My doctor has handed me a study which concludes that those who hyperthyroid are more susceptible to AF, trying to tell me why my thyroxine dose should be reduced. My TSH has been 0.002 and T4 around 22. I have been taking 175mcg daily of levothyroxine for about ten years and felt well. In March I was prescribed pseudoephedrine for sinus problems. A week after I finished the course I was taken to hospital with atrial fibrillation. the doctor has reduced my dose to 150mcg but I feel under par, unmotivated to do anything phsyical, sometimes lying on the sofa for hours with my eyes shut. I get through the day but not feeling as bright as before. My doctor, through his action of reducing my thyroxine dose, seems to blame 'hyperthyrodism' but to me, the AF was due entirely to the doctor mistakenly prescribing pseudoephedrine. My heart rate is entirely normal on 175mcg. I have monitored it for a couple of weeks. BPM Usually in high 50s and 60s. There was no T3 measure taken. Even though my TSH/T4 has always been out of range, my T3 has always been within range. How can I persuade my doctor to put me back on the dose which makes me feel well?
THYROXINE AND ATRIAL FIBRILLATION: My doctor has... - Thyroid UK
THYROXINE AND ATRIAL FIBRILLATION
Tell him you are going to be forceed by his method of adjusting your dose according to the TSH and sourcing your own medication and give him a copy of the following from an EXPERT on hormones in general. Tell him he is ruining your health and as it is 'hormone replacements' he shouldn't get confused with the condition HYPERthyroidism and HYPOthyroidism - both are at opposite ends of the spectrum.
hormonerestoration.com/Thyr...
hormonerestoration.com/Docs...
hormonerestoration.com/PCon...
excerpt:
Some recommend that the TSH should be reduced to around 1. However, the TSH is the wrong test. It is not a measure of thyroid hormone levels or effects--either in the untreated or treated state. Many, if not most of your patients on levothyroxine, dosed to "normalize" the TSH, are being undertreated. That is why they have persistent fatigue, weight gain, cold extremities, constipation, headaches, depression, etc.
thank you for your reply
Does that study say what criteria were used for diagnosing hyperthyroidism?
I very much doubt that your test results fall into the criteria used.
Have you got a link or even just details (title, authors, etc.) of the study you were given?
yes. It is from the BMJ journal, published 27th November 2012
THE SPECTRUM OF THYROID DISEASE AND RISK OF NEW ONSET ATRIAL FIBRILLATION: A LARGE POPULATION COHORT STUDY
Christian Selmer, research fellow is first named expert. Several others involved.
12 pages
It's a bit complicated for me to understand everything.
Link to study:
I am no expert, but it appears to me that the study is based on subjects not taking levothyroxine (or any other thyroid-related medicine).
Not at all sure you can say "In subject without known thyroid issues, low TSH is more likely to result in AF" and then apply it as "someone on levothyroxine with low TSH is more likely to result in AF". Further, I am not at all sure you can say that because the population risk of AF is increased 10% or 40% (low or suppressed TSH), that this risk applies to you as an individual.
Don't know how old you are, but this bit could have some relevance:
Overall, the relative risk of atrial fibrillation associated with thyroid dysfunction was highest among the younger subjects and lower in elderly subjects. This is because less of the atrial fibrillation risk is attributable to a hyperthyroid state in elderly people, whereas hyperthyroidism in younger adults is often the main cause of atrial fibrillation. This observation may be in line with the fact that the marked rise in atrial fibrillation incidence with increasing age is mainly due to increased cardiovascular comorbidity (such as hypertension, heart failure, myocardial infarction, valvular heart disease, and diabetes).
Of course, this is not to suggest that ignoring the possibility is right. Just questioning the direct application of that paper to you as an individual. I'd also be a lot happier if the paper had included FT4 and FT3 results!
The basic problem is that this study, like all studies before it and since, mixes up apples and pears. Low or suppressed TSH in therapy can come from either those who really are overdosed and need a drawback, or those who because of their particular insensitivity to T4 therapy have to have their TSH suppressed before the right levels of FT4 and FT3 can be achieved (if indeed the FT3 levels can be normalised). I've lived with one of these for 55 years, 47 of which she has had no thyroid (Hashimoto's) no detectable TSH, high normal FT4, FT3 never measured. Bones OK, AF occasional but not bad for 79 yrs and treatable by magnesium citrate. Response to therapy is an individual thing, and to blanketly condemn particular outcomes re TSH is medically ignorant and ignores the individual response.
There are any number of articles online about the interaction between levo and pseudoephedrine. I can't believe your doctor isn't aware! Print some off and take them to show him and then tell him you want your thyroxine dose increasing back to where it was!
drugs.com/drug-interactions...
I have pointed this out and he came round to the conclusion it was a combination of 'hyperthyroidism' and pseudoephedrine (prescribed by a different doctor I've never seen before), hence the reduction in my medication dose. The hospital also attributed the AF to high T4, suppressed TSH BUT, I strongly believe they were unaware of the pseudoephedrine involvement. (and there was no mention of T3) They never asked me about drugs. At the time, I never realised the significance and I doubt they had the time to go through my health records and search for anything. The hospital could find absolutely no other reason for the AF, so I presume they had to blame it on something. Although one doctor did say, casually, that AF does not normally result if blood results are just a bit higher than 'normal'
But, if you are hypo - which you obviously are because you're taking levo - you cannot become hyper. It is a physical impossibility. The thyroid cannot suddenly regenerate and start producing too much hormone. This man is a menace, he knows nothing and thinks he knows it all!
And you are neither over-medicated, nor 'hyper' unless the FT3 is over-range. If he hasn't tested that, then he has no idea what he's talking about. You could very well have a suppressed TSH, and an over-range FT4, but a conversion problem meaning that your FT3 is low. In which case, you are neither 'hyper' nor over-medicated!
Thyroid patients should not have pseudoephedrine. They are very hot on that in America. I found out to my cost when prescribed it years ago for sinusitis.
I echo most of the other respondents. There is research to show that there is a slightly increased risk of Atrial Fibrillation and Osteoporosis in hyperthyroid patients.
BUT that risk is only slightly increased if the patient is clinically hyperthyroid, not just outside the reference range. There is research to show that a population of correctly titrated patients do not have an increase in the risk of AF and O. See Effects of Long-Term Combination LT4 and
LT3 Therapy for Improving Hypothyroidism and Overall Quality of Life Southern Medical Journal • Volume 111, Number 6, June 2018 363
AS diogenes says, and more importantly for the doctor, Good Medical Practice says, the doctor has to treat you as an individual, not a population.
The Mental Capacity Act 2005 has done away with the concept that a doctor acts in your best interests. The case of Montgomery v Lanarkshire has established that a doctor has to work WITH you to establish informed consent in line with "Good Medical Practice Consent: patients and doctors making decisions together".
So if i were in your position I would speak to the doctor and say:
1)I am aware of research that shows that properly titrated patients do not have an increased risk of AF and O. (show the doctor the research)
2) I am certain my AF was due to the pseudoephedrine, (show the doctor the research drugs.com/drug-interactions... ) from natchat
3) I feel well on my dose on 175 and I have no signs or symptoms of hyperthyroidism.
4) If you reduce my dose, I will be unwell,
5) therefore there is no logical rationale to reduce my dose
6) I have weighed up the risks and benefits of reducing my dose and I have the mental capacity to make this decision about my own health.
7)Please maintain my dose of 175 now that I have stopped the pseudoephedrine and we will monitor for future AF.
I personally would make a formal complaint if the doctor does not maintain the dose of 175, but that is up to you how you proceed.
thank you very much for this guideline. I do not understand what is meant by 'titrated'.
Titrated means that the balance of a physiological function or drug dosage is continuously measured and adjusted
On my notes, my doctor refers to me as 'hyperthyroid' because of my very out of range TSH/T4. What would be the difference if I was clinically hyperthyroid. I do not understand this difference.
I am not medically qualified so this is only my understanding, but I have read a lot of books and other research papers and read the posts about this subject.
There are 2 bodies of responsible medical opinion with opposite views on the treatment of thyroid disease.
The main point of difference in the 2 bodies of thyroid doctors is that the larger body of medical opinon only refers to the reference range and not the patient and the other school looks at the whole patient including the reference ranges.
In the larger body of medical opinion, an individual does not have a thyroid disease if the individual's thyroid hormone levels are within the reference range of a population - even if the individual has a plethora of signs and symptoms of thyroid disease. The signs and symptoms, in their view, are caused a multitude of different diseases and need to be treated separately.
In the larger body of medical opinion an individual does have a thyroid disease if the individual has thyroid hormone levels outside the reference range of a population - even if the individual has NO signs and symptoms.
The larger body of medical opinion classes a person who has thyroid hormones at levels higher than the reference range of a population as biochemically thyrotoxic - even if there are no signs or symptoms of toxicity in the individual.
As each healthy person has their own set point and narrow range of thyroid hormones, it is not logical to assume that the range for the individual is as wide as that of a population.
Recent research posted on this forum confirms this logical analysis.
So it is possible that an individual can have thyroid hormones outside the reference range of a population and be healthy.
Most doctors do not take into account that thyroid hormones only have an effect inside a cell. They have no effect at all in the blood.
There are a number of points on the route from the thyroid gland to the cells where the thyroid hormone action in the cells can be reduced. This means that it is possible that the cells are not getting enough thyroid hormone in to them, despite a large amount of hormones circulating in the blood.
So you can have a large amount of thyroid hormones in the blood but they are not having enough effect in the cells for them to be toxic. This is why an individual can have thyroid hormone levels outside the reference range for a population without them being toxic.
A person would be clinically hyperthyroid if they have the signs and symptoms of thyrotoxicity.
These include but are not limited to:
Excessive sweating.
Heat intolerance.
Increased bowel movements.
Tremor (usually fine shaking)
Nervousness, agitation, anxiety.
Rapid heart rate, palpitations, irregular heart rate.
Weight loss.
Fatigue, weakness.
So my view is that a person can have as much thyroid hormone circulating in their blood as they need to make them feel well, so long as the person does not develop the signs and symptoms of thyrotoxicity above.
Because of the lack of understanding the above, most doctors think that just because an individual has a high level of thyroid hormones circulating in the blood, this automatically leads to Atrial Fibrillation and Osteoporosis.
But, because of the possibility of the thyroid hormones not having the normal action within the cells this is not automatically the case. It is the case if there is too much thyroid action in the cells, there may be an increase in the risk of AF and OP. Don't forget that AF and OP have other risk factors as well.
BUT if there are no signs and symptoms of thyrotoxicity, then you can't be being poisoned by thyroid hormones, so there is no increase in the risk of AF or OP.
Thanks for explaining that in words I understand. So helpful.
Dr Wants to reduce my Thyroxine further - aghh
Atrial Fibrillation and T3
Dose adjustment - thyroxine. 
Thyroxine induced osteoporosis?
