Guest guest Posted March 5, 2005 Report Share Posted March 5, 2005 > are.TSH is .04 {range is.35-5} > Free T4 is 12 {range is9-19} > Free T3 is 5.8 {range is 2.63-5.70} > I take 75mgs in morning and 60 mgs around 2:00 pm. > I am not sleeping,feel warm, anxious,tight chest,pulse is high at > times,blood pressure is fine and have massive ringing in my ears.I have > not seen my doctor yet...not till next week.My question is what should > my next step be???Stay at this dosage or lower my meds???The ringing ear > part I was told by an ENT a month ago to switch meds. and go back on > synthetics!!?? _____________________ First off the ENT is full of it. Ringing in the ears is a common symptom of hypothyroidism and I can't see how a pill that matches human thyroid output is going to give you these symptoms more than synthetic Synthroid. You will see from the last link that tinnitis is not listed as a hyperthyroid symptom, but as a hypothyroidism symptom. Tinnitis is a problem related to a buildup of polysaccharides, wax and other waste products in the tiny vessels in the ear. The ear is very sensitive to problems with getting blood flow to them. http://yourmedicalsource.com/library/tinnitus/TIN_causes.html http://www.aboutchronicwellness.com/symptoms.htm I don't think your dose is high enough for you to have true hyperthyroidism. The healthy human thyroid makes 3 to 5 grains and if you do not have adrenal hypofunction, anemia and other deficiencies and health issues, you cannot overdose on thyroid untill the dose gets near 180mg minimum. Your pituitary will drop TSH production to slow the thyroid down to cancel out doses less than your own healthy thyroid would make. So, what I think is driving your test numbers up and causing you the sleepless nights, anxiety, pulse problems, tinitis, etc is adrenal fatigue, or anemia, most likely. I became a total insomniac on 50 mcg of levoxyl due to adrenal problems. What happens when you have problems like anemia, adrenal fatigue, deficiencies... is that your body can't use thyroid to make energy. The chain is broken and there are insifficient resources to make energy from thyroid. So, thyroid homone builds up in the blood and can't get into tissues. This creates both hyperthyroid and hypothyroid symptoms. You will get a racing pulse, palipitations, fatigue, anxiety and at the same time have hypothryoid symptoms like tinitis and low energy due to the fact that thyroid can't get into tissues and is staying in the blood. Tissues are hypothyroid. This tends to affect muscles as they have high blood flow and so get exposed to too much thyroid. This leads to weakness, the shakes, mental disturbances, the feeling of not being able to cope. Also, when the adrenals are stressed and can't make enough cortisol for the amount of thyroid in the blood, you will loose your circadian rythem. This will result in insomnia, light restless sleep, frequent wakings in the night, going to the bathroom a lot at night, aches and misery. Your doctor will probably tell your to drop your dose significantly and then will not want to let you raise it later when your adrenals have recovered some and your hypo symptoms worsen. From my own experience, I have found that when I get in a situation where thyroid has built up in the blood, if I don't drop my thyroid dose to clear it out, it just beats my adrenals to death and sets me back physically and mentally. It seems not to get better by leaving it that way. So, my advice is to drop your dose a little untill you recover from this and you get the excess thyroid out that has built up in the blood, and you can stop beating up your adrenals, putting your muscles in a catabolic (protein wasting) state and just wearing yourself out. I would stay at this lower dose untill I recovered and stabilized. Then, I would make a tiny thyroid dose raise, no more than 1/4 grain and wait 2 to 4 weeks untill I stabilized again before making any more tiny raises. When you have health issues interfering with the body's ability to use thyroid, you need to go much more slowly with thyroid dose raises and give your body a chance to adapt before raising again. I would also use Dr. Rind's page to monitor my symptoms and adrenal situation. This will help you see if adrenal issues are the problem and when you should consider another dose raise. http://www.drrind.com/tempgraph.asp http://www.thyrophoenix.com/self_monitor.htm I do not think your dose is too high, but that you are having other problems that are making it hard to use the thyroid you are taking. I think you need to perhaps stop your thyroid for a day to clear out all the excess or lower your dose for two weeks or more to get yourself stabilized and give your adrenals a rest and allow them to catch up a bit. Probably it is the extra T3 that is causing you the problems with the adrenals or anemia. Or you made dose raises too quickly or that were too large. I do not think you have reached your optimal dose due to the tinnitis, but that you are going to have to go much more slowly getting your dose up and will have to work to reduce stress, eat frequently and have more protein, and do other things to try and improve your overall heatlh in order that you will be able to thyroid better. Tish _________________________ From " Thyroid Guardian of Health " by G. Young It is an important guidline in that if individuals are placed on and excessive dose of thyroid hormone, the temperature should become elevated within two weeks time. However, if the thyroid feedback mechanisms are working properly it is impossible to make and individual hyperthyroid untill they are given more thyroid that the gland produces--about 4-1/2 grains for a small individual and about 5 grains for the usual adult. Their basal temperature should rise up over 98.2 deg F if they are truely hyperthyroid, and thus have too much thyroid hormone. The pulse is important as well; a slow pulse is typical of pure low thyroid condition. With low adrenal function, the pulse speeds up and the rapid pulse may indicate inadequate adrenal support. The blood pressure is also an important guid line. A blood pressure with a systolic below one hundred indicates inadequate adrenal support...... Some authorities believe that if autoantibodies are present, it renders other thyroid testing invalid. Clinical symptoms remain the best indicator of adequate dosage. ________________________ Dr. Barry Peatfield from his book " The Great Thyroid Scandal " Page 87-88: The disgraceful fact is that all these measurements (except the last) may not be worth the paper they are written on; or may be so flawed that treatment based on them is bound to be wrong. So what goes wrong? And why are doctors not aware that they may be so badly off the beam? And why do so many have minds so closed? The reasons blood tests may be so flawed we need now to examine. First and foremost these are measures only of the levels of thyroid hormone in the blood. What we need to know is the level of thyroid in the tissues, and, of course, this the blood test cannot tell us. The nearest we can go is the Basal Temperature Test, or the Basal Metabolic Rate. The first we have discussed; the second is now of historical value. The patient is connected up to an oxygen uptake, carbon dioxide excretion, measuring device, and the rate of usage determines the metabolic rate. This is also subject to various errors. The amount of thyroid hormones being carried by the bloodstream varies in a highly dynamic way, and may be up at one point and down the next. The blood test is simply a two-dimensional snapshot of the situation at that moment. The slowed circulation may cause haemo-concentration from fluid loss, so that the thyroid levels are higher than they should be. (A simple way to explain this is to think of a spoonful of sugar in your cup of tea. If it is only half a cup of tea but you still put in your teaspoon of sugar, then although the amount of sugar is the same, the tea will be twice as sweet.) But the blood levels depend mostly on what's happening to the thyroid hormones. If the cellular receptors are sluggish, or resistant, or there is extra tissue fluid, together with mucopolysaccharides, the thyroid won't enter the cells as it should; so that part of the hormone is unused and left behind, giving a falsely higher reading to the blood test. It is simply building up unused hormone. This may apply to both T3 and T4. Further complications exist if the T4 + T3 conversion is not working properly, with a 5'-diodinase enzyme deficiency. There will be too much T4, and too little T3. If there is a conversion block, and a T3 receptor uptake deficiency, both T3 and T4 may be normal or even raised. The patient will be diagnosed as normal or even over-active; in spite of all other evidence to the contrary. It grieves me to report that I have intervened several times to prevent patients, diagnosed as hyperthyroid, having an under-active thyroid removed when the only evidence was the high T4 level (due to receptor resistance) and the patient was clinically obviously hypothyroid. The patients thanked me, but not the consultants. Adrenal insufficiency adds another dimension for error to the T4 and T3 tests. Adrenal insufficiency, of which more anon, will adversely affect thyroid production, conversion, tissue uptake and thyroid response. It may make a complete nonsense of the blood tests. The most commonly used test of all is the TSH. I have sadly come across very few doctors who can accept the fact that a normal, or low TSH may still occur with a low thyroid. The doctrine is high TSH = low thyroid. Normal TSH = normal thyroid. But the pituitary may not be working properly (secondary or tertiary hypothyroidism). It may not be responding to the Thyrotrophin Release Hormone(TRH) produced by the hypothalamus, which itself may not be producing enough TRH for reasons we saw earlier. The pituitary may be damaged by the low thyroid state anyway, and be sluggish in its TSH output. ______________________________ Personal correspondence from DR. Derry to Edna Kyrie of http://www.thyroidhistory.net Dear Edna The statement by C.P. Lalonde in 1948 review: " When thyroxine is administered to a thyroidectomized or myxedematous patient, it takes 250 -350 micrograms of thyroxine (3.4 grains to 4.7 grains) to maintain a normal metabolism. ( et al, 1935, Means, 1937) " C. P. Leblond. Iodine metabolism. Advanc Biol Med Phys 1:353-386, 1948. It does not say but I believe they gave it intravenously because it is so badly absorbed orally. But IV thyroxine works well. _______________________ Author: Dr PBS Fowler Date Published: 23-May-2001 Publication: Lancet 2001; 357: 619-24. Volume 357, Number 9273 23 June 2001 Title: Letter in response to Colin Dayan's article ' Interpretation of thyroid function tests'. Before the days of hormone assays, hypothyroid patients received about double the average dose of thyroxine given today, but did not develop osteoporosis or atrial fibrillation. Doses should be judged clinically rather than be governed by misinterpreted hormone results. P B S Fowler 1 Dayan CM. Interpretation of thyroid function tests. Lancet 2001; 357: 619-24. ________________________ Prognosis and treatment of COMMON THYROID DISEASES Proceedings of a Symposium held in San Francisco, California, U.S.A. - G March 1970 Editors : HERBERT A. SELENKOW AND FREDRIC HOFFMAN Thus, in the average patient requiring 280 ug T4 daily (3.7 grains), 190 ug (3 grains) are absorbed. Of this, 90-100 ug replaces the T4 normally secreted daily and the remainder provides the physiological equivalent of normal T3 secretion. ______________________ (This article shows that people got no response to thyroid hormone at doses less than 3-5 grains) Author: MONTE A. GREER, M.D. Date Published: 15-Mar-1951 Publication: The New England Journal of Medicine Volume 244 MARCH 15, 1951 Number 11 Title: THE EFFECT ON ENDOGENOUS THYROID ACTIVITY OF FEEDING DESICCATED THYROID TO NORMAL HUMAN SUBJECTS Category: research Keywords: research, GREER, EFFECT, ENDOGENOUS, THYROID, ACTIVITY, FEED, DESICCATED, NORMAL, HUMAN, SUBJECT, circulating, thyroxin, thyrotrophin, radio, iodine, index, therapeutic, accurate, euthyroid Text: 388 IT HAS been known for many years that a reciprocal relation appears to exist between the levels of circulating thyroxin and thyrotrophin in the vertebrate species so far investigated, Until recently, however, direct tests of thyroid actiyity in man have not been feasible. Within the last few years, radioactive iodine has provided a new method .for the study of thyroid function, permitting observations that would otherwise be impossible. Using shielded G-M counters, it is possible to follow directly the accumulation of radioiodine in the thyroid gland. Studies in several clinics have indicated that this method is an accurate index of thyroid function. In view of the widespread therapeutic use of thyroid medication, it was of interest to determine whether the administration of physiologic amounts of the hormone to man would produce the same compensatory depression of the thyroid gland as that observed in laboratory animals. Previous investigators, using other measures of thyroid function, have observed that the thyroid gland is depressed by thyroid feeding. Farquharson and Squiresl found that the administration of moderate doses of desiccated thyroid to apparently euthyroid " hypometabolic " subjects produced no appreciable elevation of the initially low basal metabolic rate. On the contrary, when thyroid medication was stopped, the basal metabolic rate fell rapidly below the pretreatment level and remained depressed for several weeks before gradually rising up the initial level. Riggs and his co-workers2 administered gradually increasing amounts of thyroid up to 20 to 25 gr. dally to euthyroid subjects. It was found that both the basal metabolic rate and the serum-precipitable iodine remained relatively constant until daily doses in excess of 3 to 5 gr. were given, when both. indices of thyroid activity began to rise co-comltantly. When the admmlstratlon of thyroId was abruptly stopped, the basal metabolic rate and serum-precipitable iodine fell abruptly, but transiently, to abnorncally low levels, indicating an inhibition of endogenous hormone production and a delayed return to normal thyroid function. The present investigation was designed primarily to determine how rapidly depression of the normal human thyroid gland occurs after the institution of daily physiologic doses of thyroid hormone, how much hormone is required daily to produce complete depression of the thyroid and how rapidly recovery of thyroid activity occurs after the cessation of therapy. MATERIALS AND METHODS Fortv-seven normal human volunteers, consisting chiefly of laboratory technicians, physicians and nurses, were employed. They were between 17 and 67 years of age, and all but three were women. All were clinically euthyroid so far as could be determined, although basal metabolic rates were obtained in only a few instances. About one fourth of the subjects had taken thyroid previously at one time or another; three had stopped the hormone only a few weeks before beginning the. experiment. Four had been taking 3 or more grams daily for several years, the initial study of all but one of these being made while they were still taking the hormone. Studies with radioactive iodine were made wIth a modification of the technic devIsed by Astwood and Stanley.3 The isotope with an eight day half-life, I131, was used. Following the admistratlon of a 50- microcurie tracer dose of I13l, serIal counts were made over the thyroid gland by means of an externally placed shieided gamma counter. Since the 24-hour uptake had been found to be as relIable as any index of thyroid function determined by eans of I131 only this measurement was used. The Il31 was obtained from Oak RIdge; the standardization made at that laboratory before shipment was accepted. An amount of radic:active iodine approximating 50 microcuries. was pipetted into a 50-cc. Erlenmeyer flask and diluted wIth 15 to 20 ml. of tap water. The flask was then placed in front of the shielded gamma counter, and the absolute quantity of radioactivity determined. The distance of the flask from the end of the gamma tube was measured by a ruled steel slide, at the edge of the shielding, which was connected to a thin 389 thyroid function, although without clinical evidence of hypothyroidism, was associated with normal levels of circulating thyroxin. It is interesting that subjects who had been taking desiccated thyroid for several years showed as rapid a return of thyroid function as did those subjects who had been taking the drug only a few days. This strongly indicates that chronic depression of the thyroid gland produces no permanent injury. One other interesting feature is that a " rebound " phenomenon seems concomitant with the return of the depressed thyroid glands to normal. This was especially evident in the continuously treated subjects,; two had uptakes higher than 50 per cent in the first swing of recovery, which subsequently dropped below this level. Uptakes of from 50 to 75 per cent have been observed in 5 other patients after withdrawal of thyroid hormone, which they had been taking for several years, but these were not included in the present study because only a single determination of their thyroid function was made. This rebound is presumably due to a lag in the adjustment of pituitary thyrotrophin production. The depressed pituitary may be stimulated to increased secretion of thyrotrophin as the level of circulating thyroxin falls upon cessation of therapy. However, there is perhaps a certain lag before the pituitary again becomes inhibited by increased endogenous thyroid secretion, the thyroid gland thus becoming overstimulated. This same type of delayed readjustment is probably responsible for the fall in basal metabolic rate and serum-precipitable iodine seen after the withdrawal of exogenous thyroid. It is possible that the occasional case of thyrotoxicosis seen to develop upon the withdrawal of thyroid medication from euthyroid patients may be partially explained on this basis. ..... The data presented indicate that the administration of exogenous thyroid hormone results in a corresponding depression of endogenous thyroid function, whatever the mechanism by which this is produced. Since it has been found that the serum-precipitable iodine and the basal metabolic rate do not rise in normal subjects unless thyroid in excess of 3 to 5 grains daily is given, it seems reasonable to assume that astable euthyroid level of circulating thyroxin is maintained by a depression of endogenous hormone formation equivalent to the amount administered. This stable level is probably maintained through pituitary regulation. The administration of small doses of thyroid to normal patients for the control of obesity, menstrual disturbances, " fatigue " and so forth would thus seem to be without reason or promise of therapeutic effect, since excessive amounts would be required before any elevation of the levels of circulating thyroxin and basal metabolic rate could be produced. The doses commonly administered for these disorders are certainly below what would be considered toxic levels, and the only effect to be expected would be a compensatory depression of endogenous thyroid activity. The disappointing experiences of clinicians in their attempts to treat apparently euthyroid patients for such disorders are thus readily explained. The occasional patient who complains of symptoms of hyperthyroidism while taking only 3 to 4 grains of thyroid daily may represent those persons whose thyroid glands become markedly depressed by the exhibition of 1 gr. or less of hormone daily. Three grains would thus be 390 three times their daily requirements; this might possibly give rise to symptoms of overdosage. It is of interest to consider the " increased sensitivity " of myxedematous patients to exogenous thyroid hormone. This supposition seems to have existed since the days of the first successful treatment with thyroid extract of patients with Gull's Disease. So far as the author is aware, no evidence has been published that establishes any difference in the tissue susceptibility to thyroid hormone of euthyroid subjects from that of myxedematous subjects. It is frequently stated that myxedematous patients show signs and symptoms of " toxicity " at lower dosage levels than do those with normal thyroid glands, but adequate data supporting this statement have never been presented. There is no question that small doses of hormone have a much greater effect in raising the basal metabolic rate and relieving the evidences of hypothyroidism in myxedematous than in euthyroid-patients. This is readily explained by the necessity for first equaling endogenous hormone production before any elevation of the basal metabolic rate can be produced in normal subjects. Riggs and his co-workers2 seem to be correct in assuming that the failure of the serum-precipitable iodine to rise until 3 to 5 grains of thyroid were administered daily to normal subjects was due to the necessity of first depressing endogenous thyroid activity. However, they stated that this did not adequately explain the differences between the two groups, since hypothyroid patients became " toxic " on such low doses that they could not obtain data equivalent to that on euthyroid patients who took large doses. They suggested that the thyroid gland in intact patients is capable of " breaking down " thyroid hormone, an explanation that seems unlikely in view of the evidence of Leblond and Sue7 that the thyroid gland is incapable of concentrating organically bound, iodine and that it is only when the element is available as inorganic iodide that accumulation is possible. Certainly the evidence presented by Riggs2. 8 indicated little difference in the responses of subjects with and without thyroid glands, since the basal metabolic rate increased as much for an equivalent rise in serum-precipitable iodine in normal persons as in those with myxedema. As gradually increasing doses of thyroid are given to patients with myxedema, there is a progressively diminishing augmentation of the basal metabolic rate as it approaches normal. Thus, 1 grain of thyroid taken daily will produce a much greater increment in the basal metabolic rate of an untreated myxedematous patient with a basal metabolic rate of -30 per cent than it will in a myxedematous patient already being treated with 1 grain daily who has a basal metabolic rate of -10 per cent. If the basal metabolic rate is plotted against the dose of thyroid given in myxedematous patients, a curve is seen that approaches a plateau as the metabolism returns to normal.9 It seens quite possible that if this curve were extended and thyroid given in doses equivalent to the 5 to 25 gr. administered by Riggs to normal subjects, no difference would be found between subjects with and those without thyroid glands. It would be expeeted that much larger doses of thyroid would be required to produce an equivalent rise of the metabolic rate if the subject were near the euthyroid level before treatment was begun. Such has in fact been found to be the case in investigations of intact subjects. SUMMARY The effect of exogenous thyroid hormone on the endogenous thyroid function of 47 normal human subjects has been investigated with the use of radio-active iodine. Marked depression of the subject's thyroid gland could be produced within one week by the administration of adequate daily physiologic doses of hormone. The daily amount of hormone required to produce marked thyroid depression was between land 3 grains in 93 per cent of those studied, although one girl required 9 grains. After the withdrawal of therapy, thyroid function returned to normal in most subjects within two weeks, although a few subjects showed depression for six to eleven weeks. Thyroid function returned as rapidly in those subjects whose glands had been depressed by several years of thyroid medication as it did in those whose glands had been depressed for only a few days. Thus no permanent injury to the thyroid gland seems to be produced by long-continued hormone administration. It is felt that the reduction in endogenous thyroid function was brought about through a depression of pituitary thyrotrophin secretion. It is suggested that no important difference in sensitivity to thyroid hormone exists between athyreotic and intact subjects. REFERENCES I. Farquharson, R. F., and Squires. A. H. Inhibition of secretion of thyroid gland by continued ingestion of thyroid substance. Tr. Am. Physicians 56:87-97, 1941. 2. Riggs, D. S.. Man, E. B., and Winkier, A. W. Serum iodine of euthyraid subjects treated with desiccated thyroid. j. Clin. lnvestigalion 24:722-731, 1945. 3. Astwood. E. B., and Stanley, M. M. Use of radioactive iodine a study of thyroid function in man. West. j. Surg. 55:625-639. 1947. 4. Cortell. R., and Rawson, R. W. Effect of thyroxin On response of thyroid gland to thy,otropic hormone. Endocrina/ogy 35:488-498. 1944. 5. Stanley, M. M.. and Astwood, E. B. Response of thyroid gland in normal human subjects to administration of thyrotropin, as shown by Studies with II " . Endocrinology 44:49-60. 1949. 6. Stanley, M. M. Direct estimation of rate of thyroid ho,mone formation in man: effect of iodide ion on thyroid iodine utilization. j. C/in Endocrino/. 9:941-954, 1949. 7. Le blond, C. P., and Siie, P. Iodine fluctation in thyroid as influenced by hypophysis and ulher factors. Am. j. Physiol. 134:549- 561, 1941. 8. Winkier, A. W., Riggs, D. S., and Man. E. B. Serum iodine in hypothyroidism before and during thyroid therapy. J. Clin. lnvestigalion 24:732-741.1945. 9. Means, ]. H., and Lerman, ]. Symptomatology of my:tedema: its relation to metabolic levels. time intervals and rations of thyroid. Arch. lnt. Med. 55:1-6, 1935. ___________________ Author: KENNETH STERLING Date Published: 01-Jan-1975 Publication: CRC PRESS INC CLEVELAND OHIO 1975 Title: DIAGNOSIS AND TREATMENT OF THYROID DISEASES Category: treating Keywords: Sterling, diagnosis, treat, thyroid, euthyroid, T4, T3, dose, sythetic, measure, serum, thyroid, hormone, desiccated, adult, child, PBI, TSH, heart, normal Text: 83 REPLACEMENT THERAPY OF HYPOTHYROIDISM Thus, the ultimate maintenance dose in adult myxedema is usually between 2 and 5 grains (although sometimes stated to be I to 3 grains in older texts), _______________ http://thyroid.about.com/library/derry/bl3a.htm Dr. Derry The doses a patient gets when monitored by the TSH is currently two thirds or less of the well established clinically effective doses established from 83 years of clinical experience before the TSH arrived. (5-6) For example, in a sixteen part study of the effects of desiccated thyroid on healthy prisoners Danowski et al found they tolerated dosages of 9 grains of desiccated thyroid (540 mgs which equals about 540 micrograms thyroxine) without ill effects. (9-11). On studies on obesity and thyroid hormone where the dosages for three months were between three grains and 25 grains (1500 mg of desiccated thyroid equals about 1500 micrograms of Eltroxine) (12). they said: " As in previous studies, these dosages of desiccated thyroid were well tolerated by the subjects. Occasional nervousness, increased sweating, and decreased endurance were reported. Tachycardia and slight increase in the systolic blood pressure and decreases in the diastolic blood pressure appeared in all. Electrocardiogram changes were minimal. Body weight decreased by an average of 26 pounds during the 22 weeks of treatment. " (7). _________________ Quote Link to comment Share on other sites More sharing options...
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