You don't. It's a therapeutic trial. There are several reasons however that it should be considered first, not last:

• Many people respond well to the treatment.
• It doesn't take long to see if you're on the right track.
• It's simple with few variables to manage.
• When it works it often works very well.
• The symptoms often remain improved even after the treatment is discontinued.
• T3 therapy is not foreign.
• And proper T3 is generally well tolerated.

The therapeutic trial can help distinguish between Wilson's Temperature Syndrome and other problems. It is not a cure-all. The T3 therapy can be tried in conjunction with other approaches, but doing so can sometimes add variables that confuse the therapeutic trial. It may be difficult to see how much of the patient's response, or lack thereof, is due to one approach or the other, or the combination of them. Since one can usually tell within about 2 weeks how well a patient is responding to T3 therapy, I usually like to start T3 therapy by itself at first, to more easily gauge the patient's response to it. Encouraging good health habits such as proper nutrition, exercise, and rest, is always a good idea. Discouraging harmful habits such as smoking, drug and alcohol abuse, and others is also in order.

To be sure, a lot of other problems can cause symptoms similar to Wilson's Temperature Syndrome , which can be affected in various ways. For instance, it is interesting that many diabetic patients notice that when their blood sugars are higher, their temperatures are higher; and when their blood sugars are lower, their temperatures are lower. When hypoglycemic patients have their hypoglycemic episodes, they usually if not always experience a drop in their temperatures when their blood sugar drops. I have seen the symptoms of "Wilson's Temperature Syndrome" respond sometimes to hypoglycemic diets alone; and I have seen the symptoms of "Hypoglycemia" respond sometimes to T3 therapy alone. The same could be said about antidepressants, female hormones, adrenal hormones, yeast-free diets, and a number of other approaches. So it's certainly not the only approach, it's just that in a lot of cases it's the approach to try first not last.
 

What are the substantive risks of T3 therapy (c22)? T3 is a molecule that is present from birth in every human's body, and is absolutely necessary for good health. There is nothing inherently bad about the molecule-our lives depend on it. It can't and hasn't directly damaged the tissue of your heart, brain, or other tissues. There is not a shred of evidence that suggests that thyroid hormones, when used properly, can damage the body in any way. But T3 is not candy, and T3 therapy is not completely without risk, as nothing is. The major consideration in terms of risk is cardiovascular. Cardiovascular disease is a major problem in our country. Every day many people who are not on thyroid medicine have heart attacks, strokes, and develop arrhythmias. The whole trick to T3 therapy is keeping the T3 levels steady. Unsteady T3 levels can increase a patient's chances of increased heart rate, and palpitations. And if a patient is already on the verge of having a heart attack or a stroke, these cardiovascular side effects could aggravate the situation (p142). In some cases it is difficult to avoid unsteady T3 levels, and so it might not be advisable to implement T3 therapy in those patients who may not have the cardiovascular reserve to tolerate unsteady T3 levels very well (for example, certain elderly patients) (Q17). T3 therapy is not addictive, and does not necessarily need to be taken for life. With proper T3 therapy, one does not expect drastic problems, because one does not make drastic changes, and any side effects are addressed early. The T3 should be taken as well on time as possible to minimize the chance of side effects (See Chapter 11).
 

(See c22).
 

No.
The whole advantage of T3 therapy is that patients' symptoms often remain improved even after they have discontinued T3 therapy. Sometimes the symptoms do not remain improved after the treatment has been discontinued (Q16), but it is extremely unlikely that any patient's symptoms will be persistently worse after T3 therapy than they were prior to T3 therapy.
 

(See c5).
 

Increasing the dose of T3 every three days or longer is tolerated well by 9 patients out of 10. Most patients tolerate the dose being increased every three days very well. However, about 10% of patients are one-day compensators that are likely to tolerate one-day increases better. Slow compensators usually tolerate rapid increases much better than rapid compensators tolerate slow ones. It is easier to prevent people from becoming management problems than it is to stop them from being management problems once they are.
 

This is your first clue that the patient may be a one-day compensator (p91). Such patients' negative-feedback inhibition of the pituitary gland may be so rapid that the patients can actually over-compensate, such that their temperatures can temporarily go lower than they were prior to T3 therapy. Such patients' symptoms can worsen at such a time as well. These patients are more likely to experience side effects of unsteadiness from the T3 therapy than others are. It is more difficult to keep the T3 levels steady of such patients, and so extra care should be taken to keep T3 levels as steady as possible from the start. If the patient's T3 levels become too destabilized to proceed with the T3 therapy, the patient should be weaned off the therapy. The pros and cons of the T3 therapy should be reconsidered in light of the likelihood that the patient is a one-day compensator. If the T3 therapy is re-initiated, the patient's T3 levels should first be allowed to steady down very well by keeping the patient off T3 for from 5 - 14 days. And the T3 therapy should be increased rapidly enough to take deliberate exogenous control of the thyroid system to make the transition of control as smooth as possible. If not, perhaps the one-day compensator would be better off not taking the T3 therapy at all. Remember- it is important that everything be done gradually, but not necessarily slowly.
 

Rather than to go much higher than 90 mcg's p.o. BID, it is usually best to wean off the present T3 cycle in preparation of beginning another cycle (p83)(c12). This is because the temperature can often be brought up to normal on much lower doses in subsequent cycles, when it never could be on much higher doses in previous cycles. Also, if the temperature has not been brought up to normal with 90 mcg/dose, it very often will not be even with much higher doses. This is especially true when doses close to 90 mcg have seemingly no effect on the patients' temperatures. However, when a patient's temperature is responding to each incremental dosage increase, only to predictably drop back down again each time (within about the same period of time each time-the patient's compensation time), then it may be productive to go up higher than 90 mcg/dose. The dose may be increased a step at a time, as needed, up to several increments higher if there are no side effects or complaints.

Compensation is not an infinite process, and the hope is that the patient's temperature is very close to being captured (c9). When there is a cause-effect relationship that is being demonstrated with each increase, the use of slightly higher dosages is more clearly justified.
 

It depends on whether or not the patients' temperatures are yet up to normal. If the patients' temperatures are up to normal, then the cycle should not be weaned until the patients' compensation times have passed by at least a day or two (in other words, until their temperatures have been captured). This is to ensure full benefit of the cycle (c9, Q8).

Patients who have gotten their temperatures up but who have not demonstrated a predictable compensation time, however, may need to stay up on that cycle for 3 weeks to see if their temperatures have been captured. This is because the longest compensation times are around 3 weeks, and if the patients don't compensate within 3 weeks they're probably not going to compensate. Now if the patients' temperatures haven't come up to normal, and the maximum dosage (Q8) has been reached, the patients may begin weaning the cycle right away. There is no added benefit in staying up on the cycle for 3 weeks in this circumstance. There's no point in waiting to see if their temperatures are captured when they aren't even normal (remember if the patient's temperature isn't up within a few hours of an increased dose, it probably isn't going up on that dose no matter how many weeks it's continued). It's important that progress not be delayed unnecessarily.

Patients do not necessarily need to be weaned off a cycle immediately after it is clear their temperatures have been captured. In fact, usually if the patients are feeling very well they do stay up on that plateau for a time depending on the circumstances (c8). Not uncommonly patients will say: "This is the first time that I have felt well in 20 years, so if it's all the same to you, I'd rather not wean down off the medicine right now." They are often concerned that they will start feeling badly again. But there is often so little breakthrough of the patients' symptoms that after a few months they seem to forget what it feels like to have those symptoms, and begin to gain confidence that they will be able to wean off the medicine and stay normal. This confidence is bolstered by them getting tired of taking the medicine every 12 hours, and tired of paying for it, and so the treatment is usually self-limiting with the patients becoming motivated to wean off.

Of course, if a patient begins having side effects or complaints, it may be necessary to wean the T3 at that time, even if the temperature hasn't come up.
 

It depends on how far along a patient is in treatment. For example, suppose you were tuning a radio by turning a knob and you wanted to tune in a station that was on the other end of the dial. You'd probably turn the knob more quickly at first, more slowly as you got closer to the station's frequency, and most slowly when fine-tuning. Sometimes, patients' histories suggest that it may take several cycles of T3 therapy to return a patient's temperature patterns to normal, if at all. Each cycle can take over 4 weeks. At best, such patients may be looking at 3 months worth of therapy before doing very well, so it is usually best not to dillydally. And, whereas, it is good to get as much benefit out of each cycle as possible, the preceding cycles can often be thought of as "coarse-tuning," with subsequent cycles being thought of as "fine-tuning." There is little point in fine-tuning a coarse-tuning cycle, it is usually more productive to move on to a more productive cycle. If it is likely that this is not the last cycle, it is usually best to simply decelerate the rate of wean (c12) rather than go back up a dosage increment if the temperature starts to slip a little (also see Q11).

However, what if there is a good chance that this may be the last cycle and the patient is not in a hurry to wean off the medicine? In that case, it may be best to wean down by 7.5 mcg/dose/7to 10 days to give the patient's body every opportunity to come back up on its own again.

Finally, in cases where patients go up to about 90 mcg's/dose of T3 and notice no changes whatsoever good or bad- as if they were only taking water- I will frequently try going down a 7.5 mcg dosage decrement every day if the patient has no complaints. It is usually more effective to wean off such a cycle and start another than it is to continue increasing the dose. This is because sometimes a patient can keep increasing the dose and the temperature still doesn't go up. But interestingly, when the cycle is weaned and another one is started, the temperature can frequently go up on less T3 when it never did on more. Also, it is usually better to wean off a cycle that has demonstrated no effect (in preparation of starting another), than it is to stay on that cycle for weeks hoping it will demonstrate more effect (p100). See also Q9.
 

Usually not (c12, Q10). However, if there is a good chance that this may be the last cycle it may be worth going back up an increment (or perhaps two if necessary) for a day or so to bring the temperature back up, before decelerating and continuing the wean as suggested in c12. Sometimes increasing the T3 back up one or two increments is not successful in recapturing the temperature. I believe this is usually because the T3 level has become destabilized. In such cases, it may be necessary to go back to Module 2: Cycling up (increasing the T3 according to its rules), and perhaps to give a stabilizing T4 test dose to recapture the patient's temperature and clinical status. If this approach still doesn't recapture the temperature, it probably won't be recaptured until the cycle is weaned completely and another cycle is started.
 

If it is decided that it is time for a patient to wean the T3 therapy, then it is usually best for the patient to wean all the way off. Imagine having a pile of dirt in your front yard that you want to move with a wheelbarrow to the back yard. Yes, you could wheel a full load to the back yard, dump it only halfway, and then return to the pile in the front yard for another load. But when you wheel a full load to the back yard and you dump it completely before returning for another load, you could accomplish twice as much work with much less effort. By weaning off the T3 therapy completely, the patient does not waive her chance at being able to get her temperature up on the smallest dose she can. This is no small opportunity. Generally, the lower the dose of T3 therapy, the easier it is to keep it steady, the better the patient feels, the less the chance of side effects, the less the expense incurred, and the closer the patient is to being finished with the treatment.
 

This depends on where one is in the therapy, and why the cycle was being weaned. If a cycle was being weaned because of side effects: If the side effects resolve while the patient is weaning down off the medicine, then one can stay off the treatment for 2 - 3 days before starting back up again. But what if the side effects only begin to resolve while the patient is weaning down off the T3 therapy, and resolve completely only after the patient is off the therapy for a couple of days? In that case I'd recommend the patient staying off the T3 therapy for another couple of days after that to allow the T3 to steady down further to provide a steadier T3 foundation and better start for the next cycle.

Theoretically, if someone wanted to let the T3 level steady down as much as possible, one could argue that the patient should remain off the T3 for about two weeks. Even so, most of the steadying is probably accomplished within about 10 days, so there is probably not much added benefit in staying off the T3 for much longer than that. This approach is indicated when one would like to eliminate the unsteadiness as much as possible to see if the patient will respond well to treatment. It also underscores the importance of not taking a steady start for granted, since if the T3 levels are destabilized (muddying the water, so to speak) right from the start, it would take quite a bit of time to reproduce another opportunity with that patient at so steady a start.
 

No it isn't, but patients usually feel their best when their temperatures are 98.6. Also, patients who have had their temperatures "punctuated" up to 98.6 before weaning may be less likely to relapse once the treatment has been discontinued.
 

(See c11).
 

If patients' temperatures begin to drop right away as soon as they start weaning, then it is likely that the T3 therapy is being weaned too quickly (c12). What if the patient is able to wean down several decrements, without a drop in temperature but cannot go below a certain level without the temperature dropping? In that case, it may be that the patient does not have a sufficient supply of endogenous or exogenous T4 available for conversion to T3 to maintain the present level of thyroid stimulation to the cells (the patient may be hypothyroid, see c11). What if the patient is able to wean all the way off the cycle and stay well for a period of days before the symptoms return? That suggests that the patient was almost able to maintain well off the treatment and might not have because the treatment was weaned just a little too quickly. Or the worsening of the symptoms again may be due to an actual relapse due to some precipitating factor (such as a big stress). On the other hand, what if the patient's temperature and symptoms worsen as the T3 is being weaned even though it is being weaned slowly enough and there is a sufficient supply of T4 for conversion to T3? This suggests that there may be some unaddressed factor(s) that are preventing the patient from staying improved (e.g., continuing stress). If the patient is not under a lot of stress, then some other factor may be preventing the improvement on T3 therapy to persist after the treatment has been discontinued. In such cases, one might consider adjusting some other medicines a patient may be taking (such as female hormones), and look to see what other changes can be made in other areas (p105, Q10, Q29).
 

There was a boy who was born with congenital hypothyroidism and was raised on traditional T3 (Cytomel). He was never treated with a T4-containing medicine, and so essentially never had a molecule of T4 in his body. By age 26 he had developed normally with no problems. This underscores the fact that the importance of T4 lies very much in that it is "T3 waiting to happen." Nevertheless, duration of treatment may be limited by risks of longer-term treatment (> one year or so). The potential of increased osteoporosis should be considered (especially in patients at risk). The studies that link increased osteoporosis with long-term thyroid therapy have been done with thyroid therapy managed much differently than discussed here. The studies involve patients managed with suppressive doses of T4-containing medicine, without regard to their body temperature patterns or clinical well-being. This manual should make it clear that many of these patients are perhaps being "pushed too far in the wrong direction with the wrong medicine." I would not be at all surprised if the vast majority of the patients involved were clinically hypothyroid with low body temperature patterns. Perhaps if they were caused to be clinically euthyroid with normal body temperature patterns, they would enjoy increased bone densities. T3 therapy usually lasts on the order of months, and the osteoporosis studies involved patients treated for years (e.g., 10 years). I am not concerned about increased osteoporosis in patients who are treated for months. Circumstances have been such that I have treated a few patients for more than a year, and some for a couple of years. I have done serial bone scans in a couple of these patients who I felt were at higher risk for osteoporosis. I was able to see no decreased bone density in this tiny cohort, and I wondered if it might have actually increased. But since osteoporosis is a serious condition, the potential should be seriously considered and weighed and managed accordingly.
 

They all can. The question is: Will all of the patients who do improve, remain improved as compared to the way they were before treatment? Even though many patients do enjoy persistent improvement, some of the patients will go back to feeling as they did prior to treatment. Much less than 1%, if any, will have symptoms that are persistently worse after T3 therapy than they were prior to T3 therapy (Q16).
 

If the T3 therapy improves a patient's symptoms at all, it is because it has increased the patient's body temperature patterns. That is a very good sign because it suggests that the patient's symptoms are at least to some extent temperature-mediated. During T3 therapy, it is not uncommon for a patient's temperature to drop back down again (due to compensation, see p85), or for it to become unsteady (c24), and therefore for the patient's symptoms to return. When a person first starts the T3 therapy, it is easier to keep the T3 level steady because one is building on a steady endogenous foundation of T3. For this reason, the beginning of a cycle often provides the best opportunity to see if the symptoms are temperature-mediated and T3-responsive. At that point of the cycle, if the temperature can be raised close to normal, it has a better chance of being steady also. And a temperature that is sufficiently normal and steady is what is required for clinical improvement. Of course, as a cycle wears on, and as the doses of T3 increase, the chances of "muddying the water" (making the T3 level unsteady) also increase. If the T3 therapy improves a patient's symptoms to any degree, it is likely that the symptoms are to some extent temperature-mediated. At that point it becomes less of a question as to whether the T3 therapy is on the right track. The question becomes, "Can the T3 therapy be adjusted in such a way (e.g., with increased compliance, T4 test dose, cycling the patient on and off therapy) that the patient's temperature and symptoms improve and remain improved (c28).
 

Patients' hypothyroid symptoms not improving at all with normalization of their body temperatures strongly suggests unsteady T3 levels. The purpose of going up on T3 therapy is to reset the thyroid system. It is nice when T3 levels can be held steady enough in the meantime for the patient to notice an improvement clinically while on a given cycle (p74, p76). If a patient's temperature goes up to normal but the patient is still feeling no improvement; it is very likely to be because of unsteadiness of the T3 level. This is one instance in which a T4 test dose might be illustrative. If the patient's symptoms improve within an hour or so of the test dose, then that is a good indicator that it's just a matter of the patient's T3 levels not being quite steady enough. If the patient responds tremendously well to the T4 test dose, then one could consider continuing the present T3 cycle, and using the T4 test dose prn (please repeat as necessary). But if the symptomatic resolution with the T4 test dose is not sufficient, then it would be best to wean the present T3 cycle. As patients wean off the T3 therapy, their own T3 production comes back up, and their T3 levels become more and more endogenously steady. And as they do, the patients' symptoms often begin to resolve if their temperatures hold while weaning. If their temperatures don't hold, and the patients notice no symptomatic improvement while weaning off the T3, then they will often be able to get their temperatures up on less medicine on the next cycle. With the patients on less medicine it is easier to keep T3 levels steady, and they are much more likely to notice an improvement in their symptoms. This is why I often refer to the first cycle as a "reset cycle," and why I consider a therapeutic trial of T3 as sometimes requiring two cycles (p125).
 

If this occurs at a time consistent with a patient's compensation time, then it may just be due to compensation (p85). However, if this occurs after a patient's usual compensation time has clearly passed, at a time of severe stress, it may due to a reduction of remaining endogenous T4 to T3 conversion. Finally, if it occurs after a patient's usual compensation time has clearly passed, and the patient is not under significant stress, it may be due to a "crumbling effect" from an unsteadying of T3 levels (p121). This is very unusual but does occur.

If it is due to compensation or reduced T4 to T3 conversion as mentioned above, then one may continue cycling the patient up on the T3 therapy if there are no complaints.

If it seems due to crumbling, then a T4 test dose may be helpful in steadying the patient's T3 level, and the patient's temperature may come back up. If it doesn't come back up with the T4 test dose, but the patient does notice an improvement, then continue cycling the patient up on the T3 therapy in an effort to raise the temperature back up, with T4 doses taken PRN indications of unsteadiness. If the temperature cannot be raised with this approach without the T3 level steadiness getting more and more out of control, then it may be necessary to wean off the current cycle of T3 to recapture the patient's T3 level steadiness, and then begin another cycle. This may be necessary to get the patient's temperature back up to normal, and to keep it normal, often on less medicine than the previous cycle.

Note: T3 dosage level does not always equate, for some reason, with T3 stimulation of the cell. It is clear that the effectiveness or degree of stimulation of a certain amount of T3 has something to do with its steadiness. For instance, I had one patient misunderstand the directions for taking the T3. She continued to increase the dose of T3 she was taking until she was on 800mcg per day. Yet her temperature was still low, and she wasn't having any complaints. When the error was discovered, she was gradually weaned off the T3, and after a time another cycle was started. On that cycle, she was able to get her temperature up on 150mcg per day when she never could on 800. In some cases the T3 could be increased "until the cows come home," and the patients' temperatures never would come up (this is particularly the case when there are indications of unsteady T3 levels).

Another example was a case described in the Lancet, where a woman tried to commit suicide by taking about 1600 mcg of T3 all at once. The case-study was notable in that she did not have more side effects than she did. She wasn't thrown into thyroid storm.
 

If a patient has fatigue that comes and goes at the same time each day, it may be that the T3 level is "resonating" in such a way that the T3 level is lower at that time of day. Frequently the patients report that their body temperatures drop at such times. Shifting the dosage times in relation to when the patient awakens often alleviates this problem. For example, have the patient try taking the T3 doses at 8am and 8pm, instead of 7am and 7pm. Or one could try moving the doses up an hour instead, say to 6am and 6pm.

It is helpful to determine if the slumps can be correlated to any other factors (such as meal times, diet, or sleep cycle), and making adjustments as indicated. For example, it is interesting that many diabetic patients notice that when their blood sugars are higher, their temperatures are higher; and when their blood sugars are lower, their temperatures are lower. When hypoglycemic patients have their hypoglycemic episodes, they usually if not always experience a drop in their temperatures when their blood sugar drops. I have seen the symptoms of "Wilson's Temperature Syndrome" respond sometimes to hypoglycemic diets alone; and I have seen the symptoms of "Hypoglycemia" respond sometimes to T3 therapy alone. The same could be said about antidepressants, female hormones, adrenal hormones, yeast-free diets, and a number of other approaches.
 

When patients are first started on the treatment, it is best for them to be educated well, with 2 weeks worth of instructions, and to be prescribed at least 2 weeks worth of medication. This prevents them from having to make extra phone calls and extra trips, which can be inefficient for both them and the staff. After patients are started on the T3 therapy, they should be seen back in the office in 2 weeks.

Note: In cases where patients come in taking T4-containing medicine and are instructed to wean the T4-containing medicine before the T3 therapy is initiated it may be best to schedule the following visit for 3 weeks instead of the usual 2.

After 2 weeks of being on a therapeutic trial, it is much easier to predict what course a patient's treatment is likely to take, because the patient's initial response greatly narrows the scope of likely scenarios. Predictable parameters include:

• Projected length of treatment
• Number of cycles that may be necessary
• Range of T3 dosages that may be necessary
• Expected outcomes, etc.

At that 2 week appointment, if the patient is doing well and it seems that the patient is on a predictable course, then the next appointment might be scheduled for 4 weeks (this is true for 85+% of patients). If at that 2 week appointment, it is not as easy to predict the patient's likely course, or how the patient is likely to do, scheduling the next appointment for 3 weeks would be better (very rarely, one may want to schedule the next visit less than 3 weeks out). Thereafter, the return visits might be scheduled for every 4 weeks (extending to every 6 weeks and then perhaps every 8 weeks as indicated).

This rate of office visits is in contrast to the every 6 months to every year appointments that are often scheduled for patients being treated with T4-containing medicines. Thyroid therapy need not be so static as many people consider it to be. T3 therapy is very dynamic. With T4 therapy, it takes the body over a week to convert half of the T4 given by mouth to the active hormone T3. But with T3 therapy, all of the active hormone is available immediately. That changes everything. That puts the therapy on the order of minutes, hours, days, and weeks (not months and years). If the treatment is well managed a lot can happen in a short period of time.
 

Not necessarily. The first thing that side effects suggest is an unsteady T3 level. The whole trick to T3 therapy is keeping the T3 level steady. Granted, if the level is steady but is too high or too low, then a person may have side effects. But if patients' temperatures are not above 98.6 then their T3 levels are not too high. And if their temperatures are not lower than they were before treatment, then any new complaints are not likely to be from the T3 levels being too low. If a patient is having side effects from the T3 therapy, it is usually because of T3 unsteadiness (c24, c25). This suspicion can be confirmed with a T4 test dose (p129). The most common side effects in order of appearance with increasing levels of T3 unsteadiness are fluid retention, achiness, dull headache, edginess, and then increased awareness of the heartbeat and/or increased heart rate. With T3 therapy it is important to start with steady T3 levels (c4), and then to keep the T3 levels steady thereafter with good patient compliance. When a patient begins having any side effects, the first question to be addressed is "Has the patient been able to take the medicine very much on time as directed?" Although unsteady T3 levels can develop even with good compliance, it's important to rule out poor compliance which is a likely cause that is easy and important to address (c29). Stress can also contribute to unsteady T3 levels.
 

T3 levels that are too low, too high, or unsteady can cause side effects. The body temperature patterns are useful in helping one make the distinction. The most common cause of side effects is T3 levels that are unsteady. Unsteady T3 levels are most commonly generated by not getting a good, fresh, steady start on a cycle; or by not taking the T3 compound (p112) very well on time every 12 hours. Improved compliance to dosing times may be all that is necessary to alleviate the side effects. If side effects are more severe then one should consider a T4-test dose (p129). If that doesn't work, then it would probably be best for the patient to wean gradually off the T3 therapy. If it is decided that another cycle will be started, then one should make sure that the patient remains off the T3 therapy long enough to get a good, fresh start on the next cycle (p96).
 

(See p129).
 

Now that the patient knows the clinical difference between better and worse, if she ever feels worse again, she can take another dose of T4 (PRN similar side effects or decreased symptom resolution). If she doesn't feel worse again, she shouldn't take it because it goes against what we're trying to accomplish. On a certain level of T3, if the patient ends up needing to take the T4 more than once, it commonly will be needed in a recurring interval of time (e.g. every 3 days, every 5 days, every 7days). Also, so long as the patient remains on that level of T3, the amount of T4 that is effective as a test dose shouldn't change. But if a patient is on a higher dose of T3, it may be necessary to increase the T4 test dose in a roughly proportionate manner (p132).
 

No.
Temperatures should be taken about every 3 hours, 3 times a day, starting about 3 hours after waking, but the timing is not critical. Likewise, the T4 test doses are taken only as needed according to the clinical situation, and exact timing is not critical. Some people may find that they need a T4 test dose about every 3 days, but that T4 wouldn't have to be taken every 72 hours precisely.
 

In well-selected candidates for treatment, the most common reason for difficulty is unsteady T3 levels (c25). But I'll address this question, based on the assumption that the T3 therapy has been administered as well as possible, and still does not work for a patient as hoped. Briefly, the human body is a complexly interrelated system. By affecting one area, many other areas may be affected in turn. For example, getting enough exercise, getting enough sleep, and eating well can each, individually, cause significant changes in the entire body (from bowel movements to headaches). There are many influences that can have widespread effects and that can even recalibrate the system. Such as: T3 therapy, female hormones, adrenal hormones, and other medicines. When combined, these influences can be synergistic or antagonistic. If a patient seems to be progressing nicely on T3 therapy, and that progress is inexplicably halted, it may be that there is an opposing influence that is not allowing endogenous recalibration in a certain area (see "ropes and rings" analogy in book: Wilson's Temperature Syndrome-A Reversible Thyroid Problem). For example, if a patient is taking .625 mg of Premarin each day, it may be helpful to see how well the patient does on .3mg each day. By changing the "tension" in a potentially oppositional influence, progress can often be resumed (see end of Q22). Other examples of such influences include certain blood pressure medicines and antidepressants.

Nevertheless, T3 therapy is no more a panacea than any other medical treatment. Even though it works exceptionally well for a large number of people who previously were unable to find relief, it sadly, does not work for everyone. When it is decided that an adequate therapeutic trial has been given, and the patient's symptoms have not responded, the patient will be back in a similar spot he/she was in before hearing of Wilson's Temperature Syndrome : square one, looking for a solution for his/her frustrating situation. As far as leads go, if the patient's symptoms are classic for Wilson's Temperature Syndrome, they are classic for abnormal body temperature patterns. If the patient has an abnormal body temperature pattern that does not respond to T3 therapy (very rare), then perhaps there is some other temperature-mediating factor involved. If the treatment failed because for some reason the patient could not tolerate T3 therapy (usually because of unsteadiness), then the patient may want to look toward the not too distant future. Because although T3 compounded with a sustained release agent in a capsule is a great approach, it's not perfect. The technology is already available and the application will certainly come that provides for more steady, better controlled, and better tolerated administration of T3 therapy (e.g., infusion pumps, patches, etc.).

It is important to be as supportive as possible towards patients for whom the treatment doesn't work. They can easily feel despair. I feel it is important that the patients cope as well as they can with their complaints, but I don't feel that it is warranted to tell them: "You'll have to live the rest of your life feeling the way you do." Many of the people who respond fabulously well to T3 therapy have been told that same thing in the past. But it wasn't true. Such a comment is without basis and should be avoided. It can be very destructive, and accomplishes very little. More than one patient with such symptoms has mentioned suicide. Things change and new answers come everyday, and probably will more so all the time. Wilson's Temperature Syndrome is a precedent for such simple answers.
 

A decrease in TSH and T4 levels is exactly what one would expect in a patient receiving exogenous T3 therapy. In fact, the resetting phenomenon (p48) is often not seen unless there is a decrease in T4 levels for a time. It is not alarming if their T4 levels and TSH levels are suppressed even to essentially zero, for a time (provided the patients are feeling very well without any side effects, and their temperatures are not above 98.6). Such low levels are not always necessary, but decreased T4 and TSH levels are an indication that T4 and RT3 levels are being well depleted (which is often the point of T3 therapy).

Hyperthyroidism often causes very low TSH levels and symptoms of hyperthyroidism. Yet proper T3 therapy often causes very low TSH levels without symptoms of hyperthyroidism while providing normal temperatures and a decidedly euthyroid clinical state. This shows that very low TSH levels do not necessarily equate with a hyperthyroid state. Also, there is no evidence that low TSH levels alone necessarily equate with increased osteoporosis. Some doctors have concluded that very suppressive doses of T4 given over many years without regard to patients' clinical status or body temperatures is associated with increased bone loss. But that doesn't mean it can be concluded that suppressive doses of T3 given over a period of months to produce normal body temperatures and a clinically euthyroid state also cause increased bone loss. There is no evidence that endogenous hyperthyroidism has ever been generated in a euthyroid patient with suppressive exogenous thyroid medicine. And there is no evidence that endogenous hypothyroidism has ever been generated in a euthyroid patient with exogenous thyroid medicine.
 

The thyroid blood tests are not so much to diagnose Wilson's Temperature Syndrome as they are to rule out thyroid gland dysfunction before treatment. Also, they provide a baseline against which to compare future thyroid blood tests. It is reassuring to have this baseline, because with it and post-treatment blood tests it can be demonstrated that the T3 therapy has not adversely affected endogenous thyroid gland function. Once T3 therapy is initiated, the thyroid blood tests do not significantly affect management decisions. They more reflect the changes that are occurring in the thyroid system than they are useful in directing the therapy that brings about those changes. Therefore, it is not necessary to get the thyroid tests often, if at all. But that's not to say that they are completely without value, since it is sometimes helpful to see how the blood tests reflect the effects and progress of the therapy. The thyroid tests do sometimes show some interesting trends. For example, a symptomatic patient may have a temperature of 97.8 before treatment with a T4 of 7.2 mcg/dl, a TSH of 4.1 mIU/ml, and a RT3 of 247 pg/ml. And that same patient may feel very well with a temperature of 98.6 after treatment with a T4 of 7.1 mcg/dl, a TSH of 4.2 mIU/ml, and a RT3 of 85 pg/ml. Granted RT3 levels can change quickly and readily under various circumstances, but that doesn't mean the averages can't be lower. Such interesting trends are what have led to the paradigm upon which the T3 therapy has been designed.
 

One would expect the TSH, T4, and RT3 levels to be lower, and the T3 to be higher than when the patient started T3 therapy. One would expect the T3 resin uptake test to be lower than it was, since the T3 resin uptake test is low when Total T3 by RIA (RadioImmunoAssay) is high, and it is high when Total T3 by RIA is low. The TSH, T4, and RT3 levels may be low (approaching zero), depending on the dose the patient is taking at the time of the blood tests. But suppressing T4 levels by suppressing TSH levels for a time appears to be very important in resetting the system. In other words, the suppression of T4 levels for a time is the whole point of the treatment, and in no way comes as any surprise.
 

If patients discover that they have missed a dose by an hour or so, it is usually best for them to go ahead and take the missed dosage right away. They can then get back on schedule as quickly as possible (by taking the next dosage at the same time they would have had they not missed the time) so that there is only one aberration rather than several.

However, if patients miss the dose by around 5 hours or more one might consider having them go ahead and take the medicine at that time, and then take a number of subsequent doses at equal intervals that are less than 12 hours until the patients are back on schedule. If the patients are without complaints, one might consider having the patients eliminate the missed dose completely, while staying on schedule by taking the next dose at the same time they would have had they not missed the dose. Generally, the former alternative is better in patients who are less clinically stable.
 

(See p83, c12, and Q8).
 

(See 104).