Thyroid Discussion

I do have some things to say about the science portion as well, but have to wait until I am at work and can get access to ‘my favorites’ for the medical studies I reference for T3, RT3, deiodonase interactions/conversions.

I honestly wasn’t intending this to be a sticky, nor do I really care if it becomes one. I don’t see how a discussion about the validity of STTM’s claims isn’t valid info in a sticky, nor why I couldn’t edit the first post to contain only information, but w/e.


I’m glad you mentioned this, PureChance. I’ve had doctors prescribing me anti-depressants since I was 13, and no one bothered to run a thyroid panel or testosterone blood test. Surprise surprise, my testosterone levels are messed up (151 ng/dL!!). This probably explains why anti-depressants do almost nothing for me…

I owe my life to my SO who researched side effects of cryptorchidism, i.e. hypogonadism. I mean this literally; I have been suicidal since I was 13, and it has been getting worse and worse. My doctors did nothing useful - they told me the problem was in my head, and that anti-depressants would fix me… but those did almost nothing, and often worse than nothing (e.g. killing my libido). Now I at least have a hope for a cure or at least treatment of my depression.

Do I blame my doctors for this? Not any more than I blame my parents. They all knew my medical history, and they all could have connected the dots and said “hmm, this might be a problem, let’s check his testosterone levels just in case.” Instead, they went with the easy diagnosis, as PureChance mentioned - most people are ‘just depressed’ (in their minds), so they went with the treatment that fits that bill. I made the mistake of completely trusting all of them to figure things out and do the right thing - which made me even more depressed when treatment didn’t work. That was my mistake. I’m not saying that I shouldn’t have trusted doctors at all, but I could have done independent research, and that’s what I’m doing now - which is why this thread is so useful.

I by no means think that all doctors behave in this manner, but I am worried that most do. This may work in 70%, or even 90%, of cases, but when it doesn’t work and your patient is suicidal… that’s not a sign that you should sit back and wait for the anti-depressants to work (after 4 years of not working).

Tyson: thank you for taking the time to write all of this, and I look forward to reading the rest of the science lecture :slight_smile:


I’m genuinely sorry that you have had such a rough personal experience and I see and understand your points. That does not change the thesis of what I have written thus far. Without going into personal details, let it suffice to say that I have a biography that echos some of the worst cases on this forum and would make a good number of them look like they were getting one on one, presidential, come to your house, medical care.

I would rather not have mentioned that but I think for our personal discussion it’s germane. I do want you to know that I’m no stranger to your sentiments and have spent a long, long time saying close to the same things. But…I work on both sides of the fence and can see that my point of view was myopic and, at least partially, ill informed. I just ask that you not let the inevitable negative emotions that you feel because of your personal history make you throw the baby out with the bathwater. There is a middle way.

Now to continue from the last post:

To recap, I hope that it will make sense now when I say that you can tell ALMOST (I’ll elucidate the situations in which this is not the case in a minute) everything you need to know about a persons thyroid function from a simple TSH and FT4 level.

The FT4 will tell you if a person is hypo or hyper thyroid based on the amount of hormone the gland is producing. If there is enough hormone then the non specific symptoms associated with hypothyroidism may, in fact, be caused by something else. TSH simply tells you how much of a signal the gland is getting to produce hormone.

So you will see one of several outcomes when you measure both the TSH and FT4:

  1. High TSH, low FT4: primary (the gland is the problem) hypothyroidism
  2. High TSH, high FT4: secondary or tertiary (the brain is the problem) hyperthyroidism
  3. Low TSH, high FT4: primary (usually autoimmune or ectopic or active nodular) hyperthyroidism
  4. Low-TSH, low FT4: secondary or tertiary hypothyroidism
  5. Slightly elevated TSH, normal FT4: subclinical hypothyroidism (you could argue for more tests here but understand that your symptoms are likely not caused by a lack of thyroid hormone, that’s why it’s called subclinical)

Now there are a few exceptions to those rules so don’t get all pedantic trying to find holes because I know they are there. This is just an explanation as to why in 95% of all cases you can tell what you need to know from these 2 tests alone.

So if you go to see a doc with symptoms (again these are non specific and could be a host of other things) of hypothyroidism and he runs these tests and you come back in the normal range, then yes, he is going to be resistant to your continued insistence that you have a thyroid issue and your demands to run more thyroid labs “to really see what’s going on”. Right or wrong that’s what’s happening.

I will address a few of the exceptions and then move on to treatment.

Cont. from above:

So what if you have a normal FT4, are experiencing symptoms of hypothyroidism, and have a slightly elevated TSH? This so called subclinical hypothyroidism MAY (and I can’t say that loudly enough) be due to a situation in which the peripheral conversion of T4 to T3 is impaired. That would make sense as the feedback loop is driven by T3 not T4 and a drop in T3 would therefore cause the hypothalamus to release TRH and the pituitary to increase TSH secretion in an effort to increase the T3. So what are some causes of peripheral deiodinase dysfunction? See the chart. There is also some evidence that increased chronic disease (such as liver failure and renal failure) can increase the conversion of FT4 to rT3 but that will not effect the feedback mechanism so it’s largely irrelevant.

Table 8â??3. Conditions or Factors Associated with Decreased Conversion of T4 or T3.

  1. Fetal life
  2. Caloric restriction
  3. Hepatic disease
  4. Major systemic illness
  5. Drugs:
    Propranolol (mild effect)
    Iodinated x-ray contrast agents (iopanoic acid, ipodate sodium)
  6. Selenium deficiency

So from above I would think that in most cases of people on this site/forum the only 2 you can leave as potential candidates would be caloric restriction (chronic) and major systemic illness. Maybe selenium deficiency but if you eat everyday then most likely not.

Out of time again so I’ll pick it up in a few. Sorry for the broken posts.

In issues like this, even if the exceptions are rare, the threads/forums are self selecting for those who are not doing well with standard approaches. Thus there is the appearance that things are worse then they actually are. However, for each of the effected individuals, their problem is not a statistical issue at all.

As a group, those people are have experienced ineffective health care. Some of these have more difficult things going on, some were simply not getting competent health care. Maybe a GP would have not taken on thyroid management at one point in his/her career. But after the drug rep details his T4 drug and provides a cookie cutter protocol, then you have a cookie cutter doctor.

I think that we have a good foundation for a sticky. A new and more appropriate title will be needed and my guidelines would be useful. Who will the owner? This is a long term commitment. This thread can contain ongoing discussion and the sticky can refer to this thread as a reference.

Stickies should be informative and factual and have little debate/discussion; which is bad for learning curves. A new guy reading a thread should have the facts and not the debates. The sticky should address the therapeutic pitfalls and should take a stab at best practices to some extent.

We do see lots of cases were guys are subclinical who do feel a lot better when on thyroid meds.

The sticky also needs to address the issues of iodine deficiencies. Links to other places on the web may be appropriate as well.

As for: “So the T4 is release into the circulation where it binds to carrier proteins (TBG) in much the same way T binds to SHBG.” That supports the misconception that SHBG transports testosterone. The binding energy of T to SHBG is high and SHBG-T does not release T to tissues. SHBG can transport and release estrogens due to the lower binding energies. That SHBG-E action seems to be behind the often repeated false statements of SHBG and T transport. SHBG-T does transport T to the liver to metabolized and excreted. You can’t talk about any hormone transport by proteins and then talk about T and SHBG in the same context. One can talk about how albumin transports T, but not SHBG.

I feel as though I am balanced in my approach. It just sometimes it takes making some noise and shaking things up to get some people to open their eyes to what is really happening (some people meaning the general population who are happy to have doctors make all the decisions for them).

If someone feels that what doctors say is 100% gospel, and you take a middle of the road approach to try to show them a different way of viewing the situation, there is a good chance that they will stay in their comfort zone and keep their current mindset.

If however you take the opposite point of view and successfully argue the merits of your view, then you have a chance of actually moving them along the spectrum to be more middle of the road thinkers (with a slight risk of some taking the message too literally and drifting too far over).

I recommend self empowerment. self education and then partnering with a doctor on a mutually agreeable treatment plan. The doctor is simply a paid consultant nothing more whose advice should be weighed and considered, but never considered gospel. Too many people turn off their own brain when seeing a doctor and totally abdicate any responsibility for their own health and well-being.

(MODS - please note that the links below are to a medical thyroid site. please do not delete.)

that being said, I can’t find that medical study ($#%$#%!) discussing deiodonase and how RT3 uses the same deiodonase and T4-T3 conversion plus other interesting details.

I am definitely not a medical professional, but based on what I do know, I have to disagree with the TSH/T4 blood tests confirming/proving/disproving 95% of thyroid cases and the number of potential causes of thyroid issues. support for my position is below.

I came across this in my favorites. Have you checked out this site? I haven’t read it all, and certain parts are above my level of understanding, but from what I can tell it shows that thyroid issues are significantly more complicated then TSH/T4 alone can explain, and have several additional causes.

They have a great piece reinforcing the concept that the medical system is mostly broken as it stands today and why.’t-my-doctor-know-all-of-this/

They also have great information on T3 transportation issues and how T4 is not the best indicator of Thyroid function, etc.

plus a lot more that I have not read through yet.

Since this is a site run by doctors, do you feel the information they present has a higher validity compared to STTM? because it sure seems like both sites are saying basically the exact same thing (based on my brief overview of the site)

out bodies are incredibly complex and I don’t think that we know as much as we think we do (or doctors think they do). I admit that I am way over my head. The problem is that most doctors refuse to admit that and keep stumbling along using a broken methodology. Testosterone, Cortisol, Thyroid, iron, vitamin D, vitamin B12, selenium, etc.

If you mess with one, you mess with multiple interconnected systems. focusing just on the thyroid doesn’t make sense unless you can guarantee that every other system is operating at 100%. i.e. - your TSH is fine, your free T4 is fine, your free T3 is fine, but you still have hypothyroid symptoms.

Doctor says its not your thyroid, but he can’t really say that without running Cortisol levels and RT3 levels which can have a major impact on thyroid function. which goes back to doctors jumping at the first easy answer and then failing to follow through when that doesn’t work.

what percentage of doctors do you think actually look for the root cause of an issues vs giving the patient a prescription to (possibly) relieve or mask the symptoms? In my opinion, I hope at least 10% of doctors actually look for the root cause.

The current medical establishment is focused on acute care to keep people from dying. It is not set up to help people acheive ideal health (which in turn would help keep people from needing as much acute care).

[quote]KSman wrote:
As for: “So the T4 is release into the circulation where it binds to carrier proteins (TBG) in much the same way T binds to SHBG.” That supports the misconception that SHBG transports testosterone. The binding energy of T to SHBG is high and SHBG-T does not release T to tissues. SHBG can transport and release estrogens due to the lower binding energies. That SHBG-E action seems to be behind the often repeated false statements of SHBG and T transport. SHBG-T does transport T to the liver to metabolized and excreted. You can’t talk about any hormone transport by proteins and then talk about T and SHBG in the same context. One can talk about how albumin transports T, but not SHBG.[/quote]

I have read in several places (of course I can’t find them now) by a couple of different doctors that SHBG-bound testosterone is available for use, but that it takes the body significantly longer to free the T for use compared to Free T or albumin-bound T. and there was something about a new study showing that certain cells have a place for SHBG to dock or activate something within the cell.

I don’t know which point of view is correct, I just know that there are differing opinions out there in the medical world.

I’m playing it safe right now, and think that SHBG-bound Testosterone is almost as good as permenantly bound, but may still have some effect that we don’t know about yet.

Tyson - as a side note, I appreciate the information that you have posted and do feel that it is valuable to the overall discussion and adds value to everyone who reads this site and it provides a different perspective and point of view.

I do think that some of your arguments and positions have some validity, my main concern is that they are too limiting and don’t capture the complexity of the situation.

It almost seems to easy and if it was that easy to find and fix all of the thyroid issue then boards like STTM or here wouldn’t exist.

Bio-available T [bio-T] is TT minus SHBG-T. What is there about “bio-available” that needs to be debated.

yes, but from what I have read there is discussions about what the body can and can’t use (eventuall)
free T = immediately available T
bio-available = readily avaiable T
SHBG bound T = eventually available T (possibly)

a quick google search found this (just the first site I came across).

The bond between testosterone and SHBG is so strong that the testosterone cannot enter the cells and interact with the androgen receptors, so the fraction of testosterone bound to SHBG is considered biologically unavailable, although eventually the bond will break. In contrast, free testosterone and albumin-linked testosterone are biologically available. Free testosterone readily enters cells, and the link between testosterone and albumin is so weak that it rapidly falls apart, allowing access to the cells.[/quote]

While the bond will eventually break, it isn’t easy for your body to do. SHBG isn’t immediately available for your body to use when it needs to - when your body says “oh crap, I need more T!”, SHBG is useless. What I suspect happens is that SHBG slowly releases T over time, and this released T is free (i.e. Free T) until used by your body… so measuring SHBG isn’t a very useful measure of T, but it is useful for identifying high E (high T=>E2 conversion → high E2 → high SHBG → lowered free T), which can indicate a number of issues (e.g. too low cortisol leading to higher T=>E2 conversion).

Can we discuss which symptoms would encourage a physician to dig deeper if the TSH number is just a little high?
I asked my Doc to add some thyroid labs to my last bloodwork. He asked what made me feel like I had a thyroid problem. I told him that my waking temps Were very low, 95.6 ish, I am having a super hard time losing weight, energy levels are low, and my skin is extremely dry. The metaboli issue is fairly recent. It has alwYs been very easy for to adjust my weight until last year. .
He said that temps were not a reliable indicator and that he wasn’t too worried about my TSH.
I asked him for free T3, free T4, and reverse T3. He ordered free t4 and t3 uptake.
My main issue is he metabolic sluggishness. I’m leaving a thousand calories a week on the table just with body temps alone. Am I just getting old or should I pursue deeper investigation?

in my opinion you should pursue deeper investigations. most docs will blow you off unless you are at deaths door. They are generally not much help trying to optimize your health. You have to keep pushing or keep shopping till you find a doc who is willing to partner with you.

I do not agree with the view point that something that will not happen will happen if you wait long enough.

SHBG-T is broken down in the liver and metabolized T then excreted.