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changing my synthoid dose
Two years ago I found out I had Hashimoto's. My doses started at .25. I see my doctor every 3 months for bood work. I have been taking .175 since July of this year. My regular doctor was called to active duty in the military and I was assigned to another doctor in that group. My boold work was taken on Oct. 6, 2008 and came back with a TSH reading of 0.20. The doctor I have seen for the first time wants to change the dose of Synthoid to .88. This concerns me since it has taken 2 years to reach the point I am now and she wants to drop it in half. I am concerned that this is a drastic cut in my medication. Any comments will be helpful.
How do you feel on the dose you are taking? Physicians need to start treating the patient and not the number!! Will they? Most likely not! Sad
A suppressed TSH reading is not abnormal for a hypo patient taking Synthroid. Many doctors react to it, however, by jumping to the conclusion that you have become hyper t, and reducing your meds. Of course you will suffer the consequences, if you do so. I have been through the same thing several times over a 25 year period, and you will hear similar stories from other forum members. If the doctor insisted on reducing my meds., I found a new one.
I think you will find the following info to be interesting.
The Fraser Study. Three physicians experienced in diagnosing and treating hypothyroidism assessed 148 hypothyroid patients on T4-replacement. The physicians used the Wayne clinical diagnostic index,[69] an objective tool for deciding whether a patient’s thyroid hormone therapy is adequate, excessive, or insufficient. Statistical tests showed that the three physicians’ judgment didn’t differ in classifying patients.
Among the 148 patients, 108 were clinically normal. This means they were taking enough T4 to be free from symptoms of hypothyroidism. Despite this, 53 of them (49%) had TSH levels below the lower limit of the reference range. Conventional physicians, of course, would interpret their TSH test levels as evidence that the patients were "hyperthyroid" or "thyrotoxic." This mistake is understandable when prominent endocrinologists—Dr. Anthony Toft, for example—have incorrectly termed a low TSH as a "thyrotoxic" level.[70,p.91] And probably most physicians would have required these patients to lower their dosages of T4 to raise their TSH levels—even though the patients were clinically normal. As a result of lowering their dosages, however, some of them, and perhaps all, would have begun suffering from hypothyroid symptoms and risked developing diseases from too little thyroid hormone regulation.[37]
Among the 148 patients, 18 were clinically hypothyroid. This means they were taking too little T4 to keep them from suffering from symptoms and signs of thyroid hormone deficiency. Despite being clinically hypothyroid, 3 of the 18 patients (17%) had TSH levels below the lower limit of the reference range. Most physicians would have required these patients to lower their T4 doses to raise their TSH levels. Doing so would surely worsen their symptoms and signs of hypothyroidism,[68,p.809] and would make them more susceptible to potentially fatal diseases associated with hypothyroidism.[37]
The suffering of these patients and their potential for pathology would result from the obstinate demand by the endocrinology specialty that physicians titrate hypothyroid patients’ T4 doses by their TSH levels—and only by those levels. Of course, some endocrinologists also advise other physicians to use the free T4 in making dosage decisions. The Fraser study showed that among the 18 clinically hypothyroid patients, the free T4, like the TSH, led to a false interpretation of the patients’ status. In 4 of the 18 patients (22%), the free T4 was above the upper limit of the reference range. This gave a false signal that the patients were overtreated, when it fact they were undertreated.
Results of the Fraser study should alert all physicians to the potential for harming their patients through following the practice guidelines of the endocrinology specialty. Basing their dosage decisions on TSH and free T4 levels instead of clinical assessment will leave many patients undertreated—a condition that is hazardous to the patients’ health (see following section).
I found this info on this site.
http://www.drlowe.com/frf/t4replacement/critique2.htm
I think you will find the following info to be interesting.
The Fraser Study. Three physicians experienced in diagnosing and treating hypothyroidism assessed 148 hypothyroid patients on T4-replacement. The physicians used the Wayne clinical diagnostic index,[69] an objective tool for deciding whether a patient’s thyroid hormone therapy is adequate, excessive, or insufficient. Statistical tests showed that the three physicians’ judgment didn’t differ in classifying patients.
Among the 148 patients, 108 were clinically normal. This means they were taking enough T4 to be free from symptoms of hypothyroidism. Despite this, 53 of them (49%) had TSH levels below the lower limit of the reference range. Conventional physicians, of course, would interpret their TSH test levels as evidence that the patients were "hyperthyroid" or "thyrotoxic." This mistake is understandable when prominent endocrinologists—Dr. Anthony Toft, for example—have incorrectly termed a low TSH as a "thyrotoxic" level.[70,p.91] And probably most physicians would have required these patients to lower their dosages of T4 to raise their TSH levels—even though the patients were clinically normal. As a result of lowering their dosages, however, some of them, and perhaps all, would have begun suffering from hypothyroid symptoms and risked developing diseases from too little thyroid hormone regulation.[37]
Among the 148 patients, 18 were clinically hypothyroid. This means they were taking too little T4 to keep them from suffering from symptoms and signs of thyroid hormone deficiency. Despite being clinically hypothyroid, 3 of the 18 patients (17%) had TSH levels below the lower limit of the reference range. Most physicians would have required these patients to lower their T4 doses to raise their TSH levels. Doing so would surely worsen their symptoms and signs of hypothyroidism,[68,p.809] and would make them more susceptible to potentially fatal diseases associated with hypothyroidism.[37]
The suffering of these patients and their potential for pathology would result from the obstinate demand by the endocrinology specialty that physicians titrate hypothyroid patients’ T4 doses by their TSH levels—and only by those levels. Of course, some endocrinologists also advise other physicians to use the free T4 in making dosage decisions. The Fraser study showed that among the 18 clinically hypothyroid patients, the free T4, like the TSH, led to a false interpretation of the patients’ status. In 4 of the 18 patients (22%), the free T4 was above the upper limit of the reference range. This gave a false signal that the patients were overtreated, when it fact they were undertreated.
Results of the Fraser study should alert all physicians to the potential for harming their patients through following the practice guidelines of the endocrinology specialty. Basing their dosage decisions on TSH and free T4 levels instead of clinical assessment will leave many patients undertreated—a condition that is hazardous to the patients’ health (see following section).
I found this info on this site.
http://www.drlowe.com/frf/t4replacement/critique2.htm
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