fine hand tremor then I would be concerned about having too much hormone. Ultimately it will come down to a trade off between risk and quality of life for some patients. Nothing in life is risk free, it's a question of coming to a sensible compromise and taking what steps you can to mitigate any risks. There are substantial risks in remaining clinically hypothyroid, elevated cholesterol and being unable to exercise for example.

Beware that many of the earlier studies were flawed in that they included patients that may have had concurrent parathyroid gland damage or included thyroid cancer patients whose TSH is deliberately suppressed to avoid the risk of cancer returning.

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Yes, looking at the paper, they map a correlation but there is not a direct causation in my view.

From all the other research and especially the one from this year, it appears to me that lack of TSH is not the causative factor for AF or OP. Having more T4 or T3 than you as an individual need is more of a risk factor.

This is because in theory and in law the doctor and the patient discuss the options and the risks, the patient weighs up the options and the risks and comes to a decision. They then should proceed on that decision. That's how Good Medical Practice says it should happen.

clearly there are a lot of doctors who don't do that so it important that patients have as much knowledge at their fingertips to counter anything the doctor says.

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Yes it about the patient weighing up the risks making a choice. I choose to not have fatigue, have a clear head and exercise over a theoretical minor increase in risk for AF or OP and an increase in risk of heart disease from remaining hypothyroid.

If there is that risk then the answer is not to reduce thyroid medication but to exercise regularly, take Vit D3 and K2, and monitor the heart by ECG and bones by DEXA scans.

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Thanks for that. I am hoping to have something that is not expressed as a hazard ratio because most patients see risk as a percentage. But if its a hazard ratio then I'll have to use that.

In my view just saying to patient that there is a risk of AF or OP is not sufficient. They should quantify that risk so that patients can make an informed choice as to how to proceed.

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A hazard ratio is a percentage if you multply by 100! e.g. HR 1.21 = 121% or 21% increased risk.

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healthunlocked.com/thyroidu...

My understanding from Clutter and I think helvella on a separate occasion was that the patients in this widely quoted Rotterdam study were mostly elderly and bedridden in any event. Many GPs assertions concerning the increased risk seem drawn from this study; Dr Malcolm Kendrick drmalcolmkendrick.org/2015/... would have ripped it to shreds.

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With respect to atrial fibrillation (AF), there are many more questions.

For the sake of discussion, let us accept the possible increase in risk from high or too high levothyroxine.

Does the increase in risk apply only while over-dosing on levothyroxine? Or does that increased risk continue even if the dose is reduced?

With decent monitoring for AF, would it not be reasonable to keep checking and take action if and when AF occurs? If it doesn't occur, it would seem not to be a risk factor for the individual. If it does occur, reducing dose should address (see first question above).

Do we have any idea why it would cause AF? Some mechanism that would explain the biochemistry. Seems entirely feasible to me that, for example, it could be low T3 in the heart in conjunction with sufficient or excess T4. Without knowing more, decisions are very hard to make.

We can imagine a situation in which a doctor identifies, say, a 10% risk of AF with a particular levothyroxine dose. With ten patients in front of the doctor, we could suggest one has a 100% risk and the other nine, no increased risk. There simply is no 10% risk to the nine. Yet a decision could be made to keep nine patients feeling poorly for the sake of the one. Again, give them all an increase, see who displays AF.

We allow people to climb mountains, ride Isle of Man TT races, resurrect Bluebird, go for world speed records, all of which have great risk. It is the choice of the individuals.

Why should that choice not exist simply because a doctor is involved?

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Too little or too much hormone has an effect on cardiac structure and its electrical circuits. I don't have the knowledge to describe these. Research by its nature relates risk to TSH because TSH is an indication of T3 and T4 effects, specificially on the pituitary. If you wait until AF is discovered it is too late the damage has been done but of course reducing the dose will help.

A non-medical problem with AF is that if the patient needs a cardioversion it has a big effect on their ability to get health or travel insurance. I'm sure there is information on how excess hormone affects the heart, I haven't looked at it and would find it difficult to understand, one needs a detailed knowledge of thyroid hormones and of the heart.

The bottom line is that there are risks and they are real. It helps to try and quantify the risks so they can be balanced against the benefit of resolving hypothyroid symptoms. Many illnesses carry this risk benefit trade off - a point missed by most doctors treating hypothyroidism. It shouldn't be assumed that a patient who suffers from hypothyroidism can be brought back to full normality with no increased risk. This is desired but our knowledge is not good enough to achieve this status at the moment.

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Thats my point entirely and its what the Mental Capacity Act says and its what Good Medical Practice Consent: patients and doctors making decisions together is about.

GMP Consent says at paragraph 13

"No one else can make a decision on behalf of an adult who has capacity".

A very powerful statement. This is what I want to make patients (and doctors) aware of but to have some facts and figures to help the conversation.

There is a theoretical probability of 9% that (in my view) those with higher T3 than they should have will develop AF in the future. Whereas those with insufficient T3 have 100% probability of developing brain fog, fatigue and some or all of the other symptoms together with a 25% probability of developing heart failure in the future.

Good Medical Practice allows a patient to weigh up those risks and make a decision.

Thanks for all you input it has been very useful.

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This is an older study published in the Lancet in patients who had a thyroidectomy (thyroid removed):

"Despite long-term thyroxine therapy (mean duration 7·9 [range 1-19] years) at doses (mean 191 [SD 50] μg/day) that resulted in higher serum thyroxine and lower serum thyrotropin concentrations than in the controls, the patients showed no evidence of lower bone mineral density than the controls at any site. Nor was bone mineral density correlated with dose, duration of therapy, or cumulative intake, or with tests of thyroid function. There was a decrease in bone density with age in both groups.

We suggest that thyroxine alone does not have a significant effect on bone mineral density and hence on risk of osteoporotic fractures.

"

the abstract can be found here:

thelancet.com/journals/lanc...

Hope this will be of help! :-)

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I found another article, showing that suppressed TSH is not associated with an increase in osteoporosis:

onlinelibrary.wiley.com/doi...

Patients with suppressed TSH has a slightly higher decrease in bone mineral density, but the difference between the groups were not statistically significant! :-)

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The basic problem with all trials on AF and OP versus TSH is that they mix up patients with varying responses to T4 or T4/T3 etc into those who really are overdosed and need changed dose, and those who are not. The trials treat everyone as if they each had a defined increased probability of OP and AF with suppressed TSH. This loses the point that each patient is an individual, and therefore the same parameter values can mean quite different things in two different patients. Some patients indeed could be taking too much T4 etc for their unique needs, but another patient could be taking the right amount and still having suppressed TSH. Simply put, from a statistical point of view, these trials aren't worth the paper they are written on. Only when medicine returns to the patient, and not catch-all biochemistry will proper diagnoses be made.

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Thanks for your as usual informed contribution. My main point is that most doctors are not listening to patients in the way that Good Medical Practice tells them to, so my post is about how to respond to doctors when they trot out the usual myths.

Most doctors simply close their ears to anything a patient says. I'm currently about finding ways to break that wall down. In order to do that, I think patients need to know about GMP and how to use it in the consulting room. That is why I was asking about probability percentages, even though I agree with you that doctors should look at the patient not the lab results.

It appears to me that doctors think it is easy to pull out a trial paper to support their view that they know best and will instruct the patient on what to do with their body. I think that it may useful in the context of a consulting room for patients to counter what doctors say with other trial results and their probabilities. (Not ideal in the bigger picture but in the consulting room it has to be step by step in my view). The patient can then say: I have considered what you say but these results are contrary to it, I have considered the risks of what you propose and what I propose, the risk/benefit analysis is in my favour, therefore I want to remain on the dose that keeps me healthy.

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Thanks Diogenes - is there any reliable research then on low/suppressed TSH levels and AF or osteoporosis? I have done some research into this, but unfortunately not turned up much and like you said most studies are small and patient populations not well matched.

Patients with suppressed TSH are been beaten over the head with risking AF or osteoporosis (without given any further explanation on why that should be the case), hence my interest in looking for resources on these subjects. If you have anything you could share, that would be great - thanks!

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In a word, no! The most likely OP data indicates suppressed TSH gives one extra fracture per 1000 patient years. I believe the paper rests in TU's archive. The simple matter is that as one gets older, the reasons for AF and OP due to suppressed TSH are hugely outweighed by other causes so that it simply can't be decided what an AF or OP is due to.

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in fact, that is really what I am after to counter what GPs say to patients when they want to reduce their doses.

one extra hip fracture per thousand patient years

For A &E admissions for AF, less than 2% are for patients who also have low TSH. interestingly, 11% of patients had raised TSH.

The study saw low TSH as such a low risk factor that it does not recommend routine TSH monitoring for newly admitted patients.

Validation of a Decision Rule for Selective

TSH Screening in Atrial Fibrillation Western Journal of Emergency Medicine 2015

ncbi.nlm.nih.gov/pmc/articl...

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It is this one:

Leung Angela M.. Clinical Thyroidology. July 2015, 27(7): 174-176. doi:10.1089/ct.2015;27.174-176.

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Wow, all very interesting reading. I can't believe how knowledge people are on here have. I read loads but struggle to take it all in. Holyshedballs I need some coaching from you next time I go to the doctors. I'm a confident, intelligent health professional but turn into a gibbering wreck at the drs although I am getting better at arguing my case and luckily my GP will listen. The trouble is that the GPs feel constrained by their guidelines and are frightened to go against them for fear of getting it wrong and being held accountable. At my last appointment I told the GP I wasn't going back there and would take care of myself as numerous appointments had yielded no positive results. About 18 months ago I was having auras, hypertension, high cholesterol. I wasn't allowed to drive so couldn't work, Dr thought I was having TIAS or strokes. I was put on B/P meds, statins, antidepressants (for hot flushes -didn't work), aspirin. No increase of levothyroxine. I took them for a month then gave them all up and look after myself with diet and advice from this forum. B/P is fine. Turns out these problems were caused by HRT. I aim to get nutrients and thyroid hormones optimal and then I'll research the cardiac and osteoporosis stuff as I feel at risk of these diseases from family history. Thanks all for sharing your knowledge.

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Do doctors have to follow Guidance?

In Kaur v London Borough of Ealing [2008] EWHC 2062 (Admin) Moses LJ (sitting at first instance) stated "An Authority is only entitled to depart from the statutory code for reasons which are clear and cogent (see R(Munjaz) v Mersey Care NHS Trust [2006] 2 AC 148). I suggest that that is sufficient authority also for the proposition that any authority would have to justify its departure from the non-statutory guide." (paragraph 22).

So doctors can deviate from any guidance provided that they have good reason to do so, and record that reason.

Doctors have to have due regard to guidance produced by the National Institute for Clinical and Health Excellence (NICE). Once NICE guidance is published, health professionals are expected to take it fully into account when exercising their clinical judgment. However, NICE guidance does not override the individual responsibility of health professionals to make appropriate decisions according to the circumstances of the individual patient in consultation with the patient and/or their guardian/carer.

In particular, guidance that does not recommend a treatment or procedure, or that recommends its use only in defined circumstances, is not the same as a ban on that treatment or procedure being provided by the NHS. If, having considered the guidance, a health professional considers that the treatment or procedure would be the appropriate option in a given case, there is no legal bar on the professional recommending the treatment or on the NHS funding it.

Is the statement from the British Thyroid Association national guidance that doctors have to have due regard to?

The BTA published a statement (NB the BTA have been very careful not to call it Guidance or Guidelines) to support their laboratory blood test approach. It is only 10 pages long and is not supported by a great deal of evidence. Further, it does not meet the criteria laid out in Ali v London Borough of Newham 2012.

In that case, the Judge said that in order to ascertain the weight that should be given to particular guidance it is necessary to give due regard to:

- the authorship of the guidance,

- the quality and intensity of the work done in the production of the guidance,

- the extent to which the (possibly competing) interests of those who are likely to be affected by the guidance have been recognised and weighed,

- the importance of any more general public policy that the guidance has sought to promote,

and

- the express terms of the guidance itself.

The authorship of the Guidance statement.

The author of the Guidance is the British Thyroid Association.

The BTA is “A non profit making Learned Society, membership of the BTA is restricted to professional clinical specialist doctors, retired consultants, academics, scientists, trainees, nurses and medical students in the UK who manage patients with thyroid disease and/or are researching into the thyroid and its disease in humans.” british-thyroid-association...

The BTA is not a Public Body. It is not included in the list of public bodies that the Freedom of Information Act applies to. The statement has not been required to be produced by an Act of Parliament or Regulations made under any Act of Parliament. There is no statute to require health professionals to have due regard to the statement.

Therefore the statement is not statutory guidance.

The BTA is not a Royal College, Royal Institution Chartered Institute or Regulator.

The BTA is not a Professional Body. It does not have a Code of Conduct, which if members breach, requires their expulsion from the body. A doctor does not require membership of a BTA register to call him/her self an Endocrinologist or Thyroidologist. Membership is gained by completing a form, being proposed and seconded by existing members and paying a fee, currently £55 for joint membership with the British Thyroid Foundation.

The BTA has not been charged by a Public Body to produce any guidance.

The BTA is simply an association of people.

The BTA did not consult real patient organisations; just organisations they have a close connection to.

The express terms of the statement only refer to "primary hypothyroidism", yet doctors use it as if it is about all form of thyroid problems such as:

- poor T4 to T3 conversion,

- excessive rT3 production,

- T3 resistance at the cell membrane

- T3 resistance at the nuclear membrane

etc..

In short, the statement does not carry weight and more importantly it is not logical. To use the BTA statement for all thyroid problems, let alone "primary hypothyroidism" is not logical. The Bolitho case requires doctors to carry out a course of action that is logical or face legal action for negligence.

Doctors do not have to comply with the BTA statement, they should not use it to withhold treatment or reduce a patient's dose. In fact, if they do, they could be negligent and face court action.

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I started getting what the doctor called Lone bouts of AF in my late 40's. They had no idea why. They are (for me) violent things and just awful. Cardiologist said there was nothing wrong with my heart. They would last anything up to 36hrs and then revert. I had a lot of episodes at first then they trailed off to about once a year. I had a bout in July but then I had another yesterday. I am in a bit of a state about it still because they terrify me if I'm honest and it was so soon after the last one.

I am pretty sure it's because I am hypo and not optimally medicated. They didn't diagnose hypo for many years after these things started. My treatment has been too slow to date, but I have forced the pace to pick up now. But at 100 Levo a day I don't feel well at all. I have very little energy. Yesterday I felt really miserable and exhausted all day and then it started. It might be connected to menopause, or it could be linked to both - who knows. But to only focus on over medication as a reason for AF is blinkered. They should also focus on undermedication too. For a time I self-treated with T3 only and although I ended up over medicated, I never experienced an episode of AF on it.

Not much help to the original question. I'm just feeling anxious and miserable and was searching to see if anyone else has AF episodes that might be linked to hypo levels of hormone.

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I cant help you with your AF directly only to say that being hypo is more of risk of AF than being hyper as I am sure you will corroborate. Can you get to your doctors when you have your bouts? If not can you get to A&E or call an ambulance if it happens for a sustained period?

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