James K. Rone, MD, FACP

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 AN EMAIL FROM THE WIFE OF A PATIENT DESIRING SOME ALTERNATIVE TO TESTOSTERONE REPLACEMENT IN HYPOGONDADISM

In response to your questions about Androgel vs. clomiphene directed to both me and Dr. YYYY (he passed his letter to me, suggesting that he wanted me to field this issue).

Well, as my mother used to say, “there’s more than one way to skin a cat.” Yes, there has been interest in using clomiphene to increase gonadotropin (FSH & LH) and subsequent testosterone release. Clomiphene is an antiestrogen that blocks estrogen’s inhibition of FSH & LH.

This therapeutic option has been studied mostly in the area of treating male infertility and results of studies have been mixed—yes, LH, FSH, and testosterone levels rise, but erections, sperm counts, and pregnancy rates don’t consistently improve—in some studies they do and in some (including a well-done study by the World Health Organization in 1992) they don’t. I’ve seen it stated that clomiphene is the most common drug used to stimulate sperm production in infertile men, in spite of the fact that its effectiveness has been questioned ever since 1966. In my personal clinical experience, and in all the lectures I’ve been to, and most of the articles/texts I’ve read on the subject, the preferred treatment to increase sperm production in infertile men is HCG (mimics LH) given as a shot very other day, and often HMG shots (mimicking FSH) are added later. This is far more expensive than clomiphene—but it might be a case of you get what you pay for.

Now, all of that refers the clinical problem of male infertility—that is, the man who walks into his doctor’s office complaining that he can’t get his wife or girlfriend pregnant. That is not the problem that Mr. XXXX walked in the door with. His problem was a low testosterone level, fatigue, poor libido, and impotence—in other words: “hypogonadism.” Hypogonadism might cause infertility of course, but they are not equivalent terms. Their usual treatments, and the goals of those treatments are different.

The goal when we treat infertility is to achieve a pregnancy—period, nothing else. That is a short-term goal—once the couple is pregnant we’re done and stop treatment.

The goal when we treat hypogonadism is to restore testosterone levels to normal for the LONG-TERM purpose of reducing fatigue, increasing muscles mass, strength, and exercise tolerance, decreasing body fat, increasing libido, improving erections and the sexual enjoyment, strengthening bones and preventing osteoporosis, and probably reducing the risk of heart disease. This therapy is likely life-long, not short-term like fertility treatments.

We know from long experience and good research that testosterone replacement in the form of a gel or patch or shot does all of those things in the previous paragraph well, and as far as we know, it is safe for years of use. After all, normal men are exposed to testosterone of their own making for decades presumably without adverse effect. You mention preferring a “natural” therapy. Well what isn’t natural about stimulating the testosterone receptors with testosterone, which is what’s in Androgel? The active ingredient in Androgel is a chemically identical molecule to human testosterone. Clomiphene on the other hand does not to my knowledge exist in nature and certainly not in the normal human—so, I would argue that it is less natural than Androgel. You mention Androgel side effects. Well, no drug is perfect, but the major potential adverse effects of Androgel (prostate enlargement for example) are related to elevated testosterone levels and they would occur no matter how the levels are elevated, including via clomiphene, if they are elevated excessively.

Androgel or other testosterone preparations fix all of the consequences of hypogonadism EXCEPT infertility. Infertility MUST be treated with something (like HCG or clomiphene) that stimulates internal testosterone production, because the only way to get high enough testosterone levels in the testes where sperm is made is to have it made there. Testosterone from the outside doesn’t get into the testes in sufficient concentrations.

So when the clinical problem is infertility from the beginning, or when a hypogonadism patient on testosterone replacement and his partner come in saying they definitely, right-now, want to get pregnant, then we initiate or switch over to SHORT-TERM infertility treatments and once the woman is pregnant, we go back to the LONG-TERM treatment. We don’t give HCG and HMG long term because of cost and the need for frequent injections. We don’t give clomiphene long term, even though it’s cheap and a pill, because safety and effectiveness over years and decades aren’t proven. I for one would wonder what the long-term dangers of blocking estrogen receptors would be in men. I can almost guarantee no one knows the effect of 20 years of clomiphene on bone strength, for example, in men—it’s conceivable it could cause brittleness and fractures.

You state “we want XXXX to keep fertility if he can.” To be blunt, under the modern standard of care for hypogonadism, that is not an achievable goal. It would be ideal of course, but in an ideal world he wouldn’t have ever had to come to me or Dr. YYYY in the first place. Modern, known-to-be-safe-and-effective therapy offers infertility treatment when and only when there is a stated goal that “we want to get pregnant now.” It does not offer restored fertility continuously. Obviously that is a medical advancement we should be working toward but studies and expertise to date don’t establish clomiphene as the answer.

As to Dr. Fisch and his book The Male Biological Clock—I haven’t read it so my comments have to be limited and taken with a grain of salt. I know him to be an expert on infertility, not hypogonadism in general. He has no doubt used and had success with clomiphene in infertility patients and I gather he must have then tried it in older hypogonadal men whose “biological clocks” are running out. Apparently, in his experience and opinion, there was adequate benefit and safety demonstrated in those cases. However one man’s opinion does not establish safety and efficacy and therefore standard care for the rest of us. Though it should of course spark discussion and further research.

Again, I have to be cautious commenting on a book I haven’t read, but it seems to me he’s talking about gradually declining testosterone with age. Estrogen levels increase in older men and might be expected to inhibit LH & FSH, and hence testosterone production. Blocking that estrogen with clomiphene might reverse that process.

Mr. XXXX’s situation is entirely different. He is a young man in whom this problem has come on relatively suddenly. We don’t know why his LH and FSH are low, there could be genetic factors, or head trauma could be to blame. We don’t have any special reason to believe that high estrogen levels are to blame (we could check an estrogen level—I’ve not done that in him) and unless they are, clomiphene won’t work. Also in cases where clomiphene has helped, the increased testosterone is sometimes converted to even more estrogen causing more problems—remember these are men prone to make too much estrogen in the first place, or they wouldn’t need the clomiphene.

I hope that helps. It’s a good question. To put it more simply I will not treat Mr. Crawford with clomiphene because I do not have experience and confidence with it in this situation, nor is it FDA approved for this. I do lots of things that aren’t FDA-approved—all doctors do—but if I’m going to do something off-label (as non-FDA-approved uses are termed) it has to be something I have experience and confidence in. Another doctor might feel different about clomiphene use here, and that’s fine. I consider it bad medicine for me to do things to patients without me having that experience and confidence.

Androgel and the patches both give stable serum levels of testosterone that result in better patient satisfaction. The patches sometimes cause rashes, but we might try them as they avoid the risk of transfer of the gel to women and children. Of course the gel can be used safely if care is taken (store or lock it away like any household poison; cover undried skin with a shirt; wash hands). An every-week-or-two shot is also an alternative—the serum levels fluctuate a lot so that’s why we don’t prefer them, but it would be less expensive. I advise starting the Androgel and see what you think, but let us know and we can try one of these alternatives if you prefer.

Sincerely,

jkr
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THIS IS AN EMAIL I SENT TO A PERSONAL FRIEND WHO ASKED ME WHAT I THOUGHT ABOUT A FRIEND OF HERS, A YOUNG PRE-MENOPAUSAL WOMAN, MOTHER OF A TODDLER, WHO WAS “FEELING GREAT” AFTER HAVING TESTOSTERONE PELLETS IMPLANTED.

I have reviewed the Endocrine Society’s clinical practice guidelines from 2006 for androgen (testosterone) therapy in women. These guidelines—as I told you—advised against diagnosing and treating testosterone deficiency in women. Their basis for that position was a lack of understanding of what the normal ranges of testosterone levels are for women at different points in their lives, known inaccuracies in available testosterone blood tests, and a lack of studies demonstrating safety over many years. That is, what might be safe for a week or a month or a year, might not be safe for 5 years or 10 years or 20 years.

The accuracy of testing is important—what we’re saying is that the testosterone blood tests physicians use everyday aren’t accurate enough, especially at the lower levels that are normal in women, to be trusted for identifying women who need treatment and monitoring that therapy once started to be sure enough but not too much is given. I don’t know about what testing XXXX, for example, has add, but many of these types of clinics (that prescribe testosterone and other hormones outside the recommendations of mainstream endocrinology—HRC Medical would be an example) use saliva testing. There is even less confidence among physicians as to the accuracy and usefulness of saliva testing than blood testing.

The following summarizes the Endocrine Society’s safety concerns that need further study before testosterone therapy is recommended in women:

(1) Endometrium (uterine lining)—endometrial hyperplasia, which can led to uterine cancer, SEEMS UNLIKELY in women taking testosterone, but the endometrium should be monitored in adequate long-term research studies to be sure.

(2) Breast—too much testosterone has been shown to cause breast atrophy (shrinkage); testosterone does not directly promote breast cancer, but some breast pre-cancerous lesions have the enzyme aromatase that converts testosterone to estrogen (estrogen does promote breast cancer); therefore the possibility exists that aromatization of exogenous (outside) testosterone and other androgens “could contribute to breast cancer risk for women taking them.” Actual research done in this area is as yet inconclusive and of limited quality.

(3) Cardiovascular and metabolic function—the guidelines essentially state that research is needed as to the safety of testosterone treatment in women with respect to cholesterol issues, diabetes risk, and heart disease and stroke risk.

(4) Skin and voice—it is well established that testosterone can cause facial and body hair growth in women, acne, baldness, and a deepening of the voice. No studies have been done looking at these effects in women taking testosterone in doses that maintain “normal” levels for greater than 1 year.

I think I need to emphasize that there is a very different philosophy with which I and these guidelines approach this issue, compared to you and XXXX and your friends and colleagues. I emphasize this, to point out the potential weaknesses of our assertions—namely, I and the guidelines, and most physicians follow a Hippocratic philosophy that states that we will “first do no harm.” That is, we will not give any therapy that has not been proven effective AND safe. By safe, I mean that the benefits clearly outweigh the risks—because there are ALWAYS risks. Anything that is strong enough to help is strong enough to hurt. Furthermore we need to establish exactly who should be treated, and how that treatment should be monitored for effectiveness and safety.

I and these guidelines are not saying that there might not be some benefit to testosterone supplementation in some women. I am certainly not saying that XXXX, for example, doesn’t feel better when she takes testosterone. What I am saying is that it has not been established to our satisfaction who needs this therapy to avoid real medical harm, how much should be given and how it should be monitored, and that it doesn’t do more harm than good over years and years.

I know nothing about the provider prescribing to XXXX—I will be so bold, however, as to say that there are practices that are more concerned about billing people who understandably want to feel better than they are about safety and the other issues I have discussed.

I hope this helps. I am trying to emphasize that there are no absolute right answers here. There a lot of uncertainties, and the differences are in the way we deal with the uncertainties—ignore them, or be scared off by them—truthfully the “right answer” is probably somewhere in the middle. You might take another look at The Thyroid Paradox because it talks about many of the same issues regarding the use of thyroid hormone. In the case of thyroid hormone I do treat more often than most first-do-no-harm physicians do. I do that based on many years of experience and contemplation, which I have not applied to the testosterone-in-women question, so I am ethically obligated to go along with what the mainstream guidelines say. See?

All real medicine boils down to managing uncertainty. That is, accepting the possibility of error. Malpractice lawyers fail to grasp that—but that’s another story. With regard to testosterone therapy in women—especially otherwise healthy young women—I am counseling that we should err on the side of safety, and not do it, despite the possibility of denying the patient something that might help them feel better, and enjoy other benefits. XXXX and her provider, on the other hand, are erring on the side of feeling better. Just remember: cocaine makes people feel good, but most of us don’t advocate its use for that purpose.

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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THIS WAS MY REPLY TO A PERSON IN ANOTHER STATE WHO CONTACTED ME BY EMAIL FOR A SECOND OPINION ABOUT HER HYPOGLYCEMIA EVALUATION:

Nondiabetic hypoglycemia is actually a frustrating problem for endocrinologists and their patients. Obviously hypoglycemia is a common and possibly life-threatening complication of some diabetes therapy. And some people have serious hypoglycemia problems after gastric bypass surgery for obesity.

ON the assumption that you’re not on any diabetes therapy and haven’t had obesity surgery, I will confine my discussion to other causes of “nondiabetic hypoglycemia,” which range from life-threatening insulinomas (benign or malignant pancreas tumors that secrete excess insulin), to “reactive” or “alimentary” or “postprandial” hypoglycemia which seems more common in prediabetic people and those with family histories of diabetes, to more or less normal fluctuations of blood glucose around meals that sometimes cause symptoms. There are a few other causes but that list covers the spectrum pretty well.

Obviously my comments are meant as friendly information and should not be construed as a medical evaluation or second opinion, since I don’t have access to all the information, including the most important source--a face-to-face evaluation of you. That said…

The most important determination for the endocrinologist is whether the problem is an insulinoma (big deal) or something else (not so big a deal). Usually insulinoma patients are sicker, have documented glucoses <40, and have passed out/had seizures/episodes of serious confusion. It’s these people who usually need the drastic step of a 72-hr fast--but that’s also a way of ruling out something serious if questions remain after all other evaluations. Obviously though we like to avoid doing the hospital fast in most people--I’ve only done one in my 13 years in Murfreesboro. You don’t sound that sick, and most of your glucoses have really been pretty normal. There certainly could be minor or early-stage cases where the symptoms are mild or easily masked by eating, so I’m not ruling out anything, but I think it’s statistically unlikely you’ve got an insulinoma.

Playing devil’s advocate though: pituitary tumors are genetically associated with pancreas tumors such as insulinoma and you did mention a pituitary lesion. That very easily could be a coincidence, but if you’ve ever had high calciums due to hyperparathyroidism (PARAthyroid--not thyroid) or if family members have had pituitary, hyperparathyroid, or pancreas tumors, that would up the ante.

Assuming you don’t have an insulinoma, then that leaves the rest of my list, which amounts to a spectrum of severe to mild meal-related fluctuations in blood sugar, which everyone has to some degree--just that some notice it more than others, like a lot of things. Basically sugar goes up after eating and goes down after insulin is released. If a lot of insulin is released—as happens with a high-carb meal or in prediabetes/insulin resistance—then the sugar might drop very rapidly and “overshoot” and get temporarily low enough to trigger symptoms like shaking, rapid pulse, sweating, hunger, sense of dread. This is never life-threatening and the “passing out/seizures/serious confusion” mentioned above don’t happen. However, it can be very uncomfortable, and if the person doesn’t understand what’s happening, it can be frightening.

And what does fear do? It releases adrenaline and adrenaline causes shaking, rapid pulse, sweating, hunger, and a sense of dread. In fact hypoglycemia causes adrenaline to be released (it’s a neurochemical that elevates blood sugar) and that’s what causes the symptoms I mentioned. Then fear triggers more adrenaline and more of the same symptoms—in other words the problem feeds on itself and builds to become a crisis/medical emergency that in reality amounts to nothing. And if the person is a caffeine drinker, that enhances adrenaline’s effect, making the symptoms worse. And if the person surmises or is told the problem is hypoglycemia, what do they do at the first sign of an episode? They eat a doughnut or drink a Pepsi which throws more sugar on the fire, spikes insulin, drops sugar, starting the whole thing over again. And worse yet Pepsi has caffeine in it. Worse yet, the patient starts doing finger-stick blood sugars at home--sees a normal dip in sugar (some women dip into the 40s and don’t know it)--and reacts by eating or drinking sugar. I’ve seen people become glucose invalids--tethered to glucose monitors and snacks. I strongly discourage doing home glucose monitoring unless you’re a diabetic or unless you’ve had a very severe episode that include loss of consciousness, for example. Our bodies usually can figure out what to do without too much help from us.

In my opinion and experience, most “hypoglycemia” is what I’ve just described. The cure is patient education--eliminating the fear component--and a change in diet. Lower carbs (use a book like Sugar-Busters or another low glycemic-index diet book as a guide to what food to avoid--the one with a “high glycemic index”), more protein, less caffeine and sugary soft drinks. My second step if that doesn’t fix the problem is the same diet given in 6 small meals per day which has the combined advantage of keeping some calories coming in all the time and avoid big slugs of calories that trigger the big spike in insulin. I usually see these people once--explain all this and never see them again. So, I guess they get better.

At the risk of sounding sexist—this is mostly a problem of women because most women have a smaller muscle mass and muscle stores glycogen which helps prevent drops in blood sugar. Also some women tend to more emotional on average (the “fear component”) and it’s conventional wisdom in medicine that women tend to focus on symptoms and go the doctor more than men do.

I don’t do the 2- or 3-hr glucose tolerance test for this because a lot of normal people drop their sugar under a glucose load like that. I don’t think the results are too valuable—you might ask Dr. XXXX her opinion on that before doing another one—not saying don’t do it—I’m not running the show—but as with any test I think you need to hear some justification that makes sense to you, from the ordering physician, on the basis of what exactly will be done differently in response to a given result.

That’s my take on hypoglycemia, for what it’s worth.

Now, here’s my take on endocrinologists’ management of hypoglycemia. First--it was a “fad disease” of the eighties, so some doctors just go deaf when they hear the word come out of a patient’s mouth. Second…

Let me digress, before going on—you mentioned thinking of a second opinion. Obviously you have to decide about your own comfort and confidence in your physician. I don’t know Dr. XXXX and certainly don’t know anything bad about her. Unless I’m mistaken she’s on the XXX [major medical school] faculty, which should be a good thing. I do however have some reservations about academic endocrinologists in that they are very focused on numbers and seem to forget the clinical evaluation of the patient. That is obviously a broad generalization and might or might not apply at all to your situation. However, I have personally witnessed a Mayo Clinic endocrinologist lecturing about hypoglycemia at a national meeting, spend an hour talking about insulinomas and then ignore—IGNORE—a question from a Nashville endocrinologist in the audience about reactive hypoglycemia, that is, the situation I describe in paragraphs 6, 7, and 8 above. It’s not a disease so much as it is a variation of normal physiology and so they don’t see it as worthy of consideration. It may not be a disease but it is a clinical problem that is very distressing for the patient and for the doctor the patient goes to.

What I laid out above, nobody taught me in medical school or residency or fellowship—I figured it out for myself or if any of it was taught it was in bits and pieces I had to put together. This is an example, I think, of a failing of current mainstream medicine: a lot of focus on numbers (“evidence-based medicine”) and not enough focus on the patient.

And please accept my apology for infusing politics into this—especially since I don’t know your politics—but ObamaCare won’t fix that problem, it will only make it worse.

Now, I’ve gone off on a big tangent that may or may not have anything to do with you. What gets broadly labeled “hypoglycemia” can be a serious problem but often isn’t. You didn’t tell me what set off this evaluation in the first place--that might help me assess how aggressively I think it should be pursued.

Lastly, adrenal insufficiency is a cause of serious hypoglycemia and that’s a whole nother kettle of controversial fish. As I’ve said, the cortisol of 5.1 at 11AM doesn’t mean much. The ACTH stimulation test was said to be normal. That rules out a problem in the adrenal glands and it rules out a severe long-standing problem with brain and pituitary regulation of the adrenals. It does not necessarily rule out a partial defect in that brain and pituitary regulation. This is another situation where the numbers have to be interpreted carefully in the context of what is happening with the patient. This is not an easy clear-cut evaluation either, but there are other tests that can help.

At a bare minimum I’d like to see an ACTH and cortisol drawn 1st thing in the morning (absolutely no later than 8AM). That has the advantage of telling us what the adrenals and pituitary are doing on their own at the time of day they should be working the hardest. If you get that you may fax the report to me at XXX-XXX-XXXX. If you do that also fax the full report of the ACTH stim test and any other cortisol levels.

I’m not really encouraging you to send any other reports because I think their proper interpretation will be too difficult from a distance. But certainly I’m happy to try to answer any specific questions you have.

Sorry about the tirade. I hope this is helpful more than confusing.

Best,

jkr
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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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