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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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
Read More