Having just read a post where it was stated that beta blockers inhibit T4 to T3 conversion (I’m on Beta Blockers) I did a quick search on Nebivolol (mine). That led to this paper, which interestingly says only Propanalol affects conversion, the rest apparently not.
Anyone have anything to share that says differently?
Propranolol has been specifically identified as affecting conversion, as you say. But there might be some further effects of some beta blockers.
A Review of the Pharmacokinetics of Levothyroxine for the
Treatment of Hypothyroidism.
Colucci P 1, Yue CS 2, Ducharme M 3, Benvenga S 4
European Endocrinology, 15 Mar 2013, 9(1):40-47
doi.org/10.17925/ee.2013.09... PMID: 30349610 PMCID:
PMC6193522
For instance, the administration of beta blockers such as acebutolol, oxprenolol and timolol appear to modify the extracellular distribution of T3, thereby decreasing T3 levels.
europepmc.org/article/PMC/6...
The paper referenced is somewhat old (1990):
Acute beta-blockade changes the extracellular distribution of thyroid hormones.
europepmc.org/article/MED/1...
Some more information about interactions with thyroid medicines and issues:
helvella - Thyroid Interactions
Many medicines, supplements and foods interact with thyroid hormones in various ways.
This document is intended to be a regularly updated list of recognised interactions from good sources.
As it is a new document, feedback would be very much appreciated - anything from typos, through incorrect information.
Direct link to document:
dropbox.com/scl/fi/2kcnc0v7...
Last updated 28/12/2024
Link to blog:
helvella.blogspot.com/p/hel...
Hi
It must be me, but I can't work out how to use your document to find interactions with the specific BB I take, Nebivolol. I can see it in the list of selective BBs but I can't click on that. I can find it further down with an indication it's at '5', but I can't find any reference to it there either. There are 2 links there, the first one is going to a page that's no longer there.
What am I doing wrong?
The document doesn't always give details of a specific medicine. In this example, the paper refers to "beta blockers" and then "such as".
It is only meant to be a general pointer.
Click on 5.
That takes you to the entry number 5:
5 A Review of the Pharmacokinetics of Levothyroxine for the
Treatment of Hypothyroidism.
Colucci P 1, Yue CS 2, Ducharme M 3, Benvenga S 4
European Endocrinology, 15 Mar 2013, 9(1):40-47
doi.org/10.17925/ee.2013.09... PMID: 30349610 PMCID:
PMC6193522
europepmc.org/article/PMC/6...
That paper says:
Drug interactions can also influence other PK processes. For instance, the administration of beta blockers such as acebutolol, oxprenolol and timolol appear to modify the extracellular distribution of T3, thereby decreasing T3 levels.132
I wonder what we are supposed to do then, those of us who have to take BB for Afib with high HR.
Where you able to reconnect the broken page link for one of the 2 papers under point number 5?
I've removed the broken link but not yet re-uploaded the document.
The page has entirely disappeared. Despite being a DOI link which is supposed to be a permanent link that works whatever happens...
A gremlin ate the paper.
I refused to take a beta blocker. Or did I just decline it? 
Today was 50-136. But in 2023, it was 39-210. In 2024 it changed to 40-195 early in the year, then slowly dropped further.
The changes? Increased levothyroxine from 112.5 to 125. And now on Vencamil only. (Had been making up dose with Wockhardt.)
I'm NOT saying an increase in dose will help anyone else. I simply have no other obvious changes.
I use bisoprolol now and have used nebivolol both seemingly without any problems regarding my thyroid.
I have just starting using Bisoprolol for a High Heart Rate. Only 1.25 at present and it affects the uptake of my T3. I have no thyroid and have been using Thyroid s for about 8/9 years.
It's hard to take it away from the NDT so now I am taking it at 4pm which is odd but seems to work for the heart rate. Mine was caused by taking too much T3 after covid and my NDT changed.
What do you take and when?
I take my Nebivolol at 10pm with a couple of other things. I take my NDT at 8am and 5pm.
Not sure how much interaction I'm getting at my standard dose of BB. But the GP doubled it in December and from New Year onwards I felt terrible. Like a sloth. Could barely function at all. Took a while to realise. Now I'm back down to my longer term dose I feel much better. But it is making me wonder how much of my continuing problems with lack of energy despite NDT is caused by the BB.
That's interesting, I did take mine at around 10pm but after 9 days I started itching at night so I changed it. I am not sure if it was the Biso of not?
My BP has always been fine it's just the heart rate now. How much do you take?
It's a guessing game isn't it, who is to say what percentage etc etc. A perfect nightmare.
If you are on 2 grains of Armour plus Levo you should be feeling well. I will try and let you know how it goes thanks for the posting and I hope you get better soon.
I was given atenolol for the first time, at the same time as my levothyroxine dose, during a hospital stay (despite pointing out my bradycardia). Within 12 hours I started to experience what I think was central sleep apnoea, waking (in terror) due to no respiratory drive. There's now a red flag against beta blockers for patients with sleep apnoea, and I was later diagnosed with obstructive sleep apnoea, with my CPAP machine also recording central sleep apnoea events. No change of meds, and I've not taken a beta blocker for years, but my central sleep apnoea has returned, recently, while the number of obstructive events is very low.
I had a talk on the Forum re central sleep apneoa but forgot to follow this up. Pretty sure this is a ‘thing’ even without BBs. I must follow this up. Thanks for reminding me!
I'm fairly certain I had obstructive sleep apnoea in my early 20s, when no-one would say I was overweight. I've always had a problem with nasal stuffiness. The sudden occurrence of central sleep apnoea with the commencing of the beta blocker was completely new to me. The hospital was crowded, so I was moved to the Discharge Lounge, where the problem kept occurring while I dozed in a chair. If the setup worked correctly, staff would've been asking patients to alert them of any problems. To all intents and purposes, it was just a place to dump us while the paperwork was completed, before we were allowed to escape.
Here are some A.I. responses:
The relationship between atenolol and levothyroxine in the context of central sleep apnoea (CSA) is quite interesting. Here’s what we know:
Atenolol is a beta-blocker commonly used to treat high blood pressure and heart-related conditions. While beta-blockers can have various effects on the body, their direct impact on central sleep apnoea is not well-established. Some studies suggest that beta-blockers might improve certain types of sleep-disordered breathing, but the evidence is not conclusive.
Levothyroxine is a synthetic form of the thyroid hormone used to treat hypothyroidism. Proper thyroid hormone levels are crucial for maintaining normal respiratory function. In some cases, correcting hypothyroidism with levothyroxine can improve sleep apnoea symptoms.
Interactions: There is limited research specifically addressing the concurrent use of atenolol and levothyroxine leading to CSA. However, it’s important to note that:
Beta-blockers may influence respiratory drive and airway dynamics, which could theoretically affect sleep apnoea.
Thyroid hormones play a significant role in respiratory function, and any imbalance can lead to sleep-related breathing disorders.
Clinical Observations: Some studies have indicated that patients with sleep apnoea and hypothyroidism may see improvements in their condition with appropriate thyroid hormone replacement. However, the role of atenolol in this context remains less clear.
In summary, while there is no strong evidence to suggest that taking atenolol with levothyroxine directly causes central sleep apnoea, the interplay of these medications and their effects on respiratory function can be complex.
Central sleep apnoea (CSA) can be influenced by several conditions, including hypothyroidism, hyperthyroidism, myasthenia gravis, and Lyme borreliosis. Here’s a breakdown of how each condition relates to CSA:
Hypothyroidism:
Hypothyroidism can lead to obstructive sleep apnea, which may sometimes present as central sleep apnoea. The condition can cause upper airway narrowing due to tissue deposition, affecting breathing during sleep.
Studies suggest that 10% to 25% of individuals with hypothyroidism may experience sleep apnoea symptoms. However, the relationship is complex and can vary among individuals.
Hyperthyroidism:
While hyperthyroidism is more commonly associated with sleep disturbances like insomnia, it can also contribute to sleep apnoea. An enlarged thyroid may impact the airway, leading to breathing issues during sleep.
There is evidence that thyroid imbalances can exacerbate sleep problems, although the direct link to CSA is less clear compared to hypothyroidism.
Myasthenia Gravis:
Myasthenia gravis (MG) can lead to sleep-disordered breathing, including both obstructive and central types of sleep apnoea. The condition affects the muscles involved in breathing, which can result in CSA.
Research indicates that 36% to 41% of patients with MG may experience some form of sleep apnoea, highlighting the importance of monitoring sleep quality in these individuals.
Lyme Borreliosis:
Lyme disease can affect the nervous system, potentially impacting the brain areas that regulate breathing. This can lead to sleep disturbances, including CSA.
Patients with Lyme disease may experience various sleep disorders, including insomnia and other sleep-related issues, which can complicate the presentation of CSA.
Some other key conditions and factors related to central sleep apnoea:
Heart Failure: CSA is often associated with heart failure, where the heart's ability to pump blood is compromised, affecting breathing patterns during sleep.
Stroke: A stroke can impact the brain areas responsible for regulating breathing, leading to central sleep apnoea.
High Altitude: At high altitudes, lower oxygen levels can disrupt normal breathing patterns, potentially causing CSA.
Congenital Central Hypoventilation Syndrome: This is a genetic disorder that affects the automatic control of breathing, particularly during sleep.
Brainstem Lesions: Damage to the brainstem, which controls many involuntary functions including breathing, can result in CSA.
Acromegaly: This hormonal disorder, caused by excess growth hormone, can lead to changes in the airway and breathing control.
Renal Failure: Kidney dysfunction can lead to fluid overload and other metabolic changes that may affect breathing during sleep.
Obesity: While more commonly associated with obstructive sleep apnoea, obesity can also contribute to central sleep apnoea through various mechanisms, including increased pressure on the chest and changes in respiratory control.
Crikey, mostly speculation so they always have their ‘get out clause’. Why is nothing ever properly confirmed or denied? It makes a mockery of research. No wonder we have to do so much ourselves. AND no wonder endos (in our case) get to pick and choose which research they will quote/use in their ‘game’.
However the connections are all there, in our case the common denominator is hypothyroidism - as usual.
Thanks for going to the bother of quoting all this. J am obliged. Thank you.
On the other hand, high BMI may overshadow any interest in diagnosing other potential causes. I had a trainee GP tell me that, as my thyroid levels were OK, hypothyroidism wouldn't be the cause of a particular problem.
Well of course SBT. Even back in the day when we assume more was generally known by GPs, about hypothyroidism (fondly referred to in Scotland as ‘your glands’) in 1968; I was prescribed ‘brand new’ amphetamines for unexplained weight gain. Symptoms from which I still suffer today nearly six decades later.
Even more recently I had the ‘cleaner/nurse’ (also huge as a house) tell me tentatively my issue was my weight. I nearly complained and then thought why bother.
A bit later a doctor told me my problem was not my thyroid (post diagnosis). “It’s your age. It’s your weight. It’s your posture”. Never saw him again either and he had a great reputation amongst the patients as well as the staff.
Where is there to turn when those allocated and paid for by you, cannot/will not help?
Well of course we have the Forum which is helpful in many ways. Even just shared experience but a bonus from the knowledge and experience of, dare I say ‘old hands’.
Crikey, mostly speculation so they always have their ‘get out clause’. Why is nothing ever properly confirmed or denied?
Sadly this the nature of science - there are no absolutes, there are strong correlations which could point to an effect and weaker correlations that might be less clear .
This is why it is infuriating when doctors say if you have a suppressed TSH you WILL get atrial fibrillation or you WILL get osteoporosis. But the correct answer would be you might have a higher chance of developing these conditions, but the picture is far more complex and many more factors can influence these diseases, certainly not a suppressed TSH alone.
That explains the ‘cherry picking’ of particular endocrinologist’s choices. No proof of T3 doing any good in the research they choose (never mind the inbuilt bias in much research).
I take 124 mg. levothyroxine along with 25 mg atenolol (beta-blocker). My conversion is good. TSH - 2.7, T3 (free) 2.3, reverse T3 - 21.2, T4 - 1.4 All within range.
I have always believed that all beta blockers effect conversion. I take my thyroid meds at 6am and my beta blockers at 8.30am .
Beta blockers
beta-blockers and thyroid hormone
beta blockers 
Beta blockers and hypothyroidism treatment
Beta blockers 
