Is the T3 spike relevant for those on T3 only?

[tcpace]

Prompted by another current and interesting post, I wonder if anyone can offer a view on the following, perhaps naive, questions.

If someone is on T3 only, is there any evidence showing that there's a problem if the T3 entering the bloodstream spikes and remains above the "normal" T3 range? Phrased another way, why should the T3-vs-time profile of someone on T3 only necessarily conform to the endogenous T3-vs-time profile of someone who is not taking thyroid medication? Does the body not simply regulate how much of the T3 it uses and dispose of any T3 that isn't needed?

I know that some members of this community find that a single, high dose of T3 per day suits them so doesn't this mean that they are over-range for a significant part of the day?

[radd]

tcpace,

It all depends how your body is working.

Some forum members need to take very high levels of T3 to remain well but for others such as myself, only need a little bit as more results in feeling jittery, hot and anxiety. The body will try alleviating these symptoms by reducing T3 levels into inactive metabolites. 

Good thyroid hormone function is controlled by a balance of hormone transporters, metabolism, signalling and excretion affecting both tissue and temporal regulation. Something as simple as a lack of carbs, a slow functioning liver or elevated thyroid hormones can change the whole balance to excess biologically inactive thyroid metabolites designed as a safety mechanism when thyroid hormone either exceeds required levels or the body can not use them.

So yes, some people will be fine with over range T3 levels whether it be for a short spike or a longer duration but the majority of us need to remain mindful of those ranges. Too much T3 can also alter other hormone balance and proteins such a SHBG.

[tcpace in reply to radd]

Thanks for your comments from which I assume you are not T3 only if you only need a small amount. If I'm right then my take is that you don't have much headroom on your T3 intake as most is being supplied via T4 to T3 conversion. However, for someone who is T3 only, then they presumably have a lot of headroom for their T3 intake and the limit is determined by the jittery/hot/anxiety symptoms you mention and may exceed the "normal" T3 range applicable to someone who is euthyroid.

[radd in reply to tcpace]

tcpace,

Sorry I forgot to answer but others input has reminded me.

It doesn’t matter how medicated T3 is sourced (eg T3-only, T4 conversion or NDT), the headroom limit is determined by at what levels symptoms are alleviated whilst not incurring new side effects. 

"Does the body not simply regulate how much of the T3 it uses and dispose of any T3 that isn't needed?’

It becomes more difficult to regulate those levels when using replacement meds. In healthy thyroid function both TSH and T4 conversion help adjust T3 to a measure the body is happy with and that meets overall and tissue-specific demand, but we lose the TSH when medicating thyroid hormone replacement and medicating T3-only you will also lose the T4 conversion limiting mechanism.  

And what isn't needed isn't just pee’d out but turned into inactive metabolites such as T3 sulfate, glucuronate and Triac, (that are metabolised into further metabolites that I can't remember but which helvella always reminds me 😬) resulting in both circulating and intracellular loss.

Also the decativating enzymes (deiodinases) that make the changes for loss, can alter the patterns of activating enzymes resulting in further loss. Hence the more we medicate that can't be utilised (possibly over range amounts?), the higher the ratio of loss in relation to what is being utilised at the risk of it not enough. This is why taking more thyroid hormone doesn’t necessarily make us better. 

[shaws Administrator]

Re your query, I can only refer to myself and how T3 alone works for me. I only need a low dose of 20mcg of T3 (or 25mcg - whichever is available).

T4 caused immense palpitations - especially during the night when I had to take sips of ice-cold water to try to reduce palps and even wrap around my neck an ice-cold towel. The cardiologist couldn't figure out what was happening and I had recordings from heart.

I have to take a tablet at bedtime to reduce/erase palpitations that enable me to sleep better..

I now take one dose of T3 awhen I awake with one glass of water and wait an hour before I eat. I feel fine, and am now symptom-free for 24 hours.

[tcpace in reply to shaws]

Unless I've misunderstood, you seem to be saying that the only thyroid medication you take is 1 20/25 T3 a day? If so, that's amazing unless you still have a full or half thyroid making some T4!

[tcpace]

I'm a bit puzzled by your comment. When I first went on T4 (some years ago), the initial dose prescribed was 25mcg which lowered my TSH to within "normal" range (from about 6-7). Surely that adds to the endogenous T4 rather than replacing some of it? Your thoughts and/or any references you can point to would be appreciated.

[DippyDame]

Yes....sorry, that was rather clumsy so I've deleted the reply!

Perhaps this will be clearer...

Initially, when we start taking levo, T4 from the thyroid is added to T4 from the levo....just as you point out.

However the pituitary quickly senses the added levo so TSH level drops... the thyroid then takes a step back and lowers T4 output

Consequently as glandular output falls this is gradually replaced by the exogenous T4 in levo

So levothyroxine does not top up T4 lost by the failing thyroid….it replaces it"

I expect you found you had to add to the starter dose of 25mcg, as thyroid production of T4 fell?

[tcpace in reply to DippyDame]

Thanks for the clarification DD. Re your final comment - yes, definitely!

[tattybogle]

The fT3 level 'in the blood' certainly spikes in the few hrs post dose ... however just because the blood level is briefly high (or even a bit over range) that doesn't necessarily mean the T3 level reaching the T3 receptors inside the cells spikes at the same time as the blood level does .

T3 in the blood can't do anything directly .. it can only have an effect when it fastens onto a T3 receptor inside a cell .

So we have two separate things going on

1) what the blood level is and how long that high level lasts......

2) what the level of exposure to T3 inside a cell is, and how long it's 'action' on that cell lasts for ( and remembering some cells may perhaps be getting/ taking ? more / sooner , and some less depending on ... erm ...lots of complicated stuff that i barely understand .lol)

1 and 2 are presumably very different .

1 is a simple process of "put it in the stomach and dissolve / absorb it into the blood ... fairly predictable timescale to peak level (assuming there are no gastrointestinal absorption problems)

2 ) is way more complex .. and then i get brain ache . lol.

But basically , the high peak in the blood may not always correlate nicely to when the effects are 'felt'.