By my calculations your FT4 is 68% of the range while your FT3 is only 45% of the range.
This may suggest that you have a conversion problem as usually the FT3 percent of range should be higher than your FT4 percent of range. Classic situation of conversion efficiency issue.
Typically IF symptomatic, many people find they need to have their FT4 to be 50% or a bit higher AND their FT3 to be 66.7% of the range.
Your FT4 levels seem fine if not a bit high, along with TSH (for what limited value TSH is) while your FT3 levels seem a bit low.
My guess is that your body is sensing the low thyroid at the cellular level. FT3 is the only thing that is used here. So this sense it telling the pituitary to push out TSH (thyroid stimulating hormone). And your thyroid is doing it as indicated by your FT4 levels. (your Thyroid produces both T4 and T3 but a LOT more T4 than T3).
As stated above it is worth checking your Vit D and B-12 along with Iron and ferritin. All of these can contribute to fatigue and is common to be low especially in low thyroid patients (maybe because only these folks get routinely tested for it due to the fatigue).
Other things that can cause conversion problems is high stress. Both emotionally or physically due to exercise or injury etc.
The mineral Selenium can help with conversion of the T4 to T3. But don't go overboard as too much Selenium can be toxic. But most over the counter Selenium is I think 200 mcg and seems to be OK for most people. Brazil nuts are high in Selenium.
I don't agree that these labs indicate a conversion problem. One reason is that chansat isn't on thyroid meds. I think FT3 has to be run higher in people on meds (because the hormones are no longer "on demand") than they have to be in people on no meds. Natural continuous production of T4 and conversion to T3 allows for more leeway in levels. Also, I have never encountered anyone with a conversion issue who wasn't on meds.
I would apply the same principle to people who are on T4-only meds AND feel well. Since conversion is totally natural, it's still "on demand", so levels can fluctuate more without harm.
Regardless of the cause for Free T3 being in the lower half of the range, isn't that frequently too low? Remember that the range was erroneously established, and that there has been info reported that a functional range for people with no thyroid issues would be more like the upper 60% of the current range. Also, serum thyroid levels may not reflect accurately, tissue thyroid levels. For that reason, it might be a good idea to also test for Reverse T3, along with the Free T3 and Free T4. Also maybe do some testing for basal body temperature as another good measure of tissue thyroid level. Just some thoughts.
This brings me back to a question I've asked before: Has anyone ever heard of someone who had a conversion issue ONLY? No thyroid problem, just conversion? Has anyone heard of someone not on thyroid meds who had a conversion problem only?
Thyroid symptoms can be the same as symptoms of so many other things. When do you say, "No, I do not think your thyroid is your problem."?
People who have a diagnosed thyroid disease/problem have enough trouble getting an RT3 test without being laughed out of the doctor's office. At this stage of the game, isn't telling this person to ask for RT3 a little like telling him to go out and beat his heard against the wall? There are practical considerations...
There are times when an initial thyroid screening that includes FT3 and FT4 is enough, and I think this is one of them. I certainly would not pursue thyroid at this point to the exclusion of possible iron/ferritin deficiency, vitamin D deficiency and B-12 deficiency, all of which can mimic thyroid symptoms.
I don't think I mentioned Reverse T3. Only a possibility of a conversion issue.
You make a good point about making a call that it may not be thyroid related. And you may be right that this may be one of those cases.
i also agree that Vit D, B-12 iron and ferritin should be investigated and maybe that is where the problem lies.
Are we not aware of people who have a conversion problem that are not on thyroid medicine? That is a good question. But that doesn't mean that it doesn't exist. It could simply be a function of the fact that these people never know what is wrong with them, or are never able to get sufficient testing done to even discover the conversion problem is the source of their problem. At least until a point when their thyroid gives them fits and causes them to become severely symptomatic and labs that are below range etc. But if a person never gets to that point, or is a strong enough advocate for themselves. They just accept their Dr's telling them that they are normal and they just have to live with the symptoms. Or they get diagnosed with something like chronic fatigue syndrome or fibromilygia. because they can not otherwise diagnose the problem. Just food for thought.
Given chansat blood lab results, I would agree he has a snowballs chance in H-E-Double hockey sticks of getting a Dr to prescribe a T3 medication even in a small dose. So you are probably right about beating his head against the wall.
I was the one that mentioned Reverse T3. I did so because of info that suggests that the ratio of Free T3 to Reverse T3 is the best measure of tissue thyroid levels, which is what we really need to assure as adequate. I know that some doctors probably have never ordered an RT3 test; however, a doctor that will order a Free T3 test would be more likely than most. Wouldn't hurt to push for it.
Since what I read also suggests that conversion of T4 to RT3 is affected by dieting, stress, low iron, low or high cortisol, low B12, leptin resistance, low selenium, low chromium, and low B6, among others, why would it only occur when there is another thyroid problem? I thought that it would be good to rule out/in the possibility of excessive conversion to RT3. Especially since there was some difference of opinion about whether the Free T3 level of 3.02 was adequate. If that Free T3 is adequate, then in view of the symptoms, I would check out the possibility of a low Free T3 to Reverse T3 ratio, along with other tests that were recommended.
Personally, because of the fallacy of the reference ranges for Free T3 and Free T4, I am always suspicious of a Free T3 level below the middle of the range, when it is accompanied by symptoms that can be hypo related. Of course I realize that there are other possible deficiencies that can cause symptoms similar to hypothyroidism. Those were all well covered in the thread.
I think chansat might have the best chance with his doctor if he also considers that the most common cause for diagnosed hypothyroidism is Hashimoto's Thyroiditis, and asks the doctor to also test for the thyroid antibodies associated with Hashi's. Those tests are for Thyroid Peroxidase and Thyroglobulin antibodies (TPO ab and TG ab). If Hashi's is present, it becomes much more difficult for a doctor to ignore.
I'm sure that conversion issues without thyroid issues probably do exist in some very minute portion of the population. However, my theory (yep, here she goes again!) is that poor conversion is a by-product (though not a necessary by-product) of T4 monotherapy. Now, don't interpret that to mean that it can't be caused by T3/T4 combo therapy (both synthetic and desiccated) as well...but with enough exogenous T3 administerd, the effects are pretty much obliterated. My theory continues that it has something to do with the once-a-day administration of T4 as opposed to the continuous supply that occurs naturally.
I know it was gimel who brought up RT3. I was referring to trying to get RT3 tested as beating his head against the wall. But, you're right, getting a doctor to prescribe T3 with his labs would make his head very sore, too.
Maybe a recommendation for requesting RT3 testing should come with a disclaimer..."Your doctor will probably think you're crazy, but..." Seriously, RT3 is pretty much frowned on by mainstream medicine, so people should be forewarned of the likely reception their request will get.
"Since what I read also suggests that conversion of T4 to RT3 is affected by dieting, stress, low iron, low or high cortisol, low B12, leptin resistance, low selenium, low chromium, and low B6, among others, why would it only occur when there is another thyroid problem?" Totally agree, but back to my question...there's a lot of experience here among us...I'VE yet to hear of anyone without a thyroid issue and not on meds with a conversion problem. Perhaps I should post the question. If there is no thyroid problem, evidenced by the fact that FT4 is adequate (it's more than adequate in this case), then the problem is technically metabolic, not thyroid. I'm not arguing semantcs here. My point is that if there is a conversion issue caused by any of the considerations listed above, wouldn't that have to be approached by attacking the source of the problem (i.e. low selenium, if that were the issue).
"Personally, because of the fallacy of the reference ranges for Free T3 and Free T4, I am always suspicious of a Free T3 level below the middle of the range, when it is accompanied by symptoms that can be hypo related." I agree with you completely, if the person is medicated. However, T3 is dynamic. I tend to think that it's subject to much more intraday and demand volatility in healthy people and people who do well on T4 monotherapy. Don't get me wrong...I don't like to see it in the bottom of the range, either, but a little the low side of midrange, I do not think is a problem.
My own experience bears this out. I'm on T4. Last labs, my FT3 was 1.65 (2.5-4.3). I feel great. I can only surmise that if I needed more T3, my body would convert more. My own labs freak ME out! LOL
I also agree on the antibody tests. Doctors are impressed by numbers out of range, so if you can produce some, you'll have a much easier time convincing your doctor that something is wrong. You have to test for both TPOab and TGab. Some of us with Hashi's are TPOab positive, some TGab positive and some both.
The original poster has never commented after the original post. And all the semantics have been between us.
Interesting discussion though. And should the poster ever read this thread there is a lot of information for him to consider.
The consideration of whether conversion issue is metabolic or medicine induced is a great question. That would be an awesome medical research study to conduct.
I personally have always believed that it was metabolic. And that it only was discovered when the thyroid levels got to a point that the poor efficiency of the conversion only showed up after it couldn't keep pace and resulted in the person feeling so bad that they sought out thyroid testing and ultimately medication. But I very well could be wrong.
I personally have been unable to get my FT3 levels checked. I had to beg, borrow and plead to even get an FT4 test run which showed I was towards the bottom of the range (TSH just over 1). But like so many others, I was unable to get even a small starter dose with labs within normal range. So my only choice to try has been to start taking some Selenium. And Since I've started taking 250 mcg or Selenium a day, I feel better. My hands and feet are not nearly as cold and my joints no longer ache as much nor have I been as constipated.
The only thing I can attribute these relief of symptoms is the Selenium. Nothing else has changed. So that at least now even with the low FT4 I'm being more efficiently converted into FT3. I can't explain it any other way other than a placebo effect. And even if it is in my mind, I could care less because I feel better.
"The consideration of whether conversion issue is metabolic or medicine induced is a great question. That would be an awesome medical research study to conduct." Were I a pharmaceutical company, with lots of money to spend on R&D, it would certainly be one of my projects, but weighing that against eating...well, you know where my money goes. LOL
It's interesting...I took selenium for quite a while, too. I have pituitary resistance to thyroid hormone. My pituitary lacks 5'-deiodinase, which is a selenium based enzyme. So, what the heck, right? Just after that, my FT3 went way up (for me). Like you, I had done nothing else differently. However, a couple of years later, still taking selenium, my FT3 also went way down (for anyone). I discontinued it a while ago...having labs soon, so I'll see if there was any effect.
If you feel better, who cares if it's the selenium or not? It reminds me of the old Woody Allen joke:
Woody: We've been really having a problem with my brother. He has psychological issues and thinks he's a chicken.
Friend: Oh, that must be awful. Are you taking him to a psychiatrist?
Yeah the Selenium helped. But I'm not sure it is enough.
I'd love to try a starter dose of thyroid, but can't get or convince a Dr to do it. So I guess this is as good as it gets!
I'm not 100% sure but I think the Pituitary really only "looks" at the FT4 level. So as long as the FT4 level is "good" the pituitary doesn't care that the tissue level of FT3 is sufficient. The Pituitary is one of the few tissues in the body where FT3 is not needed. Unfortunately the REST of the human body needs it.
I've never been clear on what tells or triggers the body to do the conversion. or to ramp up or down the conversion. I know it occurs. But in people that have a "conversion issue" maybe that triggering device or mechanism or whatever is messed up?
But what messes up that triggering mechanism? Is is metabolic or physiological or is it medicine dosage induced? That is the question.
I'm not sure any pharmaceutical company would even want to take this on. Because if they found out it was medicine induced. That would only hurt themselves. And Dr's will be even more reluctant to start people on thyroid medicine. On the other hand, if it proves to be metabolic, they can then have a good advertising campaign to sell some T3 medicine to overcome this "unfortunate" condition. but fortunately XYZ company is here to sell you a drug to make up for that!
A 50/50 risk reward balance is probably not worth their time or money. Not to mention those same pharma companies are also selling tons and tons of other pills to cover the multiple other symptoms the suffering patient is dealing with because no one will check or believe that they need T3 so the patient has symptoms that need to be "solved".
So again another reason big pharma will not undertake any such research. They have FAR more to lose from their bottom line than gain.
How cares about the patient. It's all about the money you know!
I started answering this yesterday, but I had to do some research first, which led me to some very interesting reading, so I never got back here.
Are you sure the pituitary doesn’t need T3? I don’t think that’s true, but it’s one of those topics that’s very hard to get a straight answer to online. I know the pituitary converts T3 for ITSELF separately from how it’s converted in the rest of the body, and it interprets that as the T3 level in the rest of the body (which is not accurate), but I don’t know if pituitary cells actually USE it or just use the information to determine how much TSH to secrete.
There are three types of deiodinases, the enzymes that catalyze the conversion of T4 to T3...D1, D2 and D3 (not to be confused with the vitamin). D1 is found peripherally, mostly in the liver and kidneys, but with many other lesser sites ubiquitous throughout the body. D3 is also peripheral, but it converts T3 to RT3. D1 and D3 are responsible for peripheral conversion and are in competition with each other for T4 to convert. The relative amounts of D1 and D3 to some extent control T3 levels. However, the feedback mechanism isn’t fully understood by anyone.
D2 is a kind of super-converter enzyme. It exists only in the pituitary and converts T4 to T3 for the pituitary only. D1 is also present in the pituitary, but D3 is not. So, the pituitary is totally blind to the amount of RT3 being produced peripherally. D2 is most active when serum T4 levels are low and is directly implicated in the control of serum TSH levels. D2 converts T4 to T3 much more efficiently than D1 does (D2 converts 80-90% of T4 to T3 as opposed to D1, which only converts 30-50%). So, the pituitary levels are almost always higher than peripheral levels, and D2 behaves exactly opposite of D1. So, when D2 is high, D1 is often low, and vice versa. Sounds like a system designed to fail, doesn’t it?
Anyway, it's D2 that my pituitary lacks and why my TSH hovers around 20.0 no matter what I do. Obviously, this could not have been the case before I was hypo, or I would have been hyper as hell with my pituitary cranking out TSH like it was going out of style. Most people with PRTH also have peripheral THR. Since both their pituitaries and their cells are resistant, they aren’t usually hyper because the peripheral resistance makes high FT3 and FT4 levels necessary. Where do I fit in? I don’t know. I certainly don’t have peripheral resistance. I’m very comfortable with very low FT3 levels. Something else yet going on?
Believe me, Big Pharma NEVER publishes the results of any study that would hurt them. Any study that would suppress sales is promptly quashed. There is no downside risk in any research they put their money into.
I wasn't going to get involved in this conversation, but now I have questions.......
"D3 is also peripheral, but it converts T3 to RT3." I thought T4 was converted to either FT3 or RT3; now you're saying that the D3 deiodinase converts T3 to RT3?
If you lack the D2 deiodinase, hence your high TSH, then it would stand to reason that I must have an overabundance of it, which would account for my super low TSH. The next obvious question is: is there a way to increase/decrease the D2 deiodinase in order to normalize TSH levels, which all the doctors want to go by?
My last test results showed my FT3 is a bit less than the upper 1/3 of its range, and I, too, feel quite comfortable with it.
I, too, would have to question the statement that the pituitary doesn't use FT3, because from everything I've read, every single cell in the body utilizes FT3; why wouldn't the pituitary use it? And if the pituitary doesn't use FT3, why does it convert T4 for its own use? What does it do with it?
Maybe flyingfool could provide a link to the source regarding that part of it, so we could put it all in context.
No, no, no, no...typo...D3 converts T4 to RT3. Too many 3s and 4s for an old lady! LOL
As far as I know, no one is manipulating any of the deiodinases. They are what they are. But, interesting point. when peripheral T3 levels are low, pituitary T3 can be high, suppressing TSH.
What does the pituitary do with the T3 it converts from T4 if it doesn't use it itself? Perhaps it just uses it as a benchmark from which it judges the T3 in the rest of the body. I don't know. I was under the impression that the pituitary does use it. I couldn't find an answer to that question...one for my endo maybe?
Okay, I did wonder if there might have been a typo there....... As an even older lady, I can get confused pretty easily....lol
If the pituitary only used T3 as a benchmark from which to judge the T3 in the rest of the body, the T3 would have "go" somewhere or it would just keep building and building in the pituitary. The fact that T3 is in and out of the system relatively quickly, and that the pituitary is constantly converting for its own use would indicate that the pituitary is either "using" the T3, or making it available for the rest of the body to use.
I, too, was under the impression that the pituitary does use the T3...... Yes, maybe a question for your endo.
It would be interesting to know if someone were doing research on how to replace the deiodinases, so proper conversion could take place. Research and more research........lol
"If the pituitary only used T3 as a benchmark from which to judge the T3 in the rest of the body, the T3 would have "go" somewhere or it would just keep building and building in the pituitary."
I've never explored this beyond T3 because it seems relatively unimportant, but the deiodination process does not stop with T3. The body not only "gets rid" of T3, it neutralizes it by converting it to T2. Then, the T2 gets converted to T1. Busy little enzymes! I believe it's a different deiodinase responsible for each step.
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