T3 Or Not T3 – Exploring The Controversy

I don’t want that synthetic stuff; I want the natural thyroid hormone.

This is probably one of the most misguided requests I get in my practice.  To make sure we’re all on the same page here, I’m talking about levothyroxine vs dessicated (pig/cow) thyroid.  First, I must reject the premise of the patient’s italicized statement above. 

Levothyroxine is Natural; Pig Thyroid Isn’t

What?!  Every other blog I’ve read says the exact opposite!

That’s because none of what you’ve read has been written by an endocrinologist (or at least not an endocrinologist worth her salt).  Among endocrinologists, it’s an open secret that levothyroxine is one of the most natural forms of hormone replacement for the human body.  When your thyroid is underactive, and your doctor puts you on a levothyroxine pill, the body cannot tell the difference between levothyroxine and thyroxine (the native hormone).  In other words, your body is perfectly happy to use levothyroxine just as it was using thyroxine when your thyroid was healthy.

Pig thyroid pills, on the other hand, contain a mixture of T4 and T3, in a ratio of roughly 4:1, respectively.  That’s a wonderful cocktail – if you’re a hypothyroid pig.  Guess what the ratio of T4:T3 is in the human body – about 15:1!  So when you take pig thyroid, you’re getting way more T3 than what the human body is accustomed to seeing on a daily basis.  Not good.  I’ll explain why shortly.

So we’ve got levothyroxine – a “synthesized” hormone that is identical to the thyroxine that your thyroid would be making if it was functioning properly.  And then we have pig thyroid, which gives you both T4 and T3 (two for the price of one!), but in a ratio that is way out of proportion for the human body.  Which of these sounds more natural so far?

Well, I’d rather get too much T3 than not enough.  After all, if my thyroid isn’t working, doesn’t that mean that I’m not making enough T4 and T3?  I have to take at least some T3, right?

You’re still skeptical – I get it.  You’ve read that T3 is the “active” form of thyroid hormone that gets inside the cells and gets the job done.  The thing is, the body is efficient at taking levothyroxine (T4) and converting it into T3.  All the different tissues in the body (liver, kidneys, muscles, brain, etc) are going to make however much T3 they need.  Are there instances in which various tissues don’t make as much T3 as they need?  Yes, but this is nowhere near as common as some of the non-evidence-based information out there would have you believe.  And when it does occur, the magnitude of the impact is probably not as vast as one might think.  If you really want to geek out on the T3 conversion issue, read Guidelines for the Treatment of Hypothyroidism: Prepared by the American Thyroid Association Task Force on Thyroid Hormone Replacement, and jump to:

13a. Do genetic variants in thyroid hormone pathway genes (deiodinases or thyroid hormone transporters) affect the serum or tissue levels of thyroid hormones in healthy euthyroid individuals or hypothyroid patients taking replacement therapy?

 

■  Summary statement

Specific polymorphisms in the deiodinases are consistently associated with very small changes in serum thyroid hormone levels. Insufficient data exist to draw any conclusion about the clinically relevant effects of deiodinase or transporter polymorphisms on tissue thyroid hormone levels.

    

If you like, there’s a plethora of scientific text you can wade through after the summary statement, but I think the more relevant issue to dive into is, why do some people feel better with pig thyroid or when we add liothyronine (T3) to their levothyroxine therapy?  And the corollary: if people like pig thyroid, why is your doctor loathe to prescribe it for you?

Five Types of People Who May Need/Like T3

  1. If someone does have one of those (not clinically diagnosable) deiodinase polymorphisms, it is certainly possible that T3 therapy provides replacement for a physiologic need.  In this case, levothyroxine alone might not cut it.
  2. Patients who have had their thyroids removed have to rely entirely on T4 to T3 conversion for their T3 needs.  In other words, an absent thyroid can’t make any T3 at all, so patients with postsurgical hypothyroidism occasionally feel better with combination T4/T3 therapy.  Contrast this to the typical patient with an under-functioning thyroid (primary hypothyroidism), who probably makes enough T3 such that exogenous (supplemental) T3 won’t make a difference.
  3. Hypothyroid patients with depression may benefit from the addition of T3 to their levothyroxine.
  4. Anyone particularly susceptible to the placebo effect will like T3.  Frankly, this encompasses almost everyone – it is rare to be immune from the placebo effect.
  5. I saved the best for last, because I believe that this is the most common reason why people like T3.  T3 is a short-acting hormone that – especially when given in supra-physiologic doses (like pig thyroid!) – tends to act as a stimulant.  This is actually true of lots of hormones when taken in higher than physiologic doses.  Ever take a whopping dose of prednisone for a few days and feel like Superman?  Do you know any body builders who juice and feel fantastic for three days after an injection of 1000mg (venti-sized dose!) of testosterone?  So, just because someone feels good on T3 does not mean that she is deficient in that hormone.  Smoking crack probably feels pretty good, but you’d never assume the addict has a “crack deficiency.”

Your Doctor isn’t Mean – She Just Cares about Your Long-Term Health

When exposed to high levels of T3, the body may exhibit symptoms of thyrotoxicosis (too much thyroid hormone).  Symptoms like heart palpitations, tremors, sweating, anxiety, and insomnia may occur even if the TSH is within the normal range.  Remember, while the TSH is usually highly accurate, if you spend part of the day with high T3 levels and part of the day with low levels, that may average out to a normal TSH.  In this case, a normal TSH does not mean you are normal. 

After longer periods of time, the heart may go into a dangerous rhythm called atrial fibrillation, the bones may become more fragile and prone to fracture, and muscles may waste.  So, while your doctor would love to fix all your symptoms right away, a stimulant that masks whatever is really going on with you is probably not the best long-term solution.

OK, I’m hearing all this, but can’t we just check a T3 level in my blood and use that to gauge whether I need T3 therapy?

Oh, were it that simple…the T3 level in your blood does not correlate well with the T3 level in all your various tissues.  Remember, each organ is making its own T3 based on its needs at that moment.  We can’t measure that.  On top of that, when on levothyroxine therapy, the blood level of T3 is usually low-normal and sometimes even slightly low.  But there has been no evidence showing that these levels correlate with any symptoms.  Bottom line: it is not helpful to check T3 levels in hypothyroid patients on levothyroxine, in an attempt to determine whether T3 therapy is indicated.

How to Broach the Subject of T3 Therapy with Your Doctor

After all that, you’re going to advise me how to actually get my doctor to prescribe T3 for me?  Did I misread the first 2/3 of this post?

No, you didn’t misread me.  After years of offering small doses of liothyronine to a subset of patients on levothyroxine – in a physiologic ratio of T4:T3 – I am disappointed with T3 therapy and skeptical that it has much benefit.  However, I do have a minority of patients who have tried T3 and have had a durable response to it.  I say “durable” because patients will often have an immediate benefit from the stimulant effect, which then wanes over the course of weeks to months.  If someone still feels better six months after starting T3, I consider that a durable response.  So, if a patient meets all of the following criteria, I may offer a trial of T3 therapy:

  • The TSH is already in the lower half of the normal range.  Sometimes (not all the time), hypothyroid symptoms will improve just by bumping the levothyroxine dose a bit to push the TSH down below 2 – 2.5.
  • There is no competing diagnosis to explain the “hypothyroid” symptoms.  For example, if a patient has sleep apnea and isn’t treating it because she doesn’t like the CPAP mask, T3 is not yet on the table.
  • The patient does not have active heart problems (angina, atrial fibrillation, etc.).
  • The patient does not have moderate-severe anxiety.  In my experience, T3 makes this worse.

If you feel you meet the above criteria, then consider broaching the subject with your doctor.  But you must understand and embrace the following bullet points before you ask:

  • If you do try T3, keep your expectations low.  Remember, you may feel better when you start it, but that feeling may disappear if the benefit was solely due to the stimulant effect.
  • If your doctor went through medical school and residency/fellowship in the 1990’s or after, chances are she has been taught that T3 is unhelpful at best, evil at worst.
  • T3 therapy is often associated with naturopathy; the naturopathic approach to hormone treatments is way out in left field and mostly antithetical to the allopathic (mainstream medicine) approach.  The number of people I’ve taken care of who have been misdiagnosed and mistreated by naturopaths should be horrifying to the lay public.  More on this in future posts.
  • Before prescribing T3, your doctor may want to probe aspects of your health and lifestyle that you feel are irrelevant to your symptoms.  I recommend you listen to your doctor, as it is impossible to be objective when it comes to your own health.  You may “know your body,” but your doctor knows hundreds – if not thousands – of bodies just like yours.  I know it’s disheartening to read that you’re not that special, but trust me, you’re not.

If you’re still reading by this point, I assume that you remain interested in discussing T3 therapy with your doctor.  Here’s how I would initiate the conversation:

Doc, I’ve been on levothyroxine for quite some time now, and I still have several symptoms that just won’t resolve, like [symptoms].  I realize that my TSH is optimized, which should mean that the treatment of my hypothyroidism is optimized.  So I’ve been thinking about what else could be causing my symptoms, and I just can’t come up with anything.  I’m getting at least 7-8 hours of sleep every night, I’m eating clean, and I exercise several times per week [this better be true].  Based on what you know about me, can you suggest any other avenues to explore that might help me figure out these symptoms?

Now you pause.  Let your doctor earn her $20 copay ($40 if she’s an endocrinologist).  Give her time to ask you questions, look at your lab work from the past couple of years, and see if perhaps there is something else to explore.  If she has some suggestions, great.  If she agrees that you are otherwise healthy, it is possible that she may actually broach the idea of a trial of T3 (this is much more likely if you have a mid-late career Endocrinologist).  If she comes up empty and basically shrugs her shoulders, then you can carefully and respectfully bring up the possibility of a trial of T3:

Doc, don’t worry about being out of ideas.  I’ve been wracking my brain for [weeks/months/years] and I haven’t come up with any competing diagnoses either.  So I wanted to get your opinion about something I read.  It was written by an endocrinologist, so I hope it’s more trustworthy than the majority of the nonsense out there on the internet.  It seems like there is a small subset of hypothyroid patients who will benefit from adding in a small dose of liothyronine to their levothyroxine.  I understand that, when used, the levothyroxine dose should remain somewhere around 10-20 times as much as the liothyronine dose, to keep the ratio close to normal for human physiology.  I also understand that it may not work, and I’m ok with that.  If it doesn’t work, then I’m happy to stop it.  What do you think?

You’ve done several things by couching your request as above.  You’ve communicated that you and your doctor are on the same team, and you’ve acknowledged that you don’t expect miracles.  You have implied that you understand how doctors feel about internet research and that you understand the limitations of such research.  You have asked your doctor to give her opinion of what you’ve read, thereby demonstrating that you respect her education and experience, and you value the doctor/patient relationship.  Now the ball is in her court.  She can agree to a trial or not.  If not, you can try to gauge if there is any wiggle room in that “no.”  But if there isn’t, you need to accept that and either forget the trial of T3, or go get a second opinion.

What do you think?  Have you tried liothyronine or talked to your doctor about it?  What has your experience been with your trial or with your doctor?  Are you a doctor who has used T3 for your patients?  Do you think it has value?  Comment below!

By interacting with me in the Comments, you agree that you have read and will abide by my Disclaimer.

25 Replies to “T3 Or Not T3 – Exploring The Controversy”

  1. Excellent, informative and entertaining summary of thyroid hormone replacement and the intricacies of T3T4. I especially like the sample script at the end. It is so important to be prepared when you meet with your doctor. This article has you more than prepared.

    1. Thanks, Dr. Scher. If people are going to ask for T3, I hope that they will do so from a position of knowledge and have realistic expectations.

  2. Thank you for the article, but you haven’t addressed why I take T3, which is as an anti-depressant adjutant. My understanding is that the level of evidence is for T3 as an anti-depressant is not great, that the mechanism of action is not understood, but that it is routinely tried in cases of recalcitrant depression, and that the evidence is clear that T4 is not helpful in these cases.

    I’m also concerned about long term T3 use in these circumstances. I’ve yet to find anything relevant on this. And periodically my doctor orders a full thyroid panel which always comes back abnormal, but is apparently “normally abnormal.”

    Also my hair fell out once, but that has not been repeated, and the dermatologist did a thyroid and told me that if it had been my thyroid, that the problem had gone away.

    1. Thanks for the comment, Christine. In my post, I do mention (in the section about who might benefit from T3) that patients with hypothyroidism and depression sometimes benefit from the addition of T3 to their T4 therapy. You don’t say whether you take T3 for hypothyroidism/depression, or just for depression. In the absence of hypothyroidism, T3 is not considered a standard pharmacologic therapy for depression. Of course, I don’t know your medical history and would not presume to make any recommendations in this venue, so I’d defer to your treating clinician.

      As for long-term use of T3, high doses over long periods of time can be irritating to the heart, muscles, and bones, among other organ systems. Low doses of T3 are much less likely to cause any long-term problems.

      1. although t3 is not a standard treatment for depression, there are a number of classic [old] papers on using it as an adjunct to antidepressants in refractory cases. these days, with so many more agents available and well-proven to be effective [both antidepressants and proven adjuncts] it is more rare that such an approach would be taken. and sometimes it does work. there is no evidence to my knowledge, btw, that t3 is better in this use than t4. i was discussing bipolar disorder with an NIMH researcher who mentioned t3 and i asked him if he had any basis to prefer it to t4, and he did not.

        HOWEVER, this brings up the possibility of patients who are mildly hypothyroid but who have “normal” thyroid studies. 4.4% of NORMAL people will have studies outside of 2 sigmas, and presumably there must be individuals whose numbers look normal but aren’t optimal for those individuals. in some individuals who have refractory depression, and who have tsh in the upper half of the range, i’ve tried adding t4 [not t3] to drive their tsh down toward 1 or so. sometimes they feel much better.

        1. I think it’s reasonable to try levothyroxine for someone with uncontrolled depression and a high-normal TSH, especially if they have positive thyroid (TPO) antibodies. As long as we’re not suppressing the TSH, there is little harm in a 6-month trial.

  3. I’m so glad to find this blog, being an endo patient myself. Before I got acquainted with skepticism, Quackwatch, etc., I fell for the T4/T3 idea, when after a thyroidectomy it took ages to feel OK again and all the “pro” patients in the forums were suggesting T3 supplementation or even dessicated thyroid. I couldn’t go to a naturopath, as there were none available in my country, so my only loss was an expensive reverse T3 lab test. Now that my skeptic muscle is trained better, I’m glad I didn’t go further with it, I’d probably get diagnosed with adrenal fatigue or Lyme, or some other imaginary disease.

    I do have a question – I was prescribed a selenium supplement to help with T4/T3 peripheral conversion (by a regular endo). Back then I must have a difficult patient with preconceived ideas about my problems, tired, depressed and anxious on top of it, so I can imagine the endo giving a placebo, but it seems it’s not entirely without scientific base. So what exactly is the evidence level for selenium supplementation in patients after thyroid removal?

    1. Great question, BL, and thanks for the kind words. The evidence for selenium improving T4 to T3 peripheral conversion in a clinically meaningful way (i.e. you will actually feel a difference) is poor.

      In my practice, I occasionally prescribe selenium for two reasons:

      – To reduce the risk of postpartum thyroiditis in a woman with a history of autoimmune thyroiditis (a woman with positive thyroperoxidase antibodies).

      – To improve symptoms in mild to moderate thyroid eye disease in a patient with Graves’-associated orbitopathy.

      Other than those situations, there isn’t much of a role for selenium, at least according to currrent evidence. Selenium does, interestingly, lower TPO antibody levels in patients with high titers; however, it has not been shown to decrease the need for thyroid hormone therapy in these patients. So it doesn’t seem to make much sense to use it just to lower the antibody level if it isn’t going to do anything tangible.

      In a thyroidectomized person, I’m not aware of any evidence that selenium is helpful.

      1. Thanks!
        One more thing about the dessicated thyroid – I always wondered about thyroid cancer patients using it so happily – shouldn’t they be worried about causing fluctuating thyroglobulin marker values? Wouldn’t you miss a recurence with this “natural” approach? Back when I read these suggestions in patient forums, this seemed to be quite a scary consequence.

        1. Another great point, BL. In theory, dessicated thyroid is even less ideal for a patient with a history of thyroid cancer (thyroid surgically removed) than it is for a patient with garden variety, primary hypothyroidism (thyroid that is underactive).

          Because most patients take dessicated thyroid once daily, and because there is so much short-acting T3 in there, they spend the first part of the day with high levels of T3, and the second part of the day with low levels. Because there is less long-acting T4 in that preparation of thyroid hormone, then there is less consistent suppression of TSH, which could (in theory), lead to more stimulation of residual thyroid cancer growth by TSH (Thyroid Stimulating Hormone). This would show up as a rising thyroglobulin level, as you suggested.

          This is all theory, as I am unaware of any data that proves patients on dessicated thyroid hormone have higher rates of thyroid cancer recurrence. But if I had thyroid cancer and a medium-high risk of recurrence based on the ATA risk stratification system, I would not take the risk of using dessicated thyroid hormone for my long-term thyroid replacement.

  4. Very interesting article. Love it. I went to a functional medicine doctor who was also a western medicine doctor prior to switching. She left me on my levothyroxine 75mcg but I also take liothyronine 5mcg daily for 5 months with no side affects. My hair loss is less on the combo. I’m 61 and I,m curious with any long term affects of this mixture. Can you comment? I would love to hear from you. Thanks

    1. Thanks for the kind words, Debbie. Functional medicine is an interesting field, as it is dominated by quacks in my area, but has the potential to be holistic in a good way if done right. As an aside, if you want to see what functional medicine can/should be, check out Dr. Bret Scher’s site. I will actually be posting my review of his book tonight (note that he and I have no financial relationship, but he is a friend).

      Regarding your thyroid question: for most people on 75mcg of levothyroxine, 5mcg of liothyronine would be considered a pretty reasonable dose. The only comment I have is that liothyronine peaks at 2-4 hours after ingestion and then wanes, such that it is best dosed twice daily if someone wants exposure to the medication throughout more of the day. Unfortunately, 5mcg is the smallest pill available, and when I ask people to split it to 2.5mcg twice a day, they usually report that it just crumbles to dust. I think some generic versions are better than others in that respect, though I don’t know which ones split nicer. Many people feel fine with just the morning hit of 5mcg, though, so if someone notices a clinical improvement on T3 that is durable, I am ok with once daily dosing.

      As for long-term ill effects, it would be unlikely to see higher rates of bone loss and heart arrhythmias with such a small dose of T3. Although there isn’t much data in this area, I wouldn’t worry much about people who take small, physiologic doses of T3. I would worry a lot more about people taking whopping doses of T3 who consistently have suppressed TSHs.

      1. Wow that was great. I was on 5mcg of the livo in the morning and then in the afternoon but more hair loss so we discontinued the afternoon dose. I will try splitting to see what happens to my pill they are quite small. I’ll check out your friend info also. Thanks.

        I also asked about compounded hormone replacement vs Premarin any opinions or references on that. Estiodiol is what I am curious about and what about progesterone? I have no ovaries or uterus since 2001. Just curious.

  5. Way back in the mid 1960s I was diagnosed as hypothyroid and put on Levothyroxin. A few years later, while living in Europe, my prescription was changed to Cytomel (T3) at lowest available dose to treat chronically low BMR. I stayed on that treatment for almost 30 years. With age either my need for T3 declined or my conversion of T4 to T3 improved or reverse T3 (never measured) improved or? Anyway I started getting too high for T3 and after some delay discontinued the medication, but not until after I had developed AFib. Have now been off any thyroid med for 20 years with quite normal health, and the Afib controlled with meds. Seems like T3 can be beneficial for quite long periods, but needs to be discontinued immediately if things change.

    1. T3 should be considered an adjunct to levothyroxine replacement, at most. It is not a replacement for T4 therapy. I agree that it should be stopped in certain situations, especially if the dose of T3 is substantial.

  6. I’ve been taking WP Thyroid, natural T4/T3 combo, for at least 2 years now. Now I’m thinking I made a mistake asking for it. (At the least, I think it makes me anxious.) I’ve been taking only 1/4 grain equivalent per day, though. Hopefully I haven’t harmed myself? Ugh. (I have Hashimoto’s, with TPO between 300 & 380 for the last few years.) Thank you for this site!

  7. I was diagnosed with mild Hashimoto’s in 2009-10. I’ve had a couple of hyperthyroid episodes – eating twice my usual amount and still losing weight fast, not able to fall asleep until 7 AM, etc., etc..
    The weird thing is, both of these episodes happened when I started taking a small amount of liothyronine (T3) in addition to the levothyroxine. I didn’t change my dose of levothyroxine. But each time I started taking liothyronine, I had a hyperthyroid episode.
    I stopped both the T3 and T4 when I started having hyperthyroid symptoms.
    But, my hyperthyroid symptoms continued for maybe 4-5 days anyway. They gradually tapered off, and I resumed the levothyroxine but not the liothyronine.
    Since T3 is short-acting, it seems weird that it would trigger a prolonged hyperthyroid episode. Maybe it somehow triggered my thyroid into dumping a lot of thyroid hormone into my blood? Have you ever noticed this happening or know why it might happen?

    1. It’s not unusual to feel thyrotoxic after being on too much thyroid hormone, even for a few days after stopping the T3. T3 would not cause the thyroid to release more hormone, but it’s certainly possible to take too much exogenous thyroid hormone.

      1. It seems weird that a small dose of liothyronine added in (probably it was 5 mg/day), would put my body into a wildly abnormal state for days after stopping it.
        I got some thyroid values measured in one of those episodes – I had stopped taking T3 and T4 and I was calming down – my TSH was about zero, and my free T3 was > 11 pg/mL.

      2. ps Maybe adding liothyronine can set off a vicious circle because it makes the thyroid more active so it pumps out more thyroid hormone …

        1. I can’t comment on your specific situation, but I can say this:

          – liothyronine would not cause the thyroid to pump out additional hormone.

          – when I see someone with a very low TSH and very high T3/T4 levels, it usually means that they are massively over-replaced with exogenous thyroid hormone or they are actually hyperthyroid.

          – it is important to distinguish between hyperthyroidism, which is the overproduction of thyroid hormone by the thyroid; and thyrotoxicosis, which is the presence of too much thyroid hormone from any cause. Thyrotoxicosis can be due to taking too much exogenous thyroid hormone or due to the thyroid cranking out too much thyroid hormone.

  8. My aging mother was doing poorly pn T4-only medication for her hypothyroidism. I advocated for her FreeT3 to be tested by her assisted living facility’s visiting physician and it was found to be low. She was given T3, and now she’s feeling better, has more energy, and is no longer sleeping 16 hours a day.

    I am on combination NDT treatment and Unithroid (T4). This combination is fantastic for me. I have been on it for now 8 years.
    Two of my three children, also (sadly) hypothyroid, are also on a combo of NDT plus Unithroid. All are doing well and my eldest sailed through college and grad school on NDT. At the age of 12, she was so depressed she could not carry out her obligations (homework, musical instrument practice). She was overweight, had no energy, her beautiful thick curly hair was falling out and breaking, she had plantar fasciitis, and had terrible well-being. NDT reversed all that. None of us but my mother began our treatment with T4-only, so apart from my mother, I can’t speak to having seen a first-hand difference. However, I’m a part of aj online forum of over 60,000 Hashimotos patients, and I can tell you with no hint of indecision that the vast majority of those in the forum have had their lives turned around by the addition of T3. Infertile women and those with no children due to multiple miscarriages have been able to bear children, even. Perhaps the fact that you haven’t seen much longterm benefit in your practice from the use of T3 is that you may not have been trained properly in its use. Surely such training is not widely available in medical schools, and is kept out of physician conferences because the conferences are underwritten by the maker of Synthroid. (And this company is also a large donor to medical schools.)

    Here is a compilation of various studies on the topic:
    stopthethyroidmadness.com/medical-research/
    While this is not the forum which asked me to serve as moderator, and I’m not fond of the angry tone of the website, the anger arises from doctors who keep their patients functionally hypothyroid with poor treatment, causijmng continued suffering and so I understand it.

    The tone of your own article is haughty and appears as though you feel you have nothing to learn from your patients. As a private piano instructor (and active classical performer) with an M.M. from a world-renowned conservatory and 28 years of teaching, I find that my students teach me all the time and that I may derive growth as a teacher from not only my professional organizations, conferences, books, and professional journals, but also, from my students themselves. I am sorry that your forays into the use of exgenous T3 to assist your patients were relatively unsuccessful. If you were to sign up for a functional medicine training on its use, you might find some benefits for your practice.

    It requires a certain humility as well as courage to be willing to venture out into a new and somewhat professionally forbidden area of medical study. I wish you and your patients the very best with their thyroid treatment.

    I also am interested to know whether you have found Levothyroxine-only treatment to eliminate symptoms in most of your hypothyroid patients, and whether you do anything to test and treat Hashimoto’s Disease?

    Thank you.

    1. First, I’m glad that you and your family members have found what works for you. To address some of your points:

      – You and the 60,000 other Hashimoto’s patients on that forum are in the echo chamber. There are a multitude of reasons why those people may feel better and, frankly, you have no idea what they are. For that matter, I would suggest that there are probably a sizable number of people who don’t feel better, hence their involvement in the forum, still searching for answers. But that is merely conjecture, since I also have no way of knowing what’s going on with these folks other than what they choose to self-report in an anonymous forum on the internet.

      – Your conspiracy theory about medical education being suppressed by the makers of Synthroid is both laughable and frightening at the same time. People really believe this nonsense? Well, I suppose so. But since I can’t prove a negative, I guess there’s no way you’ll ever come around on this one.

      – During the time I trained, we were taught why T3 was thought to be unhelpful. But as new data has emerged, doctors who are interested in continual learning (as I am) have been more open to trying it. Contrary to what you suggest, there is no magic to using T3. And yes, I learned how to do it from a real doctor, not a functional one.

      – Just as I would never presume to tell you how to teach piano just because I’m a music lover, it amazes me that you have the hubris to suggest that if only I could find the right quack to teach me how to use T3, I’d have better results. The reason T3 doesn’t usually work is because most people don’t need it. If I wanted to enter full-on quack mode, I’d jack up the dose to heroic levels that have the potential to act as a stimulant, claim success, and call it a day. But I took an oath that said something about “doing no harm.”

      – To answer your last question, I’ve written a bunch of posts that address all that:
      https://hormonesdemystified.com/the-ultimate-guide-to-thyroid-function-testing-hypothyroidism-edition
      https://hormonesdemystified.com/selenium-and-the-thyroid-secrets-your-naturopath-doesnt-want-you-to-know
      https://hormonesdemystified.com/its-not-your-thyroid

Leave a Reply

Your email address will not be published. Required fields are marked *