Thyroid madness- Everything you need to know




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 necessary because 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 some degree 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.

1.       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.
1.       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.

2.       The standard for almost all labs then shifted to the .5-5.0 as the one true range for normal.
3.       In 2002, it all changed.
a.       The American Association of Clinical Endocrinologist changed their reference range to .3-3.0 (Baskin et al. 2002)
b.      In 2003, The National Academy of Clinical Biochemistry- changed their suggested range to .5 to 2.5. (Balloch et al. 2003)
c.        (http://www.worldhealth.net/pdf/WhitePaper_GuidancePhysicians-HRT.pdf) “In2003, the consensus panel (Endocrine Society, American Association of Clinical ndocrinologists, and American Thyroid Association) recommended a target TSH range of 1.0 to 1.5 mI U per liter in patients already receiving thyroxine”
d.      In 2007, Endocrine Society changed their recommendations for labs
e.      In 2010, more research came out that suggested individual assessment of TSH values based on age, sex, and race…
f.        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.

Antibodies
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. 

Clinical- evaluation
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 maybe and no.

Maybe, if a doctor doesn’t actually diagnose you and instead relies solely 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 at all 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.

1.       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

2.       Barron et al. 1995 – Took 6 marathon runners and followed them for 4 months until 2 showed signs of overtraining which was defined 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)

3.       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.

4.       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 (3-5x3-5min 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 train hard 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:

1.       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

2.       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

3.       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 4 hours).

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.

Recovery

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 been removed.  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 destroying itself.  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.
1.       There is a genetic predisposition.
2.       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 of training?

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)


So what?
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.

STUDY-
Lastly, since almost all studies are done on old people for thyroid disease, I think it would be pretty cool if we got an actual prevalence rate for hypothyroidism in distance runners training hard.  So here’s what I’d like if you want to help clarify this issue.

If you are an elite, semi-elite, or competitive runner (regular hard training, competitive), and you want to help, then contact me (sjm1368@yahoo.com) and get in on the study.
It will consist of you going to your local Doctor or Labcorp and ordering these blood tests.

TSH
TPO (Thyroid antibody)
Free T3, Free T4.

To be in the study, let’s say you have to get the TSH test.  If you have extra money to spend, go ahead and get the other two.  If you go to www.walkinlab.com  it’s relatively cheap (around $35 for TSH, $45 for antibody, and $45ish for Free T3 and T4) and you just go to your nearest labcorp for a blood draw.
Please get blood drawn on an EASY day only, not following a hard workout.  Do not have to be fasted or anything.

If you want to participate send me an email sjm1368@yahoo.com

Why am I doing this and why should you help? If you want answers and want to help science.  It’s an easy thing to do and it fills a gap in the scientific community.  Up until now most prevalence data is on older women, so let’s see what the normal levels and prevalence is for competitive runners.

I’ll publish results  and give you a copy of the results.  All results will be kept anonymous and I will not share them with anyone. You'll simply have to sign an informed consent.

28 comments:

  1. Dwight L.9:24 AM

    Steve, one thing you didn't address that I'm curious about:

    Say you have an elite athlete whose thyroid hormones were naturally a bit low. Not unstable, and not enough to be diagnosed hypothyroid. If the athlete optimized those levels by taking T4, could he improve recovery?

    The analogy I'm thinking of here is testosterone. If you took an athlete with perfectly healthy testosterone levels and gave him a little extra testosterone, his recovery rate would improve WITHOUT approaching superphysiological levels. I'm wondering if that's what's being done here.

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  2. Anonymous4:21 PM

    We do see where your career had the highs and lows. It is just hard to see it in Rupps, Halls, and many of the other ones who are on it now.

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  3. As a hypothyroid patient, non-Hashimoto's, I concur with Steve's coverage here. Job well done, and well documented.

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  4. Steve, great article. Since you were at the Oregon project for a time, I'm wondering if you got any insights into what Rupp was taking, if that's something you know at all about. Anonymous is right, Rupp has had a pretty steady progression throughout his career and rarely has a drastically sub-par performance, which doesn't seem to match your description of someone who is running with a medicated thyroid disorder. I know Salazar is very meticulous about what his athletes do when so maybe he was able to mitigate this somehow. Anything you know and are willing to share?

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  5. THanks for the comments.

    To cover a few. Performance, I can only speak about myself truly so I don't know where the highs/lows are. Maybe Rupp in the past in college years showed this pattern.

    As far as Hall, I think the pattern is fairly obvious. Look at his 1:03-04 half marathons in some of his marathon build ups.

    I don't know if the pattern holds up for everyone. Just speaking on my experiences.

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  6. Uno2Three410:00 PM

    My own observations

    I have taken thyroid medication for 15+ years since my thyroid was removed (cancer) in 1994. I was 26 at the time.

    The past two years I have taken up jogging and run 35 to 60 minutes three times a week. Pace is non-competitive at around 11-12 minutes per mile. (fastest was around 9:50 a mile for 3.1 miles.) I record my runs and have logged over 700 miles in the past year.

    So here's what I've seen happen to my health:

    BP went from 130/90 to 110/80

    Resting Pulse went from upper 50's to mid 40's

    Weight didn't change. (Can't win them all--I'm at 315 pounds)

    Thyroid Medication has gone from 300 micrograms to 200 micrograms.

    I can't say I have given much thought to the changing thyroid dosage . . . I thought maybe it was related to the better exercise although aging may be a factor also.


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  7. Jim Collins-White3:48 AM

    I think Dwight L is onto something in his question asking about the concept of micro-dosing thyroid medication under the guidance of a medical practitioner to achieve a specific INDIVIDUALIZED level of each thyroid hormone that that specific athlete performs best at.

    1) Is this something you believe would enhance performance?
    2) do you believe this practise has occurred in elite distance running?

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    Replies
    1. Anonymous11:07 AM

      General population without thyroid health issues will test between .5-2 TSH. Generally speaking regardless of being an athlete or just someone trying to function in a day to day life will be happy and optimal in that range. Everyone should be able to have thyroid health regardless of athletic endeavors. It is a serious health issue for so many that can cause immense physical and mental issues. Would an athlete perform better if they were optimal - yes but also NO. The meds can make running more difficult as well. They can cause heart paplations, anxiety and restless/insomnia. Also just like it can take months/years of someone to find the optimal dosage it can be that way for an athlete as well.

      http://thyroid.about.com/od/hypothyroidismhashimotos/a/Editorial-Controversy-Over-Diagnosing-Hypothyroidism.htm

      Delete
  8. Can I contact you? I'm hypo cyclist with hashi @visionset on twitter. Got lots to say on subject

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  9. Anonymous5:15 PM

    Great article- someone finally sharing the truth. Good job. I know you had great career highs and lows from allergies and vocal chord dysfunction where you could not breath. All runners seem to have issues of somesort at some time. This helps explain the recovery etc. Thanks

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  10. Endocrinologist12:14 PM

    More Info: Long distance runners can have thyroid levels akin to anorexics, mimicking central hypothyroidism [ TSH not up. Lawson EA Klibanski Nat Clin Pract EndocrinolMetab $:407-414] More confusion

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  11. Very Interesting!!
    Though I am now more confused than ever. I have just been diagnosed as hypo. Had a TSH of 5.4 about a year ago and finally followed up with an endocrinolgist 2 weeks ago. He prescribed levathyroxine and ran more blood tests. The Dr. office called and said the blood tests confirmed I was hypo and that I should continue to take the medicine. (They didn't say what the actual results were or whether or not it showed antibodies.) I read another article that said that excessive cardio can cause hypo (http://www.dangerouslyhardcore.com/5343/why-women-should-not-run/) and now, after finding your article, I'm wondering if I should be taking medication if my TSH is only marginally high, especially if exercise induced the high reading!! I run, but am not really a distance runner. I compete in local 5k races and frequently place in my age group (ages 45-49), but I've never run more than a 10k. I run maybe 15 miles a week, but also take a boot camp class 3 days a week and occasionally throw in some swimming or short bike trips. Exactly how much exercise does it take to impact your TSH and how high is too high?!! I will have follow up blood tests in 5 weeks, but won't see the Dr. again for 3 months!

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  12. Very Interesting!!
    Though I am now more confused than ever. I have just been diagnosed as hypo. Had a TSH of 5.4 about a year ago and finally followed up with an endocrinologist 2 weeks ago. He prescribed levothyroxine and ran more blood tests. The Dr. office called and said the blood tests confirmed I was hypo and that I should continue to take the medicine. (They didn't say what the actual results were or whether or not it showed antibodies.) I read another article that said that excessive cardio can cause hypo (http://www.dangerouslyhardcore.com/5343/why-women-should-not-run/) and now, after finding your article, I'm wondering if I should be taking medication if my TSH is only marginally high, especially if exercise induced the high reading!! I run, but am not really a distance runner. I compete in local 5k races and frequently place in my age group (ages 45-49), but I've never run more than a 10k. I run maybe 15 miles a week, but also take a boot camp class 3 days a week and occasionally throw in some swimming or short bike trips. Exactly how much exercise does it take to impact your TSH and how high is too high?!! I will have follow up blood tests in 5 weeks, but won't see the Dr. again for 3 months!

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  13. Anonymous12:33 PM

    Very interesting article, and one thing I'd like throw in is the effect of diet on autoimmune diseases, particularly wheat and gluten products. For those who are sensitive to wheat/gluten, it increases general inflammation and may trigger autoimmune effects. It's easy to run a 3-4 week elimination diet and see if any symptoms improve. (Same goes for dairy.)

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    1. Anonymous10:53 AM

      Yes removal of Gluten from diet in a autoimmune hypothyroidism athlete is essential for performance and long term health. I removed gluten from my diet and after 6 months my thyroid antibodies went from high to normalized being I no longer have Hashimotos.

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  14. Anonymous8:29 PM

    Great article. Brings a lot of pieces together in one place. As a hypothyroid athlete, I have definitely experienced the erratic performance patterns you describe. Can make you feel like you are going crazy! I believe we need the ability to adjust replacement medication dose from day to day to support different levels and lengths of effort. Currently, it's like we are all taking one dose of insulin every day, regardless of whether we hardly eat that day or partake in a Thanksgiving feast...
    Alyson

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  15. Anonymous11:10 AM

    If you think that you may have a problem with wheat/gluten check with a registered GP and get a blood test for Coeliac disease before proceeding with an elimination diet, as diagnosis of Coeliac Disease should be done while on a diet and issues can be caused by other factors. Prevalence varies with population but is around 1 in 130 people.

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  16. Jasmin Ray3:09 PM

    I found this article very very informative. I wish I found it years ago. Ive been doing alot of research on Hypothyroidism. For years and years I haven't felt right. I felt abnormal. I felt "fat" despite feeling like I tried every diet possible. I was told it was just depression. I wasn't able to focus on any type of day to day routine. I was told I was just ADD. Then recently my hair started falling out and I was always tired I felt like I didn't want to move or get up every morning. I really felt like I was falling apart. I had no clue what could possibly be wrong with me. Every doctor just dismissed my concerns because TSH ONLY was always normal. Finally while surfing the net I found Dr. Ridha Arem's website Arem Wellness. It was very informative and then I decided to buy his books, I mean, what could it hurt? I knew I just had to see him. I flew from Washington state to Houston, Texas just for an appointment with him. It was well worth the money I have spent. I am following his instructions, taking my meds and I feel like a whole new person. I feel like I just woke up and started living again.... Every doctor is different, but when it comes to the Thyroid, I feel most don't know what they are talking about. I clearly am not cured of my hypothyroidism but I am definitely feeling alot better.

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  17. This blog gives me the information that I needed regarding sign of thyroid problems. It really helped me in knowing the whole scenario of having a thyroid problem. Appreciated what you have here, thanks a lot!

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  18. Thanks so much for this article! As having Hashi's has been a pain in the butt for me since very young, this article helps my triathlete partners (including my husband) to understand why I feel like crap after a really hard workout. Also, why it looks almost impossible for me to better my times, as I'm having such a hard time recovering. I get huge "flares" and I'm more out of training that in training. But I'm not giving up! This article will help people close to me (especially my husband) to understand that I'm trying hard and I'm just not lazy.

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  19. Anonymous3:49 PM

    I was a long distance runner - 50k at altitude, many 21ks and trail runs.. I was diagnosed as hypothyroid 3 years ago - and despite for the first time my TSH is now in the 2 range.... I now cant run more than 3k.. whilst I can weight train and cycle - I just cant run... Its difficult to find an endo that can appreciate how important it is for me to run. Thanks for this article - at least I now feel I am not crazy - nor that my symptoms are psychological.

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  20. Alice4:05 AM

    Hi,
    a very useful article, thanks. I have a guestion, and wondered if you might know the answer. I was diagnosed with hypothyroidism - Hashimoto's several years ago, have been on levothyroxine since. I feel good, gave birth to my second child in the meantime. In July I started running 3-4 times a week, quite regularly, first 5k, now 10k, sometimes more. I am a beginner, 42 years of age, never done any serious training before). I feel very good, there's just one thing - my hair started to fall out massively. Could it be connected to running? Should my dose of the med be upped? I've had my TSH and FT4 tested recently - everything is ok. Btw my endocrinologist seems not to take my hair complaints seriously, she probably thinks that as long as I still have hair everything's fine...

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  21. Alice4:17 AM

    Thanks for the article! I have a question which might sound a bit daft but is important to me. I was diagnosed with Hashimoto's hypothyrodism several years back, have been on levothyroxine since. I feel good, gave birth to my second child in the meantime. In July I started running, 3-4 times a week, first 5k then 10k and slightly more. I have not done any serious exercise before, am 42. I feel v. good, there's just one thing: my hair started to fall out massively. Could it be linked to running? Should my dose of the med be upped? I've had my TSH and FT4 levels tested recently and the results are fine. Btw my endocrinologist seems not no take this complaint seriously, she probably thinks that as long as I still have some hair, everything's great. I'd appreciate your opinion.

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    Replies
    1. Sorry to hear about your Hashimotos struggles. Likely that your Iron levels are off which is the reason for hair loss. I would have your iron checked. Having optimal Iron levels is essential for thyroid health.

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  22. Really good article. I had my thyroid removed some years ago. I tried to keep my running routine (I'm a marathon runner - PR is 3h10m), and what I noticed is that it was hard to keep training with the same frequency. I just lack stamina. The problem is that my test results (t4 and tsh levels) seem fine, though I just don't feel that fine. I wish I could just train 5 times a week like I used to and not feel super lethargic the day after. Any hints?

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  23. (I had nodules before mine were removed, btw)

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  24. As a hypo bike racer I'm always searching the internet for articles that allow me understand the condition as it relates to athletes. This is one of the best articles I've read. After quite a few years on T4/T3 my and my Endo's opinion of where my TSH should be is in agreement (~0.75). For my race seasons 2 and 3 yrs ago I ended up having to increase T4 after 6-8 wks of hard training (lots of intervals for cyclocross racing). Of course with another 6 wks to adapt to the new dosage this was not optimal as then the season was almost over. These two seasons, I got myself a coach, which led to both seasons being charaterized by overtraining. This past season (and with a new endo who happens to be Chief of Endo at the local hospital) I had a preemptive T4 dosage increase before my hard training started and it made a big difference keeping me out of the overtraining hole (once a hypo athlete is in this hole it takes a LONG time to get out of it. Each year I learn from the previous season and refine what works for me for training. This now includes i) not ramping up my training volume too quickly - slow build; ii) doing the T4 dosage increase (only for the training/racing season); iii) returning to the "offseason" dosage for 3 or more months over the winter when training is minimal; iv) keeping my base fitness higher in the lead up to the sharp end of the season; v) train every other day/no back-to-back days; vi) take a day off if you feel tired; vii) accept a slightly lower level of performance; and vii) better to be going into races slightly undertrained than slightly overtrained.
    It's a mindset that's taken me a while to get to and to shed the "more training = faster racing" general concept and training response that I got when I was younger/not hypo. Combine this with also being a Master's athlete (50) and rest and recovery (which may also equal a general training less/training smarter approach) are the keys.

    Thanks again for putting all your thoughts and findings down, it was a great read.

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