James K. Rone, MD, FACP, FACE

My Health is Not Where I Want it to Be

June 26, 2014

Tags: Thyroid

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

Possible Hypothyroidism Despite "Normal" Thyroid Function Tests

October 10, 2012

Tags: Thyroid

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

Strengths and Weakness of TSH and Other Testing in Athyrotic Patients

August 5, 2012

Tags: Thyroid

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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More Hypothyroidism with Normal Thyroid Function Tests

August 4, 2012

Tags: Thyroid

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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Hypothyroidism with Normal Thyroid Function Tests

July 27, 2012

Tags: Thyroid

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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Hypothyroidism & Chronic Fatigue Syndrome

July 26, 2012

Tags: Thyroid, Chronic fatigue syndrome, Myalgic encephalomyelitis

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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Thyroid Supplementation Questions

July 22, 2012

Tags: Thyroid

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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Patient Having Problems With Her Thyroid Supplementation

July 19, 2012

Tags: Thyroid, T3

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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Response to a frustrated thyroid patient

July 15, 2012

Tags: Thyroid

THIS IS THE FIRST IN A SERIES OF POSTS PASTED DIRECTLY AND WITH LITTLE OR NO MODIFICATION (INCLUDING POSSIBLY TYPOS) FROM MY RESPONSES TO EMAIL QUESTIONS I HAVE RECEIVED ON MEDICAL TOPICS (GENERALLY THYROID DISEASE OR OTHER AREAS OF ENDOCRINOLOGY). TO MAINTAIN THE CONFIDENTIALITY OF PERSONS INITIATING THE INQUIRIES, I WILL NOT POST THEIR QUESTIONS, NOR WILL I NECESSARILY SUMMARIZE THEM. THUS, THESE BLOG POSTS WILL BE, BY INTENT, INCOMPLETE AND DISJOINTED. IT IS MY BELIEF, HOWEVER, THAT INFORMATION CONTAINED IN THESE DISCUSSIONS, WHICH I COMPOSED FOR ONE SPECIFIC PURPOSE, MAY BE OF GENERAL INTEREST TO OTHERS, AND I PROVIDE IT FOR THAT EDUCATIONAL PURPOSE.

THIS POST IS MY RESPONSE TO A FEDERAL LAW ENFORCEMENT AGENCY EMPLOYEE WHO ASKED A COMPLEX SERIES OF QUESTIONS REGARDING HIS EXPERIENCES WITH THYROID HORMONE REPLACEMENT AND HIS EFFORTS TO FIND AN OPEN-MINDED PHYSICIAN TO WORK WITH HIM:

I’m glad we did this by email; there is a lot to think about and comment on here, and I don’t think a phone call would have done it justice.

Few comments/questions first:

1) Please tell me your age and weight—I’m going to guess you’re a big guy because you’ve been on sizable doses of thyroid hormone, yet your numbers aren’t overly high.

2) Any family history of thyroid disease?

3) I’m limited in figuring out the underlying thyroid problem here (and hence what is best to be done) because all of the objective data comes from a time when you’ve been on significant supplements. When you presented to your doctor with “symptoms of hypothyroidism” and were told your “thyroid tested normal” (I always reject the term “normal” without seeing the numbers myself)--do you happen to have those lab results? How long ago was that?

4) I should preface this next comment by asking what medical background you have? I see you’re in Medical Operations--which I presume means you are as likely an administrator as a physician. If you’re a physician, PA, or nurse, I can obviously forgive the fact that it seems like you’re doing a lot of this on your own; if not, then I would be remiss in not cautioning you that it would be better to be working with a knowledgeable provider (I realize that’s what you’re trying to do and that it is difficult to find somebody open minded who’ll take the time—I’m just saying…)

Now I’ll go through your letter and comment on certain areas, saving Dr. Holtorf and rT3 for last:

--“palpitations, weakness, eye problems, depression…” sound as much or more like HYPERthyroidism, than HYPOthyroidism, and you mention TSI antibodies, which if truly elevated define Graves’ disease (i.e., not just possible GD, but definite GD) which is the most common cause of hyperthyroidism. Not all GD is associated with elevated thyroid function tests (TFTs), but most is. That said: you were told your TFTs were normal, and most doctors don’t miss hyperthyroidism--it’s the opposite, hypothyroidism, that they miss. So, I’m not saying for sure you were hyperthyroid; just emphasizing the uncertainties we’re dealing with. Interestingly you said that you got worse as you increased your dose of desiccated thyroid (Thyroid u.s.p., which I’ll call T-usp). That would seem to also be a point in favor of hyperthyroidism--or perhaps no thyroid disease at all and the T-usp was making you hyperthyroid. Again, all I’m doing is brainstorming here.

--You mention the TSIs falling. I see TSIs in my patients fall all the time as their Graves’ disease either fluctuates or resolves, so I would caution against assuming a cause-and-effect relationship between what you did and the TSI change.

--Sounds to me like the only objective data supporting a diagnosis of hypothyroidism before you started taking T-usp for the first time was the basal body temperature (BBT). Please review pp. 36–38 of my book for a detailed discussion of BBT. As I say there—there may be something to it, but it has to be carefully and precisely done, according to rigid protocols, and other explanations for the findings need to be considered, and in my experience the use of the BBT today (which, rightly or wrong, amongst legitimate licensed physicians is almost nil) does not meet those criteria. Bottom line—it’s very shaky ground for a diagnosis that you have obviously put a lot of thought, effort, expense and thought into treating.

--I’m not going to try to comment much on the ferritin and other iron studies; obviously these things are important because iron deficiency causes anemia which causes fatigue which might mimic hypothyroidism. However, these are separate issues to be dealt with by an internist or hematologist either instead of or in addition to the thyroid problem. These things are outside my area of expertise, but I would say with a fair degree of confidence that iron studies within the normal range and an absence of anemia (do you have a CBC?) probably rule out a significant deficiency. That said, as a thyroid expect I often treat people who are “within normal range” so you might ask an internist or hematologist what they think.

--By the same token I’m not going to say too much about the adrenal studies—like the iron issues, they are separate and might be important in their own right but not as part of a thyroid evaluation. If you’ll forgive me being blunt, so-called experts (like chiropractors, for example, often present themselves) are constantly linking thyroid and adrenal problems. They are two total different systems; they are both controlled by the pituitary and they both can be attacked by autoantibodies (different autoantibodies)—so a person with pituitary disease, or rampant immune dysfunction might have both—but they by and large don’t affect each other (except in minor ways that probably aren’t relevant to your situation). It is very important to realize that adrenal testing is very complicated and affected by many variables such as time of day and stress levels. There are very specific protocols for evaluating adrenal function that endocrinologists use—most non-endocrinologists testing the adrenals don’t use these protocols and the results they get are worthless—or at best, are highly suspect. Having said that: your numbers look okay, so I wouldn’t bother worrying about them or spending money rechecking them.

--Your suppressed TSH is not mysterious at all—first of all, you have obviously been on various doses and forms of thyroid supplementation, all of which have contained the potent active hormone T3, for an extended period of time. It is possible that all this past exogenous thyroid hormone has suppressed the hypothalamic-pituitary-thyroid axis, resulting in permanent or at least persistent TSH suppression. Even if this is not a chronic problem, the dose of 3.5 grains of Naturethroid (T-usp) is equipotent to approximately 230 micrograms of Synthroid—that is a large dose—some would consider it very large.

--Now, it worries me that the “folks I am consulting with” as you put it, don’t see these doses as large. They may or may not be inappropriate—I don’t have enough information to say—but they are large. It worries me therefore that you’re consulting with people who aren’t knowledgeable enough about the management of thyroid disease to be giving out safe and effective advice. No disrespect of, or offense to anyone intended—I can only call it as I see it.

--Before focusing on rT3, let me just summarize two other things that bother me here:

1) From the information presented, I can’t say that a diagnosis of hypothyroidism has ever definitively been made—which would seem to be a prerequisite for everything else. Don’t misunderstand, as you know from my book, I am not averse to diagnosing hypothyroidism in someone with “normal” labs—but I do look at the labs, and the patient, and scratch my head about the symptoms, and try to come up with the best answer. If I’ve missed something please correct me, but I don’t think any physician (MD or DO) with the required expertise and clinical wisdom has done those things. I’m a little fuzzy on who these “biochemists from the reformist school” are, but from the description I doubt they meet my criteria outlined in the previous sentence.

2) If we assume for the moment that, in fact, you are hypothyroid and would benefit from treatment, then it bothers me that the only treatments you’ve ever been on are—from the information presented—high doses of either pure Cytomel, or T-usp with or w/o Cytomel—aka, T3 w/ or w/o T4. This is very nonstandard and it hasn’t been proven to my satisfaction that these are the best routes for you. As stated in the book, I’d start with Synthroid and move to the less standard approaches if Synthroid fails. Granted, it is often stated that Synthroid or other T4-only products are ineffective. That’s only true for those they are ineffective in, however. For millions—myself included—Synthroid and the like work just fine. It is my contention that the bad rap they get is due to the fact that mainstream doctors don’t used high enough doses (in situations that the book covers in great detail). I also believe that there are subsets of patients who do need more nonstandard approaches—but I try the safer, cheaper, simpler, better-studied first! To put it simply—if you are hypothyroid—I cannot countenance your not having at least tried a T4-only strategy.

--Dr. Holtorf and rT3: no, I was not familiar with Dr. Holtorf. I did look up his website in response to your email and scanned it briefly. In general—on the positive side—I would say his theories seem superficially to have merit and seem well documented with peer-reviewed medical research. If I were to condemn his theories I have to do the same to my own. On the negative side I would point out that anti-aging medicine is “fringe” in the minds of most physicians, and his approaches, in my opinion, are non-standard and are probably unproven to the satisfaction of the greater medical community. Theories, even those based on published research, don’t always translate to safe, effective patient care. I have no reason to question the earnestness of his and his partners’ confidence in the safety and effectiveness of their patient-care protocols. But—I do think it is unwise to try to emulate those protocols without being under the direct care of his clinic, or some qualified protégé. To use a cliché: don’t try this at home.

--I will make an additional general comment about these types of practices—which always seem to be in Southern California—that is again based on the most superficial information and should be weighed accordingly. They appear to be lucrative, often cash-paid practices aimed at making people feel better. I have no problem with that. I’m a card-carrying capitalist and if they can make a good, honest living giving patients what they want, more power to them. I would simply caution that the further a practice gets away from academic medicine, and the closer it gets to focusing on what looks, sounds, and feels really good to the public, the less scientific rigor it requires of it’s treatment protocols, and the more one ought to scrutinize its commitment to the Hippocratic principle of “first, do no harm.” I’m in the middle. I skewer academic medicine in my book. And I’ll say no more except: caveat emptor.

--Reverse T3: you are correct that the standard thought is that rT3 is a harmless, inactive metabolite of T4, and I personally have never have reason to question that. I confess to not having been aware of rT3 being an antagonist at the thyroid hormone receptor, i.e., a blocker of T3 action. I have confirmed in a standard textbook that that is in fact true; however, it is stated that very large amounts of rT3 are required, and it is also stated that rT3 is cleared very quickly from tissues (more quickly, that is, than from the blood). Meaning that while there might be some rationality to this theory, I think it remains unproven that there is a clinically significant effect in the human patient. Also, just because there are high rT3 levels in the serum—the only place Dr. Holtorf and I have the luxury of measuring them—does not mean that the same situation exists deep within the brain or a biceps muscle, for example. I would urge a healthy skepticism—but I also might start checking some rT3’s in selected patients of mine and see what I come up with.

--by the way, you mention wanting the rT3 ÷ ft3 to be 20 or higher—I think you mean ft3 ÷ rT3, which is the ratio I saw mentioned on the website, and the one that would make sense. Dr. Holtorf wants the rT3 to be lower, which in the latter equation would make the higher number.

--Finally, as to your rT3 levels and responses to these therapies: your initial elevated rT3 at the time you were on T-usp 3 grains was almost certainly due to your tissues metabolizing the 114 micrograms per day of T4 you were getting in the drug. Also, we speculated at the beginning about the possibility you might have been hyperthyroid—hyperthyroid patients have elevated rT3 levels because their tissues are inactivating the excess T4. Bottom line—there is no way to halfway reasonably interpret these data unless you are off all thyroid hormone—and I’ll bet Dr. Holtorf would agree. When you started taking the 80 mcg of Cytomel the rT3 cleared because the high dose of T3 suppressed internal T4 production—to which your lab work attests—and the breakdown of T4 is the body’s only source of rT3. That would happen to anybody on the treatment you were on, and that is Dr. Holtorf’s intended effect. It doesn’t prove anything about what, if anything, was going on before the treatment, however. See?

--rT3 is the normal garbage left behind when T4 is inactivated. Your lab’s normal range is simply the middle 95% of the values they got when they checked a bunch of rT3’s in their population; however, a physiologically normal rT3 is whatever results from the body’s processing of T4 either to or away from T3 in order to try to achieve a desired amount of T3 getting to receptors all over the body. Now, if the resulting rT3 in the serum is high at the end of all that, Dr. Holtorf’s says that’s a bad thing that makes people feel bad. He may or may not be right about that.

--I realize you felt better on the treatment—was that because you experienced the intended effect, or does a lot of T3 just give people more energy by idling the engine faster at the risk of wearing out the parts in the long run? In other words were you mildly hyperthyroid? I don’t know. On a positive note: you’re numbers really haven’t looked awful on therapy (except the low T4 while on T3 alone, which is as expected for that treatment), and I would say that all the doses you detailed to me were at the very least roughly equipotent. Highish, yes, but roughly equally high. In other words, as far as what you reported, there does seem to have been some rationality in the dosing—not a lot of wide swings.

I hope this has been more helpful than discouraging or frustrating. I’m happy for you to digest this and respond with more questions. I’d also appreciate your filling in some of the gaps by answering the questions underlined above, in addition to providing additional history that might correct any misperceptions my discussion might reflect. I’m glad you contacted me because these are very interesting issues to contemplate.

Your first email said you were “more confused than ever.” I understand. This is a confusing situation, and a big reason for that is: we don’t know what we’re treating. A basic principle in medicine is we first have to know what we’re treating before we develop a therapeutic plan. Not that we always know for sure, but we at least need to have a working hypothesis that is based on a thorough evaluation of all available objective and subjective evidence. In my opinion that hasn’t happened here, and that is why there is confusion.

What’s my advice?

You correctly interpreted my book when you decided the T3-only protocol might not be safe in the long run. It bothers me though that you stopped something that you believed in and a thought was working just on the basis of a book—mine or anyone else’s. You really do need to be partnering with a physician face to face to help steer the ship here. I do understand your dilemma. Perhaps an open minded family-medicine or integrative-medicine provider would work with you to monitor and advise and keep things from going too far awry. I don’t think you’re going to find an endocrinologist to do what you want, unless you’re just stupendously lucky.

If you were seeing me I’d say stop all thyroid hormone and get a ft4 ft3 tsh and rT3 after no less than 8 weeks—better 12 weeks. I’m not seeing you, however, and I don’t want you to be too cavalier about doing something somebody tells you to do in an email from hundreds of miles away, that is so profoundly important to your health.

If you really felt good on the Holtorf protocol, and didn’t not any problems—it is not an approach I would use even if you came to see me in the office—but could you arrange to be seen in his clinic in California, or contact them and see if they’ve “trained” anybody in your area? Again, it isn’t a therapy I advocate, but at least somebody would be advising you and taking responsibility for your care on their shoulders.

jkr

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