Thyroid disease has entered the public’s consciousness thanks to an article in the Wall Street Journal.
I debated on whether to write a blog about it or let it be. In the end, I decided it was necessarybecause of the misinformation out there on the topic. The most important thing when discussing complex issues like this, is being informed, objective, and logical. For that reason, I’m going to try and outline everything that hypothyroid entails, from diagnosis to abuse to controversies in the medical field.
As anyone knows who has read this blog, I am staunchly anti-performance enhancing drugs. So I get where people freak out when the word “hormone” is used, but I want people to realize that for some, it’s a medical necessity.
I’m not an endocrinologist, but I have had Hashimoto’s disease since I was about 14. My hope is that people get a better understanding of what thyroid issues entail and then understand where the gaps in the current treatment are, and the possible places for abuse.
While much of the public has focused on mechanisms of abuse, we’re going to start with understanding what the process of diagnosing and fixing a legitimate thyroid issue entails, before addressing the other issue.
What it is and How it’s diagnosed:
Let’s start with the biggest misunderstanding of all. How do you get diagnosed with thyroid issues? It’s a complicated mess to somedegree because there are several forms of hypothyroidism.
Hypothyroid is the condition. It is not the disease.
That’s a major distinction that should be noted.
The large majority of hypothyroidism occurs because of an autoimmune disorder (Hashimoto’s) which essentially means that your body is attacking itself. SO, your antibodies essentially attack the thyroid and if nothing is done, the thyroid is eventually “destroyed.” This would be called primary hypothyroidism because there is something wrong with the thyroid itself. Other forms include secondary hypothyroidism and tertiary hypothyroidism. Secondary refers to when the Pituitary gland is messed up and doesn’t create enough TSH (Thyroid Stimulating Hormone), and tertiary is when the hypothalamus doesn’t release enough Thyrotopin-releasing hormone (TRH) which doesn’t stimulate the pituitary to produce TSH, and so on.
That’s hypothyroidism in a nutshell. The symptoms of it are unpleasant. You can look those up yourself, but just so people understand, it goes beyond the idea of just “fatigue”. For example, hair loss, impaired cognition, inability to focus, inability to tolerate cold, depression, and on and on. In fact, occasionally, clinical depression is found to be due to a thyroid problem and not the traditional route. Bottom line, is it kind of sucks.
And it’s an every day suck. If you have overt hypothyroidism you lose ability to go through your normal everyday life, so in those cases it’s medically necessary.
Now what does the diagnosis entail.
- TSH- TSH is essentially the first marker. TSH does exactly what its name implies. It stimulates the production of T4 which is then converted to T3. It’s not the be all end all like many portray it but it’s the first marker that essentially says, “hey, something is off here.” If you stopped your diagnosis there, you’d miss a lot.
Regardless, it is the gold standard in starting thyroid diagnosis. Seems easy, if it’s outside the normal range, then start looking at other stuff and perhaps treatment.
Well, that would require consensus on what the actual normal range for TSH is. Here’s a very brief overview on the TSH wars.
- When it was first introduced, Normal range was about .5 to 5.0, with treatment not starting until you were over 10.0. So if you were in that middle ground of 5-10, you may or may not get treatment depending on other signs.
- The standard for almost all labs then shifted to the .5-5.0 as the one true range for normal.
- In 2002, it all changed.
- The American Association of Clinical Endocrinologistchanged their reference range to .3-3.0 (Baskin et al. 2002)
- In 2003, The National Academy of Clinical Biochemistry- changed their suggested range to .5 to 2.5. (Balloch et al. 2003)
“In 2003, the consensus panel (Endocrine Society, American Association of Clinical Endocrinologists, and American Thyroid Association) recommended a target TSH range of 1.0 to 1.5 mI U per liter in patients already receiving thyroxine”
- In 2007, Endocrine Society changed theirrecommendations for labs
- In 2010, more research came out that suggested individual assessment of TSH values based on age, sex, and race…
- Lastly, just go do an internet search for different labs reference ranges. Go to
the Mayo Clinic site and you get .05-5.0. Go to UNC health care and you get .6-3.3. And those are just the first two that popped up…. (http://labs.unchealthcare.org/labstestinfo/t_tests/tsh.htm)
Hopefully you see that the consensus is all over the place. The point isn’t to call into question the TSH value, but instead to show that defining what is clinical and what is not is hard based off only TSH.
To further complicate things, if you have TSH problems because of pituitary issues, then the values are all screwed up.
SOOO if a bunch of expert endocrinologists can’t even agree on what TSH level to cap hypo at, we have an issue that goes beyond track…
That’s why you look at TSH, freeT3, freeT4, and reverse T3 also. These with TSH provide a broader picture of what is going on. …but let’s continue.
So given the TSH test craziness, lets move on to diagnosis step 2. Which involves another simple blood test. This one is for two different thyroid antibodies, which essentially tells you how bad your antibodies want to destroy your thyroid. This test is pretty straight forward. Have antibodies outside of the range, and something isn’t right. The debate is if you should start treatment as soon as antibodies are out of range, or wait until thyroid has attacked itself some more before treatment.
But regardless, it’s relatively straight forward compared to TSH. Antibodies show up. Not a great sign. Probably means autoimmune disease.
TRH Stimulation test:
If we recall from our little flowchart of hormone interactions, it goes: TRH stimulates TSH which stimulates T4… So the old way (before TSH became standardized) was to simply do a TRH stimulation test. Essentially you inject some TRH hormone then every so often take blood so you can see what happens to TSH and your thyroid hormones. If they go up too much, you’ve got a certain type of problem. If they don’t go up at all, then you know there is a problem in the TRH to TSH stimulation. It’s another diagnostic tool to see if the problem is at the thyroid level, pituitary level, or hypothalamus level. The funny thing is that with the increased use of the simpler TSH test, this test isn’t used as much.
Other diagnoses also include the checking for goiters or nodules on the thyroid. Both of which can mean a problem is there. This is done both via a physical evaluation and an ultrasound. In some cases, a biopsy might be taken.
There is also a radioisotope test that can be done to look at thyroid nodules to see if there’s cancer or not.
And lastly, like many diseases, there is a clinical component to it. There’s an evaluation of the symptoms and all that jazz.
You combine all these things together and you get a diagnosis.
The problem, is that diagnosis isn’t that straight forward. You can have people with normal TSH, but have antibodies, for example. What do you do with them? That generally means they have an autoimmune disorder but it hasn’t progressed to overt hypothyroidism yet. Do you wait 5 years until their thyroid is damaged enough to start treatment, or do you treat now?
Training induced changes?
Can you fool the test?
Can someone simply overtrain and make it appear like there is a thyroid problem?
The answer is yes and no.
Yes, if a doctor doesn’t actually diagnose you and instead relies on a TSH number. If a doctor does that then manipulations of training, stress, taking certain medications, etc. can all alter TSH.
If the doctor is competent and goes through a full diagnosis, it’s much harder to create a “false” hypothyroid. The problem though goes back to what is hypothyroid, since endocrinologists can’t quite define it.
Focusing first on TSH, if we look at the research TSH changes acutely immediately after hard workouts. So if you went and did a hard workout then an hour later went and got your blood drawn, you’d see changes in TSH levels most likely. It’s not surprising. You just stressed your body and it needs time to come down to normal. A relatively short time after the workout a normal persons TSH levels are normalized. Even with a very hard workout, the swing isn’t terribly large.
In a study by Schmid et al. (1982 TSH, T3, rT3, and fT4 in maximal and submaximal physical exercise) they found that after maximal exercise in runners, TSH actually dropped before starting to return to normal. During submaximal, there was a gradual increase from 1.35 to around 1.5 at the end of exercise. So a subtle shift. Similarly, a 1971 study by Terjung found no changes in TSh, 30min, 3hrs, and 24hrs after 30min at 61%VO2max. Similarly (Dessypris et al. 1980) found no change in TSH after a marathon. A more recent(Ciloglu et al. 2005) study found that during exercise TSH levels changed from 1.69 at 45%, 1.78 at 70%, and 1.89 at 90% HR max. So again, exercise changes things acutely, but not a ton.
On the other hand, certain types of exercise has actually been shown to decrease TSH temporarily!
Given that, I would recommend getting blood work on an easy day, not following a hard workout.
What about over the long haul? It’s hard to study over months and months, but here’s the best the research gives us.
- One study tracked TSH changes in 16 professional cyclists during the Vuelta a Espana in 1998 (which maybe means these dudes were on EPO?…) Anyways. Over the 3 week T4,
free T3, and free T4 changed, which is what you’d expect, but there was no change in either TSH or free T3. Hoyos et al. (2001) http://www.karger.com/Article/FullText/48112
- Barron et al. 1995 – Took 6 marathon runners and followed them for 4 months until 2 showed signs of overtraining which wasdefined as having all physical symptoms (heavy legs, fatigue, etc.), mental symptoms (apathy), and decrease in performance that lasted at least 3 weeks. In these athletes, no change in TSH occurred. (Hypothalamic dysfunction in overtrained athletes)
- Lehman et al.1999, 1993 performed a series of studies where they tried to over train 8 runners. They took one group and increased their volume for 5 weeks, and another and increased their intensity for 4 weeks. In the volume study they went from their normal average of 86km/wk to 177km/wk. In the intensity study, they increased interval volume from 9km/wk to 23km/wk.
What they found was no change in TSH whatsoever.
- In recreational athletes, they took them and had them do 4 “units” per week of high intensity endurance running (90% of threshold) and 2 units of interval workouts (3-5×3-5min segments at 110% of 4mmol level) on a bike for 6 weeks. They then checked hormone levels and found that there were no significant changes in TSH, among other hormones (Gastmann et al. 1993)
Does this mean TSH does not change over the long term or due to overtraining? No, but it does mean that it’s more difficult than just go trainhard and have your TSH change.
The reason I mention this is because there’s this concept that if you just go train hard you can make your thyroid appear hypothyroid. We will touch on this a bit more later.
But, with TSH levels, there is a big distinction to make. If you killed yourself in training and did manage to elevate TSH, with time off it would normalize if you have no problem. If you have a legit hypothyroid issue, if you took 3 months off, your TSH would still be elevated. If you have a legit problem, no amount of rest/time off will normalize things.
But for sake of thoroughness, a ton of things can alter TSH. Just perusing through the research, here’s a few:
Can potentially depress TSH:
Birth control, glucocorticoids, aspirin, anti-depressants, depression itself, pregnancy, aging, fasting, exercise
Can potentially increase TSH:
Stress, emotional arousal, cold exposure, sleep deprivation, severe illness, iodine, lithium, and high high doses of anti-histamines.
What do you do if you have an actual thyroid problem and what does treatment entail?
If you are legitimately hypothyroid, then the solution is to take supplemental synthetic thyroid. The most prescribed drug is levothyroxine (name brand synthroid or levoxyl) which is synthetic T4. Other treatment options are synthetic T3, or dessicated pig thyroid. Most doctors simply use the synthetic T4. T4 is converted to T3 in the body. In the alternative medicine world and with some doctors, armour thyroid (dessicated pig) is big, but with most doctors they think it’s harder to control and dose.
Once you start taking the drug, it’s all about fine tuning your dose. The goal is essentially to regulate TSH to a “normal” level. The consensus by several Endocrinology societies is to try and get the TSH between 1-1.5.
How much that means depends on each person, but normal doses are in the 50-150 micrograms a day, taken in one dose.
It’s basically trial and error until you get the right dosage. It takes a long time because you can only change doses every 4 weeks (that’s the shortest it generally takes to see consistent change). In reality, most of the time you check every 2-3 months. It’s a long tedious process in most cases. Once you find the right dosage, that doesn’t mean it’s the right dosage for the long term. Instead, you have to have a blood test every 3-6 months to make sure nothing has changed.
What happens if you take too much thyroid medication?
Well if you actually have a thyroid disease, you feel horrible.
You actually take your body from a normal state, to a hyperthyroid state. What does hyperthyroid entail?
It’s basically like you are hopped up on adrenaline or caffeine all the time. Which may sound like performance enhancing, but it’s not. It’s to the extreme, not a short jolt of energy, but instead like you are the verge of a breakdown. You have crazy anxiety, inability to sleep, weight loss, increased appetite, nervousness, heart racing, your hands shake, your muscles are weak, and you generally feel like crap. And for those who know anything about overtraining, you overstimulate your sympathetic nervous system. For those who don’t know about overtraining, overstimulating your NS is one of the ways in which people theorize overtraining occurs.
So, it’s a generally unpleasant state. Thyroid is an interesting conundrum in that if you have too much or too little you get many of the same symptoms. Additionally, messing with any hormone when you don’t need it is plain dangerous. If you take synthetic thyroid and you don’t have a problem, your natural thyroid production starts to shut off. You essentially screw up how your hormones work. Over the long haul, one could only speculate what would happen, but it wouldn’t be pretty.
For that reason alone, if anyone is messing with thyroid for performance benefits, they are an idiot.
But for sake of due diligence, what if someone with a normal functioning thyroid took just a bit of synthetic thyroid and became slightly hyperthyroid. Would it help?
We can sort of investigate this by looking at subclinical hyperthyroid patients. This gives us the ability to look at patients who aren’t quite full blown hyperthyroid. It’s not a perfect comparison but it’s the best you’ll get:
- In this study, they looked at the cardiovascular effects of subclinical hyperthyroidism.
They found that it caused abnormally high resting HR (82 bpm) and increased systolic contractility and decreased diastolic relaxation. http://www.thyroid.org/wp-content/uploads/publications/clinthy/clinthy_v131.pdf#page=5
- In this one, they looked at patients who were Hypothyroid and took just a bit too much synthetic thyroid, so that they were now slightly hyper (so it’s the perfect model for our question). What were the results? There was a 9 percent reduction in bone density.http://www.sciencedirect.com/science/article/pii/0002934387902191
- This one looked at muscle performance in subclinical hyperthyroidism. What they found was that muscle strength and muscle size were reduced in subclinical hypothyroidism, and if they were put back in a normal state, it improved back to normal. http://online.liebertpub.com/doi/abs/10.1089/thy.2006.16.375
Is that a definitive analysis? Nope. The exact studies haven’t been done. But it does give a good idea of what happens when you go slightly over.
Is there a benefit?
Now that we’ve gone through legitimate thyroid disorders, potential abuse of thyroid, and all that jazz, the most important question needs to be asked.
Does it really provide a benefit? Let’s break it down.
If you are legitimately hypothyroid/autoimmune disorder:
The answer for me is obvious. Taking myself as an example, I run better than I would if I took nothing, because then my thyroid would just be attacking itself and I could barely function in life.
But, it’s not a performance enhancer. If anything, I see it as a performance hindrance. Training with a thyroid disorder is about the most complicated thing in the world. You are always on the edge of overtraining, even if your medication is spot on, and you are doing half of what your competitors are. For example, using an athlete who suffers from hypothyroidism on my college team, it’s a tough road. For this athlete, he can only run about 4 days a week, despite treating his thyroid disease AND taking almost 3 months off. He can only do 1 actual hard workout a week, and after races it takes him at least 5 days to recover. He can go from running a 4:12mile as an example, to being unable to run 800m repeats in 2:30 with ample rest.
Similarly, that is how my running was. Despite being extra vigilant on recovery, I would be wrecked after races and couldn’t workout for prolonged periods of time.
I don’t have any complaints, it just made balancing things tougher. But when I think of Anthony Famiglietti talking about how if he had taken thyroid he would have got an Olympic Trials qualifier, my response is this: if I didn’t have to take a pill and had a thyroid that secreted thyroid when it was supposed to and not have to rely on one pill taken once a day to supply my thyroid supplies, then I would have been a much better runner.
That’s the key. Just because your TSH is “optimal” doesn’t mean the hormonal system is optimal. Is a pill taken once a day that just releases stuff all at once, the same as a normal person whose thyroid secretes hormones when it is called upon to? Think of it like this, if I have a huge stress response that calls for Thyroid production, normal person gets a jolt of secreted T4, autoimmune me doesn’t really.
Who is better off?
The reality of someone who is legitimately hypothyroid is that you never know what will happen in a race either. It’s a crap shoot. Some days it’s going to be there, and some days it’s not.
Go back and look at my racing career and you get an answer to what a thyroid disorder athlete looks like. 3:47 1500m one week, 3:56 the next. Run 4:15 all out and then being able to split that in mile repeats.
That’s what happens.
That’s what it is like for a person who actually has a thyroid disorder. You can’t recover, even with pills.
Before going on, I think it’s important to note that if you look at studies, yes you will see improved performance going from overt hypothyroid to euthyroid. That’s because you are correcting a disease. I would be useless without thyroid production. With people who actually have the disease, it’s similar to asthma in a way. It will take you closer to normal, but not superhuman. For those who don’t have a disease, let’s look at the alternative to give a thorough breakdown.
How could it be abused:
Up until now, I’ve gone over the traditional route to thyroid disease. Now I want to delve into the ‘what if’ scenario. What happens if you take thyroid and you don’t need it and how could athletes potentially abuse it?
But I heard bodybuilders use it, so it must enhance performance!?
In the bodybuilding world they apparently use thyroid to cut weight because of the effects it has on metabolism.(How’d I learn bodybuilders use it…google) They essentially put themselves in a hyper state for a short time to cut fat. I have no idea why/how, but again this seems like a horrible idea. First off a runner would be sacrificing recovery (you recover worse in hyper state), and most runners are lean enough.
But the REAL reason bodybuilders and people use it is simple. It’s NOT to enhance performance.
It’s because taking Testosterone and/or HGH severely impacts the thyroid, making you temporarily hypothyroid.
You can see that in the two studies below.
Both studies found that with taking either testosterone or HGH, your TSH levels were elevated. So in order to keep order in their hormonal systems they took thyroid. In fact, look towards Major League Baseball and you can find an incidence of this in 2010.
(Also, note in that article that in 2010 WADA already looked into thyroid as performance enhancers. It’s 2013. It’s safe to say at that time they found just what they said in the WSJ article.)
So, that’s the reason your local steroid junky football player might take thyroid…because testosterone or HGH made him hypothyroid.
Interestingly, if you followed the Floyd Landis case, you know he was taking synthetic thyroid. I don’t know the details, but it makes sense because he was also on a drug program that included EPO, testosterone, and who knows what. My bet is his drug taking knocked him into hypothyroid status.
On to the next claims.
Red Blood Cell production
This is the one everyone is talking about. There are several studies out there that show a link between Thyroid and EPO. It’s easy to get distracted and start yelling blasphemy because anytime the word EPO is involved, the first thing that comes to mind is drugs! Let’s take a look:
First study:Thyroid hormone induces erythropoietin gene expression through augmented accumulation of hypoxia-inducible factor-1]
We’ll use this study as a starting point to the discussion.
First, in simple terms, EPO production essentially occurs when oxygen levels within the cell get low. The main regulator to this process is HIF-1a. If you want the full details of how this works go read my literature review from grad school as there is a section on how this works. But all you really need to know is: Low O2 triggers HIF-1a which eventually results in EPO production IF HIF-1a is
activated long enough.
So this study took cell cultures, put them in hypoxic or normoxic conditions for ~4hrs, and soaked them in either T3 or T4 for the whole time. The amount of Thyroid hormone used is also significant because I have no clue what that translates over to in terms of clinical amounts.
What’s interesting is that if you look at the study T3 + hypoxia caused an increase in EPO production in the cell. T3+normoxia caused a slight bump.. And T4+ either normoxia/hypoxia didn’t cause a bump. Just as an overview, T4 is what is prescribed to almost all hypothyroid patients. Very few people use direct T3.
The issue at hand is whether this translates from a cultured cell or isolated tissue to the whole body? It shouldn’t be surprising that putting T3 into a cell causes EPO increase. Partly because T3 is a metabolic regulator, so it acts as a stimulant to increase Oxygen demand. In a single tissue, if O2 demand is stressed, then EPO production increases. The 2nd part of the equation though is that Thyroid hormones may increase HIF-1 synthesis. That’s the issue that needs to be looked at.
The question is would that same effect occurs in a full organism? The O2 demand wouldn’t be shifted much at all in a complete organism via taking thyroid. You’d shift the O2 demand way more by jogging for a minute. So to me, that eliminates that part of the equation, but still leave the thyroids direct effect on red blood cells and RBC production. The question that needs to be answered is whether clinical amounts of T4/3 is enough, and is present in the tissues long enough. Because if we look at studies like these it’s hard to translate over.
Studies like these are essentially used to figure out cellular pathways. SO it’s important to remember in studies like this, it’s generally a non-therapeutic dose given (meaning way more than you could safely take as a human), and the exposure time is different (taking a pill vs. soaking in it for
So we’re back to square one, and I’m not well read enough to know what the exact mechanism would translate to in a functioning person. I dig around through all the research I could find, and to my knowledge there have been no studies looking at EPO increase via thyroid medication. The only studies I found showed that hypothyroid people who were anemic had an increase in RBC content once both were fixed (which shouldn’t be a surprise…)
If someone smarter than me wants to delve into this, they are more than welcome. I’ve reached out to a few expert scientists who have done the research and am waiting to hear back.
Another big one being batted around is what if I take synthetic thyroid to recover.
First, the question needs to be asked is what role does the T4/T3 play in the recovery process?
Secondly, you have to understand the dynamics. If someone is in medical need of the substance that means there own thyroid isn’t producing T4. So they rely on the pill for T4. In this circumstance, recovery is impaired. Why? Because you essentially take a pill once a day that diffuses and gives you a stream of T4. If you have a normally functioning thyroid, it doesn’t work this way. You get spurts
of T4 when needed. The body knows when to secrete it and when not to. It functions and works better.
So, if you were to abuse thyroid hormones for recovery what would it take? You’d need to time it so it helps you maximally, and you’d probably take T3 instead of T4 because T3 is generally going to give you a more rapid effect. This would be pretty dang difficult.
Subclinical Hypothyroidism debate:
If you haven’t noticed, this is the crux of the debate. What is clinical and what is not. Luckily for this debate, the vast majority of hypothyroid patients in the US are autoimmune disorders, so thankfully antibodies come into play and make life slightly easier.
But the question remains, what is subclinical?
In looking at TSH alone, it looks like it ranges anywhere from 2.5+ to 5+ in terms of TSH.
The way thyroid diseases develop is generally a long process, unless a large stressor is involved. The way it generally works is if you an autoimmune disease, your thyroid might slowly lose function over a decade. At what point do you begin treatment?
I’m not an endocrinologist. I don’t have the answers, but these are the key questions to ask.
I hope, after reading this, that you realize that if you have overt hypothyroidism, it is medically necessary to take synthetic thyroid.
In some cases you take it because your thyroid has beenremoved. In others you take it because your thyroid is destroying itself. The question is, where do we draw the line?
This is a HUGE argument within thyroid patients. Just google thyroid TSH controversy and you’ll get all sorts of patient websites. Just google it.
Genetics and a quick theory:
Before ending let’s look at how thyroiditis develops. The majority of cases (85-90%) in the U.S. are autoimmune related. Meaning that the thyroid is essentially destroyingitself. The question is how does this develop?
One thing about the autoimmune version of thyroid disease is that there is a very strong genetic component. In twin studies, there’s anywhere from 38-55% concordance rate.
So let’s look at how it develops:
Chart from: Christiakov (2005). Immunogenetics of Hashimoto’s thyroiditis. Journal of Autoimmune disease)
The first two are the interesting and important components.
- There is a genetic predisposition.
- Breakdown of immune tolerance
Why oh why would we see thyroid disease in younger people than normal?
The question needs to be asked if a large training stress COMBINED with a genetic predisposition is enough to trigger this breakdown of immune tolerance and lead to Hashimoto’s at let’s say at 20 instead of 50.
For example, if you are genetically predisposed to get it, and you are a 20yr old runner who because of the genetics is going to have Hashimoto’s develop at 50, do you instead get it at 20 because of the stress oftraining?
THAT IS THE QUESTION THAT NEEDS TO BE ASKED! To me it makes sense considering that we know that other environmental triggers can cause it.
The key though is that without the genetic predisposition, you can’t just train hard and get Hashimoto’s.
It’s just a theory at this point, but I think the thing to realize is that it has to be genetically there. You can’t just train to get it the disease. Whether it is training induced or an environmental trigger that distance running accelerates, it’s interesting to look at the idea.
The chart above also demonstrates how the body develops a thyroid problem, which is an important consideration. Thyroid disease is generally a slow progression over many years. It’s one of
the reasons why it usually is seen in women in their 50’s.
For a more thorough breakdown, read this journal article (http://www.jautoimdis.com/content/2/1/1)
If you have to have your thyroid removed, you need supplemental thyroid to function in regular life.
If you have Hashimoto’s or an autoimmune disease, you need supplemental thyroid to function in regular life because your thyroid is destroying itself…
If you are subclinical, your chances of it turning into full blown thyroiditis are increased somewhat, but should treatment begin or should you wait to see if it turns into full blown thyroiditis?
That’s the crux of the issue. I am against drug use, hard core. But there’s a lot of misinformation about what thyroid and hypothyroid entails. My hope is that people will read this and learn the process of diagnosis.
Hopefully, you also realize that this isn’t a training caused problem in people with actual thyroid diseases. And hopefully you realize that if you have a thyroid issue, taking the medication does not give you superhuman powers. It simply returns you to functioning.
Above all, the best thing you can do if you face this problem is be your own educated advocate. If you know the things outlined above, you’re not going to face a choice of whether you think you are hypothyroid or not because DR X told you yes and DR. Y told you no. You’ll know enough to get the right tests, have a thorough evaluation, and see if you have a legitimate problem or not.