James K. Rone, MD, FACP

I will take this from the beginning, assuming that I am seeing a patient not previously on thyroid replacement who has just had a total thyroidectomy. Your subject heading specifies athyreosis; however the principles and my practice are the same for a spontaneously hypothyroid patient with, say, Hashimoto's thyroiditis, except that the starting dose will be higher for the postsurgical patient, since they will obviously require full replacement—all of their thyroid needs met by exogenous replacement. As I say, most of what follows applies to both situations, although you are correct that there can be additional challenges in the athyreotic patient.

I'm going to take this from the beginning because—while your question specifies "not responding to monotherapy" (which I take to mean levothyroxine [LT4] monotherapy)—because I think "currently failing monotherapy" is different from saying "monotherapy is inappropriate." It depends on how effectively and skillfully the LT4-only treatment is being implemented. I am a firm believer based on over 30 years of doing this, that most doctors, including most endocrinologists, don't dose LT4 high enough. LT4-only Tx tends to get a bad rap on patient-oriented websites, not because it doesn't work in many, if not most, cases, but because it gets underdosed.

Why? There are a number of reasons:
—It is a common, but I believe wrong practice to monitor TSH only. I believe it is easy to miss underreplacement if you don't also look at a T4 level, usually a modern FreeT4 assay. FreeT3 is less often truly useful, although it can be very important as we will get to. So, to answer one of your questions, I usually get a TSH + FT4 + FT3, especially early on, until it is clear the additional information provided by the FT3 isn't worth the additional cost. But, I almost always get at least a TSH + FT4, even in people I've been following for years.
—And, regardless of what tests are ordered, I find it all too common that ANY level somewhere within the lab report's published reference range ("normal" range) is accepted as an indicator of adequate thyroid replacement. Often that ends up meaning dosage adjustments are stopped if the levels are JUST BARELY normal. That might be okay and it might not, and the determining factor is the patient's symptoms. If the patient feels good we're done, and if not, we're not. Although too often symptoms are ignored in the face of "normal" lab results. Endocrinologists are particularly guilty of this because we tend to be taught to treat the numbers not the patient, which flies in the face of my earlier internal medicine training to treat the patient not the numbers. The statistical disconnect is this: The lab's reference range represents what is STATISTICALLY normal for the population, NOT what is necessarily PHYSIOLOGICALLY ideal for an individual patient. That individual physiologically ideal range is always narrower than the population statistical range, usually, but not always lying within the population range. Sometimes an individual's ideal level will lie outside of the lab's reference. In fact, by statistical definition 5% of normal people will have an abnormal result on any given lab test (2.5% above, and 2.5% below).
—Relatedly, another reason LT4 gets underdosed is that low TSH's are almost universally interpreted to mean the patient is overreplaced, and same with high FT4's and FT3's. When in fact there is no question that some patient's need to be run with a low TSH or a high FT4 or FT3 (these are people with central hypothyroidism and thyroid hormone resistance, respectively).
—Lastly, it is not generally recognized that if a TSH does become suppressed by true overreplacement, or other reasons, it can be very slow to rise back to normal—leading to obsessive, repeated reductions in LT4 dose to get the TSH up. This is a good reason not to follow TSH's alone.

Okay, so I will start LT4 at some appropriate starting dose (I encourage Synthroid or one of the other branded products, but if cost is an issue, starting with generic LT4 is okay). It takes at least 5 weeks to see the full effect of any given adjustment, so it is almost never appropriate to check labs sooner than that. Generally speaking I will increase the LT4 dose in baby steps—one dosage at a time (125, to 137, to 150, to 175, etc., for example)—until the TSH is <2.0 and the FT4 is mid to high normal and the patient is no longer symptomatically hypothyroid.

If hypothyroid symptoms remain in spite of labs meeting those criteria, then I make further cautious upward adjustments, monitoring FT4, FT3, and TSH, and symptoms. If the TSH becomes low and the patient is not symptomatically HYPERthyroid, I often will not back off because of that—although I warn you most doctors will.
—if the patient is taking generic LT4 I will switch to synthroid or another name brand, and sometimes people feel better just from that.

If the above does not find a dose that resolves the hypothyroid symptoms—which is getting to the meat of your question—especially if the FT4-to-FT3 ratio is high, suggesting inadequate T4 to T3 conversion, then I will add brand-name Cytomel or generic liothyronine (LT3) 5 mcg once daily, taken first thing in the morning on an empty stomach. Depending on a number of factors I might or might not reduce the LT4 dose at the same time. If all that is added or adjusted is LT3, then labs can be checked in 3 weeks, but any adjustment in LT4 demands labs be delayed for 5 weeks or longer. When using combination therapy (LT4 + LT3) the labs I monitor are: TSH + FT4 + FT3 + SHBG, and I calculate a FT4-to-FT3 ratio.

SHBG is sex-hormone binding globulin—which is simply a protein the liver produces more of, the more the thyroid-hormone receptors deep within the nuclei of the liver cells are stimulated. This makes SHBG a sometimes useful biomarker for TISSUE thyroid levels, as opposed to SERUM levels. Remember, what we really care about in the situation you are asking about is not how much thyroid hormone is in the blood—which is what we measure out of necessity—but rather how much the thyroid hormone receptor (THR) is being stimulated deep in the body's tissues. The SHBG reflects PERIPHERAL THR stimulation, and the TSH is a reflection of BRAIN and PITUITARY THR stimulation. One thing almost no doctor considers is that the amount of thyroid hormone that adequately stimulates those BRAIN THRs, thereby suppressing TSH, is less than what it takes to adequately stimulate the PERIPHERAL THRs all over the body outside the brain. This is how you can have a low TSH, suggesting overtreatment, while the patient still feels hypothyroid because the peripheral THRs want more thyroid hormone. (This represents relatively recent research that is not widely disseminated—but was discussed in a meeting I attended in Chicago a couple of years ago, conducted simultaneously and virtually with a meeting of endocrinologists in London).

Before finishing up, let me back up and talk about the general topic of LT4 + LT3 combination therapy. As you may know, T3 is the less abundant but more potent form of thyroid hormone—it is the more active form of the hormone. The thyroid gland directly secrets about 6% of the body's daily need for T3. The rest is produced all over the body (brain, liver, kidney, muscle) via T4 to T3 conversion. For this reason, most hypothyroid patients don't need to be given LT3. Their bodies take the LT4 and convert it to however much T3 is needed by any given organ at any given time. However, some patients do benefit from the combination if they convert less efficiently—sometime the LT4 replacement will suppress conversion—and a clue to that as I've said, can be a high FT4-to-FT3 ratio (although that is not a terribly commonly used parameter by most doctors), or simply the scenario that you present: failure to respond well to monotherapy. The athyreotic patient will of course lack that small percentage of T3 that the thyroid gland directly produces, and so they are at least theoretically more likely to benefit from the combination. Some not-particularly-well-informed pundits on the Internet will argue that "natural" thyroid products that contain both T4 and T3 are always better than LT4 alone, which is simply not true. In fact, LT4 monotherapy, with the body making its own T3, mimics normal human physiology more closely (where the thyroid makes a lot of T4 and very little T3) than giving a lot of LT3 does.

There are two ways to give LT4 + LT3 combo therapy. My preference is, as I presented above, adding once daily LT3, 5 mcg, to LT4. If needed a second or even third daily dose can be added, generally taken no later than 3 p.m. so as not to disrupt sleep. Some people do okay taking the 2 or 3 LT3 pills all together in the morning for convenience and better compliance, but usually spreading the doses out through the first half of the day is more effective. Unlike LT4, LT3 does not have a long enough serum half-life to last all day on just a single dose.

The other option some patients prefer—and this isn't my first choice, but I will not uncommonly switch to this route if the response to LT4 + LT3 is inadequate, or the patient really wants to try it—is a desiccated thyroid extract (DTE) product. There are a number of these out there but the best known—and most reliably available—is Armour Thyroid. These products get their thyroid hormone from pork thyroid glands harvested from slaughter houses (the "Armour" name literally came from the Armour meat packing company). Some argue that DTE products are better because they are "natural." Not true. Whether or not they work better for some individuals, the "natural" part has nothing to do with it. The main active ingredients are chemically identical to synthetic LT4 and LT3. That said, these animal thyroid glands probably contain some minor metabolites of thyroid hormone (T1, T2, sulfated TH, etc.) that would not contaminate the synthetic products, and it is at least theoretically possible some people do detect some benefit from them. It is very unclear however that these things have any significant biologic activity.

One problem with DTE monotherapy that is clear is that it contains more T3 relative to T4 than is appropriate for humans, resulting in a low T4-to-T3 ratio. The practical result of that is that in virtually all cases in my experience, if the FT3 is adjusted to normal, then the FT4 is low, and if the FT4 is adjusted to normal, the FT3 is too high. It may in fact be that a "stimulant" effect from that extra T3 results in the "cult following" DTEs have amongst some so-called experts, but that does not make the situation safe, or physiologic, or even "natural." If a patient really wants to be be on a DTE, or seems to truly benefit from it, what I will often do is add a small dose of LT4 to the DTE, and fine-tune the two drugs to achieve a normal FT4-to-FT3 ratio. The labs I monitor for either DTE monotherapy or combined LT4 + DTE are the same as I gave above for monitoring LT4 + LT3 combo therapy, because all the issues are the same.

I hope that helps. Perhaps more than you wanted to know, but I think one of the problems with run-of-the-mill hypothyroidism management these days is that most doctors, including many endocrinologists, think it is a lot simpler than it really is.

A lady from another state contacted me by email stating that she was diagnosed with hypothyroidism at age 13, and that she had rising thyroid peroxidase antibody (TPOAb) levels, which concern her. She is frustrated because her physicians haven’t been “interested in looking at that [the antibody levels].” I don’t have details, but she reports having been on the “gamut” standard and alternative therapies for hypothyroidism, yet her health is still not where she would like it to be—her words.

What follows is an edited, and somewhat augmented, version of my reply to her, which I prefaced with the statement that there were positives and negatives in those comments regarding whether I might be able to help her, or at least provide her what she said she was looking for—essentially a partner in holistic therapy of her thyroid condition.

My positive comments, with respect helping were as follows:

If she was diagnosed with hypothyroidism at age 13, the diagnosis was likely fairly definitive, and abnormal TPOAb’s add weight to that. My point being, if there is good hard laboratory evidence of hypothyroidism and/or Hashimoto’s thyroiditis (not the same thing: hypothyroidism is a lack of thyroid hormone, which can be due to a number of causes; Hashimoto’s is an autoimmune disorder that is an important cause of hypothyroidism, though not all Hashimoto’s patients are hypothyroid), then it is much more likely that there is some relatively straightforward therapy that will help. As opposed to: well, it sounds like hypothyroidism, but the numbers don’t clearly show it. I do treat some of those people and sometimes it helps and sometimes it doesn’t. I went on to tell her—the fact she has been on some form of thyroid therapy for over 25 years makes it likely her hypothalamic-pituitary-thyroid axis has been to some degree suppressed by outside thyroid hormone. This might result in lower TSH levels than expected for any given situation, which would lead many physicians, many endocrinologists included, to undertreat.
So there are features to this individual’s story, and I’ve heard similar ones quite often, that make me think I might be able to help her, and I told her that.

Now for the negative—and I really shouldn’t say negative, I just mean, advice, counsel, constructive criticism, disclaimers… First she mentioned as part of her plea that she had been under stress for a long time. I’m unaware that there is any general recognition that a stressful lifestyle causes or worsens Hashimoto’s or hypothyroidism, except perhaps amongst certain authors and internet “experts” who may or may not really know what they’re talking about. In fact, I might argue the opposite—that hypothyroidism, causing fatigue and depression, makes life more stressful, and lessened one’s ability to cope with the ordinary stresses of life. In other words, hypothyroidism causes stress, rather than stress causing hypothyroidism.

Having said that, I will hasten to add two points: (1) a catastrophic emotional event, like the death of a spouse, or beloved pet, is well known to trigger Graves’ disease, an autoimmune thyroid disorder causing hyperthyroidism—high thyroid levels—but that type life event is different from chronic “normal” stress; and (2) one thing I do believe stress can do is elevate cortisol (a type of steroid) release from the adrenal glands, and cortisol suppresses TSH release. If TSH is suppressed, the thyroid gland might not be properly stimulated to make thyroid hormone. This would be a form of so-called “central hypothyroidism,” in which the person is hypothyroid without the expected elevation of TSH that is usually seen. This is one of the big differences in my approach to hypothyroidism from other doctors, including endocrinologists. Nobody doubts central hypothyroidism exists, but it is felt to be rare and is seldom considered. I, on the other hand, think it might be quite common and rampantly missed. And since there is no test to confirm it (the test is the TRH stimulation test, which requires a drug that is no longer available in the United States), the only thing to do if it’s suspected is to start thyroid hormone replacement and see if it helps.

So, I should modify my above statement about stress. I doubt chronic life stress causes primary hypothyroidism due to Hashimoto’s thyroiditis, but it might cause central hypothyroidism, either as a problem by itself, or one that might further worsen existing primary hypothyroidism.

I agree therefore that stress could be part of this lady’s problem; we just need to be clear what it is or isn’t doing. Also, the very stressful, busy lifestyle she described to me, can make one feel lousy for all kinds of reasons—for example, a lack of good quality exercise leading to poor physical and cardiovascular conditioning, or lack of sleep causing fatigue during the day—the lack of sleep being due to time constraints, or inability to relax due to thinking about stressful things. The point being, all the thyroid hormone in the world won’t fix those things.

She said her TPOAb’s have been climbing, and her doctors aren’t interested in looking at that. Her doctors may be right. We don’t track TPOAb’s in the same way we track, say, TSHs in thyroid patients and glucoses in diabetics. The fact that TPOAb’s (a type of thyroid antibody) are elevated tells us a person is at risk of becoming hypothyroid, or in this lady’s case (having already been diagnosed) that the cause of her hypothyroidism is autoimmune. There is no advantage, however, in continuing to check it. In fact, if a person comes to me with new hypothyroidism, I hardly ever check TPOAb’s. They don’t change anything. Unless there is some other obvious cause, like thyroid surgery, most people in the United States who are hypothyroid have Hashimoto’s. I can just assume that and don’t need to do a blood test to prove it, because the treatment is the same regardless of cause. Thyroid hormone replacement.

It would be different if there were a way to stop or reverse the autoimmune destruction of the thyroid, but there isn’t. Nothing proven safe and to work, and certainly nothing anywhere near as safe and reliable and inexpensive as thyroid hormone replacement is for most people, and I’m one of those people. Steroids might shut down TPOAb production but we wouldn’t go that route because it would be a case of the cure being worse than the disease—the steroids would cause diabetes, weight gain, osteoporosis, infections, and so forth. Now, maybe there is something out there that is safe and effective, some supplement, or diet, but we don’t know what it is yet. Until we do, giving thyroid hormone is the most reliable path to feeling better.

I and most endocrinologists do know very well that many people, like this patient, on thyroid hormone for hypothyroidism don’t feel 100 percent. To that I have two comments: (1) few things in life are perfect—that’s not a cop out; it’s wisdom and truth; and (2) I believe some of those people not feeling good on thyroid hormone aren’t on enough medication. My approach to hypothyroidism is pretty standard—that is, thyroid hormone replacement, usually with Synthroid or similar products—but I often use higher doses than most doctors are comfortable with, and I think that’s why I seem to get better symptom control in some patients than they do.

Dr. Rone Read More 

THIS PATIENT EMAILED ME ABOUT FEELING FATIGUED, MOODY, AND UNINTERESTED IN SEX 2 YEARS AFTER HER DAUGHTER WAS BORN. SHE MENTIONED HER MARRIAGE WAS ON “THIN ICE” AS WELL.

Let me start with a few general caveats and a few comments upon some of your statements, then I’ll try to provide you some helpful guidance. And please try not to take offense at anything I say—I wouldn’t be doing my best for you if I weren’t honest.

1. If there is a role for testosterone replacement in women—and there probably is, we just haven’t worked out the safety questions, the proper reasons to use it, how to dose it, and there is no practical FDA-approved product that can be adapted easily to the lower doses that would be appropriate in women compared to men—that role would not be in premenopausal menstruating women, but rather in postmenopausal women, especially those who have had a total hysterectomy (taking the ovaries, which still produce testosterone after menopause), and who are disturbed by a lack of libido, which is the main testosterone effect in women, though there may also be some role with respect to fatigue and maintenance of lean body mass (as opposed to fat mass).
2. My reason for excluding premenopausal menstruating women from this potential role for female testosterone replacement, is because the existence of mostly regular monthly menses proves the proper functioning of the brain, pituitary, and ovaries with respect to sex-steroid production—it doesn’t take much to interrupt regular menses, so if you are regular, chances are everything is running as it was physiologically intended to, and if you are not, it is extremely doubtful taking testosterone would be the solution (the opposite might even be the case).
3. By the way, the presence of underarm and pubic hair proves the presence of testosterone and/or DHEAS, the largely similar adrenal hormone, and speaks against the need for replacement of either.
4. Now, giving supplemental testosterone to a premenopausal menstruating woman, is profitable to the clinic doing it, and may well improve energy and libido, but none of that means it’s safe, especially over the long run. Cocaine makes people feel good, but most of us would agree using it is a bad idea, right? Potential side effects of testosterone replacement in young women would include acne, facial and body hair growth, clitoris enlargement, and potentially cancer promotion and potentially birth defects in a female fetus should pregnancy occur. In short, no matter how beneficial it might seem, it’s a bad idea, at least given the current state of our knowledge.
5. With regard to your situation, obviously the best outcome would be for some relatively simple to treat medical condition to turn out to be responsible for your symptoms. I’m forced to point out though that it is not at all unusual—for all kinds of reasons—for young mothers to be fatigued, irritable, distracted, and to have a low sex drive. I don’t need to tell you that having an infant or toddler in the house adds stresses, changes established lifestyles, can be exhausting (especially if you’re working outside the home as well—you don’t say), and not unusually alters the marital relationship, not always for the better. My point being: your friends who say it is “just motherhood” aren’t necessarily wrong—and you finding the answer “unacceptable” doesn’t change that, nor does the fact that your “marriage is on thin ice.” Don’t misunderstand—I’m not unsympathetic to your plight, but the acceptability of the answer is irrelevant. I’m sure many patients with cancer find that unacceptable too.
6. Along the same lines, I will freely admit that depression is diagnosed and treated in situations such as this, excessively, and often wrongly. That fact alone, however, does not automatically make the diagnosis wrong. Food for thought.
7. You mention “hormone balancing.” I don’t know what that means. It’s not a concept any real endocrinologist embraces. It is hype, a catch phrase that alternative-medicine providers—who don’t really know what they are talking about—use. To the extent that hormones need to be “balanced,” our bodies are generally much better at it than you or I or the compounding pharmacist are. (I’m not attacking you, I’m attacking practitioners who throw cool-sounding terms like that around like they mean something.)
8. Don’t be taken in by saliva hormone testing that is used and promoted by many purveyors of bio-identical hormones. Most such testing is unvalidated with respect to accurately diagnosing endocrine disorders. For the most part, real endocrine disorders are only confirmed by carefully done and timed serum testing.

Now, on to the, hopefully, helpful part of this:
1. I’ve treated a great number of patients for hypothyroidism in recent years, whose other doctors said their thyroid levels were “normal,” and it was life changing for some, not all of course. Suffice it to say—I never accept a report of “normal” thyroid functions without looking at the numbers myself. So please send me whatever thyroid test results you can get ahold of and I’ll let you know what I think—send the result and the normal range as they differ from lab to lab. Bare minimum I need a Free T4 and TSH to make a reasonable assessment—but send me whatever you have.
2. Did you experience any peripartum hemorrhage/serious delivery complications? Sometimes that damages the thyroid and other endocrine control mechanisms in ways that are not always easily discernable.
3. Did you breast feed successfully?—if so, that rules out what I was getting at in #2.
4. You mention exercising regularly and that it is mostly “cardio.” I strongly suggest adding resistance training to the mix. Endurance training as you are doing is important and valuable, but resistance training (i.e., weightlifting, and, yes, yoga and stretching to engage muscles we don’t even think about) builds muscle, improves ability to manage activities of daily living, helps weight management more so than endurance training does—and, most relevant for this discussion, the more muscle you have the less fat you have and the enzyme aromatase in fat converts testosterone to estrogen, depleting your body of testosterone.
5. And by the way, dovetailing with my earlier points, it is in fact physiologically normal for the female body to try to rid itself of testosterone, enhancing “estrogen effect” and, frankly maximizing fat deposition (within reason) to assure available caloric resources to maintain a pregnancy and nourish the infant. In other words, to repeat, this notion of supplementing testosterone in young women is just plain wrongheaded. Focusing on profit and “feeling good” over normality.
6. Also, you say you eat healthy, and perhaps you do, but I believe much of what is popularly labeled “healthy” is in fact not, or at least not the best diet for all. Consider increasing protein and fat intake, and limiting carbs, especially breads, and I have virtually eliminated high-fructose corn syrup from my diet. Hydrate well with water, and frankly black coffee is a pretty healthful drink and the caffeine may help your energy.
7. To summarize—send me your thyroid levels and I’ll advise you accordingly. No to testosterone. Yes to resistance training, perhaps yoga. Try changing up your diet since you feel lousy doing whatever it is you are doing. Don’t just assume what everybody says is healthy really is for you. And, frankly, if your marriage is on “thin ice,” regardless of the cause, I’d advise couples counseling. Can’t hurt. Read More 

THIS IS A LADY, WHO I AM PLEASED TO REPORT, READ THE BLOG AND CONTACTED ME THROUGH THE WEBSITE. SHE LIVES WITHIN DRIVING DISTANCE OF MY OFFICE AND WAS WONDERING IF IT WOULD BE WORTH MAKING AN APPT. HER STORY IS THE SAME OL' ONE--LOTS OF SYMPTOMS SUGGESTIVE OF HYPOTHYROIDISM, BUT HER THYROID FUNCTION TESTS (TFT'S) ARE "NORMAL" AND SHE KEEPS BEING TOLD IT'S NOT HER THYROID:

Good to know somebody out there is reading the blog.

If you have your lab reports available, what is your lab’s normal range for FT4? The values you documented certainly sound low-normal, I was just wondering how close to the lower normal limit they are.

The TSHs are obviously “normal” by any standard, but the question is might you have hypothyroidism due to or in addition to a defect in TSH production from the pituitary.

Any history of head injury, even something minor like knocked unconscious in an auto accident or fall?

Also, let me know all the meds you are on now.

You have enough symptoms that could be due to hypothyroidism, coupled with the lowish FT4’s and family history, that I do think a trial of thyroid replacement would be reasonable. It baffles me why “antidepressants, bcp, adhd medications” and the like are so often considered preferable to thyroid hormone, which is at least a substance that God/Mother Nature intended for us to have in our systems.

Please answer the ?’s I’ve underlined and I’ll get back to you.

***

--the 0.5 lower normal limit for FT4 is a little lower than I’m accustomed to thinking in terms of—meaning that your levels aren’t as low as I was thinking, but they are nevertheless still in the lower half of the relevant reference range. In other words I haven’t changed my mind about the possibility thyroid hormone replacement would help.
--the head injuries increase the possibility that there is a pituitary defect explaining the inappropriately normal TSHs in the face of the hypothyroidism we are postulating.
--I can’t prove this, but my feeling based on seeing a lot of patients with stories similar to yours, is that chronic pain (your headaches), narcotic use for the chronic pain, and various CNS-acting drugs, many different ones of which you are or have been on, contribute to a “soup” that hobbles TSH release—creating a central hypothyroidism-type pathophysiology.
--So, no guarantees as to our success, but I think it would be you coming to see me.

jkr
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THE FOLLOWING ARE MY RESPONSES TO A SERIES OF QUESTIONS ASKED ME BY A POST-THYROIDECTOMY PATIENT BY EMAIL:

Pardon me for starting with shameless self-promotion, but I assume since you’re contacting me you’re familiar with my book The Thyroid Paradox (2007, Basic Health Publications); if not, it addresses a lot of the issues you raise and is available from Amazon.com as a trade paperback or Kindle download; also any bookstore should be able to special order it.

I consider this book to be a good middle-of-the-road analysis of the state of modern thyroidology--criticizing what most physicians do wrong, without throwing away what they do right, which much of the hyped-up rhetoric about thyroid disease in popular books and on the internet does. In other words, I try not to throw out the baby with the bath water,

That said, I’ll address your most specific questions individually:

(1) It seems such a paradox to me to be testing the pituitary thyroid stimulating hormone in a thyroidless person

You are of course correct that TSH is a pituitary hormone—however, it is produced in response to any perceived lack of thyroid gland function by the brain, and it stimulates the thyroid gland to make thyroid hormone. Thus, TSH levels are integrally related to the proper functioning of the whole thyroid system which include the brain, pituitary and thyroid.

My disagreement with most physicians is not that they test TSH levels, but that they often only test TSH levels and ignore everything else, including FT4, FT3, and symptoms.

In other words, my position is that TSH is very useful—I just don’t assume that it tells me everything.

I know your questions relates to the athyrotic (“thyroid-less”) patient, following total thyroidectomy. Obviously in that situation the role of TSH stimulating the thyroid gland is moot--but, the pituitary still releases TSH when there is a perceived lack of thyroid hormone (in the case of the athyrotic patient, a perceived lack of Synthroid or whatever other thyroid replacement drug is being used).

So, put very simply—a patient with a high TSH is almost certainly not getting enough Synthroid—which is a very useful thing to know. Also the person not getting enough Synthroid will more often have a high TSH, and have it sooner, than an obviously low FT4 or FT3. TSH is a more sensitive test for hypothyroidism than FT4 and FT3 are. To not use it in these people would be crazy.

Now, what about monitoring for over-replacement--too much Synthroid. Almost everybody on too much thyroid medicine will have a low TSH, and they will have it before the high FT4 and FT3. In other words, TSH is also a very sensitive test for hyperthyroidism.

The problem is: TSH is NOT a very SPECIFIC test for hyperthyroidism. Other things can cause a low TSH besides too much Synthroid. That’s the mistake that gets made--almost every doctor out there--including endocrinologists--automatically assume or at least respond as if a low TSH means the person is on too much thyroid medicine and they lower the dose. That might be the right interpretation, but it might not, and the only way to know is to look at FT4, FT3, and consider the patient’s signs and symptoms.

Bottom line--TSH is a very useful test, but there are weakness which are often ignored. That is a reason to change how we think about TSH, not a reason not to use it.


(2) Shouldn't the emphasis be on the actual thyroid metabolic state reflected by serum FT4 and FT3 concentration?

It would be incorrect to assume that any given FT4 or FT3 level accurately reflects the “actual thyroid metabolic state.” And since we are talking about athyrotic patients, these levels don’t even reflect the metabolic activity of the thyroid gland to produce thyroid hormone--these levels are instead totally under the control of the Synthroid et al. prescriber’s pen or keystroke. To be clear, by “actual thyroid metabolic state” you mean the amount of thyroid hormone that is getting to the thyroid hormone receptors deep inside the nucleus of each of our cells, and the resulting intracellular actions that are triggered by those activated receptors.

Looked at that way, I think you can see that a blood level of FT4 or FT3 (which are the only measurements technically practical) does not necessarily reflect what is going on OUTSIDE the blood, deep inside cells. It’s helpful; it’s an estimate of what’s going on, but that’s all it is. That’s especially true for FT3, since much T3 is produced inside these cells and never makes it to the blood.

The fact is, just because a FT4 or FT3 blood level is “normal” doesn’t mean that cellular thyroid hormone action is normal, because there are several physical barriers and physiologic processes separating those points. Who’s to say that a low-normal FT4 of .89 is enough--maybe a high-normal level of 1.7 would be better. For that matter, who’s to say a low blood level isn’t getting the job done, or that a high level is.

“Statistically normal” which is that range printed on a lab report is not the same thing as “physiologically normal” Something else very few physicians, sadly, ever think about in my experience.

Getting back to TSH--if the pituitary is working properly (I don’t think it always is in athyrotic patients) but IF IT IS then TSH gets produced by the pituitary as a result of the brain’s perception of the adequacy of intracellular thyroid-hormone action. So really, in fact, it could be argued that the blood TSH level does, in many cases, more accurately reflect “actual thyroid metabolic state” than blood FT4 and FT3 levels. You might say that TSH reflects the “ACTUAL thyroid metabolic state,” while FT4 and FT3 reflect “POTENTIAL thyroid metabolic state.”

Bottom line--none of these tests are perfect--all have strengths and weaknesses which need to be better understood by all of us. The right answer is to evaluate them all to come up with what is never going to be any better than an estimate of what is really going on.


(3) Could you please cite any studies/information showing that a low but not suppressed TSH is acceptable as long as the free T4 and free T3 are within range and there are no hyperthyroid symptoms

As you probably know, there is a virtual obsession amongst most physicians about avoiding low, and especially undetectable TSHs. The concern is that the low TSH equals hyperthyroidism, which is of course wrong—it is a marker for it, but the problem is hyperthyroidism (too much T4 and/or T3 for the person), not low TSH. Hyperthyroidism does need to be avoided; it does do harm. There are other reasons, though, why the TSH might be low, and those other reasons are almost never considered. This obsession with avoiding low TSHs often in my experience leads to an underdosing of patients, and a lot of frustration and poor quality of life for patients—especially athyrotic ones.

I’m frankly dumbfounded why endocrinologists smarter than I am don’t see and teach the “disconnect” between “low TSH” and actual hyperthyroidism. It has a lot to do, though, with the Hippocratic principle of “first do no harm.” If we never get the TSH low then we will never do harm with hyperthyroidism. If we let TSHs get low then some of the time we might err and do harm with hyperthyroidism, and that is a possibility that mainstream medicine isn’t comfortable with.

Hopefully, most physicians out there at least see that a mildly low TSH of say 0.31 is probably okay relative to one below, say, 0.1--but alas, many do not split these hairs in actual practice.

Your specific question was about “low but not suppressed TSH” being “acceptable as long as…”

I would modify that by saying that in some but not all cases even a suppressed (undetectable, that is) TSH might be acceptable.

Unfortunately there really isn’t much literature to support this position. Common sense supports it, but the modern obsession with evidence-based medicine doesn’t give as much credence to common sense as one would like--hopefully we are seeing a slow backswing.

I will list and comment upon a few articles I referenced in my book that might be of help:

--Shimon, I., et al. “Thyrotropin Suppression by Thyroid Hormone Replacement is Correlated with Thyroxine Level Normalization in Central Hypothyroidism.” Thyroid 12 (2002): 823–827.

(This is the strongest argument for our position. Central hypothyroidism is hypothyroidism caused by a defect in TSH secretion by the pituitary--it is thought to be rare--I think it’s common but under-recognized. When I say that it’s okay for a patient to have a low or undetectable TSH, what I’m really saying is that the patient is either all or partly centrally hypothyroid, rather than pure primary hypothyroidism.)

--Zulewski, et al. “Estimation of Tissue Hypothyroidism by a New Clinical Score: Evaluation of Patients with Various Grades of Hypothyroidism and Controls.” Journal of Clinical Endocrinology and Metabolism 82 (1997): 771–777.

(Good analysis of symptoms vs. labs in the diagnosis of hypothyroidism.)

--Andersen, S., et al. “Narrow Individual Variations in Serum T4 and T3 in Normal Subjects: A Clue to the Understanding of Subclinical Thyroid Disease.” Journal of Clinical Endocrinology and Metabolism 87 (2002): 1068–1072.

--Dickey, R., L. Wartofsky, and S. Feld. “Optimal Thyrotropin Level: Normal Ranges and Reference Intervals are Not Equivalent.” Thyroid 15 (2005): 1035–1039.

(Two papers that telling us that what is “statistically” normal for the population isn’t the same as “physiologically” normal for the individual.)

--Demers, L., and C. Spencer. “Laboratory Medicine Practice Guidelines: Laboratory Support for the Diagnosis and Monitoring of Thyroid Disease.” Thyroid 13 (2003): 3–126.

(Any paper by Carol Spencer from UCLA, I believe, will be very open-minded about the weaknesses of and precautions to take when using modern thyroid function tests.)


(4) Shouldn't dosage be based more on free T4 and free T3 levels and clinical symptoms rather than so much emphasis on TSH?

Yes, it should be based on all 4 parameters: FT4, FT3, TSH, and clinical evaluation. Yes, there is too much emphasis on TSH—just don’t make the mistake of thinking that TSH is worthless.

Good questions—I hope this helps.

Best,

jkr
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THIS IS A FOLLOW UP EMAIL TO THE PARTY ADDRESSED IN MY 7/27/12 POST:

Sorry you didn’t have a good experience with Dr. XXX. He really is a top-flight endocrinologist—it’s just that you and I aren’t on the same page with many otherwise top-flight endocrinologists when it comes to hypothyroidism-diagnosis-and-treatment philosophy.

There are a few important points for you to consider--for you wife’s good, and from a practical standpoint, before you bother to travel to see me:

(1) I agree with you that a TSH of .14 does not necessarily equal a “massive overdose,” but unfortunately that’s a tough nut to crack with a lot of doctors. That is because hyperthyroidism is dangerous. I just don’t think we should be assuming that everybody with a low TSH in hyperthyroid.

(2) I’ll be blunt here: those “holistic GP’s” are wrong about a lot of things; they’re right about some things too, and as I’ve said, the mainstream is, I think, wrong about some things. One group is too aggressive with thyroid hormone and the other too cautious. My book talks a lot about this--I really think you should read it if you haven’t. Basically they’re saying that patients feel better on their treatments, but they ignore the potential for harm years down the road. Just remember feeling good, is good, but it isn’t a good physician’s only goal. It has to be at least reasonably safe. Cocaine makes people feel good, but I assume you agree people shouldn’t be using it.

(3) The reason her T4 went down on Armour is because Armour doesn’t contain enough T4 and it contains too much T3, which is a potent, more potentially dangerous form of thyroid hormone. You don’t say if a T3 was checked, but I bet it’s too high or getting close to being too high.

(4) And remember, the natural situation--that is, normal human physiology--is for there to be a lot of T4 and a little bit of T3, only enough. Proponents of T3 and Armour (hyped as “natural thyroid hormone—perhaps it is, but it does not mimic natural human thyroid status) ignore this.

(5) Again, I’ll be blunt, and this is a very important point if you decide to come see me: I think starting with Armour, and insisting on it’s continued use is a mistake. I use it occasionally, but as a last resort when other options fail. Again, the book describes this in great detail and you should read it when deciding whether you want to come to me. If you come, I very likely will insist that Armour be stopped and that we try Synthroid alone (but perhaps in higher doses than most would use). I did exactly that with a new patient on Armour yesterday.

Please consider these comments.

jkr
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THIS IS A GENTLEMAN, RETIRED MILITARY, LIVING ON THE MISSISSIPPI GULF COAST, WHO CONTACTED ME ABOUT HIS WIFE’S THYROID PROBLEMS:

Sorry you and your wife are having these difficulties.

Your email didn’t say how you found me, but you may be aware that I did my residency at Keesler Medical Center and was an endocrinologist there from 1992 to 1998—also Asst Chief of Medicine for some of that time.

To cut to the chase—I certainly agree that your wife has a compelling collection of symptoms suspicious for hypothyroidism. That doesn’t prove she is hypothyroid, but in my opinion a trial of an effective dose of thyroid hormone replacement is warranted in order to help make that determination, regardless of her labs.

The clinical scenario of hypothyroid symptoms in the face of normal thyroid function testing is a common one, and most healthcare providers—endocrinologists included—don’t do a good job of managing it, in my opinion. That said: no physician with a thorough knowledge of thyroid physiology and pathophysiology would deny that there are some situations in which hypothyroidism does manifest with little or no lab abnormality. I happen to think that situation is common, but most would say it’s rare. Rare or not, that’s not a reason not to consider it in the right setting.

I boggles me why most physicians seem so much more willing to use the latest expensive, side-effect-laden antidepressant, than thyroid hormone—a relatively inexpensive drug, with in one form or another, over a century of user experience, and it’s a molecule that either God or nature (depending on your belief system) intended to be there. I don’t dismiss the risks of inappropriate thyroid hormone use, but whatever else you want to say, it is something that is supposed to be in the human circulation.

You mention CPAP, suggesting she has sleep apnea—which is actually a condition that can blunt the rise in TSH one expects with low thyroid levels. Thus, it’s easy to speculate that her labs might not be classically indicative of hypothyroid. It is my belief that depression, antidepressant drugs, and possibly even obesity might do the same thing.

So, to summarize, I agree with your desire for a thyroid replacement trial. The next question is what form that trial should take. I occasionally use Armour thyroid but it isn’t my first choice. Most physician’s trained since the 1970s are going to consider it an obsolete drug. You don’t say why the trial XXX had was with Armour—I’m assuming there was some insistence on your part, since that’s not a drug most mainstream doctors these days would automatically reach for, even if they were inclined to use thyroid hormone.

My point being, any determination that you might be expressing that she get Armour, is automatically going to double the resistance you encounter: you’re getting resistance over treatment despite normal labs, and added resistance over the use of a drug viewed as obsolete, unfamiliar at best, dangerous or quackish at worst.

The doses of Armour she was given are very low, especially for someone weighing 200 pounds—so it does not surprise me that she got no benefit. You mention her T4 didn’t rise—my guess is her T3 did rise some, just not enough to do any good. They haven’t ever checked a T3 on her, you said—at the very least they should have when she was on Armour since T4 and T3 are active ingredients in that product.

While there are some patients who do benefit from T3 supplementation either in the form of Armour, or other products that are available, most hypothyroid patients do just fine on T4-only replacement, such as Synthroid, or other largely equivalent products. I myself have taken Synthroid with life-changing results for 20 years. I realize there is a notion floating around out there—promoted by some books and some so-called “experts” on the internet—that Synthroid doesn’t work. For most patients this is just plain wrong; however I believe that that impression has grown out of doctors’ reluctance to push Synthroid doses to high enough levels to be effective—scared off by, for example, low TSH levels.

In other words, mainstream hypothyroidism management is hampered by both a reluctance to start thyroid hormone, and a reluctance to use enough when it is started.

In short, I would advise a trial of Synthroid in gradually escalating doses. That’s not something I could order without face-to-face evaluation and follow up. After all, if we’re coloring outside the lines, it is even more important to monitor the outcomes closely to be sure we aren’t doing more harm than good—and that we are, in fact, doing some good.

I don’t know if any provider there might be willing to work with you on the basis of my comments—that’s worth a try, but I don’t have a name I can give you. You don’t say whether you have my book The Thyroid Paradox, which is all about this brick wall you’re running into. Not trying to sell you a copy, and it won’t get you a doctor, but at least you might understand the issues better.

I do have a few patients who come a long distance to see me for reasons similar to yours, so that is an option if you’re willing. If you can get somebody to draw a Free T4, Free T3, and TSH on Mrs. XXX, you could fax that to me and I might be able to give you a better idea how likely it is I think I can help, but the bottom line is, we won’t really know without trying it.

Best,

jkr
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Ms. Hagerty:

I appreciate your kind words about the book.

My father, who was a newspaper editor, was fond of saying that the British and Americans were two peoples separated by a common language. We have an example of that here: Upon my first reading of you email I’m embarrassed to say I had no clue what “ME” was. However, a brief Google search indicates to me that it is the same thing as what the US medical community calls chronic fatigue syndrome (CFS). I’ll preface my further comments by stating that I am no expert on true CFS, which (you know all this better than I, I’m sure) has very specific diagnostic criteria, and is of unknown etiology, but infectious and/or neurological causes are suspected. It is also a diagnosis of exclusion in that part of diagnosing CFS is ruling out everything else, including hypothyroidism—which can be problematic as you discovered and I discuss at length in "The Thyroid Paradox."

I agree with your statement that the list of symptoms of CFS and hypothyroidism are virtually identical, and I have no doubt that there is a subpopulation of CFS patients that are in truth undiagnosed or under-treated hypothyroidism sufferers, and that that is the cause of or at least a contributor to the fatigue. The trick of course is identifying that subpopulation—that might be done in some cases with a more open-minded interpretation of the lab work (not ruling out hypothyroidism, for example, on the basis of a TSH of 5.0, just because the lab says 5.0 is “normal”), and in other cases it might take a trial of thyroid supplementation. When we do the latter it is of course very important to stop the thyroid treatment if no clear benefit is noted after a sufficient time on a sufficient dose—which is of course evidence in favor of some non-thyroid cause of chronic fatigue.

As an aside, I also believe that a subpopulation of patients who get labeled with “fibromyalgia”—a similarly frustrating, chronic debilitating illness to CFS—actually have hypothyroidism.

Your experience wherein you felt better on an extra 12 mcg LT4 illustrates the need for careful titration of dosing, often with very small adjustments, and supports the avoidance of generic thyroid hormone replacement products, which opens us up to unacceptable variations in bioavailability. That your dose was dropped on the basis, it sounds like, of a low TSH only, resulting in a deterioration of symptom control, is alas typical on both sides of the Atlantic. As you know from the book, I believe that such determinations must be made on the basis of TSH and FT4 and FT3 and perhaps most importantly on symptoms. And I don’t mean to overstate the problem—there are experts out there besides me who recognize that there are clinical situations where it is okay to leave a patient with a low or even undetectable TSH—unfortunately, whether you’re dealing with a primary-care doc, or even a “consultant of flavour,” such willingness to look past a low TSH is, in the real world, very very rare. I smack my head against that wall every day practically.

I did not know, and thank you for telling me, that the availability of LT4 dose strengths in the UK is so limited (at most, just 25, 50, and 100 mcg tabs based on my brief online search). Fortunately, using various tricks (mixing and match full and ½ tablets of different strengths, or skipping days, or taking extra periodically) there is no dose that we have that you can’t mimic, as long as the prescribing healthcare provider bothers. Even here, with those 12 tablet sizes available, there are a lot of primary care providers who adjust (incorrectly in most cases) in 50mcg increments or the like.

Lastly, to address your main question of modulating LT4 doses based on physical activity—I do touch on this in the book as you know. What you propose is interesting, that is, upping the LT4 dose proactively in anticipation of a period of increased physical training/activity. I have never done that, but let me outline of what I can definitively say about thyroid and physical activity, most or all of which is covered in the book, I believe:

(1) Twenty years ago I published data (in a UK medical journal, by the way) that indicated an increase in thyroid hormone utilization (and thus presumably an increased LT4 dose requirement) in triathletes compared to sedentary controls (“couch potatoes”). The study could not distinguish between the observed differences being a cause of or a consequence of the improved physical conditioning—my speculation in the paper being that the alteration of thyroid hormone metabolism was what led to the improved athletic performance and endurance. To my knowledge no further research has been to settle that question. Either way though, theoretically, increased exertion might demand increased LT4 dosing. However, it is not certain that the results of this study are relevant to the “ME patient” gradually speeding up his or her life. There is a big difference between that kind of physical exertion and the running of a triathlon.

(2) I have observed that my thyroid dose has needed to be increased (based mostly on my lab results) when I am more physically active. It is possible that there were other factors—such as reflux medicine. And of course weight loss, which might result from increased activity, would tend to decrease dose requirements. So, I think the effects of increased exercise on thyroid requirements depends on the interaction of many factors—amount and type of activity (weight-lifting vs. running, for instance), duration, the conditioning of the person, diet, weight changes)

(3) I have also observed patients feeling better on LT4 and becoming more active as a result, and then seemingly having a relapse of the fatigue as a result at that increased activity—this is essentially the scenario you are painting. My interpretation of that scenario is that the patient lost musculoskeletal and cardiovascular conditioning during their period of inactivity when they were hypothyroid, and that it will take time to restore that conditioning through gradually increasing frequency and duration and intensity of exercise. It has been my feeling that no amount of thyroid hormone would solve this problem.

Might, as you suggest, the answer be a proactive increase in LT4 to stave off the renewed fatigue. I don’t know. I kind of doubt it, but I haven’t tried it, so I don’t know. Were it to be tried, I would advise no more than an increase of 12.5 mcg at a time with close monitoring of signs, symptoms, and blood tests.

I hope that helps and if you wish please feel free to share this with and recommend the book to your ME patient organizations. And put a good review of the book on Amazon if you are so inclined.

Best,
jkr
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AS MENTIONED IN THE PREAMBLE TO AN EARLIER BLOG POST, WHAT I’M DOING HERE IS SHARING FOR THE EDUCATION AND INTEREST OF THE WEB BROWSER/RESEARCHER MY REPLIES (MINIMALLY EDITED) TO INVIVIDUALS WHO HAVE CONTACTED ME OVER THE PAST COUPLE YRS WITH MEDICAL PROBLEMS AND QUESTIONS, OFTEN AFTER HAVING READ MY BOOK “THE THYROID PARADOX.” OUT OF RESPECT FOR THE PRIVACY OF THE QUESTIONERS I AM NOT INCLUDING THEIR HALF OF THE INTERACTION. THUS, WHAT APPEARS BELOW IS DISJOINTED IN PLACES AND NOT INTENDED TO BE A COMPOSITIONALLY COMPREHENSIVE ESSAY ON THE SUBJECT. NONETHELESS, I HOPE THE READER WILL FIND SOMETHING OF INTEREST AND EDUCATIONALLY VALUABLE HERE, THAT AT LEAST PROMPTS FURTHER RESEARCH.

Thanks for getting back. I’ll comment on a few points.

Your weight is normal for your height, as you probably know. The thyroid doses you’ve been using seem a little high to me for this weight, but there’s no absolute rule on that—whatever works and seems safe is the right dose.

Your father’s high-normal TSH certainly increases your risk for thyroid problems.

I agree and state, in so many words, in the book that “what’s in the blood might not be available at the cellular level,” (I said as much in my last email with respect to serum RT3 levels) and much of The Thyroid Paradox deals with the notion that TSH can be maintained in a “normal” or low range by factors other than true thyroid hormone status. So, there are certainly areas where I would agree with the work you’ve been researching. The devil, as they say, is in the details, and I do think there is a lot of unsubstantiated speculation in the material you reference. I’m not saying 100% of it is wrong. I would just submit that a wise and critical thinker must acknowledge that it is unlikely that 100% of it is correct.

To just take one small example, you state confidently that “low ferritin will suppress TSH.” I have no knowledge or experience that says that that is true. I don’t know your source, nor have I done my own literature review, so I’m not disputing you. I simply want to point out that many things that are reported in bench or animal research especially, but human studies as well, don’t necessarily translate to clinically relevant facts. If for example studies show an ASSOCIATION between low ferritin and low TSH, that does not mean that there is a CAUSE-AND-EFFECT relationship. This is a common error in viewing data and statistics (we all do it from time to time). Just remember the classic fallacy in logical thinking: post hoc ergo propter hoc--after this, therefore because of this.

(Please don’t take offense—I see from your later comments that this ferritin question is of great interest to you--again, I haven’t done the research to dispute it; I just was using that example to make a point.)

Hard to draw any helpful conclusions from those pretty benign looking TFTs other than you don’t show any classic disease pattern, which we agree doesn’t necessarily rule out disease.

The bottom half of page 128 of my book speculates that the point at which the TSH just becomes undetectable might be ideal in thyroid replacement therapy—similar to your report of Dr. Peat’s theory. I think we may have a different basis for that conclusion though.

Hypothyroidism is not a risk factor for Graves’ disease--I haven’t dug into your references to fully comprehend this contention; however, as a physician who’s seen thousands of hypothyroid patients and thousands of Graves’ patients in 20 years, I can confidently state that it is exceedingly rare for a hypothyroid patient to swing in the other direction and become hyperthyroid. To answer your question, stress does trigger Graves’ disease, probably though some dysregulation of the immune system, perhaps related to steroids.

Obviously you have to decide for yourself what to do and proceed at your own risk. There’s nothing in this email that changes my mind about not being able to advise any form of thyroid replacement under the circumstances. On the other hand I don’t wish to be responsible for taking away from you something (the Cytomel alone) that you state was helping and which you obviously have a basis for believing to be safe. Don’t misunderstand—I don’t condone that therapy, and maybe you’ll live longer without it (we’ll never know)—but nor do I want to be responsible for taking something away if we are not in the sort of face-to-face therapeutic relationship where I can participate in finding an acceptable alternative. So, as I say, you have to decide.

Not sure how much I’ve helped you here except perhaps to counsel (if you’ll excuse me using that term) you on the value of skepticism in science and medicine. My book is all about there being too much skepticism (i.e., close-mindedness) amongst physicians, esp. endocrinologists on these issues; yet not enough skepticism on the reformist side. Too much willingness to accept a particular theory—especially if it leads to a human therapeutic intervention—is at least as wrong and dangerous as not enough. I don’t have all the answers, but the truth is probably somewhere in the middle. I wish you luck in your search for health.

Best,

jkr
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MY REPLY TO A MIDDLE-AGED LADY WHO CONTACTED ME, AND IS NOW A PATIENT OF MINE, AFTER EXPERIENCING DIFFICULTY/DISSATISFACTION WITH HER THYROID HORMONE REPLACEMENT DESPITE HAVING BEEN TRIED ON SYNTHROID, ARMOUR THYROID, AND—AT THE TIME SHE CONTACTED ME—THE VERY ATYPICAL APPROACH OF GIVING T3 ONLY:

(1) If you have your thyroid function tests that were done before you were ever put on Armour Thyroid, that would be helpful.

(2) Knowing your weight would be helpful as well

(3) As you may be aware, the use of T3 therapy in general, and the use of Armour Thyroid and similar products is controversial and nonstandard, at least in the view of most physicians who treat hypothyroidism. That said, I sometimes use T3 or Armour Thyroid, and I think there are some people who do better on them, but I don’t start with them. Most people, myself included, do fine on T4 supplementation alone (Synthroid for example). T4-only is definitely simpler and safer, and is often cheaper. To jump straight to any T3-containing therapy is, to be blunt, in my opinion, bad medicine.

(4) Without knowing the thyroid levels when you had the joint pain on Armour, I can’t say why that was

(5) Synthroid takes 5 weeks to reach a steady state (buildup, that is, to whatever levels it’s going to get to) and its full effect may be delayed longer than that—so, it’s not surprising that you felt “horrible” after only 1 month on Synthroid. That doesn’t mean that a longer time on treatment, or more likely a higher dose wouldn’t have worked. Also, you went from Armour (too little T4 + too much T3, in general), to Synthroid (T4 only where T3 has to be manufactured out of the T4). As mentioned, T4 takes 5 weeks to build up—however, T3 disappears much faster than that. The T3 that you have gotten from the Armour went away after say a week or 10days. Therefore, you weren’t getting much thyroid hormone during this transition period and therefore felt bad. If your naturopath didn’t understand or explain that, then he doesn’t know enough about the pharmacology of these drugs to be doing all this.

(6) Now, you’re not doing well on the compounded T3—50mcg is a pretty decent dose—given once daily I assume? If so, and they haven’t somehow compounded it to be reliably sustained release, then is all getting absorbed and disposed of pretty quickly and therefore you probably don’t have enough thyroid hormone around in your circulation for, say, the latter 12-16 hours of the dosing interval

(7) I presume the reason you chose to go to a naturopath is a desire to pursue therapies that mimic nature as closely as possible, right? Well the human thyroid makes a whole lot of T4 and very little T3. T3 gets made by tissues all over the body depending on their needs at any given time. So, T4-only treatment actually comes closer than Armour, and its definitely closer to T3-only therapy, to the natural situation. FYI.

(8) The high normal TSH and the thyroglobulin both suggest you’re not getting enough thyroid hormone, and the low free T4 and T3 obviously suggest the same thing—so I don’t think there’s any mystery here why you don’t feel good.

(9) I think I can probably improve this situation, but I’d have to be seeing you in my office to do anything beyond just giving advice.

Hope that helps.

Best,

jkr
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