Here is yet another systmatic analysis on lots of patients. It shows that FT4 high in the reference range but not TSH is correlated with increased chance of AF. It contradicts other studies showing the opposite. Here is a beautiful example of false findings from the result of a statistical anomaly called Simpson's amalgamation paradox. First no FT3 was done, so we have no knowledge as to whether this was a factor or not. Secondly we do not know if the people with higher FT4 were all in their comfort zones and thirdly this underlines what we wrote in our latest paper about the danger of lumping everyone into a big study regardless of their individual physiology, without previous stratification to study relevant subgroups.
Clinical Thyroidology
Higher Serum FT4 Level Within the Reference Range, but Not Serum TSH, Is Associated With the Development of Atrial Fibrillation
This study looked at healthy subjects who are not on thryoid treatment and both looked at fT4 and TSH at baseline. They tend to show that higher fT4 is associated with AF over the longer term. I guess we know this, more thyroid hormone more AF. Not suprised with the lack of correlation with TSH since there is no correlation with TSH and hypothyroidism symptom resolution. TSH might be low because of suppression or because the throtrope is underperforming. There is a correlation with suppressed TSH and AF, presumably because these are usually associated with high hormone levels. The research is consistent and rational.
I understood that a study done of patients with supressed TSH following thyroid cancer demonstrated no correlation between supressed TSH and AF. I also think that whatever the studies show giveing patients the oppertunity to make thier own descions about risks and quality of life in regard to how much a patient feel they need in terms of thyroid hormones to feel well and enjoy life rather than decsions being made on our behalf about medication affecting our own bodies by doctors who for the most part seem to be just trying to prove a point rather than provide a good service. Especailly when frankly dangerous drugs are given for migraine with little or no discussion it appears, academically or otherwise.
I totally agree. Although some studies show the relative risk of AF may be 2x or 3x as high for elderly patients with a suppressed TSH this is a relative risk and not an absolute risk. The prevalence of AF is about 5% at aged 70, so if you have a TSH that is suppressed at this age your risk may go up to 15%.
This has to be balanced against the risks associated with hypothyroidism, including congestive heart disease. It also has to be balanced against the benefits of gaining a life, not going on in a vegative hypothyroid state. My approach is to use the lowest dose that resolves my symptoms provided I don't get hyperthyroid signs such as fine hand tremor, increased heart rate, insonmia or vertigo that come on with an increased dose. It's a question of informed chioce. Informed means the patient should consider potential risks (not be in denial) and the doctor should realise the blood tests do not always reflect the clinical reality. In every field of medicine these sort of compromises are made every day - except in endocrinology. Ultimately the decision is the patient's not the doctor's.
My TSH was completely supressed for many years. I am now able to do fine on a lower dose. Just looking at my latest blood test my TSH is 0.15 although this is in part due to reduced thyrotrope function (a consequence of long term TSH suppression). I am at an increased risk of AF. When I was on high dose L-T3 my GP prescribed low dose sotalol as a preventative. I try to exercise, doing 3 hours badminton twice a week and eat sensibly (sensibly includes quality patteserie a couple of times a week as far as I'm concerned). When the evidence demonstrates risks instead of going into denial it's best to accept them and see what you can do to mitigate the risks.
Scratching my head - TSH is dynamic, it changes all the time. Why would a TSH result from up to 17 years earlier be expected to correlate with Atrial Fibrillation? And was there any recognition of how TSH changes by time of day?
The normal serum TSH reference range was defined as 0.45 to 4.49 mIU/L.
Was this the actual reference range from the lab(s)? Or just an arbitrary application of a standardised range? Though if the latter, the ANALYSIS AND COMMENTARY fragment below makes little sense:
... in contrast to a Danish study that reported a protective effect of subclinical hypothyroidism on the development of AF (4), although a different serum TSH reference range was used in the latter study and so did not permit direct comparison.
Is it rational and ethical to include unpublished studies? One imagines they have not been subject to peer review - as published studies would have been.
Not expecting any answers - just lamenting the poor quality of so much that is published (despite peer review!)
Are there any general do’s and dont’s that arise from this study for us hypothyroidism and Hashimotos sufferers please?
I was diagnosed with Hashimotos about 3 years. I have been taking T4 since then and have a FT4: blood test reading of FT4: 17.13 (reference range 12-22).
My suppressed TSH is usually about 0.45 sometimes as high as 1.0 (range 0.3-4.2) after taking 100 mcg of T4 of eltroxin (started at 50 mcg went to 150 mcg now 100 mcg).
The study is statistically based. You are an individual. Individuals are not statstics and cannot be treated as such.Your body has a FT4-TSH relationship unique to you. That means that any trend in epidemiological papers that applies as a probabililty may not apply to you at all.
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New paper on TSH and FT4 reference ranges
An insight into Dr Skinner and Dr Lindner's knowledge in diagnosing and treating hypo patients. 
